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Cyclosporin A

Immunosuppressive agent CAS# 59865-13-3

Cyclosporin A

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Chemical structure

Cyclosporin A

3D structure

Chemical Properties of Cyclosporin A

Cas No. 59865-13-3 SDF Download SDF
PubChem ID 5280754 Appearance Powder
Formula C62H111N11O12 M.Wt 1202.61
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Ciclosporin A
Solubility DMSO : 62.5 mg/mL (51.97 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name 30-ethyl-33-[(E)-1-hydroxy-2-methylhex-4-enyl]-1,4,7,10,12,15,19,25,28-nonamethyl-6,9,18,24-tetrakis(2-methylpropyl)-3,21-di(propan-2-yl)-1,4,7,10,13,16,19,22,25,28,31-undecazacyclotritriacontane-2,5,8,11,14,17,20,23,26,29,32-undecone
SMILES CCC1C(=O)N(CC(=O)N(C(C(=O)NC(C(=O)N(C(C(=O)NC(C(=O)NC(C(=O)N(C(C(=O)N(C(C(=O)N(C(C(=O)N(C(C(=O)N1)C(C(C)CC=CC)O)C)C(C)C)C)CC(C)C)C)CC(C)C)C)C)C)CC(C)C)C)C(C)C)CC(C)C)C)C
Standard InChIKey PMATZTZNYRCHOR-IMVLJIQESA-N
Standard InChI InChI=1S/C62H111N11O12/c1-25-27-28-40(15)52(75)51-56(79)65-43(26-2)58(81)67(18)33-48(74)68(19)44(29-34(3)4)55(78)66-49(38(11)12)61(84)69(20)45(30-35(5)6)54(77)63-41(16)53(76)64-42(17)57(80)70(21)46(31-36(7)8)59(82)71(22)47(32-37(9)10)60(83)72(23)50(39(13)14)62(85)73(51)24/h25,27,34-47,49-52,75H,26,28-33H2,1-24H3,(H,63,77)(H,64,76)(H,65,79)(H,66,78)/b27-25+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Cyclosporin A

DescriptionImmunosuppressant; inhibits phosphatase activity of calcineurin (IC50 = 5 nM). Also inhibits formation and opening of the mitochondrial permeability transition pore (MPTP).

Cyclosporin A Dilution Calculator

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Preparing Stock Solutions of Cyclosporin A

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 0.8315 mL 4.1576 mL 8.3152 mL 16.6305 mL 20.7881 mL
5 mM 0.1663 mL 0.8315 mL 1.663 mL 3.3261 mL 4.1576 mL
10 mM 0.0832 mL 0.4158 mL 0.8315 mL 1.663 mL 2.0788 mL
50 mM 0.0166 mL 0.0832 mL 0.1663 mL 0.3326 mL 0.4158 mL
100 mM 0.0083 mL 0.0416 mL 0.0832 mL 0.1663 mL 0.2079 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Cyclosporin A

Cyclosporin A is a selective cyclophilin inhibitor with IC50 value of 7 nM [1].

Cyclophilins are isomerase enzymes and involve in a variety of functions related to cell metabolism and energy homeostasis. It has been reported that the over expression of cyclophilins were observed in inflammation or malignancy.

Cyclosporin A is a potent cyclophilin inhibitor which is responsible for the opening of the MPTP (mitochondrial permeability transition pore). When tested with retinal ganglion cells, Cyclosporin A showed a high selectivity for the expression of cyclophilin D and prolonged the cells survival [2]. In human First-Trimester Trophoblast Cells, Cyclosporin A treatment promoted cells growth and invasiveness by inhibiting Ca2+/Calcineurin/NFAT signal [3]. Cyclosporin A treatment promoted the apoptosis of T-cell by upregulating Fas/FasL and caspase activities [4]. Treated human T cells with Cyclosporin A suppressed T cell activation by inhibiting calcineurin and NFATc which are responsible for T cell function [1].

In retinal ischemia C57BL/6 mouse model, Cyclosporin A treatment significantly prevented the up regulation of cyclophilin D and ameliorated the death of neuronal cells in vivo [2].

