CN114366739A - Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer - Google Patents
Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer Download PDFInfo
- Publication number
- CN114366739A CN114366739A CN202111675425.9A CN202111675425A CN114366739A CN 114366739 A CN114366739 A CN 114366739A CN 202111675425 A CN202111675425 A CN 202111675425A CN 114366739 A CN114366739 A CN 114366739A
- Authority
- CN
- China
- Prior art keywords
- colorectal cancer
- lercanidipine
- cells
- treating
- medicament
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Pending
Links
- 229960004294 lercanidipine Drugs 0.000 title claims abstract description 57
- ZDXUKAKRHYTAKV-UHFFFAOYSA-N lercanidipine Chemical compound COC(=O)C1=C(C)NC(C)=C(C(=O)OC(C)(C)CN(C)CCC(C=2C=CC=CC=2)C=2C=CC=CC=2)C1C1=CC=CC([N+]([O-])=O)=C1 ZDXUKAKRHYTAKV-UHFFFAOYSA-N 0.000 title claims abstract description 57
- 206010009944 Colon cancer Diseases 0.000 title claims abstract description 52
- 208000001333 Colorectal Neoplasms Diseases 0.000 title claims abstract description 48
- 239000003814 drug Substances 0.000 title claims abstract description 30
- 238000002360 preparation method Methods 0.000 title claims abstract description 6
- 229940079593 drug Drugs 0.000 claims abstract description 14
- 230000009545 invasion Effects 0.000 claims abstract description 7
- 230000035755 proliferation Effects 0.000 claims abstract description 6
- 230000001617 migratory effect Effects 0.000 claims description 7
- 239000000463 material Substances 0.000 claims description 4
- 230000002265 prevention Effects 0.000 claims description 4
- 206010052360 Colorectal adenocarcinoma Diseases 0.000 claims description 3
- 239000003795 chemical substances by application Substances 0.000 claims description 3
- 230000012010 growth Effects 0.000 claims description 3
- 239000000546 pharmaceutical excipient Substances 0.000 claims description 3
- 238000010521 absorption reaction Methods 0.000 claims description 2
- 239000003623 enhancer Substances 0.000 claims description 2
- 239000000945 filler Substances 0.000 claims description 2
- 230000002401 inhibitory effect Effects 0.000 claims description 2
- 239000000314 lubricant Substances 0.000 claims description 2
- 238000001179 sorption measurement Methods 0.000 claims description 2
- 239000004094 surface-active agent Substances 0.000 claims description 2
- 238000013268 sustained release Methods 0.000 claims description 2
- 239000012730 sustained-release form Substances 0.000 claims description 2
- 239000000080 wetting agent Substances 0.000 claims description 2
- 239000011230 binding agent Substances 0.000 claims 1
- 239000007884 disintegrant Substances 0.000 claims 1
- 230000006907 apoptotic process Effects 0.000 abstract description 8
- 238000002474 experimental method Methods 0.000 abstract description 8
- 230000005012 migration Effects 0.000 abstract description 5
- 238000013508 migration Methods 0.000 abstract description 5
- 229940126585 therapeutic drug Drugs 0.000 abstract description 2
- 210000004027 cell Anatomy 0.000 description 86
- IAZDPXIOMUYVGZ-UHFFFAOYSA-N Dimethylsulphoxide Chemical compound CS(C)=O IAZDPXIOMUYVGZ-UHFFFAOYSA-N 0.000 description 6
- 230000000694 effects Effects 0.000 description 6
- 239000001963 growth medium Substances 0.000 description 6
- 239000002609 medium Substances 0.000 description 6
- 108010087230 Sincalide Proteins 0.000 description 4
- 201000011510 cancer Diseases 0.000 description 4
- 238000010609 cell counting kit-8 assay Methods 0.000 description 4
- 230000012292 cell migration Effects 0.000 description 4
- 239000012091 fetal bovine serum Substances 0.000 description 4
