WO2019208968A1 - 근육 질환 예방 및 치료용 조성물 - Google Patents
근육 질환 예방 및 치료용 조성물 Download PDFInfo
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- WO2019208968A1 WO2019208968A1 PCT/KR2019/004631 KR2019004631W WO2019208968A1 WO 2019208968 A1 WO2019208968 A1 WO 2019208968A1 KR 2019004631 W KR2019004631 W KR 2019004631W WO 2019208968 A1 WO2019208968 A1 WO 2019208968A1
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- WO
- WIPO (PCT)
- Prior art keywords
- vitamin
- dimenhydrinate
- muscle
- calcium pantothenate
- hamol
- Prior art date
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Definitions
- the present invention relates to a pharmaceutical composition for treating muscle diseases, and relates to a pharmaceutical composition for preventing or treating muscle diseases containing dimenhydrinate, hamol and / or calcium pantothenate as active ingredients.
- Skeletal muscles make up the largest part of the body, accounting for 40-50% of the total body weight, and play an important role in various metabolic functions in the body, including energy homeostasis and heat generation.
- Human muscle decreases by more than 1% per year after age 40, and by age 80, 50% of the maximum muscle mass is reduced, and muscle loss in old age is recognized as one of the most important factors that impair overall physical function.
- the body shape changes such as muscle and fat content and skeletal distortion.
- Obesity prevalence due to the decrease in old age has been continuously increasing at the level of more than 30% worldwide.
- Abnormal insulin secretion can cause muscle development problems due to poor energy supply to cells, leading to an increase in myopathy in diabetics than the general population.
- Muscular dystrophy is a major cause of poor quality of life associated with various diseases.
- Muscular dystrophy refers to a condition in which the amount and function of skeletal muscle is reduced. Muscular dystrophy is caused by a variety of causes, including aging, hormonal abnormalities, malnutrition, lack of physical activity, inflammatory and degenerative diseases, among which cancer, aging and sex hormone deficiency are known to be the main causes. Due to the development and development of various therapeutic agents, the aging population is increasing as the average life expectancy increases worldwide, and accordingly, the demand for treatment for myotropia is expected to continue to increase.
- myopathy patients the number of myoblasts decreases due to impairment of recruitment, activity or proliferation of satellite cells, stem cells of myoblasts, and the proliferation and differentiation of myoblasts decreases, thereby reducing Muscles show a decrease in muscle function due to a decrease in the size and number of muscle fibers at the histological level.
- epidemiology of sarcopenia has been actively conducted in the United States and Europe, and the interest in clinical significance of sarcopenia has recently increased.
- muscular dystrophy causes poor quality of life due to systemic weakness, impairment of activity and decreased muscle strength, but recently published studies may significantly increase the risk of osteoporotic fractures in addition to quality of life. This was reported.
- Myopathy caused by cancer is caused by malnutrition, lack of exercise, and cytokines secreted by cancer, and markedly lowered muscle mass and physical function.
- cancer-related sarcopenia is found in 14 to 78.7% of cancer patients, it is higher than 50% in gastrointestinal cancer, and about 40% in lung cancer and liver cancer.
- patients with esophageal cancer showed a shorter average of 2 years and 8 months of life expectancy and increased complications of cancer surgery compared to patients without muscular dystrophy.
- the number of patients who survived without recurrence for five years after liver cancer surgery was more than doubled in the case of myopathy without muscular dystrophy.
- Myopathy caused by the degeneration of spinal nerve, motor nerve or skeletal muscle fiber associated with muscle disease is one of the representative refractory diseases which have not yet been identified.
- studies have been conducted that the motor nerves that induce skeletal muscle contraction do not progress to skeletal muscle contraction, or the expression of proteins involved in muscle contraction in skeletal muscle is reduced or the protein is modified to contract normal skeletal muscle. This does not progress and in the long term it is known that the motor or skeletal muscle is transformed into fibrous tissue. Since the underlying cause of muscular dystrophy has not yet been identified and no method has been developed to prevent or restore motor neurodegeneration or skeletal muscle degeneration, a method for slowing the progression of muscular dystrophy is currently being developed. The research for this is being actively conducted.
- a method of suppressing muscular dystrophy caused by degeneration or progressive mutation of muscle cells which is a kind of myotropenia
- WO 2007/088123 discloses a therapeutic agent for muscular dystrophy comprising nitroxy derivatives as an active ingredient
- WO 2006/081997 discloses a therapeutic agent for muscular dystrophy comprising atactic acid or derivatives thereof as an active ingredient.
- these therapeutic agents containing a compound as an active ingredient act not only on skeletal muscles in which muscular dystrophy develops, but also on visceral or myocardial muscles not related to muscular dystrophy, which can cause a variety of side effects, and thus cannot be used for practical treatment.
- the hormonal preparations have significantly reduced side effects than the compound preparations and are biocompatible due to the characteristics of the hormonal preparations, the development of drugs for treating muscular dystrophy or myopathy using hormonal preparations has been accelerated.
- the present invention provides a pharmaceutical composition for the prevention or treatment of muscle diseases containing Dimenhydrinate, Harmol or calcium pantothenate as an active ingredient.
- the present invention also provides a pharmaceutical composition for preventing or treating muscle and fat loss due to administration of an anticancer agent comprising dimenhydrinate or calcium pantothenate as an active ingredient.
- the present invention provides a food composition for preventing or improving muscle diseases including dimenhydrinate, hamol or calcium pantothenate.
