WO2024147074A1

WO2024147074A1 - Methods for treating pots using fcrn antagonists

Info

Publication number: WO2024147074A1
Application number: PCT/IB2024/000018
Authority: WO
Inventors: Joost Johannes VAN MIDDENDORP; Tae Hwan CHUNG
Original assignee: argenx BV
Priority date: 2023-01-06
Filing date: 2024-01-05
Publication date: 2024-07-11

Abstract

Provided herein are methods of treating postural orthostatic tachycardia syndrome (POTS) using an effective amount of a human neonatal Fc receptor (FcRn) antagonist. FcRn antagonists for use in the treatment of POTS and for use in the manufacture of a medicament for the treatment of POTS are also provided herein.

Description

METHODS FOR TREATING POTS USING FCRN ANTAGONISTS CROSS REFERENCE TO RELATED APPLICATIONS [0001] This application claims the benefit of and priority to U.S. Provisional Patent Application No. 63/437,552, filed January 6, 2023, the entire contents of which are hereby incorporated by reference. FIELD [0002] The present disclosure relates to methods of treating postural orthostatic tachycardia syndrome (POTS). The methods involve use of an antagonist of human neonatal Fc receptor (FcRn), which in certain embodiments is efgartigimod. BACKGROUND [0003] Postural orthostatic tachycardia syndrome (POTS) is a form of autonomic dysregulation characterized by excessive tachycardia upon standing in the presence of orthostatic intolerance. Diagnosis is based on evaluations for excessive orthostatic tachycardia (sustained heart rate [HR] increment of not less than 30 beats/minute [bpm] within 10 minutes of standing or head-up tilt [not less than 40 bpm in 12-19 year olds]); absence of orthostatic hypotension; frequent symptoms of orthostatic intolerance during standing, with rapid improvement upon return to a supine position; duration of symptoms for no less than three months; and absence of other conditions explaining sinus tachycardia. [0004] The pathophysiology underlying POTS is heterogenous, encompassing excess sympathetic tone, impaired peripheral autonomic function, volume dysregulation, cardiovascular deconditioning, and autoimmune dysfunction. These mechanisms are not mutually exclusive but instead overlap in a complex interaction of cause and effect. Affected physiologic systems include neuropathic, cardiovascular, renal, immune, and hematologic; this widespread implication of complex systems has added a certain degree of difficulty in constructing a comprehensive framework in the understanding of POTS. Common symptoms include chronic fatigue, dizziness, sleep disturbance, headache, tremors, tachycardia, anxiety, depression, gastrointestinal disturbances, syncope, and vision changes. [0005] Many COVID-19 patients develop chronic, debilitating symptoms after recovery from acute SARS-CoV-2 infection. Multiple terms have been used to describe the constellation of symptoms, including long-COVID, long-haul COVID, and post-acute sequelae of SARS-CoV-2 syndrome. Typical symptoms of long-COVID include breathlessness, fatigue, cognitive impairment (e.g., brain fog), orthostatic intolerance, and palpitations. These symptoms are often debilitating, and most patients receive disability or modified independence. Evidence is emerging that autonomic dysfunction underlies the symptoms that persist after the acute SARS-CoV-2 infection resolves. In several case reports, POTS has been identified in patients who continue to have long-lasting symptoms after recovery from the initial SARS- CoV-2 infection. [0006] Currently, the underlying pathophysiology and effective treatments are unknown for post-COVID-19 POTS. Pharmacologic therapy mainly focuses on orthostatic symptoms, targeting blood volume expansion, and stabilizing HR and blood pressure. [0007] Accordingly, there is a need in the art for improved POTS treatment options. [0008] Therapeutic antagonism of FcRn, a major histocompatibility complex class I- like molecule that is involved in the recycling of immunoglobulin G (IgG) and is thus responsible for the long half-life of IgG, has been explored as a strategy to treat IgG-mediated autoimmune diseases such as generalized myasthenia gravis (gMG), immune thrombocytopenia (ITP), and pemphigus (pemphigus vulgaris (PV) and pemphigus foliaceus (PF)). The remarkable clinical efficacy of FcRn antagonism appears to be directly linked to early removal of pathogenic IgG autoantibodies from circulation. [0009] Pathogenic autoantibodies may play a role in the development and/or progression of POTS. By reducing pathogenic autoantibodies, FcRn antagonists may provide a safer, more effective treatment option for patients with POTS. SUMMARY [0010] The instant disclosure is broadly directed to methods for treating POTS with FcRn antagonists. [0011] The instant disclosure provides a method of treating POTS in a subject in need thereof, the method comprising administering to the subject an effective amount of a human neonatal Fc receptor (FcRn) antagonist. In some embodiments, the FcRn antagonist comprises two, three, or four FcRn binding regions. In some embodiments, the FcRn antagonist comprises or consists of a variant Fc region or FcRn binding fragment thereof. In some embodiments, the variant Fc region or FcRn binding fragment thereof binds to FcRn with a higher affinity at pH 6.0 as compared to a corresponding wild-type Fc region. In some embodiments, the variant Fc region or FcRn binding fragment thereof binds to FcRn with a higher affinity at pH 7.4 as compared to a corresponding wild-type Fc region. [0012] In some embodiments, the variant Fc region comprises or consists of a first Fc domain and a second Fc domain which form a homodimer or heterodimer. In some embodiments, the first Fc domain and/or the second Fc domain comprise amino acids Y, T, E, K, and F at EU positions 252, 254, 256, 433, and 434, respectively. In some embodiments, the first Fc domain and/or the second Fc domain comprise amino acids Y, T, E, K, F, and Y at EU positions 252, 254, 256, 433, 434, and 436, respectively. [0013] In some embodiments, the first Fc domain and/or the second Fc domain comprise an amino acid sequence independently selected from the group consisting of SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 20, and SEQ ID NO: 21. In some embodiments, the first Fc domain and the second Fc domain comprise an amino acid sequence independently selected from the group consisting of SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 20, and SEQ ID NO: 21. In some embodiments, the FcRn antagonist is efgartigimod. [0014] In some embodiments, the FcRn antagonist is an anti-FcRn antibody. [0015] In some embodiments, the FcRn antagonist is administered to the subject at a fixed dose of 20 mg to 20,000 mg or at a dose of 0.2 mg/kg to 200 mg/kg. [0016] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks. In some embodiments, the FcRn antagonist is administered intravenously at a dose of from 2 mg/kg to 200 mg/kg once weekly or once every two weeks. In some embodiments, the FcRn antagonist is administered intravenously at a dose of 3 mg/kg to 60 mg/kg once weekly or once every two weeks. In some embodiments, the FcRn antagonist is administered intravenously at a dose of 10 mg/kg to 30 mg/kg once weekly or once every two weeks. In some embodiments, the FcRn antagonist is administered intravenously at a dose of 10 mg/kg once weekly or once every two weeks. In some embodiments, the FcRn antagonist is administered intravenously at a dose of 25 mg/kg once weekly or once every two weeks. [0017] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 200 mg to 20,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 1000 mg or 2000 mg once weekly or once every two weeks. [0018] In some embodiments, the FcRn antagonist is administered for 24 weeks or less. In some embodiments, the FcRn antagonist is administered for at least 24 weeks. In some embodiments, the FcRn antagonist is administered for 52 weeks or less. In some embodiments, the FcRn antagonist is administered for at least 52 weeks. [0019] In some embodiments, the subject has one or more symptoms selected from the group consisting of fatigue, orthostatic intolerance, brain fog, exertional dyspnea, difficulty with concentration, venous pooling, exercise intolerance, palpitation, heat intolerance, nausea with or without vomiting, insomnia, anxiety, lack of appetite, chest pain, and diaphoresis. [0020] In some embodiments, the subject was diagnosed with POTS following an infection. In some embodiments, the subject was diagnosed with POTS following a COVID- 19 infection. [0021] In some embodiments, the subject shows a reduction in the Composite Autonomic Symptom Score 31 (COMPASS 31) or the Malmӧ POTS Symptom Score (MaPS) following administration of the FcRn antagonist, compared to a baseline value. In some embodiments, the COMPASS 31 or the MaPS is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the subject has a COMPASS 31 less than or equal to 35, 40, 45, 50, or 55, following administration of the FcRn antagonist. In some embodiments, the baseline value is a COMPASS 31 of about 35, 40, 45, 50, or 55. In some embodiments, the subject has a MaPS less than or equal to 90, 80, 70, 60, 50, or 40, following administration of the FcRn antagonist. In some embodiments, the baseline value is a MaPS of about 120, 110, 100, 90, 80, 70, 60, or 50. [0022] In some embodiments, the subject shows a reduction in Patient Global Impression of Severity (PGI-S) score, Patient Global Impression of Change (PGI-C) score, and/or Patient-Reported Outcomes Measurement Information System (PROMIS) Fatigue Short Form 8a score, or an increase in PROMIS Cognitive Function Short Form 6a score following administration of the FcRn antagonist, compared to a baseline value. In some embodiments, the PGI-S score, the PGI-C score, the PROMIS Fatigue Short Form 8a score, or the PROMIS Cognitive Function Short Form 6a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the subject has a PGI-S score of 1, 2, or 3, following administration of the anti-FcRn antagonist. In some embodiments, the baseline value is a PGI-S score of 3 or 4. In some embodiments, the subject has a PGI-C score of 1, 2, 3, 4, 5, or 6, following administration of the FcRn antagonist. In some embodiments, the baseline value is a PGI-C score of 2, 3, 4, 5, 6, or 7. In some embodiments, the subject has a PROMIS Fatigue Short Form 8a T-score of less than 70, 65, 60, 55, 50, 45, 40, or 35, following administration of the FcRn antagonist. In some embodiments, the baseline value is a PROMIS Fatigue Short Form 8a T-score of greater than 40, 45, 50, 55, 60, 65, 70, or 75. In some embodiments, the subject has a PROMIS Cognitive Function Short Form 6a T-score of greater than 30, 35, 40, 45, 50, 55, or 60, following administration of the FcRn antagonist. In some embodiments, the baseline value is a PROMIS Cognitive Function Short Form 6a T-score of less than 55, 50, 45, 40, 35, 30, or 25. [0023] In some embodiments, the subject shows a reduction in a serum level of total IgG, an autoantibody, a SARS CoV-2 antibody, a cytokine, or an inflammatory biochemical following administration of the FcRn antagonist, compared to a baseline value. In some embodiments, the serum level of total IgG, an autoantibody, a SARS CoV-2 antibody, a cytokine, or an inflammatory biochemical is measured 4 weeks, 12 weeks, or 24 weeks following administration of the FcRn antagonist. [0024] In some embodiments, the autoantibody is a G-protein-coupled receptor autoantibody. In some embodiments, the autoantibody is a muscarinic acetylcholine receptor (AChR) autoantibody or an adrenergic receptor autoantibody. In some embodiments, the muscarinic AChR receptor autoantibody is selected from an anti-M1 autoantibody, an anti-M2 autoantibody, an anti-M3 autoantibody, an anti-M4 autoantibody, an anti-M5 autoantibody, or any combination thereof. In some embodiments, the autoantibody is a ganglionic AChR receptor autoantibody. In some embodiments, the adrenergic receptor autoantibody is selected from an anti-α1AR autoantibody, an anti-α2AR autoantibody, an anti-β1AR autoantibody, an anti-β2AR autoantibody, or any combination thereof. In some embodiments, the post- administration serum level of the autoantibody is reduced by at least 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%, as compared to the baseline serum level of the autoantibody obtained from the subject prior to administering the FcRn antagonist. [0025] In some embodiments, the subject shows a reduction in a serum level of IL 1β, IL 21, TNFα, IFNα, CD30, CD40 L, CCL5, CRP, and/or ferritin following administration of the FcRn antagonist, compared to a baseline value. In some embodiments, the post- administration serum level of the cytokine or the inflammatory biochemical is reduced by at least 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%, as compared to the baseline serum level of the cytokine or the inflammatory biochemical obtained from the subject prior to administering the FcRn antagonist. [0026] In some embodiments, the subject shows a reduction in a serum level of total IgG following administration of the FcRn antagonist, compared to a baseline serum level of total IgG obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration serum level of total IgG is reduced by at least 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%, as compared to the baseline serum level of total IgG obtained from the subject prior to administering the FcRn antagonist. [0027] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of serum albumin that is not reduced as compared to a baseline level of serum albumin obtained from the subject prior to administering the FcRn antagonist. [0028] The instant disclosure also provides an FcRn antagonist for use in the treatment of POTS, wherein the treatment is performed according to the methods described above and herein. [0029] The instant disclosure also provides an FcRn antagonist for use in the manufacture of a medicament for the treatment of POTS, wherein the treatment is performed according to the methods described above and herein. [0030] The instant disclosure also provides a use of an FcRn antagonist for the treatment of POTS according to the methods described above and herein. [0031] The instant disclosure also provides use of an FcRn antagonist for the manufacture of a medicament for treatment of POTS, wherein the treatment is performed according to the methods described above and herein. DETAILED DESCRIPTION [0032] The present disclosure provides engineered FcRn antagonists and methods for their use in treating POTS, such as post-COVID-19 POTS. Advantageously, the methods disclosed herein permit long-term reduction of POTS symptoms and improvement in disease- related quality of life. Definitions [0033] As used herein, the term “FcRn” refers to a neonatal Fc receptor. Exemplary FcRn molecules include human FcRn encoded by the FCGRT gene as set forth in RefSeq NM 004107. The amino acid sequence of the corresponding protein is set forth in RefSeq NP_004098. [0034] As used herein, the term “FcRn antagonist” refers to any agent that binds specifically to FcRn and inhibits the binding of immunoglobulin to FcRn (e.g., human FcRn). In an embodiment, the FcRn antagonist is an Fc region (e.g., a variant Fc region disclosed herein) that specifically binds to FcRn through the Fc region and inhibits the binding of immunoglobulin to FcRn. In an embodiment, the FcRn antagonist is not a full-length IgG antibody. In an embodiment, the FcRn antagonist comprises an antigen binding site that binds a target antigen and a variant Fc region. In an embodiment, the FcRn antagonist is an Fc fragment comprising or consisting of an Fc region and lacking an antigen binding site. In an embodiment, the term “FcRn antagonist” refers to an antibody or antigen-binding fragment thereof that specifically binds to FcRn via its antigen binding domain or via its Fc region and inhibits the binding of the Fc region of immunoglobulin (e.g., IgG autoantibodies) to FcRn. [0035] As used herein, the terms “antibody” and “antibodies” include full-length antibodies, antigen-binding fragments of full-length antibodies, and molecules comprising antibody CDRs, VH regions, or VL regions. Examples of antibodies include monoclonal antibodies, recombinantly produced antibodies, monospecific antibodies, multi-specific antibodies (including bispecific antibodies), human antibodies, humanized antibodies, chimeric antibodies, immunoglobulins, synthetic antibodies, tetrameric antibodies comprising two heavy chain and two light chain molecules, an antibody light chain monomer, an antibody heavy chain monomer, an antibody light chain dimer, an antibody heavy chain dimer, an antibody light chain-antibody heavy chain pair, intrabodies, heteroconjugate antibodies, antibody-drug conjugates, single domain antibodies (sdAb), monovalent antibodies, single