GIP (1-39) - CAS 725474-97-5
Category: Inhibitor
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Molecular Formula:
C210H316N56O61S
Molecular Weight:
4633.21
COA:
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Targets:
GIP Receptor
Description:
GIP (1-39) is an endogenous truncated form of the incretin hormone GIP. GIP (1-39) has the high potency at stimulating glucose-dependent insulin secretion from rat pancreatic β-cells than GIP.
Sequence:
Tyr-Ala-Glu-Gly-xiThr-Phe-xiIle-Ser-Asp-Tyr-Ser-xiIle-Ala-Met-Asp-Lys-xiIle-Arg-Gln-Gln-Asp-Phe-Val-Asn-Trp-Leu-Leu-Ala-Gln-Lys-Gly-Lys-Lys-Ser-Asp-Trp-Lys-His-Asn
Synonyms:
Gastric Inhibitory Polypeptide (1-39)
MSDS:
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InChIKey:
URQGMGVMCZCZDR-UHFFFAOYSA-N
InChI:
InChI=1S/C210H316N56O61S/c1-18-107(10)169(266-203(320)155(102-269)260-190(307)141(85-117-58-62-122(272)63-59-117)247-197(314)150(93-166(286)287)255-202(319)154(101-268)261-207(324)171(109(12)20-3)265-200(317)143(84-115-44-25-22-26-45-115)256-208(325)172(113(16)270)262-162(279)99-229-178(295)134(67-71-163(280)281)235-173(290)110(13)231-176(293)125(216)82-116-56-60-121(271)61-57-116)205(322)233-112(15)175(292)237-138(72-79-328-17)186(303)253-148(91-164(282)283)195(312)241-132(54-35-40-77-215)187(304)264-170(108(11)19-2)206(323)244-133(55-41-78-225-210(222)223)180(297)242-136(65-69-157(218)274)184(301)243-137(66-70-158(219)275)185(302)252-149(92-165(284)285)196(313)248-142(83-114-42-23-21-24-43-114)199(316)263-168(106(8)9)204(321)257-147(89-159(220)276)194(311)249-145(87-119-96-227-127-49-30-28-47-124(119)127)192(309)246-140(81-105(6)7)189(306)245-139(80-104(4)5)188(305)232-111(14)174(291)236-135(64-68-156(217)273)183(300)238-128(50-31-36-73-211)177(294)228-98-161(278)234-129(51-32-37-74-212)179(296)239-131(53-34-39-76-214)182(299)259-153(100-267)201(318)254-151(94-167(288)289)198(315)250-144(86-118-95-226-126-48-29-27-46-123(118)126)191(308)240-130(52-33-38-75-213)181(298)251-146(88-120-97-224-103-230-120)193(310)258-152(209(326)327)90-160(221)277/h21-30,42-49,56-63,95-97,103-113,125,128-155,168-172,226-227,267-272H,18-20,31-41,50-55,64-94,98-102,211-216H2,1-17H3,(H2,217,273)(H2,218,274)(H2,219,275)(H2,220,276)(H2,221,277)(H,224,230)(H,228,294)(H,229,295)(H,231,293)(H,232,305)(H,233,322)(H,234,278)(H,235,290)(H,236,291)(H,237,292)(H,238,300)(H,239,296)(H,240,308)(H,241,312)(H,242,297)(H,243,301)(H,244,323)(H,245,306)(H,246,309)(H,247,314)(H,248,313)(H,249,311)(H,250,315)(H,251,298)(H,252,302)(H,253,303)(H,254,318)(H,255,319)(H,256,325)(H,257,321)(H,258,310)(H,259,299)(H,260,307)(H,261,324)(H,262,279)(H,263,316)(H,264,304)(H,265,317)(H,266,320)(H,280,281)(H,282,283)(H,284,285)(H,286,287)(H,288,289)(H,326,327)(H4,222,223,225)
Canonical SMILES:
CCC(C)C(C(=O)NC(CCCNC(=N)N)C(=O)NC(CCC(=O)N)C(=O)NC(CCC(=O)N)C(=O)NC(CC(=O)O)C(=O)NC(CC1=CC=CC=C1)C(=O)NC(C(C)C)C(=O)NC(CC(=O)N)C(=O)NC(CC2=CNC3=CC=CC=C32)C(=O)NC(CC(C)C)C(=O)NC(CC(C)C)C(=O)NC(C)C(=O)NC(CCC(=O)N)C(=O)NC(CCCCN)C(=O)NCC(=O)NC(CCCCN)C(=O)NC(CCCCN)C(=O)NC(CO)C(=O)NC(CC(=O)O)C(=O)NC(CC4=CNC5=CC=CC=C54)C(=O)NC(CCCCN)C(=O)NC(CC6=CNC=N6)C(=O)NC(CC(=O)N)C(=O)O)NC(=O)C(CCCCN)NC(=O)C(CC(=O)O)NC(=O)C(CCSC)NC(=O)C(C)NC(=O)C(C(C)CC)NC(=O)C(CO)NC(=O)C(CC7=CC=C(C=C7)O)NC(=O)C(CC(=O)O)NC(=O)C(CO)NC(=O)C(C(C)CC)NC(=O)C(CC8=CC=CC=C8)NC(=O)C(C(C)O)NC(=O)CNC(=O)C(CCC(=O)O)NC(=O)C(C)NC(=O)C(CC9=CC=C(C=C9)O)N
1.Impaired beta-cell function, incretin effect, and glucagon suppression in patients with type 1 diabetes who have normal fasting glucose.