- XJMOSONTPMZWPB-UHFFFAOYSA-M propidium iodide Chemical compound [I-].[I-].C12=CC(N)=CC=C2C2=CC=C(N)C=C2[N+](CCC[N+](C)(CC)CC)=C1C1=CC=CC=C1 XJMOSONTPMZWPB-UHFFFAOYSA-M 0.000 description 4
- IZTQOLKUZKXIRV-YRVFCXMDSA-N sincalide Chemical compound C([C@@H](C(=O)N[C@@H](CCSC)C(=O)NCC(=O)N[C@@H](CC=1C2=CC=CC=C2NC=1)C(=O)N[C@@H](CCSC)C(=O)N[C@@H](CC(O)=O)C(=O)N[C@@H](CC=1C=CC=CC=1)C(N)=O)NC(=O)[C@@H](N)CC(O)=O)C1=CC=C(OS(O)(=O)=O)C=C1 IZTQOLKUZKXIRV-YRVFCXMDSA-N 0.000 description 4
- 108010040476 FITC-annexin A5 Proteins 0.000 description 3
- 206010028980 Neoplasm Diseases 0.000 description 3
- 239000002246 antineoplastic agent Substances 0.000 description 3
- 230000001640 apoptogenic effect Effects 0.000 description 3
- 230000002238 attenuated effect Effects 0.000 description 3
- 208000029742 colonic neoplasm Diseases 0.000 description 3
- 238000003235 crystal violet staining Methods 0.000 description 3
- 238000001514 detection method Methods 0.000 description 3
- 230000002147 killing effect Effects 0.000 description 3
- 108010082117 matrigel Proteins 0.000 description 3
- 239000012528 membrane Substances 0.000 description 3
- 230000002829 reductive effect Effects 0.000 description 3
- 206010059866 Drug resistance Diseases 0.000 description 2
- 206010020772 Hypertension Diseases 0.000 description 2
- 229940041181 antineoplastic drug Drugs 0.000 description 2
- 238000003782 apoptosis assay Methods 0.000 description 2
- 230000008901 benefit Effects 0.000 description 2
- 239000000872 buffer Substances 0.000 description 2
- 239000006285 cell suspension Substances 0.000 description 2
- 230000003247 decreasing effect Effects 0.000 description 2
- 229940127292 dihydropyridine calcium channel blocker Drugs 0.000 description 2
- 239000002866 dihydropyridine calcium channel blocker Substances 0.000 description 2
- 238000012137 double-staining Methods 0.000 description 2
- 238000000684 flow cytometry Methods 0.000 description 2
- 230000005764 inhibitory process Effects 0.000 description 2
- 238000012986 modification Methods 0.000 description 2
- 230000004048 modification Effects 0.000 description 2
- 238000012827 research and development Methods 0.000 description 2
- 238000006467 substitution reaction Methods 0.000 description 2
- 230000004083 survival effect Effects 0.000 description 2
- 108091003079 Bovine Serum Albumin Proteins 0.000 description 1
- KCXVZYZYPLLWCC-UHFFFAOYSA-N EDTA Chemical compound OC(=O)CN(CC(O)=O)CCN(CC(O)=O)CC(O)=O KCXVZYZYPLLWCC-UHFFFAOYSA-N 0.000 description 1
- 238000002965 ELISA Methods 0.000 description 1
- 208000007530 Essential hypertension Diseases 0.000 description 1
- 206010061218 Inflammation Diseases 0.000 description 1
- 206010027476 Metastases Diseases 0.000 description 1
- 102000004142 Trypsin Human genes 0.000 description 1
- 108090000631 Trypsin Proteins 0.000 description 1
- 239000000853 adhesive Substances 0.000 description 1
- 230000001070 adhesive effect Effects 0.000 description 1
- 230000001093 anti-cancer Effects 0.000 description 1
- 230000003276 anti-hypertensive effect Effects 0.000 description 1
- 239000002220 antihypertensive agent Substances 0.000 description 1
- 229940127088 antihypertensive drug Drugs 0.000 description 1
- 239000007640 basal medium Substances 0.000 description 1
- 239000012148 binding buffer Substances 0.000 description 1
- 239000003560 cancer drug Substances 0.000 description 1
- 230000010261 cell growth Effects 0.000 description 1
- 230000004709 cell invasion Effects 0.000 description 1
- 230000004663 cell proliferation Effects 0.000 description 1
