SM19712 (free acid)
CAS No. : 194542-49-9
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| Cat. No. : | HY-120148 |
| M.Wt: | 415.85 |
| Formula: | C18H14ClN5O3S |
| Purity: | >98 % |
| Solubility: |
SM19712 free acid is an orally active, selective endothelin converting enzyme (ECE) inhibitor. SM19712 free acid inhibits conversion of big ET-1 to ET-1. SM19712 free acid attenuates colonic angiogenesis, tissue injury, inflammation, without altering colon shortening or myeloperoxidase levels in mice. SM19712 free acid can be used for the research of inflammatory bowel disease (colitis), ischemic acute renal failure, acute myocardial infarction, and myocardial ischemia/reperfusion injury[1][2][3][4][5].
In Vitro:SM19712 free acid potently inhibits ECE solubilized from rat lung microsomes with an IC50 of 42 nM[3].
SM19712 (10-300 μM) free acid shows high specificity for ECE, with no significant inhibitory activity against NEP, ACE, 13 tested receptors, or 9 tested enzymes at concentrations up to 300 μM[3].
SM19712 (1-100 μM; 6 h) free acid concentration-dependently inhibits endogenous ET-1 production in cultured porcine aortic endothelial cells with an IC50 of 31 μM[3].
SM19712 (100 μM) free acid exhibits high selectivity for endothelin-converting enzyme, with minimal inhibitory effects on neutral endopeptidase, angiotensin converting enzyme, collagenase IV, and other proteinase classes[4].
In Vivo:SM19712 (15 mg/kg; p.o.; daily; 5-6 days) free acid partially attenuates Dextran Sodium Sulfate (HY-116282C)-induced colitis in mice[1].
SM19712 (3-30 mg/kg; i.v.; single bolus 5 minutes before occlusion) dose-dependently attenuates ischemia/reperfusion-induced acute renal failure in Sprague-Dawley rats[2].
SM19712 (0.3-30 mg/kg; i.v.; single dose) free acid dose-dependently suppresses Big ET-1-induced pressor responses in rats[3].
SM19712 (10-30 mg/kg; p.o.; single dose) free acid significantly suppresses big ET-1-induced pressor responses in rats by 37.2%[3].
SM19712 (25.9 mg/kg bolus, 1.7 mg/kg/min infusion; i.v.; single bolus followed by continuous infusion; duration of experiment) free acid significantly reduces infarct size, serum ET-1 elevation, and serum CPK activity in a rabbit model of acute myocardial infarction induced by coronary occlusion and reperfusion[3].
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