Gap 26 TFA

Gap 26 TFA, a gap junction blocker, is a connexin mimetic peptide derived from the amino acid sequence 63-75 in the first extracellular loop of connexin 43, featuring the SHVR amino acid motif [1].

Gap 26 is a mimetic peptide corresponding to the residues 63-75 of connexin 43, which is a gap junction blocker.

Ac2-26 TFA, an active N-terminal peptide of annexin A1 (AnxA1), attenuates ischemia-reperfusion-induced acute lung injury. Ac2-26 also decreases AnxA1 protein expression, inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue.

MART-1 (26-35) (human) TFA is an amino acid residue of 26-35 protein.

Ac2-26 TFA, the active N-terminal peptide of Annexin A1 (AnxA1), mitigates ischemia-reperfusion-induced acute lung injury, reduces AnxA1 protein expression, and inhibits the activation of NF-κB and MAPK pathways in affected lung tissue [1].

Tat-Gap 19, a peptide inhibitor of connexin43 (Cx43) hemichannels, is derived from the HIV-1 Tat protein transduction domain fused with a nine-amino acid sequence from Cx43 residues 128-136. This compound, at a concentration of 10 µM, effectively suppresses glutamate-induced ATP release in primary rat hepatocytes, indicating inhibition of Cx43 hemichannel activity. Furthermore, Tat-Gap 19 demonstrates therapeutic potential by significantly reducing infarct volume in a mouse cerebral ischemia-reperfusion injury model following middle cerebral artery occlusion (MCAO) at a dosage of 25 mg/kg. Moreover, its intraperitoneal administration at 1 mg/kg per day ameliorates fibrosis and decreases the area of hepatic stellate cells, the precursors to myofibroblasts, expressing α-smooth muscle actin (α-SMA), in a model of thioacetamide-induced liver damage. Additionally, it enhances superoxide dismutase (SOD) activity in hepatic cells from the treated mice, indicating its antioxidative benefits.