- 239000003153 chemical reaction reagent Substances 0.000 description 1
- 229940044683 chemotherapy drug Drugs 0.000 description 1
- 230000007547 defect Effects 0.000 description 1
- 238000011161 development Methods 0.000 description 1
- 238000010586 diagram Methods 0.000 description 1
- 238000007865 diluting Methods 0.000 description 1
- 230000000857 drug effect Effects 0.000 description 1
- 210000002919 epithelial cell Anatomy 0.000 description 1
- 238000001943 fluorescence-activated cell sorting Methods 0.000 description 1
- 238000009650 gentamicin protection assay Methods 0.000 description 1
- 231100000405 induce cancer Toxicity 0.000 description 1
- 230000008595 infiltration Effects 0.000 description 1
- 238000001764 infiltration Methods 0.000 description 1
- 210000003734 kidney Anatomy 0.000 description 1
- 230000007246 mechanism Effects 0.000 description 1
- 230000009401 metastasis Effects 0.000 description 1
- 239000000203 mixture Substances 0.000 description 1
- 230000009456 molecular mechanism Effects 0.000 description 1
- 238000010899 nucleation Methods 0.000 description 1
- 230000002062 proliferating effect Effects 0.000 description 1
- 229960005322 streptomycin Drugs 0.000 description 1
- 239000000126 substance Substances 0.000 description 1
- 238000012360 testing method Methods 0.000 description 1
- 230000001225 therapeutic effect Effects 0.000 description 1
- 230000036962 time dependent Effects 0.000 description 1
- 230000001988 toxicity Effects 0.000 description 1
- 231100000419 toxicity Toxicity 0.000 description 1
- 239000012588 trypsin Substances 0.000 description 1
Images
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/33—Heterocyclic compounds
- A61K31/395—Heterocyclic compounds having nitrogen as a ring hetero atom, e.g. guanethidine or rifamycins
- A61K31/435—Heterocyclic compounds having nitrogen as a ring hetero atom, e.g. guanethidine or rifamycins having six-membered rings with one nitrogen as the only ring hetero atom
- A61K31/44—Non condensed pyridines; Hydrogenated derivatives thereof
- A61K31/4422—1,4-Dihydropyridines, e.g. nifedipine, nicardipine
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P1/00—Drugs for disorders of the alimentary tract or the digestive system
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
Landscapes
- Health & Medical Sciences (AREA)
- Pharmacology & Pharmacy (AREA)
- Veterinary Medicine (AREA)
- Chemical & Material Sciences (AREA)
- Public Health (AREA)
- General Health & Medical Sciences (AREA)
- Medicinal Chemistry (AREA)
- Animal Behavior & Ethology (AREA)
- Life Sciences & Earth Sciences (AREA)
- Chemical Kinetics & Catalysis (AREA)
- Organic Chemistry (AREA)
- Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
- General Chemical & Material Sciences (AREA)
- Engineering & Computer Science (AREA)
- Bioinformatics & Cheminformatics (AREA)
- Epidemiology (AREA)
- Pharmaceuticals Containing Other Organic And Inorganic Compounds (AREA)
Abstract
The invention discloses an application of lercanidipine in preparation of a drug for treating and/or preventing colorectal cancer, and belongs to the technical field of biological medicines. The lercanidipine can effectively inhibit proliferation, migration invasion and apoptosis of colorectal cancer cells. Experiments show that lercanidipine with the effective concentration of 2-18 mu M can effectively inhibit proliferation, migration invasion and apoptosis of colorectal cancer cells. The invention provides a novel drug for treating and/or preventing colorectal cancer, and provides a novel therapeutic drug and strategy for treating and/or preventing colorectal cancer.