chain antibodies or single-chain Fvs (scFv), camelid antibodies, affibody molecules, humanized antibodies, VHH fragments, Fab fragments, F(ab')₂ fragments, disulfide-linked Fvs (sdFv), anti-idiotypic (anti-Id) antibodies (including, e.g., anti-anti-Id antibodies), and antigen- binding fragments of any of the above. Antibodies can be of any type (e.g., IgG, IgE, IgM, IgD, IgA, or IgY), any class (e.g., IgG₁, IgG₂, IgG₃, IgG₄, IgA₁, or IgA₂), or any subclass (e.g., IgG_2a or IgG_2b) of immunoglobulin molecule. [0036] As used herein, the term “Fc domain” refers to the portion of a single immunoglobulin heavy chain comprising both the CH2 and CH3 domains of the antibody. In some embodiments, the Fc domain comprises at least a portion of a hinge (e.g., upper, middle, and/or lower hinge region) region, a CH2 domain, and a CH3 domain. In some embodiments, the Fc domain does not include the hinge region. [0037] As used herein, the term “hinge region” refers to the portion of a heavy chain molecule that joins the CH1 domain to the CH2 domain. In some embodiments, the hinge region is at most, 70 amino acid residues in length. In some embodiments, this hinge region comprises approximately 11-17 amino acid residues and is flexible, thus allowing the two N- terminal antigen binding regions to move independently. In some embodiments, the hinge region is 12 amino acid residues in length. In some embodiments, the hinge region is 15 amino acid residues in length. In some embodiments, the hinge region is 62 amino acid residues in length. Hinge regions can be subdivided into three distinct domains: upper, middle, and lower hinge domains. The FcRn antagonists of the instant disclosure can include all or any portion of a hinge region. In some embodiments, the hinge region is from an IgG1 antibody. In some embodiments, the hinge region comprises the amino acid sequence of EPKSCDKTHTCPPCP (SEQ ID NO: 31). [0038] As used herein, the term “Fc region” refers to the portion of an immunoglobulin formed by the Fc domains of its two heavy chains. The Fc region can be a wild-type Fc region (native Fc region) or a variant Fc region. A native Fc region is homodimeric. The Fc region can be derived from any native immunoglobulin. In some embodiments, the Fc region is formed from an IgA, IgD, IgE, or IgG heavy chain constant region. In some embodiments, the Fc region is formed from an IgG heavy chain constant region. In some embodiments, the IgG heavy chain constant region is an IgG1, IgG2, IgG3, or IgG4 heavy chain constant region. In some embodiments, the Fc region is formed from an IgG1 heavy chain constant region. In some embodiments, the IgG1 heavy chain constant region comprises a G1m1(a), G1m2(x), G1m3(f), or G1m17(z) allotype. See, e.g., Jefferis and Lefranc (2009) mAbs 1(4):332-338, and de Taeye et al. (2020) Front Immunol.11:740, incorporated herein by reference in their entirety. [0039] As used herein, the term “variant Fc region” refers to an Fc region with one or more alteration(s) relative to a native Fc region. Alterations can include amino acid substitutions, additions and/or deletions, linkage of additional moieties, and/or alteration of the native glycans. The term encompasses heterodimeric Fc regions where each of the constituent Fc domains is different. The term also encompasses single chain Fc regions where the constituent Fc domains are linked together by a linker moiety. [0040] As used herein, the term “FcRn binding fragment” refers to a portion of an Fc region that is sufficient to confer FcRn binding. [0041] As used herein, the term “EU position” refers to the amino acid position in the EU numbering convention for the Fc region described in Edelman, GM et al., Proc. Natl. Acad. USA, 63, 78-85 (1969) and Rabat et al., in “Sequences of Proteins of Immunological Interest,” U.S. Dept. Health and Human Services, 5th edition, 1991. [0042] As used herein, the term “baseline” refers to a measurement (e.g., IgG levels) in a patient, e.g., in a patient’s blood or urine, prior to the first administration (e.g., intravenous or subcutaneous administration) of a treatment (e.g., an FcRn antagonist). [0043] As used herein, the term “autoantibody-mediated disease” refers to any disease or disorder in which the underlying pathology is caused, at least in part, by pathogenic IgG autoantibodies. [0044] As used herein, the terms “treat,” “treating,” and “treatment” refer to therapeutic or preventative measures described herein. The methods of “treatment” employ administration of a polypeptide to a subject having a disease or disorder, or predisposed to having such a disease or disorder, in order to prevent, cure, delay, reduce the severity of, or ameliorate one or more symptoms of the disease or disorder or recurring disease or disorder, or in order to prolong the survival of a subject beyond that expected in the absence of such treatment. [0045] As used herein, the term “effective amount” in the context of the administration of a therapy to a subject refers to the amount of a therapy that achieves a desired prophylactic or therapeutic effect. [0046] As used herein, the terms “dose” or “dosing” refer to an amount of an agent administered to a subject in a single administration. [0047] As used herein, the terms “fixed dose” or “flat dose” both refer to a dose that does not vary based upon a characteristic (e.g., body mass, e.g., within a set range; sex; age, e.g., within a set range; etc.) of the subject. [0048] As used herein, the term “subject” or “patient” or “participant” includes any human or non-human animal. In an embodiment, the subject or patient or participant is a human or non-human mammal. In an embodiment, the subject or patient or participant is a human. [0049] As used herein, the term “about” or “approximately” when referring to a measurable value, such as a dosage, encompasses variations of ±5% of a given value or range, as are appropriate to perform the methods disclosed herein. Postural Orthostatic Tachycardia Syndrome [0050] Postural orthostatic tachycardia syndrome (POTS) is a form of autonomic dysregulation characterized by excessive tachycardia upon standing in the presence of orthostatic intolerance. Diagnosis is based on evaluations for excessive orthostatic tachycardia (sustained heart rate [HR] increment of not less than 30 beats/minute [bpm] within 10 minutes of standing or head-up tilt [not less than 40 bpm in 12-19 year olds]); absence of orthostatic hypotension; frequent symptoms of orthostatic intolerance during standing, with rapid improvement upon return to a supine position; duration of symptoms for no less than three months; and absence of other conditions explaining sinus tachycardia. [0051] The pathophysiology underlying POTS is heterogenous, encompassing excess sympathetic tone, impaired peripheral autonomic function, volume dysregulation, cardiovascular deconditioning, and autoimmune dysfunction. These mechanisms are not mutually exclusive but instead overlap in a complex interaction of cause and effect. Affected physiologic systems include neuropathic, cardiovascular, renal, immune, and hematologic; this widespread implication of complex systems has added a certain degree of difficulty in constructing a comprehensive framework in the understanding of POTS. Common symptoms include chronic fatigue, dizziness, sleep disturbance, headache, tremors, tachycardia, anxiety, depression, gastrointestinal disturbances, syncope, and vision changes. [0052] Many COVID-19 patients develop chronic, debilitating symptoms after recovery from acute SARS-CoV-2 infection. Multiple terms have been used to describe the constellation of symptoms, including long-COVID, long-haul COVID, and post-acute sequelae of SARS-CoV-2 syndrome. Typical symptoms of long-COVID include breathlessness, fatigue, cognitive impairment (e.g., brain fog), orthostatic intolerance, and palpitations. These symptoms are often debilitating, and most patients receive disability or modified independence. Evidence is emerging that autonomic dysfunction underlies the symptoms that persist after the acute SARS-CoV-2 infection resolves. In several case reports, POTS has been identified in patients who continue to have long-lasting symptoms after recovery from the initial SARS- CoV-2 infection. [0053] Currently, the underlying pathophysiology and effective treatments are unknown for post-COVID-19 POTS. Pharmacologic therapy mainly focuses on orthostatic symptoms, targeting blood volume expansion and stabilizing HR and blood pressure. However, POTS may be related to immune dysfunction and autoimmunity preceded by infection. Several infectious pathogens may be associated with the development of POTS, including SARS-CoV- 2. Patients with POTS have a higher prevalence of autoantibodies, including G-Protein coupled receptor (GPCR) antibodies, which could explain an increase in sympathetic tone by activating adrenergic receptors and eliciting a negative allosteric effect on muscarinic GPCRs. In a case series of 31 patients suffering from different long-COVID-19 symptoms, an unusually high number of functionally active autoantibodies targeting GPCR with chronotropic and vasoactive functions was detected in the sera of these patients (Wallukat G. et al., J Trans Autoimmun. 2021; 4:100100). Notably, adrenergic receptor autoantibodies, such as anti-α1AR, anti-α2AR, anti-β1AR, and anti-β2AR, and muscarinic receptor autoantibodies such as anti-M1, anti-M2, anti-M3, anti-M4, and anti-M5, have been detected in POTS patients pre-COVID. Other recognized autoantibodies in POTS include circulating anti-nuclear, anti-thyroid, anti-cardiac protein, anti-phospholipid, and Sjögren’s antibodies. Moreover, antiphospholipid antibodies were detected in a patient with post-COVID-19 POTS who developed clinical signs and symptoms of antiphospholipid syndrome and mast cell activation syndrome following SARS- CoV-2 infection. [0054] Patients with POTS have been shown to have higher levels of these autoantibodies than healthy subjects. The binding of these autoantibodies to adrenergic receptors has been hypothesized to cause tachycardia in some patients. These autoantibodies, acting as partial agonists, are thought to decrease the effectiveness of peripheral norepinephrine leading to an increase sympathetic response to posture resulting in postural tachycardia in the absence of hypotension. Collectively, these data suggest that POTS could be caused, at least in part, by IgG autoantibodies that induce autonomic dysfunction. [0055] The management of POTS divides into non-pharmacologic and pharmacologic approaches and is contingent on accurate diagnosis, patient education, and therapy adherence. Currently, the U.S. Food and Drug Administration has not approved any drug for POTS treatment. However, some medications are used off label to help certain POTS symptoms. Fludrocortisone, a synthetic mineralocorticoid aldosterone analog, increases salt retention and plasma volume. Adverse hypertension, hypokalemia, and headaches may be present. The alpha-1-adrenergic agonist, midodrine, causes systemic vasoconstriction leading to an increase in venous return that may be effective in hypotensive phenotypes. Limitations include frequent dosing, urinary retention, and supine hypertension. Clonidine and alpha-methyldopa are central-acting alpha-2 agonist sympatholytics that may be beneficial in hyperadrenergic subtypes with hypertension as a predominant symptom. May cause adverse sedation, cognitive clouding, and fatigue. Beta-blockers (propranolol, metoprolol) may reduce upright tachycardia without significant hemodynamic changes. However, worsening fatigue is a concern. Pyridostigmine is an acetylcholinesterase inhibitor that increases acetylcholine levels in the autonomic ganglia. In turn, this may reduce tachycardia with minimal hemodynamic effects; however worsening cramps, vomiting, and urinary symptoms often limit continued use. There is a clear need for more effective treatments, given that the currently used medications treat only the symptoms of POTS and all have side effects which prohibit their continued use. FcRn Antagonists [0056] FcRn antagonists that are useful in the methods and uses provided herein include any molecule that binds to and inhibits FcRn, including, but not limited to, any anti- FcRn antibody, any anti-FcRn binding region, or any Fc domain or Fc region. [0057] In some embodiments, the FcRn antagonists disclosed herein comprise two, three, or four FcRn binding regions, such as an Fc region. [0058] Any Fc region can be altered to produce a variant Fc region for use in the methods disclosed herein. In general, an Fc region, or FcRn binding fragment thereof, is from a human immunoglobulin. It is understood, however, that the Fc region may be derived from an immunoglobulin of any other mammalian species, including for example, a camelid species, a rodent (e.g., a mouse, rat, rabbit, guinea pig), or non-human primate (e.g., chimpanzee, macaque) species. Moreover, the Fc region or portion thereof may be derived from any immunoglobulin class, including IgM, IgG, IgD, IgA, and IgE, and any immunoglobulin isotype, including IgG1, IgG2, IgG3, and IgG4. In an embodiment, the Fc region is an IgG Fc region (e.g., a human IgG region). In an embodiment, the Fc region is an IgG1 Fc region (e.g., a human IgG1 region). In an embodiment, the Fc region is a chimeric Fc region comprising portions of several different Fc regions. Suitable examples of chimeric Fc regions are set forth in US 2011/0243966A1, which is incorporated herein by reference in its entirety. A variety of Fc region gene sequences (e.g., human constant region gene sequences) are available in the form of publicly accessible deposits. [0059] An Fc region can be further truncated or internally deleted to produce a minimal FcRn binding fragment thereof. The ability of an Fc-region fragment to bind to FcRn can be determined using any art recognized binding assay (e.g., ELISA). [0060] To enhance the manufacturability of the FcRn antagonists disclosed herein, it is preferable that the constituent Fc regions do not comprise any non-disulfide bonded cysteine residues. Accordingly, in an embodiment, the Fc regions do not comprise a free cysteine residue. [0061] Any Fc variant, or FcRn binding fragment thereof, that binds specifically to FcRn with increased affinity and reduced pH dependence relative to the native (i.e., wild-type) Fc region can be used in the methods disclosed herein. In an embodiment, the variant Fc region comprises amino acid alterations, substitutions, insertions, and/or deletions that confer the desired characteristics. In some embodiments, the FcRn antagonist comprises a variant Fc region, or FcRn binding fragment thereof, which binds to FcRn with a higher affinity at pH 5.5 as compared to a corresponding wild-type Fc region. In some embodiments, the FcRn antagonist comprises or consists of a variant Fc region, or FcRn binding fragment thereof, which binds to FcRn with a higher affinity at pH 6.0 and/or at pH 7.4 as compared to a corresponding wild-type Fc region. In some embodiments, the FcRn antagonist comprises a variant Fc region, or FcRn binding fragment thereof, which binds to FcRn with a higher affinity at both acidic and neutral pH. [0062] In some embodiments, the variant Fc region is derived from the Fc region of any native immunoglobulin. In some embodiments, the native immunoglobulin is a human immunoglobulin. In some embodiments, the immunoglobulin is IgA, IgD, IgE, or IgG. In some embodiments, the immunoglobulin is IgG. In some embodiments, the immunoglobulin is human IgA, human IgD, human IgE, or human IgG. In some embodiments, the immunoglobulin is human IgG. In some embodiments, the IgG is IgG1, IgG2, IgG3, or IgG4. In some embodiments, the human IgG is human IgG1, human IgG2, human IgG3, or human IgG4. In some embodiments, the variant Fc region varies from the human IgG1 Fc region. In some embodiments, the human IgG1 Fc region comprises a G1m1(a), G1m2(x), G1m3(f), or G1m17(z) allotype. [0063] In an embodiment, the variant Fc region, or FcRn binding fragment thereof consists of two Fc domains. [0064] In an embodiment, the variant Fc region comprises or consists of a first Fc domain and a second Fc domain which form a homodimer or heterodimer. In an embodiment, the first Fc domain and/or the second Fc domain comprise amino acids Y, T, E, K, and F at EU positions 252, 254, 256, 433, and 434, respectively. In an embodiment, the first Fc domain and/or the second Fc domain comprise amino acids Y, T, E, K, F, and Y at EU positions 252, 254, 256, 433, 434, and 436, respectively. [0065] In some embodiments, the FcRn antagonists disclosed herein comprise or consist of at least one Fc domain, wherein the amino acid sequence of the at least one Fc domain comprises or consists of the amino acid sequence of SEQ ID NO:1, provided below. Table 1.

