538925
Prostaglandin I2, Sodium Salt
Potent vasodilatory prostaglandin produced by the endothelium.
别名:
Prostaglandin I2, Sodium Salt, PGI2, Prostacyclin
InChI key
LMHIPJMTZHDKEW-XQYLJSSYSA-M
InChI
1S/C20H32O5.Na/c1-2-3-4-7-14(21)10-11-16-17-12-15(8-5-6-9-20(23)24)25-19(17)13-18(16)22;/h8,10-11,14,16-19,21-22H,2-7,9,12-13H2,1H3,(H,23,24);/q;+1/p-1/b11-10+,15-8-;/t14-,16+,17+,18+,19-;/m0./s1
assay
≥98% (HPLC)
form
crystalline solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, desiccated (hygroscopic)
solubility
water: soluble
shipped in
wet ice
storage temp.
−20°C
Quality Level
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General description
Potent vasodilatory prostaglandin produced by the endothelium. Induces vasodilation, stimulates cAMP formation. Cytoprotective and fibrinolytic. Inhibits platelet aggregation by receptor mediated stimulation of adenylate cyclase.
Biochem/physiol Actions
Cell permeable: no
Primary Target
Induces vasodilation
Induces vasodilation
Product does not compete with ATP.
Reversible: no
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). This product is rapidly hydrolyzed in acidic solutions. The half-life at pH 7.48 is between 3.5 min and 10.5 min at 25°C. At pH 12 the half-life is ~6 days at 25°C. No loss of biological activity was observed at pH 9.37 for 48 h, when stored at 0°C.
Other Notes
Vane, J.R. 1985. Adv. Prostaglandin Thromboxane Leukotriene Res.15, 11.
Moncada, S., et al. 1979. Pharmacol. Rev.30, 293.
Cho, M.J. and Allen, M.A. 1978. Prostaglandins15, 943.
Tateson, J.E., et al. 1977. Prostaglandins13, 389.
Moncada, S., et al. 1979. Pharmacol. Rev.30, 293.
Cho, M.J. and Allen, M.A. 1978. Prostaglandins15, 943.
Tateson, J.E., et al. 1977. Prostaglandins13, 389.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Harmful (C)
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
监管及禁止进口产品
此项目有
Henrike Hoermann et al.
International journal of molecular sciences, 22(22) (2021-11-28)
Vascular injury induces the exposure of subendothelial extracellular matrix (ECM) important to serve as substrate for platelets to adhere to the injured vessel wall to avoid massive blood loss. Different ECM proteins are known to initiate platelet adhesion and activation.
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