Cyclosporin C
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| Category | Cyclosporin Analogue Set |
| Catalog number | BBF-05763 |
| CAS | 59787-61-0 |
| Molecular Weight | 1218.61 |
| Molecular Formula | C62H111N11O13 |
| Purity | ≥90% by HPLC |
Ordering Information
| Catalog Number | Size | Price | Stock | Quantity |
|---|---|---|---|---|
| BBF-05763 | 20 mg | $199 | In stock |
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Add to cartDescription
A minor analogue of the cyclosporin complex produced by a number of fungal species, including trichoderma, tolypocladium, fusarium, nectria and acremonium. It has the immunosuppressant activity but has been much less extensively investigated than the major analogue, cyclosporin A. Cyclosporin C is a broad-spectrum antifungal agent against filamentous phytopathogenic fungi but no activity against bacteria or yeasts.
Specification
| Synonyms | 7-L-Threoninecyclosporin A; WF 3484 |
| Sequence | XTXLVLAALL V |
| Storage | Store at -20°C |
| IUPAC Name | (3S,6S,9S,12R,15S,18S,21S,24S,30S,33S)-30-[(1R)-1-hydroxyethyl]-33-[(E,1R,2R)-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 |
| Canonical SMILES | CC=CCC(C)C(C1C(=O)NC(C(=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)N1C)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)C(C)O)O |
| InChI | InChI=1S/C62H111N11O13/c1-25-26-27-39(14)52(76)51-56(80)66-49(42(17)74)60(84)67(18)32-47(75)68(19)43(28-33(2)3)55(79)65-48(37(10)11)61(85)69(20)44(29-34(4)5)54(78)63-40(15)53(77)64-41(16)57(81)70(21)45(30-35(6)7)58(82)71(22)46(31-36(8)9)59(83)72(23)50(38(12)13)62(86)73(51)24/h25-26,33-46,48-52,74,76H,27-32H2,1-24H3,(H,63,78)(H,64,77)(H,65,79)(H,66,80)/b26-25+/t39-,40+,41-,42-,43+,44+,45+,46+,48+,49+,50+,51+,52-/m1/s1 |
| InChI Key | JTOKYIBTLUQVQV-QRVTZXGZSA-N |
| Source | Trichoderma sp. |
Properties
| Appearance | White to Off-white Solid |
| Antibiotic Activity Spectrum | fungi |
| Boiling Point | 1316°C at 760 mmHg |
| Melting Point | 152-155°C |
| Density | 1.033 g/cm3 |
| Solubility | Soluble in ethanol, methanol, DMF, DMSO |
Reference Reading
1. Identification of cyclosporin C from Amphichorda felina using a Cryptococcus neoformans differential temperature sensitivity assay
Lijian Xu, Yan Li, John B Biggins, Brian R Bowman, Gregory L Verdine, James B Gloer, J Andrew Alspaugh, Gerald F Bills Appl Microbiol Biotechnol. 2018 Mar;102(5):2337-2350. doi: 10.1007/s00253-018-8792-0. Epub 2018 Feb 2.
We used a temperature differential assay with the opportunistic fungal pathogen Cryptococcus neoformans as a simple screening platform to detect small molecules with antifungal activity in natural product extracts. By screening of a collection extracts from two different strains of the coprophilous fungus, Amphichorda felina, we detected strong, temperature-dependent antifungal activity using a two-plate agar zone of inhibition assay at 25 and 37 °C. Bioassay-guided fractionation of the crude extract followed by liquid chromatography-mass spectrometry (LC-MS) and nuclear magnetic resonance spectroscopy (NMR) identified cyclosporin C (CsC) as the main component of the crude extract responsible for growth inhibition of C. neoformans at 37 °C. The presence of CsC was confirmed by comparison with a commercial standard. We sequenced the genome of A. felina to identify and annotate the CsC biosynthetic gene cluster. The only previously characterized gene cluster for the biosynthesis of similar compounds is that of the related immunosuppressant drug cyclosporine A (CsA). The CsA and CsC gene clusters share a high degree of synteny and sequence similarity. Amino acid changes in the adenylation domain of the CsC nonribosomal peptide synthase's sixth module may be responsible for the substitution of L-threonine compared to L-α-aminobutyric acid in the CsA peptide core. This screening strategy promises to yield additional antifungal natural products with a focused spectrum of antimicrobial activity.