[0066] In some embodiments, the FcRn antagonists disclosed herein comprise or consist of a variant Fc region comprising or consisting of a dimer of a first Fc domain and a second Fc domain, wherein the amino acid sequence of the first and second Fc domain comprises or consists of the amino acid sequence of SEQ ID NO: 1. [0067] In some embodiments, the FcRn antagonists disclosed herein comprise or consist of an amino acid sequence at least 70%, 75%, 80%, 85%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% identical to the amino acid sequence of a variant Fc region comprising or consisting of a dimer of a first Fc domain and a second Fc domain, wherein the amino acid sequence of the first and second Fc domain comprises or consists of an amino acid sequence independently selected from the group consisting of SEQ ID NOs: 2-22. In some embodiments, the dimer is a heterodimer or a homodimer. Table 2.

[0068] In an embodiment, the first Fc domain and/or the second Fc domain comprise an amino acid sequence independently selected from the group consisting of SEQ ID NOs: 2, 3, 20, or 21. In an embodiment, the first Fc domain and the second Fc domain comprise an amino acid sequence independently selected from the group consisting of SEQ ID NOs: 2, 3, 20, or 21. In some embodiments, the FcRn antagonist comprises a population of FcRn antagonist molecules. In some embodiments, a FcRn antagonist comprising a first Fc domain and a second Fc domain comprising an amino acid sequence independently selected from the group consisting of SEQ ID NOs: 2, 3, 20, or 21 is the predominant FcRn antagonist molecule in the population of FcRn antagonist molecules. In some embodiments, the predominant FcRn antagonist molecule makes up at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 96%, 97%, 98%, or 99% of the population of FcRn antagonist molecules. [0069] In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region comprises the amino acid sequence of SEQ ID NO: 2. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region consists of the amino acid sequence of SEQ ID NO: 2. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region comprises the amino acid sequence of SEQ ID NO: 3. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region consists of the amino acid sequence of SEQ ID NO: 3. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region comprises the amino acid sequence of SEQ ID NO: 20. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region consists of the amino acid sequence of SEQ ID NO: 20. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region comprises the amino acid sequence of SEQ ID NO: 21. In an embodiment, the amino acid sequence of the Fc domains of the variant Fc region consists of the amino acid sequence of SEQ ID NO: 21. [0070] In certain embodiments, the variant Fc region is a heterodimer, where the constituent Fc domains are different from each other. Methods of producing Fc heterodimers are known in the art (see, e.g., US 8,216,805, which is incorporated by reference herein in its entirety). In an embodiment, the FcRn antagonist consists of a variant Fc region, wherein the variant Fc region consists of two Fc domains which form a heterodimer, wherein the amino acid sequence of each of the Fc domains is independently selected from SEQ ID NOs: 2, 3, 20, or 21. In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a heterodimer, wherein the amino acid sequence of the first Fc domain consists of or comprises the amino acid sequence of SEQ ID NO: 2 and the amino acid sequence of the second Fc domain consists of or comprises the amino acid sequence of SEQ ID NOs: 3, 20, or 21. In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a heterodimer, wherein the amino acid sequence of the first Fc domain consists of or comprises the amino acid sequence of SEQ ID NO: 3 and the amino acid sequence of the second Fc domain consists of or comprises the amino acid sequence of SEQ ID NOs: 2, 20, or 21. In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a heterodimer, wherein the amino acid sequence of the first Fc domain consists of or comprises the amino acid sequence of SEQ ID NO: 20 and the amino acid sequence of the second Fc domain consists of or comprises the amino acid sequence of SEQ ID NOs: 2, 3, or 21. In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a heterodimer, wherein the amino acid sequence of the first Fc domain consists of or comprises the amino acid sequence of SEQ ID NO: 21 and the amino acid sequence of the second Fc domain consists of or comprises the amino acid sequence of SEQ ID NOs: 2, 3, or 20. [0071] In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a homodimer, wherein the amino acid sequence of each of the Fc domains consists of or comprises the amino acid sequence of SEQ ID NO: 2. [0072] In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a homodimer, wherein the amino acid sequence of each of the Fc domains consists of or comprises the amino acid sequence of SEQ ID NO: 3. [0073] In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a homodimer, wherein the amino acid sequence of each of the Fc domains consists of or comprises the amino acid sequence of SEQ ID NO: 20. [0074] In an embodiment, the FcRn antagonist consists of or comprises a variant Fc region, wherein the variant Fc region consists of or comprises two Fc domains which form a homodimer, wherein the amino acid sequence of each of the Fc domains consists of or comprises the amino acid sequence of SEQ ID NO: 21. [0075] In some embodiments, the FcRn antagonist comprises glycanation on one or both of the Fc domains. In some embodiments, the FcRn antagonist molecules comprise glycanation at EU position 297 on one or both of the Fc domains. In some embodiments, the glycanation comprises an N-glycan. In some embodiments, the N-glycan comprises a G0F N- glycan, G1F N-glycan, G2F N-glycan, or G0 N-glycan. [0076] In some embodiments, FcRn antagonist comprises or consists of a population of FcRn antagonists, wherein at least 33%, at least 34%, at least 35%, at least 36%, at least 37%, at least 38%, at least 39%, at least 40%, at least 41%, at least 42%, at least 43%, at least 44%, at least 45%, at least 46%, at least 47%, at least 48%, at least 49%, at least 50%, at least 51%, at least 52%, at least 53%, at least 54%, at least 55%, at least 56%, or at least 57% of the population of Fc domains of the FcRn antagonists comprise galactose. In some embodiments, the population comprises or consists of FcRn antagonists, wherein at least 88%, at least 89%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% of the population of Fc domains of the FcRn antagonists comprise fucose. [0077] In some embodiments, the FcRn antagonist lacks an amino acid at EU position 441 of one or both Fc domains. In some embodiments, the FcRn antagonist comprises glycine and lysine at EU positions 440 and 441, respectively. In some embodiments, the FcRn antagonist lacks amino acids at EU positions 440 and 441. In some embodiments, the FcRn antagonist comprises amidated proline at EU position 439. In some embodiments, the FcRn antagonist lacks amino acids at EU positions 440 and 441 and comprise amidated proline at EU position 439. [0078] In some embodiments, the FcRn antagonist comprises aspartate, lysine, threonine, histidine, threonine, and cysteine at EU positions 221, 222, 223, 224, 225, and 226, respectively. In some embodiments, the FcRn antagonist lacks an amino acid at EU positions 221, and comprises lysine, threonine, histidine, threonine, and cysteine at EU positions 222, 223, 224, 225, and 226, respectively. In some embodiments, the FcRn antagonist lacks amino acids at EU positions 221 and 222, and comprises threonine, histidine, threonine, and cysteine at EU positions 223, 224, 225, and 226, respectively. In some embodiments, the FcRn antagonist lacks amino acids at EU positions 221-224, and comprises threonine and cysteine at EU positions 225 and 226, respectively. In some embodiments, the FcRn antagonist lacks amino acids at EU positions 221, 222, 223, 224, 225, and 226. [0079] In some embodiments, the FcRn antagonist is a population of FcRn antagonist molecules. In some embodiments, the population of FcRn antagonist molecules comprises one or more of the FcRn antagonists described herein. In some embodiments, the FcRn antagonist is any of those described in U.S. Patent Application No. 63/383,599, filed on November 14, 2022, incorporated herein by reference in its entirety. In some embodiments, the FcRn antagonist is a population of FcRn antagonists as described in U.S. Patent Application No. 63/383,599, filed on November 14, 2022, incorporated herein by reference in its entirety. [0080] In an embodiment, the FcRn antagonist is efgartigimod (CAS Registry No. 1821402-21-4). The term “efgartigimod” as used herein is interchangeable with “efgartigimod alfa.” In some embodiments, efgartigimod is efgartigimod alfa-fcab. [0081] In an embodiment, the anti-FcRn antibody is nipocalimab (M281), rozanolixizumab (UCB7665), orilanolimab (ALXN1830/SYNT001), or batoclimab (IMVT- 1401/RVT1401/HBM9161). [0082] In an embodiment, an antibody that binds specifically to FcRn and inhibits the binding of the Fc region of immunoglobulin to FcRn is nipocalimab, also known as M281. Nipocalimab is a full-length “Fc dead” IgG1 monoclonal antibody. Nipocalimab has been administered as an intravenous infusion in Phase 2 clinical trials for the treatment of myasthenia gravis (MG), warm autoimmune hemolytic anemia (WAIHA), and hemolytic disease of fetus and newborn (HDFN). Nipocalimab comprises the light chain (SEQ ID NO: 23) and heavy chain (SEQ ID NO: 24) sequences set forth in Table 3 below (VL region of SEQ NO: 23 and VH region of SEQ ID NO: 24 are underlined): Table 3. Heavy chain and light chain sequences of nipocalimab

[0083] In an embodiment, an antibody that binds specifically to FcRn and inhibits the binding of the Fc region of immunoglobulin to FcRn is rozanolixizumab, also known as UCB 7665. Rozanolixizumab is a full-length humanized IgG4 monoclonal antibody. Rozanolixizumab has been administered as a subcutaneous infusion in ongoing clinical trials for MG, immune thrombocytopenia (FTP), and chronic inflammatory demyelinating polyneuropathy (CIDP). Rozanolixizumab comprises the light chain (SEQ ID NO: 25) and heavy chain (SEQ ID NO: 26) sequences set forth in Table 4 below (VL region of SEQ NO: 25 and VH region of SEQ ID NO: 26 are underlined): Table 4. Heavy chain and light chain sequences of rozanolixizumab

[0084] In an embodiment, an antibody that binds specifically to FcRn and inhibits the binding of the Fc region of immunoglobulin to FcRn is orilanolimab, also known as SYNT001. Orilanolimab is another full-length humanized IgG4 monoclonal antibody. Orilanolimab has been administered as an intravenous infusion in Phase 2 clinical trials for treatment of WAIHA. Orilanolimab comprises the light chain (SEQ ID NO: 27) and heavy chain (SEQ ID NO: 28) sequences set forth in Table 5 below (VL region of SEQ NO: 27 and VH region of SEQ ID NO: 28 are underlined): Table 5. Heavy chain and light chain sequences of orilanolimab

[0085] In an embodiment, an antibody that binds specifically to FcRn and inhibits the binding of the Fc region of immunoglobulin to FcRn is batoclimab, also known as IMVT1401/RVT1401/HBM9161. Batoclimab is another full-length “Fc dead” IgG1 monoclonal antibody. Batoclimab has been administered as a subcutaneous injection in ongoing Phase 2 clinical trials for treatment of MG and Graves’ ophthalmopathy. Batoclimab comprises the light chain (SEQ ID NO: 29) and heavy chain (SEQ ID NO: 30) sequences set forth in Table 6 below (VL region of SEQ NO: 29 and VH region of SEQ ID NO: 30 are underlined): Table 6. Heavy chain and light chain sequences of batoclimab