Description
Technical Field
The invention belongs to the technical field of biological medicines, and particularly relates to application of lercanidipine in preparation of a medicine for treating and/or preventing colorectal cancer.
Background
Colorectal cancer is one of the most common malignant tumors, and according to the global cancer data statistics report of 2020, the morbidity and mortality of the colorectal cancer are third and second in the world respectively, and the overall survival rate is poor. The colorectal cancer is in the colorectal due to the fact that the diseased part of the colorectal cancer is in the colorectal, the early development stage of the colorectal cancer is quite secret, so that the patient is often in the middle and late stage when the patient is diagnosed, and the advanced colorectal cancer is difficult to treat due to high metastasis and high infiltration of the colorectal cancer; at the same time, the difficulty of colorectal cancer treatment is exacerbated by the resistance of colorectal cancer cells to chemotherapeutic drugs. Drug resistance has become an important joint for overcoming colorectal cancer, two major problems of reversing drug resistance and searching for new anticancer drugs become the current colorectal cancer treatment, the drugs used on the market have definite drug effect, mechanism, safety and stability, and if the drugs with strong anticancer effect can be found, the research and development cost of the anticancer drugs can be greatly reduced, the research and development period can be shortened, the clinical colorectal cancer treatment selection can be increased, the rapid application of the drugs can be facilitated, and patients can benefit. Under the circumstances, it is urgent to find more stable, effective and safe anti-colorectal cancer drugs.
Lercanidipine (Lercanidipine) is a lipophilic third-generation dihydropyridine-calcium channel blocker (DHP-CCB), which has a good and durable antihypertensive effect in the treatment of hypertension, either alone or in combination, and is a first-line antihypertensive drug for the treatment of essential hypertension; meanwhile, lercanidipine has better tolerance and lower incidence of side effects, and particularly shows lower toxicity of kidney than other medicines. Lercanidipine has been studied intensively in terms of anti-hypertension, anti-inflammation, etc., but no report has been made on the therapeutic effect of lercanidipine on colorectal cancer so far, and the molecular mechanism thereof is not clear.
Disclosure of Invention
The invention aims to overcome the defects in the prior art and provides the application of lercanidipine in preparing medicaments for treating and/or preventing colorectal cancer.
The above object of the present invention is achieved by the following technical solutions:
application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer.
The structural formula of lercanidipine is shown as the formula (I):
the effective concentration of the lercanidipine is preferably 2-18 mu M.
The drug for treating and/or preventing colorectal cancer is preferably a drug capable of inhibiting growth, proliferation and/or migration invasion of colorectal cancer cells.
The colorectal cancer is preferably at least one of colorectal adenocarcinoma and colon cancer.
A medicament for the treatment and/or prevention of colorectal cancer comprising lercanidipine.
The medicine for treating and/or preventing colorectal cancer further comprises pharmaceutically acceptable auxiliary materials.
The pharmaceutically acceptable auxiliary material is preferably at least one of a sustained-release agent, an excipient, a filler, an adhesive, a wetting agent, a disintegrating agent, an absorption enhancer, an adsorption carrier, a surfactant and a lubricant.
The administration form of the medicament for treating and/or preventing colorectal cancer preferably includes, but is not limited to, oral administration.
Compared with the prior art, the invention has the following advantages and effects:
the lercanidipine can effectively inhibit proliferation, migration invasion and apoptosis of colorectal cancer cells. Experiments show that lercanidipine with the effective concentration of 2-18 mu M can effectively inhibit proliferation, migration invasion and apoptosis of colorectal cancer cells. The invention provides a novel drug for treating and/or preventing colorectal cancer, and provides a novel therapeutic drug and strategy for treating and/or preventing colorectal cancer.
Drawings
Figure 1 is a structural formula diagram of lercanidipine.
FIG. 2 is a graph showing the effect of lercanidipine treatment time and treatment concentration on the proliferative capacity of DLD-1 cells, HT-29 cells, and HCT-116 cells.
