Gap19 TFA, a peptide derived from nine amino acids of the Cx43 cytoplasmic loop (CL), is a potent and selective connexin 43 (Cx43) hemichannel blocker. Gap19 TFA inhibits hemichannels caused by preventing intramolecular interactions of the C-terminus (CT) with the CL. Gap19 TFA is not blocking GJ channels or Cx40/pannexin-1 hemichannels. Gap19 TFA has protective effects against myocardial[1][2].
Gap19 TFA (250 μM; for 30 min ) decreases mitochondrial potassium uptake[1]. Gap19 TFA (400 μM) inhibits unitary hemichannel currents in HeLa-Cx43 cells[2]. Gap19 TFA (100 μM) inhibits hemichannel unitary currents in ventricular cardiomyocytes[2]. Gap19 TFA (250 μM, 30 min) protects against myocardial ischemia/reperfusion injury in vitro and in vivo[2].
Gap19 TFA (iv; 25 mg/kg; 10 min before ligation) significantly reduces the infarct size by approximately one-fifth[2]. Animal Model: C57/BL6 mice[2]
[1]. Boengler K, et al. Connexin 43 impacts on mitochondrial potassium uptake. Front Pharmacol. 2013 Jun 6;4:73. [2]. Wang N, et al. Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury. Basic Res Cardiol. 2013 Jan;108(1):309.