Pharmaceutical Compositions [0086] In an aspect, the instant disclosure provides pharmaceutical compositions comprising an FcRn antagonist for use in methods of treating POTS. In certain embodiments, these compositions comprise or consist of a variant Fc region, or FcRn binding fragment thereof, that binds specifically to FcRn, particularly human FcRn, with increased affinity and reduced pH dependence relative to a native Fc region. In other embodiments, the FcRn antagonist composition is an antibody or antigen-binding fragment thereof that binds specifically to FcRn via its antigen binding domain and inhibits the binding of Fc region of immunoglobulin to FcRn. In general, these FcRn antagonists inhibit the binding of Fc- containing agents (e.g., antibodies and immunoadhesins) to FcRn in vivo, which results in an increased rate of degradation of the Fc-containing agents and, concomitantly, a reduced serum level of these agents. [0087] In an embodiment, the FcRn antagonist is efgartigimod. Efgartigimod (ARGX- 113) is a modified human immunoglobulin (Ig) gamma (IgG) 1-derived Fc of the za allotype that binds with nanomolar affinity to human FcRn. Efgartigimod encompasses the IgG1 Fc- region and has been engineered using ABDEG™ technology to increase its affinity for FcRn at both physiological and acidic pH. The increased affinity for FcRn of efgartigimod at both acidic and physiological pH results in a blockage of FcRn-mediated recycling of IgG. [0088] Due to its increased affinity for FcRn at both acidic and neutral pH, efgartigimod blocks the FcRn/IgG complex from forming, which results in degradation of endogenous IgGs, including autoantibodies that cause IgG-mediated autoimmune diseases. This blocking of FcRn by efgartigimod results in a rapid and profound reduction in autoantibody levels, which underlies the therapeutic strategy for the treatment of autoimmune indications where IgG autoantibodies are expected to have a central role in the disease pathology. [0089] Efgartigimod is under development for both the intravenous (IV) and subcutaneous (SC) administration route. [0090] For IV administration, in certain embodiments, efgartigimod may be administered in a formulation comprising sodium phosphate, sodium chloride, L-arginine hydrochloride, and polysorbate 80. In certain embodiments, efgartigimod may be administered in a formulation comprising about 25 mM sodium phosphate, about 100 mM sodium chloride, and about 150 mM L-arginine hydrochloride (pH 6.7), with about 0.02% (w/v) polysorbate 80. In certain embodiments, efgartigimod may be administered in a formulation comprising 25 mM sodium phosphate, 100 mM sodium chloride, and 150 mM L-arginine hydrochloride (pH 6.7), with 0.02% (w/v) polysorbate 80. In certain embodiments, efgartigimod may be administered in a formulation comprising about 25 mM sodium phosphate, about 100 mM sodium chloride, and about 150 mM L-arginine hydrochloride (pH 6.7), with about 0.02% (w/v) polysorbate 80, via intravenous infusion in a total volume of about 250 mL over a period of about 2 hours. In certain embodiments, efgartigimod may be administered in a formulation comprising 25 mM sodium phosphate, 100 mM sodium chloride, and 150 mM L-arginine hydrochloride (pH 6.7), with 0.02% (w/v) polysorbate 80, via intravenous infusion in a total volume of 250 mL over a period of 2 hours. See, e.g., WO2019110823A1, which is incorporated by reference herein in its entirety. [0091] In certain embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising about 25 mM sodium phosphate, about 100 mM sodium chloride, and about 150 mM L-arginine hydrochloride with a pH of about 6.7, with about 0.02% (w/v) polysorbate 80, diluted for intravenous infusion to a total volume of about 125 mL over a period of about 1 hour. In certain embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising 25 mM sodium phosphate, 100 mM sodium chloride, and 150 mM L-arginine hydrochloride with a pH of 6.7, with 0.02% (w/v) polysorbate 80, diluted for intravenous infusion to a total volume of 125 mL over a period of 1 hour. [0092] In certain embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising about 4 mM sodium phosphate, about 146 mM sodium chloride, about 24 mM L-arginine, and about 0.0032% (w/v) polysorbate 80, with a pH of about 6.7. This formulation is administered via intravenous infusion in a total volume of about 125 mL over a period of about 1 hour. In certain embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising 4 mM sodium phosphate, 146 mM sodium chloride, 24 mM L-arginine, and 0.0032% (w/v) polysorbate 80, with a pH of 6.7. This formulation is administered via intravenous infusion in a total volume of 125 mL over a period of 1 hour. [0093] In certain embodiments, efgartigimod is administered via IV infusion and is provided in a sterile, colorless, clear concentrate solution at a concentration of about 20 mg/mL. In certain embodiments, efgartigimod is administered via IV infusion and is provided in a sterile, colorless, clear concentrate solution at a concentration of 20 mg/mL. [0094] In certain embodiments, efgartigimod is administered via IV infusion and is provided in a vial (e.g., a single-dose vial). In certain embodiments, a vial of efgartigimod contains about 400 mg of efgartigimod at a concentration of about 20 mg/mL. In certain embodiments, a vial of efgartigimod contains 400 mg of efgartigimod at a concentration of 20 mg/mL. In certain embodiments, each mL of solution in a vial of efgartigimod contains about 31.6 mg L-arginine hydrochloride, about 0.2 mg polysorbate 80, about 5.8 mg sodium chloride, about 2.4 mg sodium phosphate dibasic anhydrous, about 1.1 mg sodium phosphate monobasic monohydrate, and water for injection, USP, at a pH of about 6.7. In certain embodiments, each mL of solution in a vial of efgartigimod contains 31.6 mg L-arginine hydrochloride, 0.2 mg polysorbate 80, 5.8 mg sodium chloride, 2.4 mg sodium phosphate dibasic anhydrous, 1.1 mg sodium phosphate monobasic monohydrate, and water for injection, USP, at a pH of 6.7. [0095] In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of about 10 mg/kg as an IV infusion. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of about 10 mg/kg as an IV infusion over about one hour. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of about 10 mg/kg as an IV infusion over about one hour once weekly. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of about 10 mg/kg as an IV infusion over about one hour once weekly for about 4 weeks. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of 10 mg/kg as an IV infusion. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of 10 mg/kg as an IV infusion over one hour. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of 10 mg/kg as an IV infusion over one hour once weekly. In certain embodiments, for patients weighing under 120 kg, efgartigimod is administered at a dose of 10 mg/kg as an IV infusion over one hour once weekly for 4 weeks. In certain embodiments, for patients weighing 120 kg or more, efgartigimod is administered at a dose of about 1200 mg per IV infusion. In certain embodiments, for patients weighing 120 kg or more, efgartigimod is administered at a dose of 1200 mg per IV infusion. [0096] For SC administration, in certain embodiments, efgartigimod may be administered alone. Alternatively, for SC administration, in certain embodiments, efgartigimod may be administered co-formulated with hyaluronidase, for example, in particular, rHuPH20. The co-formulated material will allow SC dosing of larger volumes. [0097] In some embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising about 20 mM L-histidine, about 100 mM sodium chloride, about 60 mM sucrose, about 10 mM L-methionine, and about 0.04% (w/v) polysorbate 20, wherein the formulation has a pH of about 6.0. In some embodiments, the formulation comprises about 180 mg/mL efgartigimod. In some embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising 20 mM L- histidine, 100 mM sodium chloride, 60 mM sucrose, 10 mM L-methionine, and 0.04% (w/v) polysorbate 20, wherein the formulation has a pH of 6.0. In some embodiments, the formulation comprises 180 mg/mL efgartigimod. [0098] In some embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising about 20 mM L-histidine, about 50 mM L-arginine, about 100 mM sodium chloride, about 60 mM sucrose, about 10 mM L-methionine, and about 0.04 (w/v) polysorbate 80, wherein the formulation has a pH of about 6.0. In some embodiments, the formulation comprises about 200 mg/mL efgartigimod. In some embodiments, efgartigimod may be administered in a formulation comprising an aqueous solution comprising 20 mM L-histidine, 50 mM L-arginine, 100 mM sodium chloride, 60 mM sucrose, 10 mM L-methionine, and 0.04 (w/v) polysorbate 80, wherein the formulation has a pH of 6.0. In some embodiments, the formulation comprises 200 mg/mL efgartigimod. [0099] rHuPH20 is the active ingredient of Halozyme’s commercial product HYLENEX® recombinant (hyaluronidase human injection), referred to as HYLENEX®, which was approved by FDA for marketed use in the U.S. in December 2005. HYLENEX® is a tissue permeability modifier indicated as an adjuvant in SC fluid administration for achieving hydration, to increase the dispersion and absorption of other injected drugs, and in SC urography, for improving resorption of radiopaque agents. [00100] rHuPH20 is a recombinant enzyme human hyaluronidase produced by genetically engineered Chinese hamster ovary (CHO) cells containing a deoxyribonucleic plasmid encoding a soluble fragment of human hyaluronidase (posterior head protein 20 [PH20]). [00101] The HZ202 rHuPH20 DS is currently registered in HYLENEX® and other biologic drug products co-formulated with rHuPH20 DS. As such, in certain embodiments HZ202 rHuPH20 DS is used in the efgartigimod / rHuPH20 co-formulated product for SC administration (i.e., efgartigimod PH20 SC). [00102] Provided in the co-formulations, combinations, uses and methods herein are soluble hyaluronidases. Soluble hyaluronidases include any that, upon expression, are secreted from a cell and exist in soluble form. Such soluble hyaluronidases include, but are not limited to, bacterial soluble hyaluronidases, non-human soluble hyaluronidases, such as bovine PH20 and ovine PH20, human soluble PH20, and variants thereof. Generally soluble forms of PH20 are produced using protein expression systems that facilitate correct N-glycosylation to ensure the polypeptide retains activity, since glycosylation is important for the catalytic activity and stability of hyaluronidases. Such cells include, for example Chinese Hamster Ovary (CHO) cells (e.g., DG44 CHO cells). [00103] rHuPH20 refers to the composition produced upon expression in a cell, such as a CHO cell, of nucleic acid encoding residues 36-482 of SEQ ID NO:32, generally linked to the native or a heterologous signal sequence (residues 1-35 of SEQ ID NO:32). rHuPH20 is produced by expression of a nucleic acid molecule, such as encoding amino acids 1-482 (set forth in SEQ ID NO:32) in a mammalian cell. Translational processing removes the 35 amino acid signal sequence. As produced in the culture medium there is heterogeneity at the C- terminus such that the product, designated rHuPH20, includes a mixture of species that can include any one or more of the polypeptides 36-480, 36-481, and 36-482 of SEQ ID NO:32, and some shorter polypeptides, in various abundance. Typically, rHuPH20 is produced in cells that facilitate correct N-glycosylation to retain activity, such as CHO cells (e.g., DG44 CHO cells). In some embodiments, one of the most abundant species is the 446 amino acid polypeptide corresponding to residues 36-481 of SEQ ID NO:32. Also included are polypeptides that are soluble or secreted upon expression in a mammalian cell and have at least 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or more sequence identity with residues 36-482 of SEQ ID NO:32. [00104] In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 20 mg to about 20,000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 200 mg to about 20,000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 300 mg to about 6000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 750 mg to about 3000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 1000 mg to about 2500 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from about 1000 mg to about 2000 mg. [00105] In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 20 mg to 20,000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 200 mg to 20,000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 300 mg to 6000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 750 mg to 3000 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 1000 mg to 2500 mg. In some embodiments, the pharmaceutical formulation comprises an FcRn antagonist in an amount from 1000 mg to 2000 mg. [00106] In some embodiments, the pharmaceutical formulation comprises about 1000 mg or about 2000 mg of an FcRn antagonist. In some embodiments, the pharmaceutical formulation comprises 1000 mg or 2000 mg of an FcRn antagonist. In some embodiments, the FcRn antagonist is efgartigimod. [00107] In some embodiments, the pharmaceutical formulation comprises efgartigimod in an amount from about 800 mg to about 1200 mg. In some embodiments, the pharmaceutical formulation comprises efgartigimod in an amount from 800 mg to 1200 mg. [00108] In some embodiments, the pharmaceutical formulation comprises about 1000 mg efgartigimod. In some embodiments, the pharmaceutical formulation comprises 1000 mg efgartigimod. [00109] In some embodiments, the pharmaceutical formulation comprises from about 10 mg/mL to about 200 mg/mL efgartigimod. In some embodiments, the pharmaceutical formulation comprises from 10 mg/mL to 200 mg/mL efgartigimod. [00110] In some embodiments, the pharmaceutical formulation comprises about 20 mg/mL efgartigimod. In some embodiments, the pharmaceutical formulation comprises 20 mg/mL efgartigimod. [00111] In some embodiments, the pharmaceutical formulation comprises about 180 mg/mL efgartigimod. In some embodiments, the pharmaceutical formulation comprises 180 mg/mL efgartigimod. [00112] In some embodiments, the pharmaceutical formulation further comprises hyaluronidase. In some embodiments, the hyaluronidase is recombinant human hyaluronidase PH20 (rHuPH20). [00113] The hyaluronidase can be present in the pharmaceutical formulation in any suitable amount. In an embodiment, the amount of hyaluronidase enzyme is from about 1000 U/mL to about 3000 U/mL. In an embodiment, the amount of hyaluronidase enzyme is about 1000 U/mL, about 1500 U/mL, about 2000 U/mL, about 2500 U/mL, or about 3000 U/mL. In an embodiment, the amount of hyaluronidase enzyme is 2000 U/mL. [00114] In some embodiments, the rHuPH20 is present in the pharmaceutical formulation in an amount of about 11,000 U. In some embodiments, the rHuPH20 is present in the pharmaceutical formulation in an amount of 11,000 U. [00115] In some embodiments, the pharmaceutical formulation comprises at least about 5 U to at least about 100,000 U of an endoglycosidase hydrolase enzyme. In some aspects, the pharmaceutical formulation comprises at least about 5 U, at least about 10 U, at least about 20 U, at least about 30 U, at least about 40 U, at least about 50 U, at least about 75 U, at least about 100 U, at least about 200 U, at least about 300 U, at least about 400 U, at least about 500 U, at least about 750 U, at least about 1000 U, at least about 2000 U, at least about 3000 U, at least about 4000 U, at least about 5000 U, at least about 6000 U, at least about 7000 U, at least about 8000 U, at least about 9000 U, at least about 10,000 U, at least about 20,000 U, at least about 30,000 U, at least about 40,000 U, at least about 50,000 U, at least about 60,000 U, at least about 70,000 U, at least about 80,000 U, at least about 90,000 U, or at least about 100,000 U of an endoglycosidase hydrolase enzyme. [00116] In some embodiments, the pharmaceutical formulation comprises about 20,000 U of an endoglycosidase hydrolase enzyme. In some embodiments, the pharmaceutical formulation comprises at least about 500 U/mL to at least about 5000 U/mL of an endoglycosidase hydrolase enzyme. In some embodiments, the pharmaceutical formulation comprises at least about 1500 U/mL, at least about 1600 U/mL, at least about 1700 U/mL, at least about 1800 U/mL, at least about 1900 U/mL, at least about 2000 U/mL, at least about 2100 U/mL, at least about 2200 U/mL, at least about 2300 U/mL, at least about 2400 µM, at least about 2500 µM, at least about 3000 µM, at least about 3500 µM, at least about 4000 µM, at least about 4500 U/mL, or at least about 5000 U/mL of an endoglycosidase hydrolase enzyme. In some embodiments, the pharmaceutical formulation comprises about 2000 U/mL of an endoglycosidase hydrolase enzyme. [00117] In some embodiments, the endoglycosidase hydrolase enzyme cleaves hyaluronic acid at a hexosaminidic β (1–4) or (1–3) linkage. In some embodiments, the endoglycosidase hydrolase enzyme comprises a catalytic domain of hyaluronidase PH-20 (HuPH20), HYAL1, HYAL2, HYAL3, HYAL4, or HYALPS1. In some embodiments, the endoglycosidase hydrolase enzyme comprises an amino acid sequence having at least about 70%, at least about 75%, at least about 80%, at least about 85%, at least about 90%, at least about 95%, at least about 96%, at least about 97%, at least about 98%, at least about 99%, or about 100% sequence identity to amino acids 36-490 of SEQ ID NO: 32. In some embodiments, the endoglycosidase hydrolase enzyme comprises a hyaluronidase. In some embodiments, the endoglycosidase hydrolase enzyme comprises a hyaluronidase selected from the group consisting of HuPH20, HYAL1, HYAL2, HYAL3, HYAL4, any variant, and any isoform thereof. In some embodiments, the endoglycosidase hydrolase enzyme comprises rHuPH20 or a fragment thereof. [00118] In some embodiments, the endoglycosidase hydrolase enzyme comprises a modified hyaluronidase comprising one or more amino acid substitutions relative to a wild- type hyaluronidase selected from the group consisting of HuPH20, HYAL1, HYAL2, HYAL3, HYAL4, HYALPS1, or a fragment thereof. In some embodiments, the endoglycosidase hydrolase enzyme comprises a modified hyaluronidase comprising one or more amino acid substitution in an alpha-helix region relative to a wild-type hyaluronidase selected from the group consisting of HuPH20, HYAL1, HYAL2, HYAL3, HYAL4, HYALPS1, or a fragment thereof. In some embodiments, the endoglycosidase hydrolase enzyme comprises a modified hyaluronidase comprising one or more amino acid substitution in linker region relative to a wild-type hyaluronidase selected from the group consisting of HuPH20, HYAL1, HYAL2, HYAL3, HYAL4, HYALPS1, or a fragment thereof. In some embodiments, the endoglycosidase hydrolase enzyme comprises a modified hyaluronidase, wherein one or more N-terminal and/or C-terminal amino acids are deleted relative to a wild-type hyaluronidase selected from the group consisting of HuPH20, HYAL1, HYAL2, HYAL3, HYAL4, HYALPS1, or a fragment thereof. In some embodiments, the endoglycosidase hydrolase enzyme comprises a modified rHuPH20, wherein the modified rHuPH20 comprises: i. one or more amino acid substitution in an alpha-helix region, a linker region, or both an alpha- helix region and a linker region relative to wild-type rHuPH20; ii. deletion of one or more N- terminal amino acid, one or more C-terminal amino acid, or one or more N-terminal amino acid and one or more C-terminal amino acid relative to wild-type rHuPH20; or iii. both (i) and (ii). [00119] "Hyaluronidase," as used herein, refers to an enzyme capable of catalyzing the cleavage of hyaluronan. Hyaluronan is a repeating polymer of N-acetyl-glucosamine and glucuronic acid, which is present in the subcutaneous space and contributes to the soluble gel- like component of the extracellular matrix of the skin and is restored by rapid turnover (resynthesis). In some embodiments, the hyaluronidase comprises rHuPH20, which is a glycosylated 447-amino acid single chain polypeptide that depolymerizes hyaluronan in the subcutaneous space locally at the site of injection in the skin. Depolymerization of hyaluronan by hyaluronidase is accomplished by hydrolysis of the polysaccharide polymer. Depolymerization of hyaluronan results in a transient reduction in the viscosity of the gel-like phase of the extracellular matrix and increased hydraulic conductance that facilitates the dispersion and absorption of the coadministered therapeutic agent. Thus, a hyaluronidase, e.g., rHuPH20, can improve the speed and ease of subcutaneous delivery of injectable biologics and drugs by acting as a permeation enhancer. In certain embodiments, the hyaluronidase comprises ENHANZE™. [00120] In any of the above embodiments, the pharmaceutical formulation may be a unit dosage form. [00121] In an embodiment, the unit dosage form comprises the FcRn antagonist as a dry formulation for dissolution such as a lyophilized powder, freeze-dried powder, or water-free concentrate. In