FIG. 3 is a graph showing the effect of lercanidipine at various concentrations on the migratory ability of DLD-1 cells.
FIG. 4 is a graph showing the effect of lercanidipine at various concentrations on the migratory ability of HT-29 cells.
FIG. 5 is a graph showing the effect of lercanidipine at various concentrations on the migratory ability of HCT-116 cells.
FIG. 6 is a graph showing the results of crystal violet staining of varying concentrations of lercanidipine on the migratory capacity of DLD-1 cells, HT-29 cells and HCT-116 cells.
FIG. 7 is a graph showing the results of crystal violet staining of varying concentrations of lercanidipine on the invasive potential of DLD-1 cells, HT-29 cells, and HCT-116 cells.
FIG. 8 is a graph of flow cytometry detection results of lercanidipine at different concentrations on apoptosis in DLD-1 cells, HT-29 cells, and HCT-116 cells.
Detailed Description
The present invention will be described in further detail with reference to examples and drawings, but the present invention is not limited thereto.
Example 1
(1) Experimental Material
Human colorectal adenocarcinoma epithelial cells (DLD-1), human colon cancer cells (HT-29) and human colon cancer cells (HCT-116) were purchased from ATCC; lercanidipine is available from Selleck Chemicals (Huston, TX, USA) and has a formula shown in FIG. 1; the CCK-8 kit was purchased from the institute of Homon chemistry, Japan; 1640 basal medium, fetal bovine serum, penicillin-streptomycin, PBS buffer (pH7.4) were purchased from Gibco, USA; DMSO was purchased from sigma, USA, lercanidipine was dissolved in DMSO and stored at a storage concentration of 10mM in a freezer at-80 deg.C; the Annexin V-FITC/PI fluorescence double-staining apoptosis detection kit is purchased from Nanjing Kai Biotech development Co., Ltd, China; transwell cells and matrigel were purchased from Corning, United States.
(2) CCK-8 experiment
At 50. mu.L/1000 cells per wellRespectively inoculating DLD-1 cells, HT-29 cells and HCT-116 cells into a 96-well plate, and diluting 10mM lercanidipine into a culture medium containing lercanidipine by using a 1640 complete culture medium after the cells are attached to the wall; wherein the concentration of lercanidipine in the culture medium containing lercanidipine is respectively 4 μ M, 8 μ M, 12 μ M, 16 μ M, 20 μ M, 24 μ M, 28 μ M, 32 μ M and 36 μ M, 50 μ L of the culture medium containing lercanidipine is added into each well according to different concentration gradients, and the culture medium without lercanidipine is used as a control, so as to obtain cell treatment groups with the concentration of lercanidipine respectively 0, 2 μ M, 4 μ M, 6 μ M, 8 μ M, 10 μ M, 12 μ M, 14 μ M, 16 μ M and 18 μ M. Add 10. mu.L of CCK-8 reagent to each well at 0, day 1, day 2, day 3, day 4 and day 5 according to CCK-8 kit instructions and 5% CO at 37 deg.C2Incubate for 2 hours in an incubator and detect at 450nm using an enzyme linked immunosorbent assay.
The results are shown in fig. 2, and the killing effect (cell proliferation inhibition) of lercanidipine on colorectal cancer cells (DLD-1, HT-29, HCT-116) is significantly increased with increasing lercanidipine concentration and treatment time (the survival cells are decreased and the OD450 readings are significantly decreased in the lercanidipine-treated group compared to the control group), indicating that the killing effect of lercanidipine on DLD-1 cells, HT-29 cells and HCT-116 cells is dose-and time-dependent (the longer the time, the higher the lercanidipine drug concentration, the stronger the killing effect on colorectal cancer cells).
