JKC 363Potent and selective MC4 receptor antagonist CAS# 436083-30-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 436083-30-6 | SDF | Download SDF |
PubChem ID | 118856394 | Appearance | Powder |
Formula | C69H91N19O16S2 | M.Wt | 1506.72 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 1 mg/ml in water | ||
Sequence | XEHXRWGCPPKD (Modifications: Disulfide bridge between 1 - 8, X-1 = Mpr, X-4 = D-2-Nal, Asp-12 = C-terminal amide) | ||
SMILES | C1CC(N(C1)C(=O)C2CCCN2C(=O)C3CSSCCC(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NC(C(=O)NCC(=O)N3)CC4=CNC5=CC=CC=C54)CCCNC(=N)N)CC6=CC7=CC=CC=C7C=C6)CC8=CNC=N8)CCC(=O)O)C(=O)NC(CCCCN)C(=O)NC(CC(=O)N)C(=O)O | ||
Standard InChIKey | RFMOGPSXMCHBKU-CLMJCUFPSA-N | ||
Standard InChI | InChI=1S/C69H91N19O16S2/c70-23-6-5-14-45(61(96)86-51(68(103)104)32-55(71)89)82-65(100)53-16-8-25-87(53)67(102)54-17-9-26-88(54)66(101)52-36-106-105-27-22-56(90)79-47(20-21-58(92)93)62(97)85-50(31-42-34-74-37-78-42)64(99)83-48(29-38-18-19-39-10-1-2-11-40(39)28-38)63(98)81-46(15-7-24-75-69(72)73)60(95)84-49(59(94)77-35-57(91)80-52)30-41-33-76-44-13-4-3-12-43(41)44/h1-4,10-13,18-19,28,33-34,37,45-54,76H,5-9,14-17,20-27,29-32,35-36,70H2,(H2,71,89)(H,74,78)(H,77,94)(H,79,90)(H,80,91)(H,81,98)(H,82,100)(H,83,99)(H,84,95)(H,85,97)(H,86,96)(H,92,93)(H,103,104)(H4,72,73,75)/t45-,46-,47-,48+,49-,50-,51-,52-,53-,54-/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 | Potent and selective melanocortin MC4 receptor antagonist (IC50 values are 0.5 and 44.9 nM at MC4 and MC3 respectively) that antagonizes the effects of α-MSH. Suppresses thyrotropin-releasing hormone (TRH) release, attenuates food intake and reduces formalin-induced pain in vivo. |
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Evidence for an interaction between CB1 cannabinoid and melanocortin MCR-4 receptors in regulating food intake.[Pubmed:15033920]
Endocrinology. 2004 Jul;145(7):3224-31.
Melanocortin receptor 4 (MCR4) and CB(1) cannabinoid receptors independently modulate food intake. Although an interaction between the cannabinoid and melanocortin systems has been found in recovery from hemorrhagic shock, the interaction between these systems in modulating food intake has not yet been examined. The present study had two primary purposes: 1) to examine whether the cannabinoid and melanocortin systems act independently or synergistically in suppressing food intake; and 2) to determine the relative position of the CB(1) receptors in the chain of control of food intake in relation to the melanocortin system. Rats were habituated to the test environment and injection procedure and then received intracerebroventicular injections of various combinations of the MCR4 receptor antagonist JKC-363, the CB(1) receptor agonist Delta(9)-tetrahydrocannabinol, the MCR4 receptor agonist alpha-MSH, or the cannabinoid CB(1) receptor antagonist SR 141716. Food intake and locomotor activity were then recorded for 120 min. When administrated alone, SR 141716 and alpha-MSH dose-dependently attenuated baseline feeding, whereas sub-anorectic doses of SR 141716 and alpha-MSH synergistically attenuated baseline feeding when combined. Delta(9)-Tetrahydrocannabinol-induced feeding was not blocked by alpha-MSH, whereas SR 141716 dose-dependently attenuated JKC-363-induced feeding. Locomotor activity was not significantly affected by any drug treatment, suggesting that the observed effects on feeding were not due to a nonspecific reduction in motivated behavior. These findings revealed a synergistic interaction between the cannabinoid and melanocortin systems in feeding behavior. These results further suggested that CB(1) receptors are located downstream from melanocortin receptors and CB(1) receptor signaling is necessary to prevent the melanocortin system from altering food intake.