an embodiment, the dry formulation is comprised in a hermetically sealed container such as a vial, an ampoule, or a sachet. [00122] In an embodiment, the unit dosage form comprises the FcRn antagonist as a liquid formulation, e.g., injection or infusion solution. In an embodiment, the liquid formulation is comprised in a hermetically sealed container such as a vial, a sachet, a pre-filled syringe, a pre-filled autoinjector, or a cartridge for a reusable syringe or applicator. [00123] In an embodiment, the unit dosage per vial may contain 0.5 ml, 1 ml, 2 ml, 3 ml, 4 ml, 5 ml, 6 ml, 7 ml, 8 ml, 9 ml, 10 ml, 15 ml, or 20 ml of an FcRn antagonist ranging from about 500 to about 2500 mg or from about 1000 mg to about 2000 mg. In an embodiment, these preparations can be adjusted to a desired concentration by adding a sterile diluent to each vial. [00124] The formulations disclosed herein include bulk drug compositions useful in the manufacture of pharmaceutical compositions (e.g., compositions that are suitable for administration to a subject or patient) which can be used in the preparation of unit dosage forms. In an embodiment, a composition of the invention is a pharmaceutical composition. Such compositions comprise a prophylactically or therapeutically effective amount of one or more prophylactic or therapeutic agents (e.g., an FcRn antagonist of the invention or other prophylactic or therapeutic agent), and a pharmaceutically acceptable carrier. In an embodiment, the pharmaceutical compositions are formulated to be suitable for subcutaneous administration to a subject. Methods [00125] In an aspect, methods for treating POTS using an FcRn antagonist are provided. In certain embodiments, the POTS is post-COVID-19 POTS. As used herein, the term “post- COVID-19 POTS” refers to POTS which develops in a subject after having COVID-19. In certain embodiments, the FcRn antagonist is efgartigimod. An important goal and feature of the methods disclosed herein is improvement in one or more symptoms in POTS patients. Symptoms in POTS patients include autonomic symptoms, including but not limited to, orthostatic intolerance, vasomotor, secretomotor, gastrointestinal, bladder, and pupillomotor symptoms. Other symptoms in POTS patients include symptoms related to orthostatic intolerance, such as tachycardia, palpitations, dizziness, and presyncope. Other symptoms in POTS patients include symptoms unrelated to orthostatic intolerance, such as gastrointestinal symptoms, insomnia, and concentration difficulties. Other goals and features of the methods disclosed herein include, but are not limited to, reduced fatigue and improvement in disease- related quality of life. Effective treatment of POTS using an FcRn antagonist may include at least one of the elements of the group consisting of: improvement in COMPASS 31 score and/or improvement in MaPS score, improvement in PGI-S score, improvement in PGI-C score, and/or reduced fatigue. [00126] COMPASS 31 is a questionnaire that measures autonomic symptom burden based on the well-established 169-item Autonomic Symptom Profile (ASP) and the validated 84-question scoring instrument, the Composite Autonomic Symptom Score (COMPASS). Prior studies in patients with POTS support the ability of this assessment to measure autonomic symptom burden in patients relative to controls and over time. The 31-item questionnaire requires approximately 10 minutes to administer and addresses 6 domains: orthostatic intolerance, vasomotor, secretomotor, bladder, pupillomotor, and gastrointestinal-mixed upper and diarrhea. Higher scores indicate a mover severe degree of autonomic symptoms. Elevations in COMPASS 31 have also been found in patients post-COVID-19 with evidence of POTS and other forms of dysautonomia. [00127] The MaPS questionnaire was developed specifically for patients with POTS by investigators at the Skåne University Hospital, Lund University in Malmö, Sweden to assess the severity of the most common symptoms found in patients with POTS based on clinical experience and literature. The score consists of 12 questions that assess symptom burden related (tachycardia, palpitations, dizziness, presyncope) and unrelated to orthostatic intolerance (GI symptoms, insomnia, concentration difficulties). The maximum score is 120 points, with higher scores indicating more severe symptoms. In general, patients with POTS score >40 points, whereas healthy controls have lower values. A score of >90 points indicates debilitating/severe symptoms. This 12-item evaluation score is being evaluated in a case- control study in patients with POTS compared to healthy controls. MaPS is expected to provide an accurate assessment of POTS symptoms over time. [00128] The PGI-S and PGI-C questionnaires are simple, valid, participant-rated, single- item global measures of their perceived condition. PGI-S measures severity of disease symptoms over the past 7 days, rated on a 4-point Likert scale, with scores ranging from 1 (no symptoms) to 4 (severe). PGI-C measures change in the overall status from the beginning of the study to timepoint, rated on a 7-point Likert scale, with scores ranging from 1 (much better) to 7 (much worse). [00129] In some embodiments, reduced fatigue is assessed by PROMIS Fatigue score. PROMIS is a publicly available system of highly reliable, precise patient-reported health status measures of physical, mental, and social well-being. PROMIS instruments measure concepts including pain, fatigue, and physical function. PROMIS Fatigue Short Form 8a assesses the impact and perceived fatigue during the last 7 days. This validated 8-question scale has 5 response options, with scores ranging from 1 to 5. Scores are converted to a T-score, and higher scores indicate higher fatigue levels. A decrease in score (negative change from baseline) indicates improvement in fatigue. PROMIS Cognitive Function Short Form 6a: assesses the frequency of cognitive difficulties experienced in the past 7 days. The questionnaire comprises 6 questions on subjective cognitive difficulties regarding a patient’s concentration, memory, language, mental acuity, and perceived changes in cognitive functioning. The participant marks their response on a 5-point Likert scale, with lower scores indicating worse perceived cognitive functioning. [00130] In some embodiments, the POTS may be characterized by sustained heart rate increase of ≥30 beats per minute (bpm) within 10 minutes of standing or head-up tilt in a subject. In some embodiments, the POTS may be characterized by sustained heart rate increase of ≥40 bpm within 10 minutes of standing or head-up tilt in a subject, particularly in a subject aged 12 to 19 years old. In some embodiments, the subject is aged 12 to 20 years old. In some embodiments, the subject is aged 18 to 20 years old. In some embodiments, the POTS may be characterized heart rate reaching >120 bpm within 10 minutes of standing or head-up tilt in a subject. In some embodiments, the heart rate increase is in the absence of sustained 20 mmHg decrease in systolic blood pressure (SBP). In some embodiments, each of the above measurements is measured by tilt table or orthostatic vital sign measurement. [00131] In some embodiments, the POTS may be characterized by one or more of the following symptoms in a subject: fatigue, orthostatic intolerance, brain fog, exertional dyspnea, difficulty with concentration, venous pooling, exercise intolerance, palpitation, heat intolerance, nausea with or without vomiting, insomnia, anxiety, lack of appetite, chest pain, and diaphoresis. In some embodiments, the POTS may be characterized by two or more of the above symptoms. In some embodiments, the POTS may be characterized by three or more of the above symptoms. In some embodiments, the symptoms last longer than 12 weeks after either diagnosis of COVID-19 or after hospital discharge for COVID-19. [00132] In some embodiments, the POTS may be characterized by a COMPASS 31 score ≥35. [00133] In some embodiments, the POTS may be characterized by serum total IgG ≥6 g/L in a subject. In some embodiments, the POTS may be characterized by serum total IgG ≥4 g/L in a subject. [00134] In some embodiments, the subject has not been diagnosed with, or received treatment for, one or more of the following conditions before the subject was diagnosed with COVID-19: peripheral neuropathy, POTS, myalgic encephalomyelitis encephalitis/chronic fatigue syndrome, Ehlers-Danlos syndrome confirmed by genetic testing, autonomic neuropathy, multiple sclerosis, stroke, spinal cord injury, any known lesions in the central nervous system by imaging or neurological exam, or has HIV disease or common variable immunodeficiency. In some embodiments, the subject has not been diagnosed with, or received treatment for, any of the following conditions before the subject was diagnosed with COVID- 19: peripheral neuropathy, POTS, myalgic encephalomyelitis encephalitis/chronic fatigue syndrome, Ehlers-Danlos syndrome confirmed by genetic testing, autonomic neuropathy, multiple sclerosis, stroke, spinal cord injury, any known lesions in the central nervous system by imaging or neurological exam, or has HIV disease or common variable immunodeficiency. [00135] In some embodiments, the subject has no history of, or is currently being treated for, one or more of the following conditions: clinically significant ongoing cardiac arrythmia, heart failure, myocarditis, pulmonary embolism requiring anticoagulation, pulmonary fibrosis, or critical illness-related polyneuropathy or myopathy. In some embodiments, the subject has no history of, or is currently being treated for, any of the following conditions: clinically significant ongoing cardiac arrythmia, heart failure, myocarditis, pulmonary embolism requiring anticoagulation, pulmonary fibrosis, or critical illness-related polyneuropathy or myopathy. [00136] In some embodiments, the subject has no history of, of malignancy unless considered cured by adequate treatment with no evidence of recurrence for ≥3 years before the first administration of IMP. In some embodiments, subjects do have basal cell or squamous cell skin cancer, carcinoma in situ of the cervix, carcinoma in situ of the breast, or incidental histological finding of prostate cancer (TNM stage T1a or T1b). [00137] In some embodiments, the subject does not have significant uncontrolled active or chronic bacterial, viral, or fungal infection or positive SARS-CoV-2 PCR test. In some embodiments, the subject has no positive serum test for hepatitis B virus (HBV) that is indicative of an acute or chronic infection, unless associated with a negative HB surface antigen (HBsAg) or negative HBV DNA test, hepatitis C virus (HCV) based on HCV antibody assay unless a negative RNA test is available, or HIV. In some embodiments, the subject does not have total IgG <4 g/L. [00138] In some embodiments, the FcRn antagonist is administered at a fixed dose of about 20 mg to about 20,000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of about 200 mg to about 20,000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of about 300 mg to about 6000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of about 750 mg to about 3000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of about 1000 mg to about 2500 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of about 1000 mg to about 2000 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00139] In some embodiments, the FcRn antagonist is administered at a fixed dose of 20 mg to 20,000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of 200 mg to 20,000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of 300 mg to 6000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of 750 mg to 3000 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of 1000 mg to 2500 mg. In some embodiments, the FcRn antagonist is administered at a fixed dose of 1000 mg to 2000 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00140] In some embodiments, the FcRn antagonist is administered at a fixed dose of about 20 mg, about 50 mg, about 100 mg, about 200 mg, about 250 mg, about 300 mg, about 500 mg, about 750 mg, about 1000 mg, about 1500 mg, about 2000 mg, about 2500 mg, about 3000 mg, about 4000 mg, about 5000 mg, about 6000 mg, about 7000 mg, about 8000 mg, about 9000 mg, about 10,000 mg, about 11,000 mg, about 12,000 mg, about 13,000 mg, about 14,000 mg, about 15,000 mg, about 16,000 mg, about 17,000 mg, about 18,000 mg, about 19,000 mg, or about 20,000 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00141] In some embodiments, the FcRn antagonist is administered at a fixed dose of 20 mg, 50 mg, 100 mg, 200 mg, 250 mg, 300 mg, 500 mg, 750 mg, 1000 mg, 1500 mg, 2000 mg, 2500 mg, 3000 mg, 4000 mg, 5000 mg, 6000 mg, 7000 mg, 8000 mg, 9000 mg, 10,000 mg, 11,000 mg, 12,000 mg, 13,000 mg, 14,000 mg, 15,000 mg, 16,000 mg, 17,000 mg, 18,000 mg, 19,000 mg, or 20,000 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00142] In some embodiments, the FcRn antagonist is administered at a dose of about 0.2 mg/kg to about 200 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of about 2 mg/kg to about 200 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of about 2 mg/kg to about 120 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of about 3 mg/kg to about 60 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of about 10 mg/kg to about 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00143] In some embodiments, the FcRn antagonist is administered at a dose of 0.2 mg/kg to 200 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of about 2 mg/kg to about 200 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of 2 mg/kg to 120 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of 3 mg/kg to 60 mg/kg. In some embodiments, the FcRn antagonist is administered at a dose of 10 mg/kg to 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00144] In some embodiments, the FcRn antagonist is administered at a dose of about 0.2 mg/kg, about 0.5 mg/kg, about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 12.5 mg/kg, about 15 mg/kg, about 17.5 mg/kg, about 20 mg/kg, about 25 mg/kg, about 30 mg/kg, about 35 mg/kg, about 40 mg/kg, about 45 mg/kg, about 50 mg/kg, about 55 mg/kg, about 60 mg/kg, about 65 mg/kg, about 70 mg/kg, about 75 mg/kg, about 80 mg/kg, about 85 mg/kg, about 90 mg/kg, about 95 mg/kg, about 100 mg/kg, about 110 mg/kg, about 120 mg/kg, about 130 mg/kg, about 140 mg/kg, about 150 mg/kg, about 160 mg/kg, about 170 mg/kg, about 180 mg/kg, about 190 mg/kg, or about 200 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00145] In some embodiments, the FcRn antagonist is administered at a dose of 0.2 mg/kg, 0.5 mg/kg, 1 mg/kg, 2 mg/kg, 3 mg/kg, 4 mg/kg, 5 mg/kg, 6 mg/kg, 7 mg/kg, 8 mg/kg, 9 mg/kg, 10 mg/kg, 12.5 mg/kg, 15 mg/kg, 17.5 mg/kg, 20 mg/kg, 25 mg/kg, 30 mg/kg, 35 mg/kg, 40 mg/kg, 45 mg/kg, 50 mg/kg, 55 mg/kg, 60 mg/kg, 65 mg/kg, 70 mg/kg, 75 mg/kg, 80 mg/kg, 85 mg/kg, 90 mg/kg, 95 mg/kg, 100 mg/kg, 110 mg/kg, 120 mg/kg, 130 mg/kg, 140 mg/kg, 150 mg/kg, 160 mg/kg, 170 mg/kg, 180 mg/kg, 190 mg/kg, or 200 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00146] In some embodiments, the FcRn antagonist is administered intravenously. In some embodiments, the FcRn antagonist is administered intravenously once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00147] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 0.2 mg/kg to about 200 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 2 mg/kg to about 200 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 2 mg/kg to about 120 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 3 mg/kg to about 60 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 10 mg/kg to about 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00148] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 0.2 mg/kg to 200 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 2 mg/kg to 200 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 2 mg/kg to 120 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 3 mg/kg to 60 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 10 mg/kg to 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00149] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 0.2 mg/kg, about 0.5 mg/kg, about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 12.5 mg/kg, about 15 mg/kg, about 17.5 mg/kg, about 20 mg/kg, about 25 mg/kg, about 30 mg/kg, about 35 mg/kg, about 40 mg/kg, about 45 mg/kg, about 50 mg/kg, about 55 mg/kg, about 60 mg/kg, about 65 mg/kg, about 70 mg/kg, about 75 mg/kg, about 80 mg/kg, about 85 mg/kg, about 90 mg/kg, about 95 mg/kg, about 100 mg/kg, about 110 mg/kg, about 120 mg/kg, about 130 mg/kg, about 140 mg/kg, about 150 mg/kg, about 160 mg/kg, about 170 mg/kg, about 180 mg/kg, about 190 mg/kg, or about 200 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00150] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 0.2 mg/kg, 0.5 mg/kg, 1 mg/kg, 2 mg/kg, 3 mg/kg, 4 mg/kg, 5 mg/kg, 6 mg/kg, 7 mg/kg, 8 mg/kg, 9 mg/kg, 10 mg/kg, 12.5 mg/kg, 15 mg/kg, 17.5 mg/kg, 20 mg/kg, 25 mg/kg, 30 mg/kg, 35 mg/kg, 40 mg/kg, 45 mg/kg, 50 mg/kg, 55 mg/kg, 60 mg/kg, 65 mg/kg, 70 mg/kg, 75 mg/kg, 80 mg/kg, 85 mg/kg, 90 mg/kg, 95 mg/kg, 100 mg/kg, 110 mg/kg, 120 mg/kg, 130 mg/kg, 140 mg/kg, 150 mg/kg, 160 mg/kg, 170 mg/kg, 180 mg/kg, 190 mg/kg, or 200 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00151] In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 10 mg/kg to about 30 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 10 mg/kg to about 25 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 10 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 15 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 20 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 25 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of about 30 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 10 mg/kg to 30 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 10 mg/kg to 25 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 10 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 15 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 20 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 25 mg/kg. In some embodiments, the FcRn antagonist is administered intravenously once weekly or once every two weeks at a dose of 30 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00152] In some embodiments, the FcRn antagonist is administered intravenously once every two weeks for 52 weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00153] In some embodiments, the FcRn antagonist is administered subcutaneously. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00154] In some embodiments, FcRn antagonist is administered subcutaneously at a fixed dose of about 20 mg to about 20,000 mg. In some embodiments, FcRn antagonist is administered subcutaneously at a fixed dose of about 100 mg to about 10,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 1000 mg to 2000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00155] In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of about 20 mg, about 50 mg, about 100 mg, about 250 mg, about 500 mg, about 750 mg, about 1000 mg, about 1500 mg, about 2000 mg, about 3000 mg, about 4000 mg, about 5000 mg, about 6000 mg, about 7000 mg, about 8000 mg, about 9000 mg, about 10,000 mg, about 11,000 mg, about 12,000 mg, about 13,000 mg, about 14,000 mg, about 15,000 mg, about 16,000 mg, about 17,000 mg, about 18,000 mg, about 19,000 mg, or about 20,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00156] In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 20 mg, 50 mg, 100 mg, 250 mg, 500 mg, 750 mg, 1000 mg, 1500 mg, 2000 mg, 3000 mg, 4000 mg, 5000 mg, 6000 mg, 7000 mg, 8000 mg, 9000 mg, 10,000 mg, 11,000 mg, 12,000 mg, 13,000 mg, 14,000 mg, 15,000 mg, 16,000 mg, 17,000 mg, 18,000 mg, 19,000 mg, or 20,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 1000 mg or 2000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00157] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly or every two weeks at a fixed dose of about 750 mg to about 3000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly or every two weeks at a fixed dose of about 1000 mg to about 2000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of about 1000 mg or about 2000 mg once weekly or every two weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00158] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly or every two weeks at a fixed dose of 750 mg to 3000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once weekly. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once every two weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once every three weeks. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 750 mg to 3000 mg once monthly. