CGRP 8-37 (human)CGRP1 receptor antagonist CAS# 119911-68-1 |
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| Cas No. | 119911-68-1 | SDF | Download SDF |
| PubChem ID | 71308663 | Appearance | Powder |
| Formula | C139H230N44O38 | M.Wt | 3125.64 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Calcitonin Gene-Related Peptide 8-37 (human) | ||
| Solubility | H2O : ≥ 20 mg/mL (6.40 mM) *"≥" means soluble, but saturation unknown. | ||
| Sequence | VTHRLAGLLSRSGGVVKNNFVPTNVGSKAF (Modifications: Phe-30 = C-terminal amide) | ||
| SMILES | CC(C)CC(C(=O)NC(CC(C)C)C(=O)NC(CO)C(=O)NC(CCCNC(=N)N)C(=O)NC(CO)C(=O)NCC(=O)NCC(=O)NC(C(C)C)C(=O)NC(C(C)C)C(=O)NC(CCCCN)C(=O)NC(CC(=O)N)C(=O)NC(CC(=O)N)C(=O)NC(CC1=CC=CC=C1)C(=O)NC(C(C)C)C(=O)N2CCCC2C(=O)NC(C(C)O)C(=O)NC(CC(=O)N)C(=O)NC(C(C)C)C(=O)NCC(=O)NC(CO)C(=O)NC(CCCCN)C(=O)NC(C)C(=O)NC(CC3=CC=CC=C3)C(=O)N)NC(=O)CNC(=O)C(C)NC(=O)C(CC(C)C)NC(=O)C(CCCNC(=N)N)NC(=O)C(CC4=CNC=N4)NC(=O)C(C(C)O)NC(=O)C(C(C)C)N | ||
| Standard InChIKey | NDACAFBDTQIYCQ-YVQXRMNASA-N | ||
| Standard InChI | InChI=1S/C139H230N44O38/c1-66(2)48-86(161-102(193)60-155-113(197)74(17)159-120(204)87(49-67(3)4)168-118(202)83(40-31-45-152-138(147)148)163-123(207)90(53-80-57-151-65-158-80)173-136(220)111(77(20)188)182-131(215)105(145)69(7)8)121(205)169-88(50-68(5)6)122(206)176-96(64-186)129(213)165-84(41-32-46-153-139(149)150)119(203)175-94(62-184)115(199)156-58-101(192)154-59-104(195)177-107(71(11)12)134(218)179-108(72(13)14)133(217)166-82(39-28-30-44-141)117(201)171-91(54-98(142)189)125(209)172-92(55-99(143)190)124(208)170-89(52-79-36-25-22-26-37-79)126(210)180-109(73(15)16)137(221)183-47-33-42-97(183)130(214)181-110(76(19)187)135(219)174-93(56-100(144)191)127(211)178-106(70(9)10)132(216)157-61-103(194)162-95(63-185)128(212)164-81(38-27-29-43-140)116(200)160-75(18)114(198)167-85(112(146)196)51-78-34-23-21-24-35-78/h21-26,34-37,57,65-77,81-97,105-111,184-188H,27-33,38-56,58-64,140-141,145H2,1-20H3,(H2,142,189)(H2,143,190)(H2,144,191)(H2,146,196)(H,151,158)(H,154,192)(H,155,197)(H,156,199)(H,157,216)(H,159,204)(H,160,200)(H,161,193)(H,162,194)(H,163,207)(H,164,212)(H,165,213)(H,166,217)(H,167,198)(H,168,202)(H,169,205)(H,170,208)(H,171,201)(H,172,209)(H,173,220)(H,174,219)(H,175,203)(H,176,206)(H,177,195)(H,178,211)(H,179,218)(H,180,210)(H,181,214)(H,182,215)(H4,147,148,152)(H4,149,150,153)/t74-,75-,76+,77+,81-,82-,83-,84-,85-,86-,87-,88-,89-,90-,91-,92-,93-,94-,95-,96-,97-,105-,106-,107-,108-,109-,110-,111-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Peptide antagonist for CGRP1 receptors. |
CGRP 8-37 (human) Dilution Calculator
CGRP 8-37 (human) Molarity Calculator
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Human alpha-calcitonin gene-related peptide (CGRP)-(8-37), but not -(28-37), inhibits carotid vasodilator effects of human alpha-CGRP in vivo.[Pubmed:1915584]
Eur J Pharmacol. 1991 Jul 9;199(3):375-8.
