Candesartan Cilexetil (TCV-116) is an angiotensin II receptor antagonist (IC50: 0.26 nM). After hydrolysis of candesartan cilexetil to candesartan during gastrointestinal absorption, candesartan selectively competes with angiotensin II for the binding of the angiotensin II receptor subtype 1 (AT1) in vascular smooth muscle, blocking angiotensin II-mediated vasoconstriction and inducing vasodilatation.

Ang II receptor:0.26 nM

给药5小时后,Candesartan（1 mg/kg,p.o.）在第1和第7天,与依那普利（10 mg/kg,p.o.）以相同的程度降低血压.Candesartan使肾血流量显著增加,但心脏指数无变化.在DCM大鼠的心肌中,Candesartan剂量依赖性地提高功能标记并上调血管紧张素（1-7）,ACE2和MAS1.在Candesartan处理的大鼠中,Candesartan使各种ER应激、凋亡标志物及凋亡细胞的数目降低.在扩张型心肌病的大鼠中,Candesartan剂量依赖性地显示对血管紧张素-II的阻断作用.

Candesartan的前药经胃肠道吸收酯水解活化为Candesartan。Candesartan阻断血管紧张素II对血管紧张素II类型1受体的影响。

Kinetic Methods: In a typical kinetic run, 2.00 mL of assay buffer (20 mM HEPES, 0.5 mM EDTA, 0.035% SDS, pH 7.8) and Suc-Leu-Leu-Val-Tyr-AMC in DMSO are added to a 3 mL fluorescence cuvette, and the cuvette is placed in the jacketed cell holder of a fluorescence spectrophotometer. Reaction temperature is maintained at 37℃ by a circulating water bath. After the reaction solution has reached thermal equilibrium (5 minutes), 1 μL?10 μL of the stock enzyme solution is added to the cuvette. Reaction progress is monitored by the increase in fluorescence emission at 440 nm (λex= 380 nm) that accompanies cleavage of AMC from peptide-AMC substrates.