Non-competitive nicotinic cholinergic antagonist that selectively inhibits nicotinic-stimulated catecholamine secretion from chromaffin cells and noradrenergic neurons (IC50 ~ 200 nM). It blocks nicotinic-induced cationic signaling (IC50 ~ 200 - 250 nM) and inhibits nicotinic-agonist induced desensitization of catecholamine release, and also stimulates mast cell release of histamine via a separate mechanism.
CAT No: R1008
CAS No: 142211-96-9
Synonyms/Alias: Catestatin;142211-96-9;Chromogranin A344-364;EX-A6265;AKOS024457258;PD079356;G83769;
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M.F/Formula | C107H173N37O26S |
M.W/Mr. | 2425.8 |
Sequence | One Letter Code:RSMRLSFRARGYGFRGPGLQL Three Letter Code:H-Arg-Ser-Met-Arg-Leu-Ser-Phe-Arg-Ala-Arg-Gly-Tyr-Gly-Phe-Arg-Gly-Pro-Gly-Leu-Gln-Leu-OH |
Labeling Target | Nicotinic receptor |
Appearance | White lyophilised solid |
Purity | >98% |
Activity | Antagonist |
Length | 21 |
InChI | InChI=1S/C107H173N37O26S/c1-57(2)45-72(95(162)137-70(35-36-81(109)148)93(160)141-77(102(169)170)47-59(5)6)130-84(151)53-127-101(168)80-30-20-43-144(80)85(152)54-128-89(156)67(27-17-40-122-105(114)115)134-97(164)75(48-61-21-11-9-12-22-61)132-83(150)52-126-90(157)74(50-63-31-33-64(147)34-32-63)131-82(149)51-125-88(155)66(26-16-39-121-104(112)113)133-86(153)60(7)129-91(158)68(28-18-41-123-106(116)117)136-98(165)76(49-62-23-13-10-14-24-62)140-100(167)79(56-146)143-96(163)73(46-58(3)4)139-92(159)69(29-19-42-124-107(118)119)135-94(161)71(37-44-171-8)138-99(166)78(55-145)142-87(154)65(108)25-15-38-120-103(110)111/h9-14,21-24,31-34,57-60,65-80,145-147H,15-20,25-30,35-56,108H2,1-8H3,(H2,109,148)(H,125,155)(H,126,157)(H,127,168)(H,128,156)(H,129,158)(H,130,151)(H,131,149)(H,132,150)(H,133,153)(H,134,164)(H,135,161)(H,136,165)(H,137,162)(H,138,166)(H,139,159)(H,140,167)(H,141,160)(H,142,154)(H,143,163)(H,169,170)(H4,110,111,120)(H4,112,113,121)(H4,114,115,122)(H4,116,117,123)(H4,118,119,124)/t60-,65-,66-,67-,68-,69-,70-,71-,72-,73-,74-,75-,76-,77-,78-,79-,80-/m0/s1 |
InChI Key | HCEYIDADOJWYIM-DIWOTYQXSA-N |
Isomeric SMILES | C[C@@H](C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N[C@@H](CC1=CC=C(C=C1)O)C(=O)NCC(=O)N[C@@H](CC2=CC=CC=C2)C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N3CCC[C@H]3C(=O)NCC(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H](CC(C)C)C(=O)O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CC4=CC=CC=C4)NC(=O)[C@H](CO)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CCSC)NC(=O)[C@H](CO)NC(=O)[C@H](CCCNC(=N)N)N |
BoilingPoint | N/A |
References | CST is a biologically highly active peptide. It was originally found to be a non-competitive nicotinic cholinergic antagonist which inhibits catecholamine release from noradrenergic neurons, PC12 and bovine chromaffin cells by an autocrine negative feedback loop and nicotine-induced desensitization of catecholamine release. Furthermore, CST causes release of histamine from peritoneal and pleural mast cells, vasodilation in rats and humans, induces chemotaxis of human monocytes and acts as an antibacterial peptide. CST also exerts effects on the cardiovascular system. In particular, it abolishes isoproterenol-induced positive inotropic and lusitropic effects in the rat heartand regulates blood pressure by acting as an inhibitor of peripheralas well as centralnicotinic-cholinergic receptors and β-adrenoceptors. The significance of CST in the regulation of blood pressure should be emphasized by the facts that lower plasma levels of CST are a risk factor for the development of hypertension in humans, that a naturally occurring human variant of CST alters autonomic function and blood pressure and that arterial hypertension of chga knockout mouse is rescued by exogenous injection of CST. Furthermore, CST acts as an insulin-sensitizing peptide, inhibits gluconeogenesis and lipogenesis and stimulates fatty acid oxidation. And finally, CST is a potent angiogenic cytokine which acts via a basic fibroblast growth factor-dependent mechanism. Catestatin-like immunoreactivity in the rat eye Catestatin is a peptide which is a potent inhibitor of catecholamine secretion and played essential functions in the cardiovascular system. Previous research found that dramatic changes of catestatin were associated with hemodynamics in acute myocardial infarction (AMI) during the first week after the AMI symptoms onset, but whether catestatin is also involved in the pathophysiological progression after AMI and then a predictor for outcomes is not clear. Correlation of Plasma Catestatin Level and the Prognosis of Patients with Acute Myocardial Infarction |
Melting Point | N/A |
4. Low bone turnover and low BMD in Down syndrome: effect of intermittent PTH treatment
5. The spatiotemporal control of signalling and trafficking of the GLP-1R
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