Cyclosporin A has also been reported to inhibit the entry of hepatitis B and C virus through interfering NTCP reportor [5]. In CRC cell lines (CACO-2, HT-29, HCT-116 and LOVO), Cyclosporin A treatment also could impair cell growth via without calcineurin pathway while the mechanism was still undermined [6].

References:
[1].  Minguillon, J., et al., Concentrations of cyclosporin A and FK506 that inhibit IL-2 induction in human T cells do not affect TGF-beta1 biosynthesis, whereas higher doses of cyclosporin A trigger apoptosis and release of preformed TGF-beta1. J Leukoc Biol, 2005. 77(5): p. 748-58.
[2].  Kim, S.Y., et al., Inhibition of cyclophilin D by cyclosporin A promotes retinal ganglion cell survival by preventing mitochondrial alteration in ischemic injury. Cell Death Dis, 2014. 5: p. e1105.
[3].  Du, M.R., et al., Cyclosporin A promotes growth and invasiveness in vitro of human first-trimester trophoblast cells via MAPK3/MAPK1-mediated AP1 and Ca2+/calcineurin/NFAT signaling pathways. Biol Reprod, 2008. 78(6): p. 1102-10.
[4].  Gao, J., et al., Mitochondrial permeability transition pore in inflammatory apoptosis of human conjunctival epithelial cells and T cells: effect of cyclosporin A. Invest Ophthalmol Vis Sci, 2013. 54(7): p. 4717-33.
[5].  Nkongolo, S., et al., Cyclosporin A inhibits hepatitis B and hepatitis D virus entry by cyclophilin-independent interference with the NTCP receptor. J Hepatol, 2014. 60(4): p. 723-31.
[6].  Werneck, M.B., et al., Cyclosporin A inhibits colon cancer cell growth independently of the calcineurin pathway. Cell Cycle, 2012. 11(21): p. 3997-4008.

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References on Cyclosporin A

Pharmacokinetic comparison of cyclosporin A and tacrolimus in graft-versus-host disease prophylaxis.[Pubmed:28343273]

Ann Hematol. 2017 Jun;96(6):935-942.

A number of studies were published with contradictory results comparing tacrolimus (Tac) and cyclosporine A (CsA) for graft-versus-host disease (GVHD) prophylaxis, but there are only few that accounted for pharmacokinetic (PK) parameters. In this study, we created a model based on median concentrations, variability of concentrations, and failures to maintain target levels that distinguished patients with low, intermediate, and high risks of acute GVHD (hazard ratios (HR) 1.77, 95%CI 1.36-2.32, p < 0.0001). This model was used to compare 95 patients with CsA and 239 with Tac GVHD prophylaxis. In the multivariate analysis, incorporating PK risk, no differences were observed for grade II-IV acute GVHD (HR 0.73, 95%CI 0.48-1.10, p = 0.13), but grade III-IV acute GVHD was lower in the Tac group (HR 0.47, 95%CI 0.28-0.78, p = 0.004). The observed difference was due to patients with high PK risk (HR 0.377, 95%CI 0.19-0.75, p = 0.005), but not with low and intermediate PK risk (p > 0.05). Patients in the Tac group had better GVHD relapse-free survival (HR = 0.659, p = 0.01) and comparable overall survival (p > 0.05). In conclusion, PK risk should be accounted for in comparisons of GVHD prophylaxis regimens with calcineurin inhibitors, and Tac was superior to CsA in patients with high, but not intermediate and low PK risk.

Production of the immunosuppressant cyclosporin A by a new soil isolate, Aspergillus fumigatus, in submerged culture.[Pubmed:27995310]

Appl Microbiol Biotechnol. 2017 Apr;101(8):3305-3317.

Cyclosporin A (CyA) has received meticulous attention owing to its immunosuppressive and biological activities. In this study, a soil isolate, capable of producing CyA, was named Zag1 strain and identified as Aspergillus fumigatus based on macroscopic and microscopic characteristics, 18S rDNA sequence, and phylogenetic characteristic analysis. To maximize the production of CyA, the fungal culture was grown under various fermentation conditions including selection of the cultivation medium, agitation rate, fermentation time, incubation temperature, pH value, inoculum nature, and medium volume. A simple medium (pH 5.0) containing 5% maltose as a carbon source and 2% potassium nitrate as a nitrogen source favored the highest CyA production when the fermentation process was maintained at 120 rpm for 9 days and at 30 degrees C using 3% standard inoculum of 5-day-old. The final CyA titer under these conditions was intensified to 2.23-3.31-fold, as compared with the amount obtained with seven types of basal media. A. fumigatus Zag1 appears to possess a good biotechnological potential for CyA production under favorable culture conditions.