2. Lethal and Sublethal Toxicity Assessment of Cyclosporin C (a Fungal Toxin) against Plutella xylostella (L.)
Jianhui Wu, Xiaochen Zhang, Muhammad Hamid Bashir, Shaukat Ali Toxins (Basel). 2022 Jul 28;14(8):514. doi: 10.3390/toxins14080514.
Secondary metabolites/toxins produced by Purpeocillium lilacinum (Hypocreales; Phiocordycipitaceae), a well-known insect pathogen, can be used for the management of different insect pests. We report the lethal and sublethal effects of cyclosporin C (a toxin produced by P. lilacinum) against a major vegetable pest, Plutella xylostella, at specific organismal (feeding rate, larval growth, adult emergence, fecundity, and adult longevity) and sub-organismal levels (changes in antioxidant and neurophysiological enzyme activities). The toxicity of cyclosporin C against different larval instars of P. xylostella increased with increasing concentrations of the toxin and the maximum percent mortality rates for different P. xylostella larval instars at different times were observed for the 300 µg/mL cyclosporin C treatment, with an average mortality rate of 100% for all larval instars. The median lethal concentrations (LC50) of cyclosporin C against the first, second, third, and fourth larval instars of P. xylostella 72 h post-treatment were 78.05, 60.42, 50.83, and 83.05 μg/mL, respectively. Different concentrations of cyclosporin C caused a reduction in the average leaf consumption and average larval weight. Different life history parameters, such as the pupation rate (%), adult emergence (%), female fecundity, and female longevity were also inhibited when different concentrations of cyclosporin C were applied topically. The cyclosporin C concentrations inhibited the activities of different detoxifying (glutathione S-transferase, carboxylesterase, and acetylcholinesterase) and antioxidant enzyme (superoxide dismutase, catalase, and peroxidase) activities of P. xylostella when compared to the control. These findings can serve as baseline information for the development of cyclosporin C as an insect control agent, although further work on mass production, formulation, and field application is still required.
3. Cyclosporin C(2) and C(0) concentration monitoring in stable, long-term heart transplant recipients receiving metabolic inhibitors
John E Ray, Anne M Keogh, Andrew J McLachlan, Fatemah Akhlaghi J Heart Lung Transplant. 2003 Jul;22(7):715-22. doi: 10.1016/s1053-2498(02)00649-6.
Background: Cyclosporin (CsA) dose selection is complicated by significant pharmacokinetic variability between patients. Although therapeutic drug monitoring (TDM) has proven to be a useful tool for dose individualization, the search for an effective and practical measure of clinical effect has uncovered a number of options. Monitoring the CsA concentration in a blood sample taken 2 hours after the dose (C(2)) has been utilized but has not been rigorously evaluated in all clinical situations. The aim of this study was to evaluate C(2) and trough (C(0)) CsA concentrations as surrogate markers of area under the concentration-time curve (AUC) in stable, long-term heart transplant recipients receiving CsA alone or with diltiazem and/or ketoconazole. Methods: CsA blood concentration-time data were collected at steady state for 47 stable heart transplant recipients after the morning dose of Neoral. CsA concentration in whole blood was quantitated using the EMIT immunoassay. Patients were stratified into 4 groups, depending on the long-term concomitant administration of drugs known to inhibit CsA metabolism, as part of their routine therapy: Group A (n = 11), CsA alone; Group B (n = 10), CsA with slow-release diltiazem; Group C (n = 13), CsA with ketoconazole; and Group D (n = 12), CsA with a combination of diltiazem and ketoconazole. Results: In Group A, C(2) correlated poorly with AUC(0-5) (r(2) = 0.197; p = 0.17), whereas C(0) (trough blood sample) showed a stronger correlation (r(2) = 0.710; p = 0.001). Correlations of C(0) and C(2) with AUC(0-5) were the same, but weaker in patients receiving CsA and diltiazem (r(2) = 0.650; p = 0.005); however, C(2) correlated strongly with AUC(0-5) in patients receiving ketoconazole (r(2) = 0.870; p < 0.0001) or ketoconazole with diltiazem (r(2) = 0.898; p < 0.0001). C(0) was a poor predictor of AUC(0-5) in the latter 2 groups. Conclusions: C(2) showed a strong correlation with AUC(0-5) in cardiothoracic transplant recipients receiving CsA with ketoconazole, but not with CsA alone or diltiazem. TDM using C(2) as an estimate of AUC requires further evaluation before being applied in long-term, stable cardiac transplant patients, as it may lead to inappropriate dose adjustment of CsA in patients receiving concomitant metabolic inhibitors.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
