1001015-18-4

CORM-401 is an oxidant-sensitive CO-releasing molecule. CORM-401 induces NO increase in the regulation of endothelial calcium signalling. CORM-401 reduces TNF-α/CHX and H2O2-induced ROS production. CORM-401 uncouples mitochondrial respiration and inhibits glycolysis[1][2][3].

CORM-401 (Mn(CO)4(S2CNMe(CH2CO2H))) is a manganese-containing carbon monoxide-releasing molecule (CORM) th at generates at least three molar equivalents of CO. Due to reversible binding of COCORM-401 is relatively stable in solution (0.33 mol eq of CO loss after 4 h in PBS; [CORM-401] = 1 mM at time zero)while increased CO release occurs in the presence of a CO receptor or a ligand to prevent the rebinding of CO (3.2 mol eq of CO transferred to iron with a t1/2 of 0.8 min in the presence of 44 μM myoglobin; [CORM-401] = 10 μM at time zero). CO administration by CORM-401 is reported to uncouple mitochondrial respiration and inhibit glycolysis in human endothelial cells (10-100 μM)and relax isolated r at aortic rings (25 μM) pre-contracted with phenylephrine.

[1] Kaczara P, et al. CORM-401 induces calcium signalling, NO increase and activation of pentose phosphate pathway in endothelial cells. FEBS J. 2018 Apr;285(7):1346-1358. DOI:10.1111/febs.14411
[2] Babu D, et al. Differential Effects of CORM-2 and CORM-401 in Murine Intestinal Epithelial MODE-K Cells under Oxidative Stress. Front Pharmacol. 2017 Feb 8;8:31. DOI:10.3389/fphar.2017.00031
[3] Kaczara P, et al. Carbon monoxide released by CORM-401 uncouples mitochondrial respiration and inhibits glycolysis in endothelial cells: A role for mitoBKCa channels. Biochim Biophys Acta. 2015 Oct;1847(10):1297-309. DOI:10.1016/j.bbabio.2015.07.004