[Effect of Rabbit Anti-human Thymocyte Immunoglobulin Combined with Cyclosporin A on Severe Aplastic Anemia].[Pubmed:28024501]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2016 Dec;24(6):1824-1827.

OBJECTIVE: To study the efficacy and safety of anti-human thymocyte immunoglobulin(ATG-F) combined with Cyclosporin A(CsA) on patients with severe aplastic anemia (SSA), so as to provide support for clinical work. METHODS: From January 2010 to December 2015, 78 patients with SAA admitted in our hospital were divided into 2 groups: ATG-F+CsA group(40 cases) and ATG-F group(38 cases). After treatment for 6 months, the effective rate, side reaction rate and time of effect initiation were compared between 2 groups. The follow-up results were compared between 2 groups. RESULTS: The effective rate and side reaction rate in ATG-F+CsA group were 100.00% and 32.50% respectively, those in ATG-F group were 94.74% and 44.74% respectively and without statistical significant difference(P>0.05). In ATG-F+CsA group, the time of effect initiation in cured patients, remission and obvious inprovement were (44.9+/-15.4) d, (68.8+/-15.9) d and (85.4+/-17.6) d; in ATG-F group, patients with those were (59.6+/-11.5) d, (94.7+/-17.8) d and (119.8+/-21.4) d respectively, the difference showed statistical significance(P<0.05). The follow-up results were not statistically significantly different between 2 groups(P>0.05). CONCLUSION: ATG-F combined with CsA can shorten the time of effect initiation, and demonstrates reliable safety.

Cyclosporin-A potently induces highly cardiogenic progenitors from embryonic stem cells.[Pubmed:19094963]

Biochem Biophys Res Commun. 2009 Jan 30;379(1):115-20.

Though cardiac progenitor cells should be a suitable material for cardiac regeneration, efficient ways to induce cardiac progenitors from embryonic stem (ES) cells have not been established. Extending our systematic cardiovascular differentiation method of ES cells, here we show efficient and specific expansion of cardiomyocytes and highly cardiogenic progenitors from ES cells. An immunosuppressant, cyclosporin-A (CSA), showed a novel effect specifically acting on mesoderm cells to drastically increase cardiac progenitors as well as cardiomyocytes by 10-20 times. Approximately 200 cardiomyocytes could be induced from one mouse ES cell using this method. Expanded progenitors successfully integrated into scar tissue of infracted heart as cardiomyocytes after cell transplantation to rat myocardial infarction model. CSA elicited specific induction of cardiac lineage from mesoderm in a novel mesoderm-specific, NFAT independent fashion. This simple but efficient differentiation technology would be extended to induce pluripotent stem (iPS) cells and broadly contribute to cardiac regeneration.

Evidence that cyclosporin A and dexamethasone inhibit allergic airway eosinophilic inflammation via suppression of interleukin-5 synthesis by T cells.[Pubmed:9723954]

Br J Pharmacol. 1998 Aug;124(7):1425-32.

1. We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusing interleukin (IL)-5-producing T cell clones. Using that murine model, we performed this study to delineate the mechanism of Cyclosporin A and dexamethasone to inhibit allergic airway eosinophilic inflammation. 2. The ovalbumin-reactive murine T cell clones, FJ17, produced IL-2, IL-4 and IL-5 upon stimulation with relevant antigen. In FJ17-transferred mice, messenger RNA (mRNA) of IL-2 and IL-5 expressed in the lungs, the number of eosinophils in bronchoalveolar lavage fluid (BALF) was increased and the bronchial responsiveness to acetylcholine was enhanced after antigen provocation. 3. Cyclosporin A (10, 100 ng ml(-1)) and dexamethasone (10, 100 ng ml(-1) suppressed the production of IL-5 as well as IL-2 and IL-4 by FJ17 in vitro. 4. Subcutaneously administered Cyclosporin A (30 mg kg(-1)) and dexamethasone (10 mg kg(-1)) inhibited antigen-induced mRNA expression of IL-2 and IL-5, increase of BALF eosinophils and bronchial hyperresponsiveness of FJ17-transferred mice in vivo. The number of BALF eosinophils was correlated with the bronchial responsiveness to acetylcholine (r=0.672). 5. The results clearly indicated that the suppression of IL-5 synthesis by T cells is involved in the effects of Cyclosporin A and dexamethasone to inhibit allergic airway eosinophilic inflammation.