(3) Cell scratch test
Taking cells with good growth state (DLD-1 cells, HT-29 cells and HCT-116 cells), digesting, counting, adjusting cell density, respectively inoculating appropriate amount of DLD-1 cells, HT-29 cells and HCT-116 cells into 6-well plate (2 mL complete culture medium per well), setting 3 multiple wells for each group, setting control wells, 37 deg.C, 5% CO2The culture was carried out in a constant temperature incubator overnight. The wells were streaked with a 10. mu.L pipette tip to create gaps between cells, the complete medium was aspirated, washed 2 times with PBS buffer (pH7.4), the gaps and detached cells were cleaned as thoroughly as possible, and 2mL of 1640 complete medium containing 2% FBS and corresponding lercanidipine concentrations (0. mu.M, 8. mu.M, 16. mu.M) was added. Marking a mark on the back of the 6-hole plate in the vertical direction to ensure that the positions of photographing are consistent,microscopic photographs were taken every 24 hours (i.e., day 0, day 1, and day 2) to record the growth of cells and the size of gaps in the streaks in each group, and the inhibition of colorectal cancer cell migration by lercanidipine at different concentrations was determined based on the gap distance.
(4) Cell migration invasion assay
Appropriate numbers of DLD-1 cells, HT-29 cells and HCT-116 cells were resuspended in serum-free 1640 base medium containing varying concentrations of lercanidipine (0. mu.M, 8. mu.M, 16. mu.M) and added to the corresponding upper Transwell chamber, and 1640 complete medium containing 20% FBS was added to the lower chamber. Then, the plate was incubated at 37 ℃ for 24 hours in an incubator, and subjected to crystal violet staining detection. For the invasion experiment, matrigel (corning, usa) was diluted with a base medium 1640 without FBS at a ratio of 1:25 and applied uniformly to the upper membrane surface of a Transwell chamber before seeding cells, and cells were seeded after the matrigel was solidified, in the same manner as in the cell migration experiment.
(5) Apoptosis assay
Cells (DLD-1 cells, HT-29 cells and HCT-116 cells) were cultured in lercanidipine 1640 complete medium at concentrations of 0. mu.M, 8. mu.M and 16. mu.M for 48 hours, and cells were collected gently with trypsin without EDTA according to the instructions of Annexin V-FITC/PI fluorescence double-staining apoptosis assay kit, and resuspended in an appropriate amount of binding buffer to obtain a cell suspension. Add 5. mu.L each of Annexin V-FITC and Propidium Iodide (PI) to the cell suspension in the dark and mix well, then react at room temperature for 5-15 min to ensure adequate binding of the dye. Within 1 hour, the number of apoptotic cells was determined by flow cytometry and FACS Calibur system (BD Biosciences).
The results are shown in FIGS. 3-5. As can be seen from FIGS. 3-5, the scratch width of 8 μ M, 16 μ M lercanidipine-treated DLD-1 cells, HT-29 cells, and HCT-116 cells was significantly wider than that of 0 μ M lercanidipine-treated cells, indicating that lercanidipine significantly attenuated the migratory capacity of cancer cells (DLD-1 cells, HT-29 cells, and HCT-116 cells). As can be seen from FIG. 6, in the cell migration experiment, the number of cells that migrated from the upper surface to the lower surface of the Transwell chamber membrane of DLD-1 cells, HT-29 cells and HCT-116 cells was greatly reduced as the treatment concentration of lercanidipine was increased, indicating that lercanidipine significantly attenuated the migratory ability of cancer cells (DLD-1 cells, HT-29 cells and HCT-116 cells); from FIG. 7, it can be seen that in the cell invasion experiment, as the treatment concentration of lercanidipine was increased, the number of DLD-1 cells, HT-29 cells and HCT-116 cells invading from the upper surface to the lower surface of the Transwell chamber membrane was greatly reduced, indicating that lercanidipine significantly attenuated the invasive ability of colorectal cancer cells; from FIG. 8, it can be seen that in the apoptosis experiment, with the increase of the treatment concentration of lercanidipine, the number of cells in which DLD-1 cells, HT-29 cells and HCT-116 cells were apoptotic after the drug treatment was greatly increased, as indicated by the increase of the proportion of apoptotic cells to the total number of cells, indicating that lercanidipine can significantly induce cancer cells (DLD-1 cells, HT-29 cells and HCT-116 cells) to undergo apoptosis.
