| Description |
Gap19, a peptide derived from nine amino acids of the Cx43 cytoplasmic loop (CL), is a potent and selective connexin 43 (Cx43) hemichannel blocker. Gap19 inhibits hemichannels caused by preventing intramolecular interactions of the C-terminus (CT) with the CL. Gap19 is not blocking GJ channels or Cx40/pannexin-1 hemichannels. Gap19 has protective effects against myocardial[1][2].
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| Related Catalog |
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| Target |
Cx43 Hemichannel[1]
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| In Vitro |
Gap19 (250 μM; for 30 min ) decreases mitochondrial potassium uptake[1]. Gap19 (400 μM) inhibits unitary hemichannel currents in HeLa-Cx43 cells[2]. Gap19 (100 μM) inhibits hemichannel unitary currents in ventricular cardiomyocytes[2]. Gap19 (250 μM, 30 min) protects against myocardial ischemia/reperfusion injury in vitro and in vivo[2].
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| In Vivo |
Gap19 (iv; 25 mg/kg; 10 min before ligation) significantly reduces the infarct size by approximately one-fifth[2]. Animal Model: C57/BL6 mice[2] Dosage: 25 mg/kg Administration: IV; 10 min before ligation Result: Significantly reduced the infarct size by approximately one-fifth.
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| References |
[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.
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