Inhibition of the mitochondrial permeability transition by cyclosporin A during long time frame experiments: relationship between pore opening and the activity of mitochondrial phospholipases.[Pubmed:8845372]

Biochemistry. 1995 Dec 19;34(50):16440-9.

Inhibition of the mitochondrial permeability transition pore by Cyclosporin A or trifluoperazine is transient on the time scale of cell injury studies (hours). However, these agents act synergistically and produce long-lasting inhibition when used in combination. The cause of this synergism has been investigated from the perspective of the known action of trifluoperazine as an inhibitor of mitochondrial phospholipase A2. Free fatty acids, which are phospholipase reaction products, facilitate pore opening in a concentration-dependent manner (I50 approximately 2 nmol/mg of mitochondrial protein). Endogenous and exogenous fatty acids are similarly effective. Fatty acids of differing structure are also similarly effective, but long-chain alcohols and alkanes are ineffective. Free fatty acids accumulate in Cyclosporin A-treated mitochondria when Ca2+ plus tert-butyl hydroperoxide or Ca2+ plus N-ethylmaleimide is present, but do not accumulate when Ca2+ plus inorganic phosphate is present. In the presence of Cyclosporin A, bovine serum albumin markedly delays pore opening induced by tert-butyl hydroperoxide or N-ethylmaleimide, but has little effect on pore opening induced by inorganic phosphate, which is subject to long-lasting inhibition by Cyclosporin A without trifluoperazine. Free fatty acid accumulation is thus a factor which limits pore inhibition by Cyclosporin A. However, trifluoperazine has no effect on free fatty acid accumulation in intact, cyclosporin-inhibited mitochondria and thus does not act by inhibiting phospholipases. Comparing the actions of free fatty acids, trifluoperazine, long-chain acyl cations, and other effectors on the pore suggests that a more negative membrane surface potential favors pore opening and a more positive potential favors a closed pore. Expected surface potential effects of trifluoperazine can explain the synergism between this compound and Cyclosporin A as pore inhibitors. Surface potential may influence the pore through the voltage-sensing element which responds to transmembrane potential. The present data also suggest that long-lived, solute-selective forms of the pore exist when it is opened in the presence of inhibitors. The implications of these findings for pore regulation and for the use of Cyclosporin A to identify pore opening as a component of cell injury mechanisms are discussed.

Calcineurin phosphatase activity in T lymphocytes is inhibited by FK 506 and cyclosporin A.[Pubmed:1373887]

Proc Natl Acad Sci U S A. 1992 May 1;89(9):3686-90.

The immunosuppressive agents Cyclosporin A (CsA) and FK 506 bind to distinct families of intracellular proteins (immunophilins) termed cyclophilins and FK 506-binding proteins (FKBPs). Recently, it has been shown that, in vitro, the complexes of CsA-cyclophilin and FK 506-FKBP-12 bind to and inhibit the activity of calcineurin, a calcium-dependent serine/threonine phosphatase. We have investigated the effects of drug treatment on phosphatase activity in T lymphocytes. Calcineurin is expressed in T cells, and its activity can be measured in cell lysates. Both CsA and FK 506 specifically inhibit cellular calcineurin at drug concentrations that inhibit interleukin 2 production in activated T cells. Rapamycin, which binds to FKBPs but exhibits different biological activities than FK 506, has no effect on calcineurin activity. Furthermore, excess concentrations of rapamycin prevent the effects of FK 506, apparently by displacing FK 506 from FKBPs. These results show that calcineurin is a target of drug-immunophilin complexes in vivo and establish a physiological role for calcineurin in T-cell activation.

Description

Cyclosporin A is an immunosuppressant which binds to the cyclophilin and inhibits phosphatase activity of calcineurin with an IC50 of 5 nM. Cyclosporin A also inhibits CD11a/CD18 adhesion.

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