The above embodiments are preferred embodiments of the present invention, but the present invention is not limited to the above embodiments, and any other changes, modifications, substitutions, combinations, and simplifications which do not depart from the spirit and principle of the present invention should be construed as equivalents thereof, and all such changes, modifications, substitutions, combinations, and simplifications are intended to be included in the scope of the present invention.
Claims (9)
1. Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer.
2. Use according to claim 1, wherein lercanidipine has the formula (i):
3. the use according to claim 1, wherein the effective concentration of lercanidipine is 2 to 18 μ M.
4. The use according to claim 1, wherein the medicament for the treatment and/or prevention of colorectal cancer is a medicament capable of inhibiting the growth, proliferation and/or migratory invasion of colorectal cancer cells.
5. The use of claim 1, wherein the colorectal cancer is at least one of colorectal adenocarcinoma and colon carcinoma.
6. A medicament for the treatment and/or prevention of colorectal cancer, comprising lercanidipine.
7. The medicament for treating and/or preventing colorectal cancer according to claim 6, wherein the medicament for treating and/or preventing colorectal cancer further comprises pharmaceutically acceptable auxiliary materials.
8. The drug for treating and/or preventing colorectal cancer according to claim 7, wherein the pharmaceutically acceptable excipient is at least one of a sustained release agent, an excipient, a filler, a binder, a wetting agent, a disintegrant, an absorption enhancer, an adsorption carrier, a surfactant, and a lubricant.
9. The medicament for the treatment and/or prevention of colorectal cancer according to claim 6,
the administration form of the medicament for treating and/or preventing colorectal cancer includes, but is not limited to, oral administration.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202111675425.9A CN114366739A (en) | 2021-12-31 | 2021-12-31 | Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202111675425.9A CN114366739A (en) | 2021-12-31 | 2021-12-31 | Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CN114366739A true CN114366739A (en) | 2022-04-19 |
Family
ID=81142017
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CN202111675425.9A Pending CN114366739A (en) | 2021-12-31 | 2021-12-31 | Application of lercanidipine in preparation of medicine for treating and/or preventing colorectal cancer |
Country Status (1)
| Country | Link |
|---|---|
| CN (1) | CN114366739A (en) |
Citations (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN102470129A (en) * | 2009-07-09 | 2012-05-23 | Cbt发展有限公司 | Combined preparation for use as a medicament |
| WO2015163706A1 (en) * | 2014-04-25 | 2015-10-29 | 아주대학교산학협력단 | Composition for preventing or treating cancers, containing proteasome inhibitor and dihydropyridine-based compound as active ingredients |
| US20200129492A1 (en) * | 2017-07-03 | 2020-04-30 | Menri Group Ltd. | Treatment of cancer with dihydropyridines |
| CN111803497A (en) * | 2020-09-02 | 2020-10-23 | 中国科学院昆明动物研究所 | Application of lercanidipine drugs in preparation of drugs for treating human glioma |
-
2021
- 2021-12-31 CN CN202111675425.9A patent/CN114366739A/en active Pending
Patent Citations (4)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN102470129A (en) * | 2009-07-09 | 2012-05-23 | Cbt发展有限公司 | Combined preparation for use as a medicament |
| WO2015163706A1 (en) * | 2014-04-25 | 2015-10-29 | 아주대학교산학협력단 | Composition for preventing or treating cancers, containing proteasome inhibitor and dihydropyridine-based compound as active ingredients |
| US20200129492A1 (en) * | 2017-07-03 | 2020-04-30 | Menri Group Ltd. | Treatment of cancer with dihydropyridines |
| CN111803497A (en) * | 2020-09-02 | 2020-10-23 | 中国科学院昆明动物研究所 | Application of lercanidipine drugs in preparation of drugs for treating human glioma |