- Dimenhydrinate, hamol and calcium pantothenate of the present invention have the effect of promoting the proliferation and differentiation of myoblasts alone, in particular, combining them has an effect of synergistically increasing the proliferation and differentiation of myoblasts. Therefore, they can be usefully used for the prevention or treatment of muscle diseases in combination with each or several, and can also be used for the prevention or treatment of muscle and fat reduction due to the administration of anticancer drugs.
- FIG. 1 is a photograph and a graph confirming the effect of promoting the proliferation of myoblasts by the treatment of dimenhydrinate (OC-501) of the present invention.
- Figure 2 is a photograph confirming the effect of promoting the differentiation of myoblasts by the dimenhydrinate treatment of the present invention:
- Figure 3 is a diagram confirming the expression level of muscle cell differentiation markers myogenin (Myogenin) and MHC (myosin heavy chain) by Western blot analysis.
- Figure 4 is a photograph and graph confirming the proliferation promoting effect of myoblasts by the treatment of the lower mole (OC-503) of the present invention.
- Figure 5 is a photograph confirming the effect of promoting differentiation of myoblasts by the molar treatment of the present invention:
- FIG. 6 is a diagram confirming the expression level of myogenin (Myogenin) and MHC (myosin heavy chain), the muscle cell differentiation markers by Western blot analysis.
- Myogenin myogenin
- MHC myosin heavy chain
- Figure 7 is a photograph and graph confirming the effect of promoting proliferation of myoblasts by calcium pantothenate (OC-504) treatment of the present invention.
- FIG. 9 is a diagram confirming the expression level of muscle cell differentiation markers myogenin (Myogenin) and MHC (myosin heavy chain) by Western blot analysis.
- Figure 10 is a diagram confirming the cytotoxicity to myoblasts when treated in combination with dimenhydrinate, hamol and calcium pantothenate.
- Figure 11 is a diagram confirming the effect of increasing the proliferation of myoblasts when treated in combination with dimenhydrinate and calcium or pantothenate.
- Figure 12 is a diagram confirming the effect of increasing the proliferation of myoblasts when treated with a combination of dimenhydrinate and calcium or pantothenate.
- Figure 13 is a diagram confirming the effect of increasing the proliferation of myoblasts when the treatment of calcium and pantothenate, dimenhydrinate, hypo- and calcium pantothenate.
- Figure 14 is a diagram confirming the effect of differentiation of myoblasts when treated with a combination of dimenhydrinate and calcium or pantothenate:
- FIG. 15 is a diagram confirming the degree of differentiation of myoblasts through the expression levels of myogenin and MHC, which are differentiation markers of muscle cells, when treated with a combination of dimenhydrinate and calcium or pantothenate.
- 16 is a diagram confirming the effect of promoting myoblast differentiation due to the calcium pantothenate treatment group and the combination treatment of dimenhydrinate and calcium pantothenate by microscope and Western blot analysis.
- 17 is a diagram confirming the muscle regeneration effect by the combination of dimenhydrinate and calcium pantothenate.
- 18 is a diagram confirming the early recovery effect of muscle fibers by the combination of dimenhydrinate and calcium pantothenate.
- 19 is a diagram showing the process of causing cancer-related muscular dystrophy and the schedule of administration of dimenhydrinate and calcium pantothenate.
- 20 is a diagram confirming the effect on cancer-associated muscle and fat reduction by the combination of dimenhydrinate and calcium pantothenate.
- the present invention relates to a pharmaceutical composition for preventing or treating muscle diseases containing dimenhydrinate, Harmol or calcium pantothenate as an active ingredient.
- the dimenhydrinate may be a compound of molecular formula C 24 H 28 ClN 5 O 3 and a molecular weight of 469.97 g / mol represented by Formula 1:
- the lower mole may be a compound having the molecular formula C 12 H 10 N 2 O and a molecular weight of 198.225 g / mol represented by Formula 2:
- the calcium pantothenate is a calcium salt of water-soluble vitamin B5, which may be a compound having the molecular formula C 18 H 32 CaN 2 O 10 and a molecular weight of 476.536 g / mol represented by the following Chemical Formula 3:
- the calcium pantothenate may comprise a vitamin, wherein the vitamin may be a water soluble vitamin selected from vitamin C, vitamin B1, vitamin B2, vitamin B6, vitamin H, vitamin PP or pro-vitamin B5 or mixtures thereof.
- the vitamin may be a fat-soluble vitamin selected from vitamin A, vitamin D, vitamin E, vitamin K1 or carotene or mixtures thereof, more preferably vitamin B2 (riboflavin, vit B2).
- the dimenhydrinate, lower and calcium pantothenate may be included at 250 nM to 20 ⁇ M, respectively, and the lower mole may be included at 500 nM to 10 ⁇ M and the calcium pantothenate at 500 nM to 20 ⁇ M.
- the pharmaceutical composition of the present invention may include dimenhydrinate and lower, dimenhydrinate and calcium pantothenate, lower and calcium pantothenate, or dimenhydrinate, lower and calcium pantothenate as active ingredients, Dimenhydrinate 5 ⁇ M + Hamol 250nM, Dimenhydrinate 5 ⁇ M + Hamol 500nM, Dimenhydrinate 5 ⁇ M + Calcium Pantothenate 5 ⁇ M, Dimenhydrinate 5 ⁇ M + Calcium Pantothenate 10 ⁇ M, Dimenhydrinate 10 ⁇ M + Hamol 250nM, Dimenhydrin Nate 10 ⁇ M + Hamol 500nM, Dimenhydrinate 10 ⁇ M + Calcium Pantothenate 5 ⁇ M, Dimenhydrinate 10 ⁇ M + Calcium Pantothenate 10 ⁇ M, Hamol 250nM + Calcium Pantothenate 5 ⁇ M, Hamol 250nM + Calcium Pantothenate 10 ⁇ M, Hamol 500nM + Calcium Pantothenate 5 ⁇ M, 500nM Calcium Pantothenate 10 ⁇ M, Dimenhydrinate 5 ⁇ M +
- the muscle disease may be a muscle disease due to muscle function decline, muscle wasting or muscle degeneration, and may include atony, muscular atrophy, muscular dystrophy, workhorse disease, cachexia and It may be any one or more selected from the group consisting of sarcopenia, and more preferably is myopathy due to aging or cancer.