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly or every two weeks at a fixed dose of 1000 mg to 2000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously at a fixed dose of 1000 mg or 2000 mg once weekly or every two weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00159] In some embodiments, the FcRn antagonist is first administered subcutaneously at a fixed dose of about 1000 mg twice on the same day. In some embodiments, the FcRn antagonist is first administered subcutaneously at a fixed dose of 1000 mg twice on the same day. In some embodiments, the FcRn antagonist is efgartigimod. [00160] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 750 mg to about 1750 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 800 mg to about 1200 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 750 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 800 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 1000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 1200 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 1250 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 1500 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of about 1750 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00161] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 750 mg to 1750 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 800 mg to 1200 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 750 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 800 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 1000 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 1200 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 1250 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 1500 mg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a fixed dose of 1750 mg. In some embodiments, the FcRn antagonist is efgartigimod. [00162] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of about 10 mg/kg to about 25 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of about 10 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of about 15 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of about 20 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of about 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00163] In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of 10 mg/kg to 25 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of 10 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of 15 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of 20 mg/kg. In some embodiments, the FcRn antagonist is administered subcutaneously once weekly at a dose of 25 mg/kg. In some embodiments, the FcRn antagonist is efgartigimod. [00164] In some embodiments, the FcRn antagonist is first administered intravenously and is subsequently administered subcutaneously. In some embodiments, the FcRn antagonist is first administered intravenously and is subsequently administered subcutaneously at fixed dose of 100 mg to 10,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is first administered intravenously and is subsequently administered subcutaneously at fixed dose of 1000 mg or 2000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00165] In some embodiments, one or more doses of the FcRn antagonist are administered intravenously and subsequent doses of the FcRn antagonist are administered subcutaneously. In some embodiments, one or more doses of the FcRn antagonist are administered intravenously and subsequent doses of the FcRn antagonist are administered subcutaneously at fixed dose of 100 mg to 10,000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, one or more doses of the FcRn antagonist are administered intravenously and subsequent doses of the FcRn antagonist are administered subcutaneously at fixed dose of 1000 mg or 2000 mg once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. In some embodiments, the FcRn antagonist is efgartigimod. [00166] In some embodiments, the FcRn antagonist is administered for 6, 12, 24, 39, or 52 weeks or less. In some embodiments, the FcRn antagonist is administered for 24 weeks or less. In some embodiments, the FcRn antagonist is administered for 52 weeks or less. In some embodiments, the FcRn antagonist is administered for at least 6, 12, 24, 39, or 52 weeks. In some embodiments, the FcRn antagonist is administered for at least 24 weeks. In some embodiments, the FcRn antagonist is administered for at least 52 weeks. [00167] In some embodiments, the FcRn antagonist is rozanolixizumab. In some embodiments, rozanolixizumab is administered subcutaneously or intravenously. In some embodiments, rozanolixizumab is administered at a dose of about 0.2 mg/kg to about 200 mg/kg or at a fixed dose of about 20 mg to about 20,000 mg administered once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. [00168] In some embodiments, rozanolixizumab is administered once weekly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00169] In some embodiments, rozanolixizumab is administered once every two weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00170] In some embodiments, rozanolixizumab is administered once every three weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00171] In some embodiments, rozanolixizumab is administered once every four weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00172] In some embodiments, rozanolixizumab is administered once monthly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00173] In some embodiments, the FcRn antagonist is nipocalimab. In some embodiments, nipocalimab is administered subcutaneously or intravenously. In some embodiments, nipocalimab is administered at a dose of about 0.2 mg/kg to about 200 mg/kg or at a fixed dose of about 20 mg to about 20,000 mg administered once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. [00174] In some embodiments, nipocalimab is administered once weekly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00175] In some embodiments, nipocalimab is administered once every two weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00176] In some embodiments, nipocalimab is administered once every three weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00177] In some embodiments, nipocalimab is administered once every four weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00178] In some embodiments, nipocalimab is administered once monthly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00179] In some embodiments, the FcRn antagonist is orilanolimab. In some embodiments, orilanolimab is administered subcutaneously or intravenously. In some embodiments, orilanolimab is administered at a dose of about 0.2 mg/kg to about 200 mg/kg or at a fixed dose of about 20 mg to about 20,000 mg administered once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. [00180] In some embodiments, orilanolimab is administered once weekly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00181] In some embodiments, orilanolimab is administered once every two weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00182] In some embodiments, orilanolimab is administered once every three weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00183] In some embodiments, orilanolimab is administered once every four weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00184] In some embodiments, orilanolimab is administered once monthly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00185] In some embodiments, orilanolimab is administered intravenously at a dose of about 30 mg/kg once weekly for three weeks and then at a dose of 10 mg/kg administered intravenously every other week. [00186] In some embodiments, the FcRn antagonist is batoclimab. In some embodiments, batoclimab is administered subcutaneously or intravenously. In some embodiments, batoclimab is administered at a dose of about 0.2 mg/kg to about 200 mg/kg or at a fixed dose of about 20 mg to about 20,000 mg administered once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. [00187] In some embodiments, batoclimab is administered once weekly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00188] In some embodiments, batoclimab is administered once every two weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00189] In some embodiments, batoclimab is administered once every three weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00190] In some embodiments, batoclimab is administered once every four weeks at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00191] In some embodiments, batoclimab is administered once monthly at a dose of about 1 mg/kg, about 2 mg/kg, about 3 mg/kg, about 4 mg/kg, about 5 mg/kg, about 6 mg/kg, about 7 mg/kg, about 8 mg/kg, about 9 mg/kg, about 10 mg/kg, about 11 mg/kg, about 12 mg/kg, about 12.5 mg/kg, about 13 mg/kg, about 14 mg/kg, about 15 mg/kg, about 16 mg/kg, about 17 mg/kg, about 18 mg/kg, about 19 mg/kg, about 20 mg/kg, about 21 mg/kg, about 22 mg/kg, about 23 mg/kg, about 24 mg/kg, about 25 mg/kg, about 26 mg/kg, about 27 mg/kg, about 28 mg/kg, about 29 mg/kg, about 30 mg/kg, about 31 mg/kg, about 32 mg/kg, about 33 mg/kg, about 34 mg/kg, about 35 mg/kg, about 36 mg/kg, about 37 mg/kg, about 38 mg/kg, about 39 mg/kg, about 40 mg/kg, about 41 mg/kg, about 42 mg/kg, about 43 mg/kg, about 44 mg/kg, about 45 mg/kg, about 46 mg/kg, about 47 mg/kg, about 48 mg/kg, about 49 mg/kg, about 50 mg/kg, about 51 mg/kg, about 52 mg/kg, about 53 mg/kg, about 54 mg/kg, about 55 mg/kg, about 56 mg/kg, about 57 mg/kg, about 58 mg/kg, about 59 mg/kg, about 60 mg/kg, about 61 mg/kg, about 62 mg/kg, about 63 mg/kg, about 64 mg/kg, about 65 mg/kg, about 66 mg/kg, about 67 mg/kg, about 68 mg/kg, about 69 mg/kg, about 70 mg/kg, about 71 mg/kg, about 72 mg/kg, about 73 mg/kg, about 74 mg/kg, about 75 mg/kg, about 76 mg/kg, about 77 mg/kg, about 78 mg/kg, about 79 mg/kg, about 80 mg/kg, about 81 mg/kg, about 82 mg/kg, about 83 mg/kg, about 84 mg/kg, about 85 mg/kg, about 86 mg/kg, about 87 mg/kg, about 88 mg/kg, about 89 mg/kg, about 90 mg/kg, about 91 mg/kg, about 92 mg/kg, about 93 mg/kg, about 94 mg/kg, about 95 mg/kg, about 96 mg/kg, about 97 mg/kg, about 98 mg/kg, about 99 mg/kg, or about 100 mg/kg. [00192] In some embodiments, the method further comprises administering to the subject an additional therapeutic compound. In some embodiments, the method further comprises administering to the subject an effective amount of one or more of the following: an aldosterone analog, an α1-adrenergic agonist, an α2-adrenergic agonist, a beta-blocker, and an acetylcholinesterase inhibitor. In some embodiments, the method further comprises administering to the subject an effective amount of one or more of the following compounds: fludrocortisone, midodrine, clonidine, alpha-methyldopa, propranolol, metoprolol, and pyridostigmine. [00193] In an embodiment, the method further comprises administering to the subject an effective amount of a corticosteroid and/or an immunosuppressive agent. In an embodiment, the method further comprises administering to the subject an effective amount of a corticosteroid. In an embodiment, method further comprises administering to the subject an effective amount of a glucocorticoid. In an embodiment, the method further comprises administering to the subject an effective amount of a glucocorticoid intravenously and/or administering to the subject an effective amount of a glucocorticoid orally. In an embodiment, the method further comprises administering to the subject an effective amount of a glucocorticoid intravenously and administering to the subject an effective amount of a glucocorticoid orally. [00194] In an embodiment, the method further comprises administering to the subject an effective amount of prednisone. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 7.5 mg/day to 75 mg/day, to a maximum of 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 8 mg/day to 72 mg/day, to a maximum of 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 9 mg/day to 66 mg/day, to a maximum of 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 10 mg/day to 60 mg/day, to a maximum of 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 0.5 mg/kg/day to 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 0.6 mg/kg/day to 1 mg/kg/day. In an embodiment, the method further comprises administering to the subject prednisone at a dose of 0.6 mg/kg/day to 1 mg/kg/day, to a maximum of 80 mg/day. In an embodiment, the prednisone is administered orally. [00195] In an embodiment, the method further comprises administering to the subject an effective amount of methylprednisolone. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 100 mg to 1250 mg, for up to three days. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 150 mg to 1200 mg, for up to three days. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 200 mg to 1100 mg, for up to three days. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 500 mg to 1000 mg, for up to three days. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 0.25 g/day to 0.5 g/day. In an embodiment, the method further comprises administering to the subject methylprednisolone at a dose of 0.25 g/day to 0.5 g/day, for one to three days. In an embodiment, the methylprednisolone is administered intravenously. [00196] In an embodiment, the method further comprises administering to the subject an effective amount of prednisone orally and an effective amount of methylprednisolone intravenously. In an embodiment, the method further comprises administering to the subject prednisone orally at a dose of 10 mg/day to 60 mg/day, to a maximum of 1 mg/kg/day, and methylprednisolone intravenously at a dose of 500 mg to 1000 mg, for up to three days. In an embodiment, the method further comprises administering to the subject prednisone orally at a dose of 0.5 mg/kg/day to 1 mg/kg/day, and methylprednisolone intravenously at a dose of 500 mg to 1000 mg, for up to three days. In an embodiment, the method further comprises administering to the subject prednisone orally at a dose of 0.6 mg/kg/day to 1 mg/kg/day, to a maximum of 80 mg/day, and methylprednisolone intravenously at a dose of 0.25 g/day to 0.5 g/day, for one to three days. [00197] In an embodiment, the method further comprises administering to the subject an effective amount of a B-lymphocyte targeting biologic. Examples of B-lymphocyte targeting biologics include, without limitation, belimumab, rituximab, and obinutuzumab. In an embodiment, the method further comprises administering to the subject an effective amount of belimumab. In an embodiment, the method further comprises administering to the subject belimumab intravenously at a dose of 10 mg/kg once every two weeks for three doses, then once every four weeks for subsequent doses. In an embodiment, the method further comprises administering to the subject belimumab intravenously at a dose of 10 mg/kg once every two weeks for three doses, then once every four weeks for subsequent doses, and a mycophenolic acid analog. In an embodiment, the method further comprises administering to the subject belimumab intravenously at a dose of 10 mg/kg once every two weeks for three doses, then once every four weeks for subsequent doses, and cyclophosphamide. In an embodiment, the method further comprises administering to the subject belimumab intravenously at a dose of 10 mg/kg once every two weeks for three doses, then once every four weeks for subsequent doses, and cyclophosphamide at a dose of 500 mg once every two weeks for six months. In an embodiment, the method further comprises administering to the subject an effective amount of rituximab. In an embodiment, the method further comprises administering to the subject rituximab at a dose of 1 g on days 1 and 15 as add-on therapy for refractory cases or for corticosteroid minimization. In an embodiment, the method further comprises administering to the subject an effective amount of obinutuzumab. [00198] In an embodiment, when the subject is administered the FcRn antagonist, the dose of prednisone is tapered over 12 weeks to a dose of 7.5 mg/day. In an embodiment, the initial oral prednisone dose is at 0.5 mg/kg/day to 1 mg/kg/day, not to exceed 60 mg/day. [00199] In some embodiments, treatment of POTS is characterized by the subject exhibiting a reduction in the Composite Autonomic Symptom Score 31 (COMPASS 31) compared to a baseline COMPASS 31 score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 10% reduction in the COMPASS 31 score as compared to a baseline COMPASS 31 score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 20%, greater than 30%, greater than 40%, or greater than 50% reduction in COMPASS 31 score as compared to a baseline COMPASS 31 score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline COMPASS 31 score of about 35, 40, 45, 50, or 55. In some embodiments, the subject has a COMPASS 31 score less than or equal to 35, 40, 45, 50, or 55, following administration of the FcRn antagonist. In some embodiments, the COMPASS 31 score is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the COMPASS 31 score is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00200] In some embodiments, treatment of POTS is characterized by the subject exhibiting a reduction in the Malmӧ POTS Symptom Score (MaPS) compared to a baseline MaPS score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 10% reduction in the MaPS score as compared to a baseline MaPS score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 20%, greater than 30%, greater than 40%, or greater than 50% reduction in MaPS score as compared to a baseline MaPS score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline MaPS score of about 120, 110, 100, 90, 80, 70, 60, or 50. In some embodiments, the subject has a MaPS score less than or equal to 90, 80, 70, 60, 50, or 40, following administration of the FcRn antagonist. In some embodiments, the MaPS score is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the MaPS score is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00201] In some embodiments, treatment of POTS is characterized by the subject exhibiting a reduction in the Patient Global Impression of Severity (PGI-S) score, compared to a baseline PGI-S score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits a 1, 2, or 3 point reduction in the PGI-S score as compared to a baseline PGI-S score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline PGI-S score of 3 or 4. In some embodiments, the subject has a PGI-S score of 1, 2, or 3, following administration of the FcRn antagonist. In some embodiments, the PGI-S score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the PGI-S score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00202] In some embodiments, treatment of POTS is characterized by the subject exhibiting a reduction in the Patient Global Impression of Change (PGI-C) score, compared to a baseline PGI-C score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits a 1, 2, 3, 4, 5, or 6 point reduction in the PGI-C score as compared to a baseline PGI-C score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline PGI-C score of 2, 3, 4, 5, 6, or 7. In some embodiments, the subject has a PGI-C score of 1, 2, 3, 4, 5, or 6, following administration of the FcRn antagonist. In some embodiments, the PGI-C score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the PGI-C score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00203] In some embodiments, treatment of POTS is characterized by the subject exhibiting a reduction in the Patient-Reported Outcomes Measurement Information System (PROMIS) Fatigue Short Form 8a score, compared to a baseline PROMIS Fatigue Short Form 8a score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the PROMIS Fatigue Short Form 8a score is a raw PROMIS Fatigue Short Form 8a score. In some embodiments, the PROMIS Fatigue Short Form 8a score is a PROMIS Fatigue Short Form 8a T-score. In some embodiments, the subject exhibits greater than 10% reduction in the PROMIS Fatigue Short Form 8a score as compared to a baseline PROMIS Fatigue Short Form 8a score from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 20%, greater than 30%, greater than 40%, or greater than 50% reduction in PROMIS Fatigue Short Form 8a score as compared to a baseline PROMIS Fatigue Short Form 8a score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline PROMIS Fatigue Short Form 8a T-score of greater than 40, 45, 50, 55, 60, 65, 70, or 75. In some embodiments, the subject has a PROMIS Fatigue Short Form 8a T-score of less than 70, 65, 60, 55, 50, 45, 40, or 35, following administration of the FcRn antagonist. In some embodiments, the PROMIS Fatigue Short Form 8a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the PROMIS Fatigue Short Form 8a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00204] In some embodiments, treatment of POTS is characterized by the subject exhibiting an increase in the PROMIS Cognitive Function Short Form 6a score, compared to a baseline PROMIS Cognitive Function Short Form 6a score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the PROMIS Cognitive Function Short Form 6a score is a raw PROMIS Cognitive Function Short Form 6a score. In some embodiments, the PROMIS Cognitive Function Short Form 6a score is a the PROMIS Cognitive Function Short Form 6a T-score. In some embodiments, the subject exhibits greater than 10% increase in