GaP19 trifluoroacetate salt

Gap 19 is a nonapeptide derivative of connexin43 (Cx43) and an inhibitor of Cx43 hemichannels.1,2 It suppresses the membrane charge transfer (Qm) in HeLa cells expressing Cx43 (IC50 = ~6.5 µM), as well as Cx43 hemichannel currents in isolated guinea pig cardiomyocytes when used at a concentration of 100 µM.1 Gap 19 inhibits glutamate-induced ATP release, a marker of Cx43 hemichannel activity, in primary mouse astrocytes.2 In vivo, Gap 19 (300 µg/kg, i.c.v.) decreases cortical neuronal loss, infarct volume, and the number of errors in a foot fault test in a mouse model of cerebral ischemia and reperfusion injury induced by middle cerebral artery occlusion (MCAO).3 It also reduces infarct size in a mouse model of myocardial ischemia and reperfusion injury induced by ligation of the left anterior descending (LAD) artery when administered at a dose of 25 mg/kg.1WARNING This product is not for human or veterinary use.

[1] NAN WANG. Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury.[J]. Basic Research in Cardiology, 2013, 108 1: 309. DOI: 10.1007/s00395-012-0309-x
[2] VERÓNICA ABUDARA. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes.[J]. Frontiers in Cellular Neuroscience, 2014: 306. DOI: 10.3389/fncel.2014.00306
[3] BEILEI CHEN . Inhibition of Connexin43 hemichannels with Gap19 protects cerebral ischemia/reperfusion injury via the JAK2/STAT3 pathway in mice[J]. Brain Research Bulletin, 2019, 146: Pages 124-135. DOI: 10.1016/j.brainresbull.2018.12.009