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Cyclosporin H

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Chemical Structure| 83602-39-5 同义名 : 5-(N-methyl-D-valine)-Cyclosporin A;Sandoz 37-839;5-(N-methyl-D-valine)-Cyclosporin A, Cyclosporin H, Sandoz 37-839
CAS号 : 83602-39-5
货号 : A219301
分子式 : C62H111N11O12
纯度 : 99%+
分子量 : 1202.611
MDL号 : MFCD04039488
存储条件：

粉末 Keep in dark place,Inert atmosphere,Store in freezer, under -20°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(87.31 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 As an initial signal in the innate immunity, the formyl peptide stimulates leukocyte chemotaxis, induces acute and chronic inflammation, and stimulates the release of a number of the cytokine storm mediators from monocytes, neutrophils and endothelial cells by acting through the formyl peptide receptor (FPR). Cyclosporin H, a potent anti-inflammatory compound, acts as a specific competitive antagonist of formyl peptides on FPR on phagocytic: leukocytes. Cyclosporin H completely blocked neutrophil chemotaxis induced by the standard formyl peptide, f-MLF, as well as the bacteria-derived or host-derived formyl peptide[1]. Cyclosporin H (8 to 800 nM) concentration-dependently inhibited histamine and leukotriene C4 release from purified and unpurified basophils activated by FMLP. Furthermore, Cyclosporin H inhibited tritiated FMLP binding to human polymorphonuclear leukocytes with a concentration required to inhibit binding by 50% of approximately 0.54 nM[2]. In vivo treatment by Cyclosporin H in the mouse model of HINI Swine flu influenza infection for 5 days markedly reduced lung inflammation and endothelial cell damage[1].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

0.83mL

0.17mL

0.08mL

4.16mL

0.83mL

0.42mL

8.32mL

1.66mL

0.83mL
参考文献

[1]Elgebaly SA, Elbayoumi T, Kreutzer DL. CYCLOSPORIN H: A NOVEL ANTI-INFLAMMATORY THERAPY FOR INFLUENZA FLU PATIENTS. J Egypt Soc Parasitol. 2017 Apr;47(1):25-33

[2]de Paulis A, Ciccarelli A, de Crescenzo G, Cirillo R, Patella V, Marone G. Cyclosporin H is a potent and selective competitive antagonist of human basophil activation by N-formyl-methionyl-leucyl-phenylalanine. J Allergy Clin Immunol. 1996 Jul;98(1):152-64