Non-Patent Citations (1)
| Title |
|---|
| 张舒民等: "《医养结合医师手册》", vol. 1, 吉林大学出版社, pages: 151 * |
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| Jiao et al. | Activation of PI3 kinase/Akt/HIF-1α pathway contributes to hypoxia-induced epithelial-mesenchymal transition and chemoresistance in hepatocellular carcinoma | |
| Xu et al. | TGF-β plays a vital role in triple-negative breast cancer (TNBC) drug-resistance through regulating stemness, EMT and apoptosis | |
| Grasset et al. | Matrix stiffening and EGFR cooperate to promote the collective invasion of cancer cells | |
| Ganguly et al. | Secretory mucin 5AC promotes neoplastic progression by augmenting KLF4-mediated pancreatic cancer cell stemness | |
| Hirsch et al. | Metformin selectively targets cancer stem cells, and acts together with chemotherapy to block tumor growth and prolong remission | |
| Liu et al. | Combined niclosamide with cisplatin inhibits epithelial-mesenchymal transition and tumor growth in cisplatin-resistant triple-negative breast cancer | |
| Elkashty et al. | Cancer stem cells enrichment with surface markers CD271 and CD44 in human head and neck squamous cell carcinomas | |
| Wu et al. | Cinnamaldehyde induces apoptosis and reverses epithelial-mesenchymal transition through inhibition of Wnt/β-catenin pathway in non-small cell lung cancer | |
| Chang et al. | Effect of antisense hypoxia-inducible factor 1α on progression, metastasis, and chemosensitivity of pancreatic cancer | |
| Ma et al. | Epithelial–mesenchymal transition plays a critical role in drug resistance of hepatocellular carcinoma cells to oxaliplatin | |
| Feng et al. | DAPT, a γ-secretase inhibitor, suppresses tumorigenesis, and progression of growth hormone-producing adenomas by targeting notch signaling | |
| Deng et al. | WIP1 promotes cancer stem cell properties by inhibiting p38 MAPK in NSCLC | |
| Fan et al. | Metformin suppresses the esophageal carcinogenesis in rats treated with NMBzA through inhibiting AMPK/mTOR signaling pathway | |
| Liu et al. | Tumor‐associated macrophage‐derived transforming growth factor‐β promotes colorectal cancer progression through HIF1‐TRIB3 signaling | |
| Marín-Ramos et al. | NEO212 inhibits migration and invasion of glioma stem cells | |
| Cavnar et al. | Modeling selective elimination of quiescent cancer cells from bone marrow | |
| Dai et al. | Activation of transmembrane receptor tyrosine kinase DDR1-STAT3 cascade by extracellular matrix remodeling promotes liver metastatic colonization in uveal melanoma | |
| Rossini et al. | Combined targeting of EGFR and HER2 against prostate cancer stem cells | |
| Wang et al. | Dihydroartemisinin prevents distant metastasis of laryngeal carcinoma by inactivating STAT3 in cancer stem cells | |
| Xu et al. | Sufentanil combined with parecoxib sodium inhibits proliferation and metastasis of HER2-positive breast cancer cells and regulates epithelial-mesenchymal transition | |
| Wang et al. | Cinnamaldehyde suppressed EGF-induced EMT process and inhibits ovarian cancer progression through PI3K/AKT pathway | |
| Wang et al. | Metformin downregulates the expression of epidermal growth factor receptor independent of lowering blood glucose in oral squamous cell carcinoma | |
| Al-Kharashi et al. | High DNMT1 expression in stromal fibroblasts promotes angiogenesis and unfavorable outcome in locally advanced breast cancer patients | |
| Hsieh et al. | Acquisition of an enhanced aggressive phenotype in human lung cancer cells selected by suboptimal doses of cisplatin following cell deattachment and reattachment | |
| Olmedo et al. | Mitochondria in oral cancer stem cells: Unraveling the potential drug targets for new and old drugs |
Legal Events
| Date | Code | Title | Description |
|---|---|---|---|
| PB01 | Publication | ||
| PB01 | Publication | ||
| SE01 | Entry into force of request for substantive examination | ||
| SE01 | Entry into force of request for substantive examination |