- the dimenhydrinate, hamol and / or calcium pantothenate of the present invention may enhance muscle mass or muscle strength or improve muscle function through promoting proliferation and differentiation of myoblasts.
- the dimenhydrinate, hamol and / or calcium pantothenate of the present invention may prevent or treat a decrease in muscle or fat due to anticancer treatment.
- the anticancer treatment may be one or more selected from the group consisting of an anticancer agent, a chemotherapeutic agent, an immunotherapy agent, an antibacterial agent, a radiotherapy agent and an antiviral agent, and a photodynamic therapy, and the anticancer agent is 5-FU (5-fluorouracil).
- an anticancer agent a chemotherapeutic agent, an immunotherapy agent, an antibacterial agent, a radiotherapy agent and an antiviral agent, and a photodynamic therapy
- the anticancer agent is 5-FU (5-fluorouracil).
- the present invention includes all of the dimenhydrinates, hamols and calcium pantothenates represented by the formulas (1) to (3), as well as pharmaceutically acceptable salts thereof, and possible solvates, hydrates, racemates or stereoisomers that can be prepared therefrom. Include.
- Dimenhydrinate, Hamol and calcium pantothenate represented by Formulas 1 to 3 of the present invention can be used in the form of pharmaceutically acceptable salts, and acid addition salts formed by pharmaceutically acceptable free acids are useful as salts.
- Acid addition salts include inorganic acids such as hydrochloric acid, nitric acid, phosphoric acid, sulfuric acid, hydrobromic acid, hydroiodic acid, nitrous acid or phosphorous acid and aliphatic mono and dicarboxylates, phenyl-substituted alkanoates, hydroxy alkanoates and alkanes. Obtained from non-toxic organic acids such as dioates, aromatic acids, aliphatic and aromatic sulfonic acids.
- Such pharmaceutically toxic salts include sulfate, pyrosulfate, bisulfate, sulfite, bisulfite, nitrate, phosphate, monohydrogen phosphate, diaidogen phosphate, metaphosphate, pyrophosphate chloride, bromide and iodide.
- the acid addition salts according to the present invention are dissolved in conventional methods, for example, the dimenhydrinate, hamol and calcium pantothenate represented by the formulas (1) to (3) in an excess of aqueous acid solution, and the salts are water miscible organic solvents, for example For example, it can be prepared by precipitation using methanol, ethanol, acetone or acetonitrile. In this mixture, the solvent or excess acid may be evaporated to dryness, or the precipitated salt may be prepared by suction filtration.
- Bases can also be used to make pharmaceutically acceptable metal salts.
- An alkali metal or alkaline earth metal salt is obtained by, for example, dissolving a compound in an excess of alkali metal hydroxide or alkaline earth metal hydroxide solution, filtering the insoluble compound salt, and evaporating and drying the filtrate.
- the metal salt it is pharmaceutically suitable to prepare sodium, carpal or calcium salts.
- Corresponding silver salts are also obtained by reacting alkali or alkaline earth metal salts with a suitable negative salt (eg, silver nitrate).
- the pharmaceutical composition of the present invention may further include known muscle disease therapeutic agents in addition to dimenhydrinate, hamol and calcium pantothenate as active ingredients, and may be used in combination with other known treatments for the treatment of these diseases.
- the present invention relates to a pharmaceutical composition for preventing or treating muscle and fat loss caused by anticancer agent, comprising dimenhydrinate or calcium pantothenate as an active ingredient.
- prevention means any action that inhibits or delays the development, spread and recurrence of muscle disease by administration of the pharmaceutical composition according to the present invention
- treatment means the dimenhydrinate of the present invention.
- Those skilled in the art to which the present invention pertains can refer to the data presented by the Korean Medical Association, etc., to know the exact criteria of the disease in which the composition of the present invention is effective, and to determine the extent of improvement, improvement and treatment. will be.
- the term "therapeutically effective amount" as used in combination with an active ingredient in the present invention means an amount effective for preventing or treating a target disease, and the therapeutically effective amount of the composition of the present invention may be various factors, for example, a method of administration. It may vary depending on the purpose, location of the patient and the condition of the patient. Therefore, when used in humans, the dosage should be determined in an appropriate amount in consideration of both safety and efficiency. It is also possible to estimate the amount used in humans from an effective amount determined through animal testing. Such considerations when determining the effective amount include, for example, Hardman and Limbird, eds., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 10th ed. (2001), Pergamon Press; And E.W. Martin ed., Remington's Pharmaceutical Sciences, 18th ed. (1990), Mack Publishing Co.
- the pharmaceutical composition of the present invention is administered in a pharmaceutically effective amount.
