Global InformationHMR 1883 information
 | This article may be too technical for most readers to understand. (March 2011) |
HMR 1883 (1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenyl]sulfonyl-3 methylthiourea) and its sodium salt HMR 1098, are experimental anti-arrhythmic drugs classified as sulfonylthiourea compounds.[1] Their main purpose is to treat ventricular fibrillation caused by myocardial ischemia. They were synthesized via structural modifications to glibenclamide, an antidiabetic drug.[1] Both HMR 1883 and glibenclamide act by inactivating the ATP-sensitive potassium channels (KATP) responsible for potassium efflux.[2] Unlike glibenclamide, HMR 1883 has been suggested to target selectively the Kir6.2/SUR2A KATP subtype, found mostly in the membranes of cardiac cells.[3] However, data showing that HMR 1098 inhibits the Kir6.2/SUR1 KATP subtype found in insulin-secreting pancreatic beta cells challenges this view.[4]
- ^ a b Heinrich C. Englert, Uwe Gerlach, Heinz Goegelein, Jens Hartung, Holger Heitsch, Dieter Mania, and Sabine Scheidler. 2001. Cardioselective KATP Channel Blockers Derived from a New Series of m-Anisamidoethylbenzenesulfonylthioureas J. Med. Chem. 44 (7):1085–1098
- ^ Billman, G. E., Englert, H. C., & Schoelkens, B. A. (1998) HMR 1883, a novel cardioselective inhibitor of the ATP- sensitive potassium channel; Part II: effects on susceptibility to ventricular fibrillation induced by myocardial ischemia in conscious dogs. J Pharmacol Exp Therap 286, 1465−1473
- ^ Suzuki, M., Li, R. A., Miki, T., Uemura, H., Sakamoto, N., Ohmoto-Sekine, Y., Tamagawa, M., Ogura, T., Seino, S., Marban, E., & Nakaya, H. (2001). Functional roles of cardiac and vascular ATP-sensitive potassium channels clarified by Kir6.2-knockout mice. Circ Res 88, 570−577.
- ^ Hai Xia Zhang, Alejandro Akrouh, Harley T Kurata, Maria Sara Remedi, Jennifer S Lawton, Colin G Nichols. 2011. HMR 1098 is not an SUR isotype specific inhibitor of heterologous or sarcolemmal KATP channels. J. Mol. Cell. Cardiol. 50(3):552-560