For research use only. Not for therapeutic Use.
Gap 27, a synthetic connexin43 mimetic peptide, is a gap junction inhibitor. Gap 27 possesses conserved sequence homology to a portion of the second extracellular loop leading into the fourth transmembrane connexin segment[1][2].
Gap 27 causes a remarked decrease in the number of both TRAP-positive mononuclear and multinucleated rat osteoclasts cultured on bovine bone slices. The activity of the remaining osteoclasts is found to be diminished by measuring the percentage of osteoclasts with actin rings of all TRAP-positive cells. In addition, the resorbed area in the treated cultures is greatly diminished[1]. Incubation of the carotid artery with the gap junction inhibitor Gap 27 (500 μM) essentially abolishes the hyperpolarization to acetylcholine but it is without effect on that to levcromakalim. In the guinea-pig isolated internal carotid artery, Gap 27 inhibits acetylcholine-induced, endothelium-dependent hyperpolarizations[2].
Gap 27 (300 μM) inhibits relaxation by 40% in thoracic aorta and the superior mesenteric artery. Gap 27 also attenuates the endothelium-dependent component of the relaxation induced by ATP in thoracic aorta. [3].
| Catalog Number | I013646 |
| CAS Number | 198284-64-9 |
| Molecular Formula | C60H101N15O17 |
| Purity | ≥95% |
| Reference | [1]. Ilvesaro J, et al. Connexin-mimetic peptide Gap 27 decreases osteoclastic activity. BMC Musculoskelet Disord. 2001;2:10. [2]. Edwards G, et al. Role of gap junctions in the responses to EDHF in rat and guinea-pig small arteries. Br J Pharmacol. 1999 Dec;128(8):1788-94. [3]. Chaytor AT,e t al. Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J Physiol. 1998 Apr 15;508 ( Pt 2):561-73. |