- pharmaceutically effective amount refers to an amount sufficient to treat the disease at a reasonable benefit / risk ratio applicable to medical treatment and not to cause side effects
- the effective dose level refers to Factors including health condition, type of muscle disease, cause of muscle disease, severity, drug activity, sensitivity to drug, method of administration, time of administration, route of administration and rate of release, duration of treatment, combination or concurrent use of the drug, and It may be determined according to factors well known in other medical fields.
- the compositions of the present invention may be administered as individual therapeutic agents or in combination with other therapeutic agents, may be administered sequentially or simultaneously with conventional therapeutic agents, and may be administered in single or multiple doses. Taking all of the above factors into consideration, it is important to administer an amount that can achieve the maximum effect with a minimum amount without side effects, which can be readily determined by one skilled in the art.
- compositions of the present invention may include carriers, diluents, excipients, or combinations of two or more thereof conventionally used in biological preparations.
- pharmaceutically acceptable means to exhibit a characteristic that is not toxic to cells or humans exposed to the composition.
- the carrier is not particularly limited so long as it is suitable for in vivo delivery of the composition, for example, Merck Index, 13th ed., Merck & Co. Inc.
- Compounds, saline solution, sterile water, Ringer's solution, buffered saline solution, dextrose solution, maltodextrin solution, glycerol, ethanol and one or more of these components can be mixed and used as needed. Conventional additives can be added.
- diluents, dispersants, surfactants, binders and lubricants may be additionally added to formulate into main dosage forms, pills, capsules, granules or tablets such as aqueous solutions, suspensions, emulsions and the like.
- it may be preferably formulated according to each disease or component by a suitable method in the art or using a method disclosed in Remington's Pharmaceutical Science (Mack Publishing Company, Easton PA, 18th, 1990).
- the pharmaceutical composition may be one or more formulations selected from the group consisting of oral formulations, external preparations, suppositories, sterile injectable solutions and sprays, with oral or injectable formulations being more preferred.
- the term "administration" means providing a given substance to an individual or patient in any suitable manner, and according to the method desired, non-oral administration (eg, intravenous, subcutaneous, intraperitoneal). Or topically injectable formulations) or orally, and the dosage varies depending on the weight, age, sex, health condition, diet, time of administration, method of administration, rate of excretion and severity of the patient.
- Liquid preparations for oral administration of the composition of the present invention include suspensions, solvents, emulsions, syrups, and the like, and various excipients such as wetting agents, sweeteners, fragrances, and preservatives, in addition to water and liquid paraffin, which are commonly used simple diluents.
- Formulations for parenteral administration include sterile aqueous solutions, non-aqueous solvents, suspensions, emulsions, lyophilized formulations, suppositories, and the like.
- the pharmaceutical composition of the present invention may be administered by any device in which the active substance may migrate to the target cell.
- Preferred modes of administration and preparations are intravenous, subcutaneous, intradermal, intramuscular, drip and the like.
- Injections include non-aqueous solvents such as aqueous solvents such as physiological saline solution and ring gel solution, vegetable oils, higher fatty acid esters (e.g., oleic acid), and alcohols (e.g., ethanol, benzyl alcohol, propylene glycol, glycerin, etc.).
- aqueous solvents such as physiological saline solution and ring gel solution
- vegetable oils e.g., oleic acid
- alcohols e.g., ethanol, benzyl alcohol, propylene glycol, glycerin, etc.
- Stabilizers e.g.
- Preservatives eg, mercury nitrate, chimerosal, benzalkonium chloride, phenol, cresol, benzyl alcohol, etc. may be included.
- the term "individual” means monkeys, cows, horses, sheep, pigs, chickens, turkeys, quails, cats, dogs, mice, mice, rabbits, including humans who may or may not develop the muscle disease. Or any animal, including guinea pigs, and by effectively administering the pharmaceutical composition of the present invention to an individual, the above diseases can be effectively prevented or treated.
- the pharmaceutical composition of the present invention can be administered in parallel with existing therapeutic agents.
- the pharmaceutical composition of the present invention may further include a pharmaceutically acceptable additive, wherein the pharmaceutically acceptable additive may include starch, gelatinized starch, microcrystalline cellulose, lactose, povidone, colloidal silicon dioxide, calcium hydrogen phosphate, Lactose, mannitol, syrup, gum arabic, pregelatinized starch, corn starch, powdered cellulose, hydroxypropyl cellulose, oppadry, sodium starch glycolate, carnauba lead, synthetic aluminum silicate, stearic acid, magnesium stearate, aluminum stearate, stearic acid Calcium, sucrose, dextrose, sorbitol, talc and the like can be used.
- the pharmaceutically acceptable additive according to the present invention is preferably included 0.1 parts by weight to 90 parts by weight based on the composition, but is not limited thereto.
- the present invention relates to a pharmaceutical composition for preventing or treating muscle and fat loss caused by anticancer agent, comprising dimenhydrinate or calcium pantothenate as an active ingredient.
- the calcium pantothenate may comprise a vitamin, wherein the vitamin may be a water soluble vitamin selected from vitamin C, vitamin B1, vitamin B2, vitamin B6, vitamin H, vitamin PP or pro-vitamin B5 or mixtures thereof.
- the vitamin may be a fat-soluble vitamin selected from vitamin A, vitamin D, vitamin E, vitamin K1 or carotene or mixtures thereof, more preferably vitamin B2 (riboflavin, vit B2).
- the present invention relates to a food composition for the prevention or improvement of muscle diseases, including dimenhydrinate, hamol or calcium pantothenate.
- the calcium pantothenate may comprise a vitamin, wherein the vitamin may be a water soluble vitamin selected from vitamin C, vitamin B1, vitamin B2, vitamin B6, vitamin H, vitamin PP or pro-vitamin B5 or mixtures thereof.