the PROMIS Cognitive Function Short Form 6a score as compared to a baseline PROMIS Cognitive Function Short Form 6a score from the subject prior to administering the FcRn antagonist. In some embodiments, the subject exhibits greater than 20%, greater than 30%, greater than 40%, or greater than 50% increase in PROMIS Cognitive Function Short Form 6a score as compared to a baseline PROMIS Cognitive Function Short Form 6a score obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the subject has a baseline PROMIS Cognitive Function Short Form 6a T-score of less than 55, 50, 45, 40, 35, 30 or 25. In some embodiments, the subject has a PROMIS Cognitive Function Short Form 6a T-score of greater than 30, 35, 40, 45, 50, 55, or 60, following administration of the FcRn antagonist. In some embodiments, the PROMIS Cognitive Function Short Form 6a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. In some embodiments, the PROMIS Cognitive Function Short Form 6a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following an initial administration of the FcRn antagonist. [00205] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of a serum autoantibody that is reduced as compared to a baseline level of the serum autoantibody obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the serum autoantibody is reduced by at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or 100%, as compared to the baseline level of the serum autoantibody obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the serum autoantibody is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post-administration level of the serum autoantibody is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. In some embodiments, the serum autoantibody is a G-protein- coupled receptor autoantibody. In some embodiments, the autoantibody is a muscarinic acetylcholine receptor (AChR) autoantibody or an adrenergic receptor autoantibody. In some embodiments, the muscarinic AChR receptor autoantibody is selected from an anti-M1 autoantibody, an anti-M2 autoantibody, an anti-M3 autoantibody, an anti-M4 autoantibody, an anti-M5 autoantibody, or any combination thereof. In some embodiments, the autoantibody is a ganglionic AChR receptor autoantibody. In some embodiments, the adrenergic receptor autoantibody is selected from an anti-α1AR autoantibody, an anti-α2AR autoantibody, an anti- β1AR autoantibody, an anti-β2AR autoantibody, or any combination thereof. [00206] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of a SARS-CoV-2 antibody that is reduced as compared to a baseline level of the SARS-CoV-2 antibody obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the SARS-CoV-2 antibody is reduced by at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or 100%, as compared to the baseline level of the SARS-CoV-2 antibody obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the SARS-CoV-2 antibody is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post-administration level of the SARS-CoV-2 antibody is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. [00207] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of a serum complement that is reduced as compared to a baseline level of the serum complement obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the serum complement is reduced by at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or 100%, as compared to the baseline level of the serum complement obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of the serum complement is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post-administration level of the serum complement is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. In some embodiments, the serum complement is selected from the group consisting of C3, C4, CH50, and C1q-binding circulating immune complexes. [00208] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of circulating immune complexes that is reduced as compared to a baseline level of circulating immune complexes obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the circulating immune complexes are selected from the group consisting of C3, C4, CH50, and C1q-binding circulating immune complexes. In some embodiments, the post-administration level of circulating immune complexes is reduced by at least 10%, at least 25%, at least 50%, at least 75%, at least 80%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%, as compared to the baseline level of circulating immune complexes obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post- administration level of circulating immune complexes is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post- administration level of circulating immune complexes is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. [00209] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of serum IgG that is reduced as compared to a baseline level of serum IgG obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of serum IgG is reduced by at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or 100%, as compared to the baseline level of serum IgG obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post- administration level of serum IgG is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post- administration level of serum IgG is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. [00210] In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of cytokine or inflammatory biochemical that is reduced as compared to a baseline level of cytokine or inflammatory biochemical obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post- administration level of cytokine or inflammatory biochemical is reduced by at least 10%, at least 20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, or 100%, as compared to the baseline level of cytokine or inflammatory biochemical obtained from the subject prior to administering the FcRn antagonist. In some embodiments, the post-administration level of cytokine or inflammatory biochemical is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post-administration level of cytokine or inflammatory biochemical is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. In some embodiments, the cytokine or inflammatory biochemical is selected from the group consisting of IL 1β, IL 21, TNFα, IFNα, CD30, CD40 L, CCL5, CRP, and ferritin. [00211] In some embodiments, after administering the FcRn antagonist to the subject, the level of albumin is not decreased in the subject following administration of the FcRn antagonist compared to a baseline level of albumin. In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of albumin that is not decreased as compared to a baseline level of albumin obtained from the subject prior to administering the FcRn antagonist. In an embodiment, an albumin reduction of less than about 1%, 2%, 3%, 4%, or 5% compared to baseline albumin level is observed. In an embodiment, an albumin reduction of less than about 10% compared to baseline albumin level is observed. In some embodiments, the post-administration level of albumin is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post-administration level of albumin is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. [00212] In some embodiments, after administering the FcRn antagonist to the subject, the level of serum albumin is not reduced in the subject following administration of the FcRn antagonist compared to a baseline level of serum albumin. In some embodiments, after administering the FcRn antagonist to the subject, the subject exhibits a post-administration level of serum albumin that is not reduced as compared to a baseline level of serum albumin obtained from the subject prior to administering the FcRn antagonist. In an embodiment, a serum albumin reduction of less than about 1%, 2%, 3%, 4%, or 5% compared to baseline serum albumin level is observed. In an embodiment, a serum albumin reduction of less than about 10% compared to baseline serum albumin level is observed. In some embodiments, the post-administration level of serum albumin is measured 4 weeks, 12 weeks, or 24 weeks after administering the FcRn antagonist to the subject. In some embodiments, the post- administration level of serum albumin is measured 4 weeks, 12 weeks, or 24 weeks after an initial administration of the FcRn antagonist to the subject. [00213] In an embodiment, the subject is any human or non-human animal. In an embodiment, the subject is a human or non-human mammal. In an embodiment, the subject is a human. EXAMPLES [00214] The following examples are offered by way of illustration, and not by way of limitation. Example 1: Investigation of efficacy and safety of efgartigimod in adult patients with post-COVID-19 postural orthostatic tachycardia syndrome (POTS) [00215] POTS in patients who continue to have long-lasting symptoms after recovery from the initial SARS-CoV-2 infection has been identified in several case reports. A POTS diagnosis is based on evaluations for excessive orthostatic tachycardia (sustained heart rate [HR] increment of not less than 30 beats/minute [bpm] within 10 minutes of standing or head- up tilt [≥40 bpm in 12 to 19 year olds]); absence of orthostatic hypotension; frequent symptoms of orthostatic intolerance during standing, with rapid improvement upon return to a supine position; duration of symptoms for ≥3 months; and absence of other conditions explaining sinus tachycardia. Patients who develop POTS after COVID-19 are designated in this study as having post-COVID-19 POTS. [00216] Currently, the underlying pathophysiology and effective treatments are unknown for post-COVID-19 POTS. Pharmacologic therapy mainly focuses on orthostatic symptoms, targeting blood volume expansion and stabilizing HR and blood pressure; however, POTS may be related to immune dysfunction and autoimmunity preceded by infection. Several infectious pathogens may be associated with the development of POTS, including SARS-CoV- 2. Patients with POTS have a higher prevalence of autoantibodies, including ganglionic AChR antibody G-protein coupled receptor (GPCR) antibodies, which could increase sympathetic tone by activating adrenergic receptors. Patients with POTS have been shown to have higher levels of these autoantibodies than healthy subjects. The binding of these autoantibodies to adrenergic receptors has been hypothesized to cause tachycardia in some patients. These autoantibodies, acting as partial agonists, are thought to decrease the effectiveness of peripheral norepinephrine leading to an increased sympathetic response to posture resulting in postural tachycardia in the absence of hypotension. [00217] Collectively, these data suggest that post-COVID-19 POTS could be caused by IgG autoantibodies that induce autonomic dysfunction. The aim of this phase 2 study is to evaluate if efgartigimod is safe and efficacious in treating the autonomic symptoms and clinical manifestations of autonomic dysfunction in patients diagnosed with POTS after COVID-19. A. Study design Overall design [00218] This is a randomized, double-blinded, placebo-controlled, parallel-group, phase 2 study. The total study duration is approximately 36 weeks comprising: - Screening period of approximately 4 weeks - Treatment period of 24 weeks - Follow-up period of approximately 8 weeks (60 days) for participants who do not roll over to an open-label extension (OLE) study. [00219] The study population is adult patients with new-onset POTS post-COVID-19. Participants will be randomized to receive efgartigimod IV 10 mg/kg or matching placebo in a 2:1 ratio, respectively. IMP (efgartigimod or matching placebo) is administered during the treatment period in an approximately 1-hour IV infusion once weekly by site staff or a home nurse. At week 24, eligible participants may roll over into a single-arm OLE. Selection of primary and secondary endpoints [00220] This study aims to evaluate the efficacy and safety of weekly infusions of efgartigimod IV 10 mg/kg compared to matched-placebo IV in adult participants with post- COVID-19 POTS. The study design is randomized, double-blinded, and placebo-controlled to evaluate the effect of efgartigimod administered as an IV infusion compared to placebo. The study consists of a treatment period where all participants will receive weekly IV infusions for 24 weeks. As there are no standardized approved therapies for post-COVID-19 POTS, the comparison to placebo is justified. [00221] The primary endpoints are the safety and tolerability of efgartigimod in participants with post-COVID-19 POTS and efficacy as assessed by change from baseline to week 24 in COMPASS 31 and the MaPS. Safety and tolerability are included as a primary endpoint as efgartigimod has not been previously administered in this patient population. [00222] COMPASS 31 is a quantitative measure of autonomic symptoms developed for use in autonomic research and clinical practice (Sletten DM, et al., Mayo Clin Proc. 2012; 87(12):1196-1201). It is a self-rated questionnaire with 31 questions in 6 domains (orthostatic intolerance, vasomotor, secretomotor, gastrointestinal, bladder, and pupillomotor). [00223] The MaPS score, recently reported by Fedorowski and colleagues, is a dedicated POTS symptom scoring questionnaire (Johansson M, et al., JACC Case Rep. 2021; 3(4):573- 580). The score consists of 12 questions that assess symptom burden related and unrelated to orthostatic intolerance (related: tachycardia, palpitations, dizziness, presyncope; unrelated: gastrointestinal (GI) symptoms, insomnia, concentration difficulties). [00224] The COMPASS 31 and MaPS questionnaires were chosen to provide a comprehensive assessment of autonomic (COMPASS 31) and POTS-specific symptoms (MaPS). COMPASS 31 is a validated measure of autonomic symptoms in a common disease of dysautonomia, small fiber polyneuropathy. Prior studies in patients with POTS support the ability of this assessment to measure autonomic symptom burden in patients relative to controls and over time. Elevations in COMPASS 31 have also been found in patients post-COVID-19 with evidence of POTS and other forms of dysautonomia. The MaPS questionnaire was developed specifically for patients with POTS by investigators at the Skåne University Hospital, Lund University in Malmö, Sweden. The 12-item evaluation score is being evaluated in a case-control study in patients with POTS compared to healthy controls (A. Fedorowski, unpublished data, 2022). MaPS is expected to provide an accurate assessment of POTS symptoms over time. Further validation of the score will be accomplished by its comparison to COMPASS 31 and the other measures included in this study. [00225] All secondary endpoints complement the primary efficacy endpoints and provide additional information on efficacy, including measures of patients’ assessment of disease severity and change over time (PGI-S and PGI-C) and an established assessment of fatigue (PROMIS Fatigue), which is a common symptom among patients with POTS. End of study [00226] The end of study is defined as the date of the last participant’s last visit. A participant will have completed the study if the treatment period (or follow-up period, if applicable) has been completed. - Participants rolling over to the OLE study will have completed this study at week 24. - Participants not rolling over to the OLE study will have completed this study after the safety follow-up visit (SFV) or early discontinuation visit (EDV), as applicable. B. Study population [00227] Prospective approval of protocol deviations to recruitment and enrollment criteria, also known as protocol waivers or exemptions, is not permitted. Inclusion criteria [00228] Participants are eligible for study inclusion only if all of the following criteria apply: - Reached age of consent when signing the informed consent form; - Capable of giving signed informed consent, which includes compliance with the requirements and restrictions listed in the informed consent form and this protocol; - Diagnosed with new-onset POTS post-COVID-19 established by the following: o Prior COVID-19 confirmed by documentation of historical PCR test; o Tilt table or orthostatic vital sign measurements during screening consistent with consensus criteria: sustained HR increase of ≥30 bpm within 10 min of standing or head-up tilt (≥40 bpm for individuals aged 18 to 19 years) and/or HR reaching >120 bpm within 10 min; absence of sustained 20 mmHg decrease in systolic blood pressure (SBP); o Ongoing symptoms of POTS confirmed by the investigator with at least 3 symptoms in each of the following areas lasting longer than 12 weeks after either diagnosis of COVID-19 or after hospital discharge for COVID-19: ^ Vasomotor symptoms: fatigue, orthostatic intolerance, brain fog, exertional dyspnea, difficulty with concentration, venous pooling, and exercise intolerance; ^ Sympathetic over-compensation symptoms: palpitation, heat intolerance, nausea with or without vomiting, insomnia, anxiety, lack of appetite, chest pain, and diaphoresis; - COMPASS 31 ≥35 at screening; - Agree to use contraceptives consistent with local regulations regarding the methods of contraception for those participating in clinical studies and the following: o Female participants of childbearing potential must have a negative serum pregnancy test at screening and a negative urine pregnancy test at baseline before receiving IMP; - Body mass index (BMI) <35 kg/m². Exclusion criteria [00229] Participants are excluded from the study if any of the following criteria apply: - Diagnosis of or receiving treatment for the following conditions before COVID-19: peripheral neuropathy, POTS, myalgic encephalomyelitis encephalitis/chronic fatigue syndrome, Ehlers-Danlos syndrome confirmed by genetic testing, autonomic neuropathy, multiple sclerosis, stroke, spinal cord injury, or any known lesions in the central nervous system by imaging or neurological exam; - History of or currently being treated for clinically significant ongoing cardiac arrythmia, heart failure, myocarditis, pulmonary embolism requiring anticoagulation, pulmonary fibrosis, or critical illness-related polyneuropathy or myopathy; - Known autoimmune disease that, in the investigator’s judgment, would interfere with an accurate assessment of clinical symptoms of post-COVID-19 POTS or puts the participant at undue risk; - Known HIV disease or common variable immunodeficiency; - History of malignancy unless considered cured by adequate treatment with no evidence of recurrence for ≥3 years before the first administration of IMP. Adequately treated participants with the following cancers may be included at any time: o Basal cell or squamous cell skin cancer; o Carcinoma in situ of the cervix; o Carcinoma in situ of the breast; o Incidental histological finding of prostate cancer (TNM stage T1a or T1b); - Clinically significant uncontrolled active or chronic bacterial, viral, or fungal infection or positive SARS-CoV-2 PCR test at screening; - Positive serum test at screening for an active infection with any of the following: o Hepatitis B virus (HBV) that is indicative of an acute or chronic infection, unless associated with a negative HB surface antigen (HBsAg) or negative HBV DNA test; o Hepatitis C virus (HCV) based on HCV antibody assay unless a negative RNA test is available; o HIV; - A medical condition that could confound the results of the study or put the participant at undue risk in the investigator’s judgment; - Clinically significant disease, recent major surgery (within 3 months of screening), or intends to have surgery during the study; or any other condition that in the opinion of the investigator could confound the results of the study or put the participant at undue risk; - Total IgG <4 g/L at screening; - Received within 12 weeks or 5 half-lives (whichever is longer) before screening an investigational product; - Received within 12 weeks before screening either intravenous immunoglobulin (Ig) IV or SC or plasmapheresis/plasma exchange (PLEX); - Received a live or live-attenuated vaccine less than 4 weeks before screening; - Known hypersensitivity to IMP or 1 of its excipients; - Previously participated in an efgartigimod clinical study and received at least 1 dose of IMP; - Currently participating in another interventional clinical study; - History (within 12 months of screening) of or current alcohol, drug, or medication abuse; - Pregnant or lactating or intends to become pregnant during the study; - Unwilling to remain on a stable regimen of medications during the study; - Unwilling to avoid initiation of new physical rehabilitation or other physician- prescribed exercise programs during the 24-week treatment period. C. IMP(s) and concomitant therapy [00230] Investigational medicinal product (IMP) is defined as any investigational intervention(s), marketed product(s), placebo, or medical device(s) intended to be administered to a study participant according to the study protocol. IMP(s) administered [00231] The IMP in this study includes efgartigimod IV and matching placebo (with the same formulation but without the active ingredient of efgartigimod), as described in Table S1: Table S1. IMP(s) administered