Human alpha-calcitonin gene-related peptide-(8-37) alone (up to doses of 30 nmol kg-1 min-1) had no significant effects on blood pressure, heart rate or common or internal carotid haemodynamics, although it caused significant, reversible, inhibition of the hypotensive, tachycardic, and common and internal carotid vasodilator effects of human alpha-CGRP (0.03 nmol kg-1 min-1) in conscious, Long Evans rats. Human alpha-CGRP-(28-37) up to doses of 300 nmol kg-1 min-1 had no cardiovascular effects itself and did not influence responses to human alpha-CGRP. These results are consistent with the carotid haemodynamic effects of human alpha-CGRP being due largely to activation of the CGRP1-receptor subtype.
Reversal of the inhibitory effects of calcitonin gene-related peptide (CGRP) and amylin on insulin secretion by the 8-37 fragment of human CGRP.[Pubmed:8517876]
Biochem Pharmacol. 1993 Jun 9;45(11):2343-7.
The 8-37 fragment of human calcitonin gene-related peptide [(8-37)hCGRP] antagonizes the effects of calcitonin gene-related peptide (CGRP) and amylin in a number of tissues. We have studied the influence of (8-37)hCGRP on the effects of both CGRP and amylin on insulin secretion. In the perfused rat pancreas, homologous CGRP and amylin, at 75 pM, exerted comparable inhibitory effects on the insulin response to 9 mM glucose (ca. 70%; P < 0.025). These effects were antagonized by (8-37)hCGRP (1 microM). Our results suggest that CGRP and amylin act on the B-cell, at least in part, through a common receptor.
BIBN4096BS and CGRP(8-37) antagonize the relaxant effects of alpha-CGRP more than those of beta-CGRP in human extracranial arteries.[Pubmed:15983761]
Naunyn Schmiedebergs Arch Pharmacol. 2005 May;371(5):383-92.
We hypothesize that dilatation of extracranial arteries during migraine could be caused by CGRP. We compared the relaxant effects of alpha-calcitonin gene-related peptide (alpha-CGRP) and beta-calcitonin gene-related peptide (beta-CGRP) and the antagonism by BIBN4096BS and CGRP(8-37) on rings of human temporal and occipital arteries precontracted with KCl. beta-CGRP relaxed temporal (-logEC50M = 8.1) and occipital arteries (-logEC50M = 7.6) with 19-fold and 29-fold lower potencies respectively than alpha-CGRP. Nearly maximal effective concentrations of alpha-CGRP (4 nM) and beta-CGRP (50 nM) caused stable relaxations of the temporal artery for 4 h without fading. BIBN4094BS antagonized the effects of alpha-CGRP (pK(B) = 10.1 and 9.9, respectively) more than beta-CGRP (pK(B) = 9.3 and 9.2 respectively) on both temporal and occipital arteries. CGRP(8-37) antagonized the effects of alpha-CGRP (pK(B) = 6.6 and 6.4 respectively) more than beta-CGRP (pK(B) = 5.7 and 5.5 respectively) on both temporal and occipital arteries. Antagonism of the relaxant effects of alpha-CGRP (4 nM) and beta-CGRP (50 nM) by BIBN4096BS (10 and 100 nM) was reversible for beta-CGRP, but irreversible for alpha-CGRP, 1 h after BIBN4096BS washout. We conclude that alpha-CGRP and beta-CGRP interact either at different binding sites of the same CGRP receptor system or all together with different receptor systems in human extracranial arteries. BIBN4096BS binds more firmly to the receptor activated by alpha-CGRP than to the receptor activated by beta-CGRP.
BIBN4096BS is a potent competitive antagonist of the relaxant effects of alpha-CGRP on human temporal artery: comparison with CGRP(8-37).[Pubmed:11976276]
Br J Pharmacol. 2002 May;136(1):120-6.