- the vitamin may be a fat-soluble vitamin selected from vitamin A, vitamin D, vitamin E, vitamin K1 or carotene or mixtures thereof, more preferably vitamin B2 (riboflavin, vit B2).
- the dimenhydrinate, lower and calcium pantothenate may be included at 250 nM to 20 ⁇ M, respectively, and the lower mole may be included at 500 nM to 10 ⁇ M and the calcium pantothenate at 500 nM to 20 ⁇ M.
- the pharmaceutical composition of the present invention may include dimenhydrinate and lower, dimenhydrinate and calcium pantothenate, lower and calcium pantothenate, or dimenhydrinate, lower and calcium pantothenate as active ingredients, Dimenhydrinate 5 ⁇ M + Hamol 250nM, Dimenhydrinate 5 ⁇ M + Hamol 500nM, Dimenhydrinate 5 ⁇ M + Calcium Pantothenate 5 ⁇ M, Dimenhydrinate 5 ⁇ M + Calcium Pantothenate 10 ⁇ M, Dimenhydrinate 10 ⁇ M + Hamol 250nM, Dimenhydrin Nate 10 ⁇ M + Hamol 500nM, Dimenhydrinate 10 ⁇ M + Calcium Pantothenate 5 ⁇ M, Dimenhydrinate 10 ⁇ M + Calcium Pantothenate 10 ⁇ M, Hamol 250nM + Calcium Pantothenate 5 ⁇ M, Hamol 250nM + Calcium Pantothenate 10 ⁇ M, Hamol 500nM + Calcium Pantothenate 5 ⁇ M, 500nM Calcium Pantothenate 10 ⁇ M, Dimenhydrinate 5 ⁇ M +
- the dimenhydrinate, hamol and / or calcium pantothenate of the present invention may enhance muscle mass or muscle strength through promoting proliferation and differentiation of myoblasts.
- the muscle disease may be a muscle disease due to muscular dysfunction, muscle wasting, or muscle degeneration, and may be any one or more selected from the group consisting of dystonia, muscular dystrophy, muscular dystrophy, hard work, cachexia and myotropia, More preferably, it is myopathy due to aging or cancer.
- the said dimenhydrinate, a lower molar, or calcium pantothenate may be added as it is, or it may be used with another food or food component, and it can use suitably according to a conventional method.
- the composition may include a food acceptable additive in addition to the active ingredient, the amount of the active ingredient may be appropriately determined according to the purpose of use (prevention, health or therapeutic treatment).
- food supplement used in the present invention means a component that can be added to food supplements, and can be appropriately selected and used by those skilled in the art as being added to prepare a health functional food of each formulation.
- food additives include flavors such as various nutrients, vitamins, minerals (electrolytes), synthetic and natural flavors, colorants and fillers, pectic acid and salts thereof, alginic acid and salts thereof, organic acids, protective colloidal thickeners. , pH regulators, stabilizers, preservatives, glycerin, alcohols, carbonation agents used in carbonated beverages, and the like, but is not limited to the kind of food additives of the present invention by the above examples.
- the food composition of the present invention may include a health functional food.
- a health functional food refers to a food prepared and processed in the form of tablets, capsules, powders, granules, liquids and pills using raw materials or ingredients having useful functions for the human body.
- 'functional' means to obtain a useful effect for health purposes such as nutrient control or physiological action on the structure and function of the human body.
- the health functional food of the present invention can be prepared by a method commonly used in the art, and the preparation can be prepared by adding raw materials and ingredients commonly added in the art.
- the formulation of the health functional food can also be prepared without limitation as long as the formulation is recognized as a health functional food.
- Food composition of the present invention can be prepared in various forms of formulation, unlike the general medicine has the advantage that there is no side effect that can occur when taking a long-term use of the drug as a raw material, and excellent portability, the present invention Dietary supplements are available as supplements to enhance the effectiveness of anticancer drugs.
- compositions comprising the dimenhydrinate, hamol or calcium pantothenate of the present invention as an active ingredient can be prepared by mixing known additives with other suitable auxiliary ingredients that may be contained in the health functional food according to the choice of those skilled in the art.
- suitable auxiliary ingredients include meat, sausages, breads, chocolates, candy, snacks, confectionery, pizza, ramen, other noodles, gums, dairy products, including ice cream, various soups, beverages, teas, drinks, alcoholic beverages and Vitamin complexes, and the like, can be prepared by adding the extract according to the present invention as a main ingredient juice, tea, jelly and juice.
- Mouse myoblast C2C12 was seeded in 96-well plates at 1.5 ⁇ 10 3 cells / well, and then cultured in DMEM medium containing 10% fetal bovine serum (FBS) at 37 ° C. and 5% CO 2 for one day at low density. . The medium was then replaced with DMEM medium containing 400 nM H 2 O 2 and dimenhydrinate (OC-501) 0 nM, 250 nM, 500 nM, 1 ⁇ M, 2.5 ⁇ M, 5 ⁇ M, 10 ⁇ M or 20 ⁇ M, respectively. After 16 hours of replacement, the wells were treated with MTT reagent and incubated in a dark incubator for 3 hours. The supernatant was removed and treated with 100 ⁇ l of DMSO in the wells, then the optical density (OD) was measured at 595 nm, and the cells were checked under a microscope.