[00232] The 10 mg/kg efgartigimod dose is based on body weight, and the maximum total dose per efgartigimod infusion is 1200 mg for participants who weigh ≥120 kg. The dose level will be recalculated for bodyweight changes of ±10%. [00233] Any medication or vaccine (including over-the-counter or prescription medicines, vitamins, and/or herbal supplements) that the participant receives within 30 days of signing the informed consent form (ICF) or receives during the study participation must be recorded. Prohibited medications [00234] The following medications/treatments are prohibited while the participant receives IMP: - Subcutaneous or intravenous immunoglobulin; - PLEX; - Live or live-attenuated vaccines; - IV saline bolus treatments for volume expansion for treating POTS symptoms.

⁰ ₇ 1_. 8₂ 1₈ 3₈ 0₃

¹ ₇ 1_. 8₂ 1₈ 3₈ 0₃

² ₇ 1_. 8₂ 1₈ 3₈ 0₃

³ ₇ 1_. 8₂ 1₈ 3₈ 0₃

Questionnaires 00235] Questionnaires are administered before any other study assessment and may be ompleted up to 1 day before the visit. COMPASS 31 00236] COMPASS 31 is an easily scored questionnaire to evaluate the severity and istribution of autonomic symptoms in various autonomic nerve disorders, providing clinically elevant scores of autonomic symptom severity. The questionnaire is based on the well-established 69-item Autonomic Symptom Profile (ASP) and the validated 84-question scoring instrument,he Composite Autonomic Symptom Score (COMPASS). The COMPASS 31 questionnaire has een previously used to assess patients with POTS. 00237] The 31-item questionnaire requires approximately 10 minutes to administer and ddresses 6 domains: orthostatic intolerance, vasomotor, secretomotor, bladder, pupillomotor, and astrointestinal-mixed upper and diarrhea. 00238] Higher scores indicate a more severe degree of autonomic symptoms. MaPS 00239] The MaPS has been developed to assess the severity of the most common symptoms ound in patients with POTS based on clinical experience and literature (A. Fedorowski, npublished data, 2022). The score consists of 12 questions that assess symptom burden related tachycardia, palpitations, dizziness, presyncope) and unrelated to orthostatic intolerance (GI ymptoms, insomnia, concentration difficulties). 00240] Participants grade their symptoms for the past 7 days using a visual analog scale VAS) ranging from 0 (no symptoms) to 10 (worst possible). The maximum score is 120 points, with higher scores indicating more severe symptoms. In general, patients with POTS score >40 oints, whereas healthy controls have lower values. A score >90 points indicates ebilitating/severe symptoms. PGI-S and PGI-C 00241] The PGI-S and PGI-C questionnaires are simple, valid, participant-rated, single-tem global measures of their perceived condition. PGI-S: severity of disease symptoms over the ast 7 days are rated on a 4-point Likert scale, with scores ranging from 1 (no symptoms) to 4 severe). PGI-C: change in the overall status from the beginning of the study to timepoint is rated n a 7-point Likert scale, with scores ranging from 1 (much better) to 7 (much worse). PROMIS 00242] PROMIS is a publicly available system of highly reliable, precise patient-reported ealth status measures of physical, mental, and social well-being. PROMIS instruments measure oncepts, including pain, fatigue, and physical function. 00243] PROMIS Fatigue Short Form 8a: assesses the impact and perceived fatigue duringhe last 7 days. This validated 8-question scale has 5 response options, with scores ranging from 1o 5. Scores are converted to a T-score, and higher scores indicate higher fatigue levels. A decreasen score (negative change from baseline) indicates improvement in fatigue. 00244] PROMIS Cognitive Function Short Form 6a: assesses the frequency of cognitive ifficulties experienced in the past 7 days. The questionnaire comprises 6 questions on subjective ognitive difficulties regarding a patient’s concentration, memory, language, mental acuity, and erceived changes in cognitive functioning. The participant marks their response on a 5-point Likert scale, with lower scores indicating worse perceived cognitive functioning. Exit Interview 00245] Trained independent moderators interview approximately 15 to 20 participants overhe telephone within 14 days after the week 24 visit. Participants respond to open-ended questions n their experience with post-COVID-19 POTS and provide their perspectives on the relevance, ompleteness, and comprehensibility of questionnaires implemented during the study. Participation in the interview is optional. 6MWT 00246] The 6MWT measures the distance walked in 6 minutes. Data can also be collected n the participant’s blood oxygen saturation and perception of dyspnea during exertion. The tests conducted following guidelines established by the American Thoracic Society. Quantitative autonomic testing 00247] Quantitative autonomic testing evaluates disorders associated with autonomic ervous system dysfunction. The tests are fully quantitative and clinically validated and include eep breathing, Valsalva maneuver, head-up tilt, and active stand for this study. The participant erforms these tests during the morning. 00248] Head-up tilt test stimulates the autonomic nervous system with orthostatic stress by assive movement from supine to upright tilt to evaluate adrenergic function. 00249] Active stand test detects autonomic dysfunction, variants of orthostatic ypotension, POTS, and orthostatic hypertension. 00250] Deep breathing tests cardiac parasympathetic functions, evaluating changes in thenstant HR provoked by “deep” breathing at 6 breaths/min. The test is performed with the articipant supine and relaxed. RSA amplitude is defined as the difference in HRs measured etween the end of expiration and the end of inspiration. 00251] Valsalva maneuver evaluates the sympathetic adrenergic functions using the blood ressure responses and parasympathetic functions using HR responses. Valsalva maneuver onsists of forced expiration against the resistance with the expiratory pressure during strain at 40 mmHg for 15 seconds. The test is performed with the participant supine and relaxed. Cutaneous Nerve/Skin Biopsy 00252] Optional cutaneous nerve skin biopsies may be taken from participants who have rovided additional consent to the procedure. Each biopsy is a punch biopsy of approximately 3 mm in size and will be obtained from the skin tissue of the leg unilaterally. The biopsy samples re processed and stained to evaluate intraepidermal small fiber density and sudomotornnervation, which is a postganglionic sympathetic fiber. The test is quantitative and normative alues exist based on sex and age. E. Pharmacokinetics 00253] Blood samples for PK analysis are collected at the time points described in Table S2 predose (within the 2 hours before IMP infusion) and within the 30 minutes after the end of thenfusion. Efgartigimod serum concentrations are determined using a validated method. F. Pharmacodynamics 00254] Blood samples for determination of total IgG levels in serum for PD evaluation are ollected at the time points described in Table S2 predose (within the 2 hours before IMPnfusion). Total IgG levels are determined using validated methods at a central laboratory. G. Biomarkers 00255] Serum, plasma, and whole blood samples are collected at the time points describedn Table S2 to identify putative biomarkers and explore their relationship with clinical effects. These analyses are exploratory as no biomarker has been validated for post-COVID-19 POTS. Immunological profiling 00256] The impact of efgartigimod treatment on immune parameters will confirm the drug mode of action, identify previously unknown pathways and drug targets, and define molecular and ellular biomarkers associated with treatment response. 00257] Specific analyses may include: Serum autoantibodies and SARS-CoV-2 antibodies; Chemokines, cytokines, and other inflammatory biochemical biomarkers; Single-cell RNA sequencing. Serum autoantibodies and SARS-CoV-2 antibodies 00258] In the absence of validated assays for detecting autoantibodies in post-COVID-19 POTS, explorative serum sample analyses will be performed. These assays may include, but are ot limited to, ELISA-based assays and functional cell-based bioassays. Such functional assays rovide a highly specific platform appropriate for identifying (dys-)functional antibodies in omplex biological samples. Serum samples may be used to conduct autoantibody discovery nalyses, e.g., phage-display screening, and evaluate the association of newly identified utoantibodies and clinical outcomes. SARS-CoV-2 antibody levels are analyzed to enrich thenterpretation of autoimmune responses in participants with post-COVID-19 POTS. Chemokines, cytokines, and other inflammatory biochemical biomarkers 00259] Abnormal concentrations were observed in inflammatory cytokines in patients with POTS who have elevated G-protein-coupled receptor autoantibodies. Inflammatory biomarker nalysis includes, but may not be limited to, IL 1β, IL 21, TNFα, IFNα, CD30, CD40 L, CCL5 RANTES), CRP, and ferritin. Single-cell RNA sequencing 00260] Longitudinal single-cell RNA sequencing is used to assess changes in transcription rofiles and examine the cellular heterogeneity of the immune system, T- and B-cell repertoire iversity, antigen specificity, and inflammatory markers at single-cell resolution over time ompared to baseline. These analyses characterize the cellular pathological mechanism by nvestigating cellular differentiation and interactions, identifying large cell type-based markers and athways for understanding the pathogenic, autoimmune events in post-COVID-19 POTS. Further, such markers may aid in designing innovative patient-centric, molecular pathology-driven linical studies. 00261] Peripheral blood mononuclear cells collected and isolated from whole blood are nalyzed. H. Immunogenicity assessments 00262] Blood samples are collected predose (within the 2 hours before IMP infusion) athe time points described in Table S2 to evaluate the serum levels of ADA against efgartigimod. 00263] Samples are analyzed by the designated laboratory in a tiered approach using alidated immunogenicity assays. Initially, samples are screened for a positive assay response (tier ). Screened positive samples are then tested in a confirmation assay (tier 2). Finally, a titration ofhe ADA response is performed in positive tier 2 samples to characterize the magnitude of the ntibody response (tier 3). . Health economics or medical resource utilization and health economics 00264] The PROMIS Global Health Scale (GHS) is a quality-of-life questionnaire that measures global physical health (GPH) and global mental health (GMH). The questionnaire omprises 10 questions on overall physical health, physical function, pain, and fatigue (GPH), uality of life, mental health, satisfaction with social activities, and emotional problems (GMH). The participant marks their response on a 5-point Likert scale, with lower scores indicating poorer ealth. 00265] The EQ-5D-5L questionnaire is a standardized test recognized by many health uthorities as a generic measure of health status for clinical and economic appraisal. The escriptive system comprises 5 dimensions: mobility, self-care, usual activities, pain/discomfort, nd anxiety/depression. Scores for each dimension include 5 levels: no problem, slight problem, moderate problem, severe problem, extreme problem. 00266] A visual analog scale (VAS) is included in the EQ-5D-5L. Participants mark their ealth status from 0 (the worst health you can imagine) to 100 (the best health you can imagine). . Objectives and endpoints Table S3. Objectives and endpoints

* * * 00267] The invention is not to be limited in scope by the specific embodiments described erein. Indeed, various modifications of the invention in addition to those described will become pparent to those skilled in the art from the foregoing description and accompanying figures. Such modifications are intended to fall within the scope of the appended claims.

Claims

Claims . A method of treating postural orthostatic tachycardia syndrome (POTS) in a subject in needhereof, the method comprising administering to the subject an effective amount of a human eonatal Fc receptor (FcRn) antagonist. . The method of claim 1, wherein the FcRn antagonist comprises two, three, or four FcRn inding regions. . The method of claim 1 or 2, wherein the FcRn antagonist comprises or consists of a variant Fc region or FcRn binding fragment thereof. . The method of claim 3, wherein the variant Fc region or FcRn binding fragment thereof inds to FcRn with a higher affinity at pH 6.0 as compared to a corresponding wild-type Fc region. . The method of claim 3 or 4, wherein the variant Fc region or FcRn binding fragment thereof inds to FcRn with a higher affinity at pH 7.4 as compared to a corresponding wild-type Fc region. . The method of any one of claims 3-5, wherein the variant Fc region comprises or consists f a first Fc domain and a second Fc domain which form a homodimer or heterodimer. . The method of claim 6, wherein the first Fc domain and/or the second Fc domain comprise mino acids Y, T, E, K, and F at EU positions 252, 254, 256, 433, and 434, respectively. . The method of claim 6 or 7, wherein the first Fc domain and/or the second Fc domain omprise amino acids Y, T, E, K, F, and Y at EU positions 252, 254, 256, 433, 434, and 436, espectively. . The method of any one of claims 6-8, wherein the first Fc domain and/or the second Fc omain comprise an amino acid sequence independently selected from the group consisting of SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 20, and SEQ ID NO: 21.

0. The method of any one of claims 6-9, wherein the first Fc domain and the second Fc domain omprise an amino acid sequence independently selected from the group consisting of SEQ ID NO: 2, SEQ ID NO: 3, SEQ ID NO: 20, and SEQ ID NO: 21. 1. The method of any one of claims 1-10, wherein the FcRn antagonist is efgartigimod. 2. The method of claim 1 or 2, wherein the FcRn antagonist is an anti-FcRn antibody. 3. The method of any one of claims 1-12, wherein the FcRn antagonist is administered to the ubject at a fixed dose of 20 mg to 20,000 mg or at a dose of 0.2 mg/kg to 200 mg/kg. 4. The method of any one of claims 1-13, wherein the FcRn antagonist is administeredntravenously once weekly or once every two weeks. 5. The method of claim 14, wherein the FcRn antagonist is administered intravenously at a ose of from 2 mg/kg to 200 mg/kg once weekly or once every two weeks. 6. The method of claim 14 or 15, wherein the FcRn antagonist is administered intravenously t a dose of 3 mg/kg to 60 mg/kg once weekly or once every two weeks. 7. The method of any one of claims 14-16, wherein the FcRn antagonist is administeredntravenously at a dose of 10 mg/kg to 30 mg/kg once weekly or once every two weeks. 8. The method of any one of claims 14-17, wherein the FcRn antagonist is administeredntravenously at a dose of 10 mg/kg once weekly or once every two weeks. 9. The method of any one of claims 14-17, wherein the FcRn antagonist is administeredntravenously at a dose of 25 mg/kg once weekly or once every two weeks.

0. The method of any one of claims 1-13, wherein the FcRn antagonist is administered ubcutaneously once weekly, once every two weeks, once every three weeks, once every four weeks, once monthly, or once every six weeks. 1. The method of claim 20, wherein the FcRn antagonist is administered subcutaneously at a ixed dose of 200 mg to 20,000 mg once weekly, once every two weeks, once every three weeks, nce every four weeks, once monthly, or once every six weeks.

2. The method of claim 20 or 21, wherein the FcRn antagonist is administered subcutaneously t a fixed dose of 750 mg to 3000 mg once weekly, once every two weeks, once every three weeks, nce every four weeks, once monthly, or once every six weeks.

3. The method of any one of claims 20-22, wherein the FcRn antagonist is administered ubcutaneously at a fixed dose of 1000 mg or 2000 mg once weekly or once every two weeks.

4. The method of any one of claims 1-23, wherein the FcRn antagonist is administered for 24 weeks or less.

5. The method of any one of claims 1-23, wherein the FcRn antagonist is administered for ateast 24 weeks.

6. The method of any one of claims 1-23, wherein the FcRn antagonist is administered for 52 weeks or less.

7. The method of any one of claims 1-23, wherein the FcRn antagonist is administered for ateast 52 weeks.

8. The method of any one of claims 1-27, wherein the subject has one or more symptoms elected from the group consisting of fatigue, orthostatic intolerance, brain fog, exertional dyspnea, ifficulty with concentration, venous pooling, exercise intolerance, palpitation, heat intolerance, ausea with or without vomiting, insomnia, anxiety, lack of appetite, chest pain, and diaphoresis.

9. The method of any one of claims 1-28, wherein the subject was diagnosed with POTS ollowing an infection. 0. The method of any one of claims 1-29, wherein the subject was diagnosed with POTS ollowing a COVID-19 infection. 1. The method of any one of claims 1-30, wherein the subject shows a reduction in the Composite Autonomic Symptom Score 31 (COMPASS 31) or the Malmӧ POTS Symptom Score MaPS) following administration of the FcRn antagonist, compared to a baseline value. 2. The method of claim 31, wherein the COMPASS 31 or the MaPS is measured 2 weeks, 4 weeks, 8 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. 3. The method of claim 31 or 32, wherein the subject has a COMPASS 31 less than or equalo 35, 40, 45, 50, or 55, following administration of the FcRn antagonist. 4. The method any one of claims 31-33, wherein the baseline value is a COMPASS 31 of bout 35, 40, 45, 50, or 55. 5. The method of claim 31 or 32, wherein the subject has a MaPS less than or equal to 90, 80, 0, 60, 50, or 40, following administration of the FcRn antagonist. 6. The method of claim 31, 32, or 35, wherein the baseline value is a MaPS of about 120, 110, 00, 90, 80, 70, 60, or 50. 7. The method of any one of claims 1-36, wherein the subject shows a reduction in Patient Global Impression of Severity (PGI-S) score, Patient Global Impression of Change (PGI-C) score, nd/or Patient-Reported Outcomes Measurement Information System (PROMIS) Fatigue Short Form 8a score, or an increase in PROMIS Cognitive Function Short Form 6a score following dministration of the FcRn antagonist, compared to a baseline value.

8. The method of claim 37, wherein the PGI-S score, the PGI-C score, the PROMIS Fatigue Short Form 8a score, or the PROMIS Cognitive Function Short Form 6a score is measured 2 weeks, 4 weeks, 12 weeks, 18 weeks, or 24 weeks following administration of the FcRn antagonist. 9. The method of claim 37 or 38, wherein the subject has a PGI-S score of 1, 2, or 3, following dministration of the anti-FcRn antagonist. 0. The method of any one of claims 37-39, wherein the baseline value is a PGI-S score of 3 r 4. 1. The method of claim 37 or 38, wherein the subject has a PGI-C score of 1, 2, 3, 4, 5, or 6, ollowing administration of the FcRn antagonist. 2. The method of claim 37, 38, or 41, wherein the baseline value is a PGI-C score of 2, 3, 4, , 6, or 7. 3. The method of claim 37 or 38, wherein the subject has a PROMIS Fatigue Short Form 8a T-score of less than 70, 65, 60, 55, 50, 45, 40, or 35, following administration of the FcRn ntagonist. 4. The method of claim 37, 38, or 43, wherein the baseline value is a PROMIS Fatigue Short Form 8a T-score of greater than 40, 45, 50, 55, 60, 65, 70, or 75. 5. The method of claim 37 or 38, wherein the subject has a PROMIS Cognitive Function Short Form 6a T-score of greater than 30, 35, 40, 45, 50, 55, or 60, following administration of the FcRn antagonist. 6. The method of claim 37, 38, or 45, wherein the baseline value is a PROMIS Cognitive Function Short Form 6a T-score of less than 55, 50, 45, 40, 35, 30, or 25.

7. The method of any one of claims 1-46, wherein the subject shows a reduction in a serumevel of total IgG, an autoantibody, a SARS CoV-2 antibody, a cytokine, or an inflammatory iochemical following administration of the FcRn antagonist, compared to a baseline value. 8. The method of claim 47, wherein the serum level of total IgG, an autoantibody, a SARS CoV-2 antibody, a cytokine, or an inflammatory biochemical is measured 4 weeks, 12 weeks, or 4 weeks following administration of the FcRn antagonist. 9. The method of claim 47 or 48, wherein the autoantibody is a G-protein-coupled receptor utoantibody. 0. The method of any one of claims 47-49, wherein the autoantibody is a muscarinic cetylcholine receptor (AChR) autoantibody or an adrenergic receptor autoantibody. 1. The method of claim 50, wherein the muscarinic AChR receptor autoantibody is selected rom an anti-M1 autoantibody, an anti-M2 autoantibody, an anti-M3 autoantibody, an anti-M4 utoantibody, an anti-M5 autoantibody, or any combination thereof. 2. The method of any one of claims 47-51, wherein the autoantibody is a ganglionic AChR eceptor autoantibody. 3. The method of claim 50, wherein the adrenergic receptor autoantibody is selected from an nti-α1AR autoantibody, an anti-α2AR autoantibody, an anti-β1AR autoantibody, an anti-β2AR utoantibody, or any combination thereof. 4. The method of any one of claims 1-53, wherein the subject shows a reduction in a serumevel of IL 1β, IL 21, TNFα, IFNα, CD30, CD40 L, CCL5, CRP, and/or ferritin following dministration of the FcRn antagonist, compared to a baseline value. 5. An FcRn antagonist for use in the treatment of POTS, wherein the treatment is performed ccording to the method of any one of claims 1-54.

6. An FcRn antagonist for use in the manufacture of a medicament for the treatment of POTS, wherein the treatment is performed according to the method of any one of claims 1-54. 7. Use of an FcRn antagonist for the treatment of POTS according to the method of any one f claims 1-54. 8. Use of an FcRn antagonist for the manufacture of a medicament for treatment of POTS, wherein the treatment is performed according to the method of any one of claims 1-54.