Urantide

Urantide acts as selective and competitive urotensin-II (UT) receptor antagonist (pKB = 8.3), which blocks hU-II induced contractions in thoracic aorta ex vivo, and has no effect on noradrenaline or endothelin 1-induced contraction or on acetylcholine-induced relaxation. It behaves as a partial agonist in a calcium mobilization assay (in CHO cells expressing hUT receptors).

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CAT#	R1053
CAS	669089-53-6
Background	Urantide is a GPR14 antagonist peptide derived from human UII and is currently considered to be the predominant GPR14 antagonist, exhibiting an antagonistic effect that is 50-100-fold stronger compared with that of other chemical compounds. >> Read More
Synonyms/Alias	1: PN: WO2005023845 SEQID: 1 Claimed Protein; L-α-Aspartyl-3-mercapto-L-valyl-L-phenylalanyl-D-tryptophyl-L-ornithyl-L-tyrosyl-L-cysteinyl-L-valine Cyclic (2→7)-Disulfide;
M.F/Formula	C51H66N10O12S2
M.W/Mr.	1075.26
Sequence	DXFWXYCV(Modifications: X-2 = Pen, X-5 = Orn, Trp-4 = D-Trp, Disulfide bridge: 2-7)
Labeling Target	Urotensin-II (UT) receptor
Activity	Antagonist

CAT#	Product Name	M.W	Molecular Formula	Inquiry
R1003	[Orn5]-URP	1003.2	C48H62N10O10S2	Inquiry

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Storage	-20°C
InChI	InChI=1S/C51H66N10O12S2/c1-27(2)41(50(72)73)60-48(70)39-26-74-75-51(3,4)42(61-43(65)33(53)24-40(63)64)49(71)58-37(21-28-11-6-5-7-12-28)45(67)57-38(23-30-25-54-34-14-9-8-13-32(30)34)47(69)55-35(15-10-20-52)44(66)56-36(46(68)59-39)22-29-16-18-31(62)19-17-29/h5-9,11-14,16-19,25,27,33,35-39,41-42,54,62H,10,15,20-24,26,52-53H2,1-4H3,(H,55,69)(H,56,66)(H,57,67)(H,58,71)(H,59,68)(H,60,70)(H,61,65)(H,63,64)(H,72,73)/t33-,35-,36-,37-,38+,39-,41-,42-/m0/s1
InChI Key	VXLUBANOZQJZFE-QVKHRKAHSA-N
Isomeric SMILES	CC(C)[C@@H](C(=O)O)NC(=O)[C@@H]1CSSC([C@H](C(=O)N[C@H](C(=O)N[C@@H](C(=O)N[C@H](C(=O)N[C@H](C(=O)N1)CC2=CC=C(C=C2)O)CCCN)CC3=CNC4=CC=CC=C43)CC5=CC=CC=C5)NC(=O)[C@H](CC(=O)O)N)(C)C
References	In vivo daily administration of urantide for three days resulted in reduced blood TG, TC, HDL and LDL levels in rat aortic tissue, in addition to the downregulation of the expression of the inflammatory mediators CRP and MCP-1, thus improving the symptoms of AS. These effects were identified to be time-dependent. Urantide improves atherosclerosis by controlling Creactive protein, monocyte chemotactic protein1 and transforming growth factor-β expression in rats Urantide, a hU-II analogue, is a potent UT receptor antagonist that could block hU-II-induced contractions in the rat isolated thoracic aorta and displaces 125I-hU-II binding on UT receptor transfected CHO/K1 cells. Though our preliminary studies have shown that urantide had a protective effect against myocardial IR injury in rats and mice, the cardioprotection property needed to be confirmed by further study. The post-receptorial mechanism of urantide on myocardial IR injury is still not clear. It is currently known that protein kinase C (PKC) and phosphtidylinositol 3′-kinase – Akt (PI3K–Akt) signaling pathways are involved in protection against myocardial IR injury. The present study was therefore designed to confirm the protective effect of urantide against myocardial IR injury in rats and to investigate whether PKC and PI3K–Akt signaling pathways are involved in the protective effects of urantide. Protective effect of urantide against ischemia–reperfusion injury via protein kinase C and phosphtidylinositol 3′-kinase – Akt pathway