- FBS fetal bovine serum
- Mouse myoblast C2C12 was dispensed in a 12-well plate at 0.7 ⁇ 10 5 cells / well and then cultured to a cell density of 70-80%. The cells are then washed with PBS before the medium is washed with 2% horse serum, 400 ⁇ M H 2 O 2 , and dimenhydrinate (OC-501) 0 nM (DMSO), 500 nM, 5 ⁇ M, 10 ⁇ M or 20 ⁇ M. Each was replaced with the included DMEM medium (differentiation medium). The medium induced differentiation for 5-7 days with every other day. After differentiation, cells were identified under a microscope (4X and 10X magnification), and cells were disrupted and Western blot analysis was performed using differentiation markers Myogenin and myosin heavy chain (MHC) antibodies.
- MHC myogenin and myosin heavy chain
- dimenhydrinate promoted the differentiation of myoblasts (FIG. 2), and particularly increased promotion of differentiation at 5 ⁇ M (FIG. 3).
- Mouse myoblast C2C12 was seeded in 96-well plates at 1.5 ⁇ 10 3 cells / well, and then cultured in DMEM medium containing 10% fetal bovine serum (FBS) at 37 ° C. and 5% CO 2 for one day at low density. . The medium was then replaced with DMEM medium containing 400 nM of H 2 O 2 and 0 nM, 250 nM, 500 nM, 1 ⁇ M, 2.5 ⁇ M, 5 ⁇ M, 10 ⁇ M or 20 ⁇ M, respectively. After 16 hours of replacement, the wells were treated with MTT reagent and incubated in a dark incubator for 3 hours. The supernatant was removed and treated with 100 ⁇ l of DMSO in the wells, then the optical density (OD) was measured at 595 nm, and the cells were checked under a microscope.
- FBS fetal bovine serum
- Mouse myoblast C2C12 was dispensed in a 12-well plate at 0.7 ⁇ 10 5 cells / well and then cultured to a cell density of 70-80%. The cells are then washed with PBS before the medium is washed with 2% horse serum, 400 ⁇ M of H 2 O 2 , and small (OC-503) 0 nM (DMSO), 500 nM, 1 ⁇ M, 2.5 ⁇ M, 5 ⁇ M or 10 ⁇ M. Each was replaced with the included DMEM medium (differentiation medium). The medium induced differentiation for 5-7 days with every other day. After differentiation, the cells were identified under a microscope, and cells were disrupted and Western blot analysis was performed using differentiation markers Myogenin and mycein heavy chain (MHC) antibodies.
- MHC myogenin and mycein heavy chain
- Mouse myoblast C2C12 was seeded in 96-well plates at 1.5 ⁇ 10 3 cells / well, and then cultured in DMEM medium containing 10% fetal bovine serum (FBS) at 37 ° C. and 5% CO 2 for one day at low density. . Thereafter, the medium was replaced with DMEM medium containing 400 nM H 2 O 2 and calcium pantothenate (OC-504) 0 nM, 250 nM, 500 nM, 1 ⁇ M, 2.5 ⁇ M, 5 ⁇ M, 10 ⁇ M or 20 ⁇ M, respectively. After 16 hours of replacement, the wells were treated with MTT reagent and incubated in a dark incubator for 3 hours. The supernatant was removed and treated with 100 ⁇ l of DMSO in the wells, then the optical density (OD) was measured at 595 nm, and the cells were checked under a microscope.
- FBS fetal bovine serum
- Mouse myoblast C2C12 was dispensed in a 12-well plate at 0.7 ⁇ 10 5 cells / well and then cultured to a cell density of 70-80%. The cells were then washed with PBS and the medium was washed with 2% horse serum, 400 ⁇ M H 2 O 2 , and calcium pantothenate (OC-504) 0 nM (DMSO), 500 nM, 2.5 ⁇ M, 5 ⁇ M, 10 ⁇ M or Each was replaced with DMEM medium (differentiation medium) containing 20 ⁇ M. The medium induced differentiation for 5-7 days with every other day. After differentiation, cells were identified under a microscope (4X and 10X magnification), and cells were disrupted and Western blot analysis was performed using differentiation markers Myogenin and myosin heavy chain (MHC) antibodies.
- MHC myogenin and myosin heavy chain
- the C2C12 cell line was dispensed at 1.5 ⁇ 10 3 cells / well in a 96-well plate, then treated with a combination of dimenhydrinate (OC-501), hamol (OC-503) and calcium pantothenate (OC-504) (OC -501 5 ⁇ M + OC-503 250nM, OC-501 5 ⁇ M + OC-503 500nM, OC-501 5 ⁇ M + OC-504 5 ⁇ M, OC-501 5 ⁇ M + OC-504 10 ⁇ M, OC-501 10 ⁇ M + OC-503 250nM, OC -501 10 ⁇ M + OC-503 500nM, OC-501 10 ⁇ M + OC-504 5 ⁇ M, OC-501 10 ⁇ M + OC-504 10 ⁇ M, OC-503 250nM + OC-504 5 ⁇ M, OC-503 250nM + OC-504 5 ⁇ M, OC-503 250nM + OC-504 10 ⁇ M, OC-503 500 nM + OC-50
- Mouse myoblast C2C12 was seeded in 96-well plates at 1.5 ⁇ 10 3 cells / well, and then cultured in DMEM medium containing 10% fetal bovine serum (FBS) at 37 ° C. and 5% CO 2 for one day at low density. .