Greenbaum CJ1, Prigeon RL, D'Alessio DA. Diabetes. 2002 Apr;51(4):951-7.
We have recently described a novel phenotype in a group of subjects with type 1 diabetes that is manifested by glucose >11.1 mmol/l 120 min after an oral glucose load, but with normal fasting glucose levels. We now describe the metabolic characteristics of these subjects by comparing parameters of islet hormone secretion and glucose disposal in these subjects to age-matched nondiabetic control subjects. The patients with type 1 diabetes had fasting glucose, insulin, and glucagon values similar to those of control subjects. Additionally, the insulin secretory response to intravenous arginine at euglycemia was similar in the control and diabetic groups (264 +/- 33.5 and 193 +/- 61.3 pmol/l; P = 0.3). However, marked differences in beta-cell function were found in response to hyperglycemia. Specifically, the first-phase insulin response was lower in diabetic subjects (329.1 +/- 39.6 vs. 91.3 +/- 34.1 pmol/l; P < 0.001), as was the slope of glucose potentiation of the insulin response to arginine (102 +/- 18.
2.Functional expression of the rat pancreatic islet glucose-dependent insulinotropic polypeptide receptor: ligand binding and intracellular signaling properties.
Wheeler MB1, Gelling RW, McIntosh CH, Georgiou J, Brown JC, Pederson RA. Endocrinology. 1995 Oct;136(10):4629-39.
Incretins are endogenous peptides released from the gastrointestinal tract into the circulation during a meal that potentiate glucose-stimulated insulin secretion. At present, there are two established incretins: glucose-dependent insulinotropic polypeptide (GIP) and the truncated glucagon-like peptides (tGLPs), which are now being investigated for use in the treatment of diabetes mellitus. In the present study we cloned a rat islet GIP receptor complementary DNA (GIP-R1) to answer several important questions regarding the ligand-binding and intracellular signaling properties of the GP receptor. GIP-R1, when expressed transiently in monkey kidney (COS-7) or stably in Chinese hamster ovary (CHO-K1) cells, demonstrated comparable high affinity binding for either synthetic porcine (sp) GIP or synthetic human (sh) GIP. The IC50 values for displacement of [125I]spGIP in CHO-K1 cells were 2.6 +/- 0.8 and 3.1 +/- 0.9 nM for two different preparations of shGIP, and 3.
3.[GIP receptor knockout mice].
Naitoh R1, Tsukiyama K, Yamada Y. Nihon Rinsho. 2004 Jun;62(6):1077-84.
Gastric inhibitory polypeptide(GIP) is a gastrointestinal peptide hormone, which is secreted from duodenal endocrine K cells after absorption of glucose or fat. It is well known as an incretin. To determine the further role of GIP in vivo, we generated GIP receptor-knockout mice. The mice showed higher blood glucose levels with impaired initial insulin response after oral glucose load. Even after high-fat diet, knockout mice lack compensatory insulin secretion, and showed no hyper-insulinemia. Moreover, knockout mice fed a high-fat diet were clearly protected from both the obesity and the insulin resistance. Therefore, GIP directly links glucose tolerance and over-nutrition to obesity and it is a potential target for the treatment for the metabolic syndrome.
4.Antagonism of gastric inhibitory polypeptide (GIP) by palmitoylation of GIP analogues with N- and C-terminal modifications improves obesity a
Pathak V1, Gault VA1, Flatt PR1, Irwin N2. Mol Cell Endocrinol. 2015 Feb 5;401:120-9. doi: 10.1016/j.mce.2014.10.025. Epub 2014 Nov 6.
Compromise of gastric inhibitory polypeptide (GIP) receptor signalling represents a possible therapeutic strategy for the treatment of obesity-related diabetes. This study has characterised and evaluated the C-terminally fatty acid derivatised GIP analogues, GIP(3-30)Cex-K(40)[Pal] and Pro(3)GIP(3-30)Cex-K(40)[Pal], as potential GIP inhibitors. Both GIP analogues lack the two N-terminal amino acids cleaved by DPP-4 and have addition of nine amino acids from the C-terminal of exendin(1-39), Cex. GIP(3-30)Cex-K(40)[Pal] and Pro(3)GIP(3-30)Cex-K(40)[Pal] effectively (p < 0.01 to p < 0.001) inhibited GIP-induced cAMP production and insulin secretion in vitro. In normal mice, GIP(3-30)Cex-K(40)[Pal] and Pro(3)GIP(3-30)Cex-K(40)[Pal] displayed a significant (p < 0.05 to p < 0.001) and prolonged inhibitory effect on GIP-induced glucose-lowering and insulin-releasing actions. When injected once daily for 21 days in obese-diabetic high fat fed mice, both GIP(3-30)Cex-K(40)[Pal] and Pro(3)GIP(3-30)Cex-K(40)[Pal] significantly reduced body weight (p < 0.
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CAS 725474-97-5 GIP (1-39)

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