Description

Ac-DEVD-CMK (Caspase-3 Inhibitor III) is a selective and irreversible caspase-3 inhibitor. Ac-DEVD-CMK significantly inhibits apoptosis induced by high levels of glucose or 3,20-dibenzoate (IDB; HY-137295). Ac-DEVD-CMK can be used in a variety of experimental approaches to inhibit apoptosis[1][2][3].—Metabolism-sugar/lipid metabolism–C21H31ClN4O11—-[1]Eon Jeong Nam, et al. Syndecan-1 limits the progression of liver injury and promotes liver repair in acetaminophen-induced liver injury in mice. Hepatology. 2017 Nov;66(5):1601-1615.|[2]Lu Cai, et al. Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes. 2002 Jun;51(6):1938-48.|[3]M M Mocanu, et al. Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury. Br J Pharmacol. 2000 May;130(2):197-200.|[4]M Blanco-Molina, et al. Ingenol esters induce apoptosis in Jurkat cells through an AP-1 and NF-kappaB independent pathway. Chem Biol. 2001 Aug;8(8):767-78.|[5]Eon Jeong Nam, et al. Syndecan-1 limits the progression of liver injury and promotes liver repair in acetaminophen-induced liver injury in mice. Hepatology. 2017 Nov;66(5):1601-1615.|[6]Hung KC, et al. Citrate-Induced p85α⁻PTEN Complex Formation Causes G2/M Phase Arrest in Human Pharyngeal Squamous Carcinoma Cell Lines. Int J Mol Sci. 2019 Apr 29;20(9):2105.|[7]Nam EJ, et al. Syndecan-1 limits the progression of liver injury and promotes liver repair in acetaminophen-induced liver injury in mice. Hepatology. 2017 Nov;66(5):1601-1615.–285570-60-7–550.94—-ClCC([C@H](CC(O)=O)NC([C@H](C(C)C)NC([C@H](CCC(O)=O)NC([C@@H](NC(C)=O)CC(O)=O)=O)=O)=O)=O–Metabolic Disease–10 mM in DMSO–Apoptosis;Caspase–Caspase 3–Apoptosis–Peptides