- FBS fetal bovine serum
- the medium was then combined with 400 ⁇ M of H 2 O 2 with dimenhydrinate (OC-501), Hamol (OC-503), and calcium pantothenate (OC-504), OC-501 5 ⁇ M + OC-503 250 nM, OC -501 5 ⁇ M + OC-503 500nM, OC-501 5 ⁇ M + OC-504 5 ⁇ M, OC-501 5 ⁇ M + OC-504 10 ⁇ M, OC-501 10 ⁇ M + OC-503 250nM, OC-501 10 ⁇ M + OC-503 500nM, OC -501 10 ⁇ M + OC-504 5 ⁇ M, OC-501 10 ⁇ M + OC-504 10 ⁇ M, OC-503 250 nM + OC-504 5 ⁇ M, OC-503 250 nM + OC-504 10 ⁇ M, OC-503 500nM + OC-504 10 ⁇ M, OC-501
- the wells were treated with MTT reagent and incubated in a dark incubator for 3 hours.
- the supernatant was removed and treated with 100 ⁇ l of DMSO in the wells, then the optical density (OD) was measured at 595 nm, and the cells were checked under a microscope.
- Mouse myoblast C2C12 was dispensed in a 12-well plate at 0.7 ⁇ 10 5 cells / well and then cultured to a cell density of 70-80%. The cells were then washed with PBS and the medium was washed with 2% horse serum, 400 ⁇ M of H 2 O 2 , and dimenhydrinate (OC-501), hamol (OC-503) and calcium pantothenate (OC -504) OC-501 5 ⁇ M + OC-503 250nM, OC-501 5 ⁇ M + OC-503 500nM, OC-501 5 ⁇ M + OC-504 5 ⁇ M, OC-501 5 ⁇ M + OC-504 10 ⁇ M, OC-501 10 ⁇ M + OC-503 250nM, OC-501 10 ⁇ M + OC-503 500nM, OC-501 10 ⁇ M + OC-504 5 ⁇ M, OC-501 10 ⁇ M + OC-504 5 ⁇ M, OC-501 10 ⁇ M + OC-504 10 ⁇ M, OC-503
- the medium induced differentiation for 5-7 days with every other day. After differentiation, cells were identified under a microscope (4X and 10X magnification), and cells were disrupted and Western blot analysis was performed using differentiation markers Myogenin and myosin heavy chain (MHC) antibodies.
- MHC myogenin and myosin heavy chain
- Mesenchymal stem cells were isolated on the third day after the cobratoxin was inserted into the tibialis anterior muscle of the mouse. After 2 days, 10 ⁇ M of dimenhydrinate (OC-501) and pantothenic acid were isolated. Western blot analysis was performed using the differentiation markers PAX7 (paired box protein-7) and MYF5 (Myogenic factor 5) antibodies with 5 ⁇ M of calcium (OC-504), respectively or in combination, and after differentiation, cells were microscopically examined. Confirmation (4X and 10X magnification).
- mpk (mg / kg) of dimenhydrinate (OC-501) and calcium pantothenate (OC-504) were added to the tibialis anterior muscle of the mouse, respectively, for 3 to 3 days after stabbing cobratoxin. And 15 or 30 mpk (mg / kg) in combination, and the day after the mice were sacrificed to determine the degree of muscle regeneration.
- Cancer-related myotropenia was induced by administering 5-FU (5-fluorouracil), an anticancer agent, to mice transplanted with colorectal cancer cells CT26.
- 5-FU 5-fluorouracil
- dimenhydrinate OC-501
- calcium pantothenate OC-504
- MRI was measured every week in OC-501 and 504 alone and combination groups. Changes in muscle and fat were measured (FIG. 19).
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Abstract
Description
Claims (21)
- 디멘하이드리네이트(Dimenhydrinate), 하몰(Harmol) 또는 판토텐산 칼슘(calcium pantothenate)을 유효성분으로 함유하는 근육 질환의 예방 또는 치료용 약학조성물.
- 제 1항에 있어서, 디멘하이드리네이트 및 하몰, 디멘하이드리네이트 및 판토텐산 칼슘, 하몰 및 판토텐산 칼슘, 또는 디멘하이드리네이트, 하몰 및 판토텐산 칼슘을 유효성분으로 포함하는, 근육 질환의 예방 또는 치료용 약학조성물.
- 제 1항에 있어서, 근육 질환은 근기능 저하, 근육 소모 또는 근육 퇴화로 인한 근육 질환인, 근육 질환의 예방 또는 치료용 약학조성물.
- 제 1항에 있어서, 근육 질환은 긴장감퇴증(atony), 근위축증(muscular atrophy), 근이영양증(muscular dystrophy), 근무력증(myasthenia), 악액질(cachexia) 및 근감소증(sarcopenia)으로 이루어진 군으로부터 선택되는 어느 하나 이상인, 근육 질환의 예방 또는 치료용 약학조성물.
- 제 7항에 있어서, 근감소증은 노화 또는 암에 의한 것인, 근육 질환의 예방 또는 치료용 약학조성물.
- 제 1항에 있어서, 비타민 C, 비타민 B1, 비타민 B2, 비타민 B6, 비타민 H, 비타민 PP 또는 프로-비타민 B5 또는 이들의 혼합물로부터 선택된 수용성 비타민을 추가로 포함하는, 근육 질환의 예방 또는 치료용 약학조성물.
- 제 1항에 있어서, 비타민 A, 비타민 D, 비타민 E, 비타민 K1 또는 카로텐 또는 이들의 혼합물로부터 선택된 지용성 비타민을 추가로 포함하는, 근육 질환의 예방 또는 치료용 약학조성물.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘을 유효성분으로 포함하는, 항암제 투여로 인한 근육 및 지방 감소의 예방 또는 치료용 약학조성물.