Release of CGRP during migraine may produce harmful dilatation of cranial arteries, thereby possibly causing pain. We have compared the antagonism by BIBN4096BS and CGRP(8-37) of the relaxant effects of alpha-CGRP on rings of human temporal artery. alpha-CGRP relaxed the arteries precontracted with 9 - 24 mM KCl (-logEC50=9.4) nearly as efficaciously as sodium nitroprusside (10 microM). BIBN4096BS (0.1 - 100 nM) antagonized the effects of alpha-CGRP in surmountable manner with slopes of Schild-plots not different from unity. -LogKB values of 10.1 and 10.4 were estimated for BIBN4096BS when administered before or during the KCl-contracture respectively. BIBN4096BS (1 microM) did not modify the relaxant effects of papaverine and sodium nitroprusside. CGRP(8-37) (1 - 10 microM) antagonized the effects of alpha-CGRP in a surmountable manner with slopes of Schild-plots not different from unity. -LogKB values of 6.6 and 6.7 were estimated for CGRP(8-37) administered before or during the KCl-contracture respectively. The high affinity of BIBN4096BS for CGRP receptors of human temporal artery makes it an excellent tool to explore the hypothesis of CGRP-evoked cerebral vasodilation in migraine.
Calcitonin gene-related peptide as a GH secretagogue in human and rat pituitary somatotrophs.[Pubmed:9757038]
Brain Res. 1998 Oct 5;807(1-2):203-7.
To elucidate the role of calcitonin gene-related peptide (CGRP) in regulating pituitary function, we investigated the effects of CGRP and the related peptide adrenomedullin (AdM) on the secretion of growth hormone (GH) in vitro from human pituitary adenoma cells, rat pituitary tumor (GH3) cells, and normal rat pituitary cells. In 3 of 5 human somatotroph adenomas, GH secretion was stimulated by CGRP (1-100 nM). In one case of somatotroph adenoma, GH release was observed following the addition of 10 nM GHRH and 10 nM CGRP. The addition of CGRP or AdM (1 pM-10 nM) evoked GH secretion from GH3 cells with a bell-shaped distribution curve. CGRP (100 pM) caused the maximum increase of GH secretion (172+/-14 (mean+/-S.D.)% of control). The addition of CGRP8-37, an antagonist of CGRP type 1 receptors, inhibited the stimulatory effect of AdM but did not inhibit the effect of CGRP. The addition of CGRP and AdM evoked moderate GH secretion from normal rat pituitary cells. These results suggested that CGRP is a new GH secretagogue in human and rat pituitary tumor cells.
Structural determinants for binding to CGRP receptors expressed by human SK-N-MC and Col 29 cells: studies with chimeric and other peptides.[Pubmed:9756381]
Br J Pharmacol. 1998 Aug;124(8):1659-66.
Structure-activity relationships for the binding of human alpha-calcitonin gene-related peptide 8-37 (halphaCGRP8-37) have been investigated at the CGRP receptors expressed by human SK-N-MC (neuroblastoma) and Col 29 (colonic epithelia) cells by radioligand binding assays and functional assays (halphaCGRP stimulation of adenylate cyclase). On SK-N-MC cells the potency order was halphaCGRP8-37 > halphaCGRP19-37 = AC187 > rat amylin8-37 > halpha[Tyr0]-CGRP28-37 (apparent pKBs of 7.49+/-0.25, 5.89+/-0.20, 6.18+/-0.19, 5.85+/-0.19 and 5.25+/-0.07). The SK-N-MC receptor appeared CGRP1-like. On Col 29 cells, only halphaCGRP8-37 of the above compounds was able to antagonize the actions of halphaCGRP (apparent pKB=6.48+/-0.28). Its receptor appeared CGRP2-like. halpha[Ala11,18]-CGRP8-37, where the amphipathic nature of the N-terminal alpha-helix has been reduced, bound to SK-N-MC cells a 100 fold less strongly than halphaCGRP8-37. On SK-N-MC cells, halphaCGRP8-18,28-37 (M433) and mastoparan-halphaCGRP28-37 (M432) had apparent pKBs of 6.64+/-0.16 and 6.42+/-0.26, suggesting that residues 19-27 play a minor role in binding. The physico-chemical properties of residues 8-18 may be more important than any specific side-chain interactions. M433 was almost as potent as halphaCGRP8-37 on Col 29 cells (apparent pKB=6.17+/-0.20). Other antagonists were inactive.
Pharmacological characterization of CGRP receptors mediating relaxation of the rat pulmonary artery and inhibition of twitch responses of the rat vas deferens.[Pubmed:9605575]
Br J Pharmacol. 1998 Apr;123(8):1673-83.