- 제 11항에 있어서, 비타민 C, 비타민 B1, 비타민 B2, 비타민 B6, 비타민 H, 비타민 PP, 프로-비타민 B5, 비타민 A, 비타민 D, 비타민 E, 비타민 K1 또는 카로텐 또는 이들의 혼합물로부터 선택된 비타민을 추가로 포함하는, 항암제 투여로 인한 근육 및 지방 감소의 예방 또는 치료용 약학조성물.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘을 포함하는 근육 질환의 예방 또는 개선용 식품 조성물.
- 제 13항에 있어서, 디멘하이드리네이트 및 하몰, 디멘하이드리네이트 및 판토텐산 칼슘, 하몰 및 판토텐산 칼슘, 또는 디멘하이드리네이트, 하몰 및 판토텐산 칼슘을 포함하는, 근육 질환의 예방 또는 개선용 식품 조성물.
- 제 13항에 있어서, 근육 질환은 근기능 저하, 근육 소모 또는 근육 퇴화로 인한 근육 질환인, 근육 질환의 예방 또는 개선용 식품 조성물.
- 제 13항에 있어서, 근육 질환은 긴장감퇴증, 근위축증, 근이영양증, 근무력증, 악액질 및 근감소증으로 이루어진 군으로부터 선택되는 어느 하나 이상인, 근육 질환의 예방 또는 개선용 식품 조성물.
- 제 13항에 있어서, 비타민 C, 비타민 B1, 비타민 B2, 비타민 B6, 비타민 H, 비타민 PP, 프로-비타민 B5, 비타민 A, 비타민 D, 비타민 E, 비타민 K1 또는 카로텐 또는 이들의 혼합물로부터 선택된 비타민을 추가로 포함하는, 근육 질환의 예방 또는 개선용 식품 조성물.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘의 근육 질환의 예방 또는 치료 용도.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘의 항암제 투여로 인한 근육 및 지방 감소 치료 용도.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘을 이용한 근육 질환의 치료 방법.
- 디멘하이드리네이트, 하몰 또는 판토텐산 칼슘을 이용한 항암제 투여로 인한 근육 및 지방 감소증의 치료 방법.
Priority Applications (11)
Application Number | Priority Date | Filing Date | Title |
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AU2019261476A AU2019261476B2 (en) | 2018-04-25 | 2019-04-17 | Composition for preventing and treating muscular disease |
CN201980002035.XA CN110636847B (zh) | 2018-04-25 | 2019-04-17 | 用于预防及治疗肌肉疾病的组合物 |
US16/607,266 US11364244B2 (en) | 2018-04-25 | 2019-04-17 | Compositions for treatment of muscular disorders |
JP2020547090A JP7250810B2 (ja) | 2018-04-25 | 2019-04-17 | 筋肉疾患の予防及び治療用組成物 |
EP19789574.1A EP3607949A4 (en) | 2018-04-25 | 2019-04-17 | COMPOSITION FOR THE PREVENTION AND TREATMENT OF MUSCLE DISEASES |
CA3090241A CA3090241C (en) | 2018-04-25 | 2019-04-17 | Composition for preventing and treating muscular disease |
AU2021269368A AU2021269368A1 (en) | 2018-04-25 | 2021-11-17 | Composition for preventing and treating muscular disease |
AU2021269360A AU2021269360A1 (en) | 2018-04-25 | 2021-11-17 | Composition for preventing and treating muscular disease |
US17/744,339 US20220265663A1 (en) | 2018-04-25 | 2022-05-13 | Composition for Treatment of Muscular Disorders |
JP2023046074A JP2023078374A (ja) | 2018-04-25 | 2023-03-22 | 筋肉疾患の予防及び治療用組成物 |
AU2023255014A AU2023255014A1 (en) | 2018-04-25 | 2023-10-27 | Composition for preventing and treating muscular disease |
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- 2019-04-17 CN CN201980002035.XA patent/CN110636847B/zh active Active
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- 2019-04-17 KR KR1020190044769A patent/KR102204204B1/ko active IP Right Grant
- 2019-04-17 EP EP19789574.1A patent/EP3607949A4/en active Pending
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- 2019-04-17 WO PCT/KR2019/004631 patent/WO2019208968A1/ko unknown
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AU2021269360A1 (en) | 2021-12-16 |
JP7250810B2 (ja) | 2023-04-03 |
EP3607949A4 (en) | 2021-03-17 |
KR102295305B1 (ko) | 2021-08-30 |
CA3090241A1 (en) | 2019-10-31 |
KR20200105785A (ko) | 2020-09-09 |
JP2023078374A (ja) | 2023-06-06 |
AU2019261476B2 (en) | 2021-11-18 |
AU2019261476A1 (en) | 2020-07-23 |
US20220265663A1 (en) | 2022-08-25 |
CN110636847A (zh) | 2019-12-31 |
CA3090241C (en) | 2023-03-28 |
EP3607949A1 (en) | 2020-02-12 |
AU2023255014A1 (en) | 2023-11-16 |
KR102295317B1 (ko) | 2021-08-30 |
JP2021515025A (ja) | 2021-06-17 |
US11364244B2 (en) | 2022-06-21 |
KR20200105786A (ko) | 2020-09-09 |
CN110636847B (zh) | 2023-06-09 |
US20200246343A1 (en) | 2020-08-06 |
CA3188049A1 (en) | 2019-10-31 |
KR102204204B1 (ko) | 2021-01-18 |
KR20190124143A (ko) | 2019-11-04 |
AU2021269368A1 (en) | 2021-12-16 |
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