1. CGRP receptors mediating vasorelaxation of the rat isolated pulmonary artery and inhibition of contractions of the rat isolated prostatic vas deferens were investigated using CGRP agonists, homologues and the antagonist CGRP8-37. 2. In the pulmonary artery, human (h)alpha-CGRP-induced relaxation of phenylephrine-evoked tone was abolished either by removal of the endothelium or by NG-nitro-L-arginine (10(-5) M). The inhibitory effect of NG-nitro-L-arginine was stereoselectively reversed by L- but not by D-arginine (10(-4) M). Thus, CGRP acts via nitric oxide released from the endothelium. 3. In the endothelium-intact artery, halpha-CGRP, hbeta-CGRP and human adrenomedullin (10(-10) - 3 x 10(-7) M), dose-dependently relaxed the phenylephrine-induced tone with similar potency. Compared with halpha-CGRP, rat amylin was around 50 fold less potent, while [Cys(ACM2,7)] halpha-CGRP (10(-7) - 10(-4) M) was at least 3000 fold less potent. Salmon calcitonin was inactive (up to 10(-4) M). 4 Human alpha-CGRP8-37 (3 x 10(-7) - 3 x 10(-6) M) antagonized halpha-CGRP (pA2 6.9, Schild plot slope 1.2+/-0.1) and hbeta-CGRP (apparent pKB of 7.1+/-0.1 for halpha-CGRP8-37 10(-6) M) in the pulmonary artery. Human beta-CGRP8-37 (10(-6) M) antagonized halpha-CGRP responses with a similar affinity (apparent pKB 7.1+/-0.1). Human adrenomedullin responses were not inhibited by halpha-CGRP8-37 (10(-6) M). 5. In the prostatic vas deferens, halpha-CGRP, hbeta-CGRP and rat beta-CGRP (10(-10) - 3 x 10(-7) M) concentration-dependently inhibited twitch responses with about equal potency, while rat amylin (10(-8) - 10(-5) M) was around 10 fold less potent and the linear analogue [Cys(ACM2,7)] halpha-CGRP was at least 3000 fold weaker. Salmon calcitonin was inactive (up to 10(-4) M). 6 The antagonist effect of halpha-CGRP8-37 (10(-5) 3 x 10(-5)) in the vas deferens was independent of the agonist, with pA2 values against halpha-CGRP of 6.0 (slope 0.9+/-0.1), against hbeta-CGRP of 5.8 (slope 1.1+/-0.1), and an apparent pKB value of 5.8+/-0.1 against both rat beta-CGRP and rat amylin. Human beta-CGRP8-37 (3 x 10(-5) - 10(-4) M) competitively antagonized halpha-CGRP responses (pA2 5.6, slope 1.1+/-0.2). The inhibitory effect of halpha-CGRP on noradrenaline-induced contractions in both the prostatic and epididymal vas deferens was antagonized by halpha-CGRP8-37 (pA2 5.8 and 5.8, slope 1.0+/-0.2 and 1.0+/-0.3, respectively). 7 The effects of halpha-CGRP and halpha-CGRP8-37 in both rat pulmonary artery and vas deferens were not significantly altered by pretreatment with peptidase inhibitors (amastatin, bestatin, captopril, phosphoramidon and thiorphan, all at 10(-6) M). The weak agonist activity of [Cys(ACM2,7)] halpha-CGRP in the vas deferens was not increased by peptidase inhibitors. 8 These data demonstrate that two different CGRP receptors may exist in the rat pulmonary artery and vas deferens, a CGRP1 receptor subtype in the rat pulmonary artery (CGRP8-37 pA2 6.9), while the lower affinity for CGRP8-37 (pA2 6.0) in the vas deferens is consistent with a CGRP2 receptor.
Pharmacology of receptors for calcitonin gene-related peptide and amylin.[Pubmed:8578616]
Trends Pharmacol Sci. 1995 Dec;16(12):424-8.
Calcitonin gene-related peptide (CGRP), a widespread neuropeptide with multiple actions, has substantial homology with amylin, a peptide implicated in insulin-resistant diabetes, and adrenomedullin, a recently discovered potent vasodilator. There is controversy over the existence of CGRP receptor subtypes, and whether independent receptors exist for amylin and adrenomedullin. In this article, the current status of CGRP receptor classification is reviewed by David Poyner, taking particular account of species differences, and evidence is presented supporting the existence of multiple receptors for CGRP, as well as independent binding sites for amylin.