Melanocortin receptor agonists and antagonists modulate nociceptive sensitivity in the mouse formalin test.[Pubmed:14660013]
Eur J Pharmacol. 2003 Dec 15;482(1-3):127-32.
A number of studies suggest the involvement of melanocortins in nociception, and although the mechanism through which this occurs is still unknown, experimental evidence would suggest an involvement of melanocortin MC(4) receptors. We investigated the effect of melanocortin receptor agonist and antagonists on nociceptive behaviour induced by formalin in the mouse. The intrathecal injection of the melanocortin receptor agonist MTII ([Ac-Nle(4),Asp(5),D-Phe(7),Lys(10)]cyclo-alpha-MSH-(4-10) amide) (5 nmol; P<0.05) significantly increased nociception in both phases of the formalin test, whereas the synthetic melanocortin receptor antagonists, SHU9119 ([Ac-Nle(4),Asp(5),D-2-Nal(7),Lys(10)]cyclo-alpha-MSH-(4-10) amide) (5 nmol), HS014 ([Ac-Cys(11),D-2-Nal(14),Cys(18)]beta-MSH-(11-22)amide) (5 nmol), and JKC-363 (cyclic [Mpr(11),D-Nal(14),Cys(18),Asp(22)-NH(2)]beta-MSH-11-22)) (5 nmol), and the endogenous receptor antagonist Agouti-related protein (AgRP) (1.5 nmol) were effective in reducing nociception in the late phase of the formalin test (50-60% of reduction in licking/flinching response; P<0.05). The present findings further support the involvement of the melanocortin system in the control of nociception. Moreover, considering that melanocortin MC(4) receptors are the only melanocortin subtype receptors present in the spinal cord, we can assume that the activity of the peptides in the formalin model is mediated through melanocortin MC(4) receptors.
Effects of melanocortin receptor ligands on thyrotropin-releasing hormone release: evidence for the differential roles of melanocortin 3 and 4 receptors.[Pubmed:11963824]
J Neuroendocrinol. 2002 Apr;14(4):276-82.
The hypothalamic melanocortin system is important in the central regulation of food intake and body weight. We have previously demonstrated that intracerebroventricular administration of alpha-melanocyte stimulating hormone (alpha-MSH), a nonselective MC3 and MC4 receptor agonist, stimulated plasma thyroid-stimulating hormone, and agouti-related protein (AgRP), an MC3 and MC4 receptor antagonist, suppressed it. In this study, we investigated the effects of MC3 and MC4 receptor (MC3-R and MC4-R) selective agonists and antagonists on the release of thyrotropin-releasing hormone (TRH) from hypothalamic explants in vitro. alpha-MSH stimulated TRH release from the rat hypothalamic explants (alpha-MSH 100 nm 230 +/- 22.9% basal, P < 0.005). In contrast, gamma 2-MSH, a selective MC3-R agonist, suppressed TRH release (gamma 2-MSH 10 microns 76.2 +/- 7.4% basal, P < 0.05). AgRP (83-132), a nonselective MC3/4-R antagonist, induced no change in TRH release whilst JKC-363 (cyclic [Mpr11, D-Nal14, Cys18, Asp22-NH2]-beta-MSH 11-22), a selective MC4-R antagonist, suppressed it (JKC-363 10 nm 57.2 +/- 11.5% basal, P < 0.05). Both AgRP (83-132) and JKC-363 blocked alpha-MSH stimulated TRH release but only AgRP (83-132) blocked the inhibitory effect of gamma 2-MSH on TRH release. These data suggest differential roles for the MC3 and MC4 receptors in TRH release; MC3-R agonism inhibiting and MC4-R agonism stimulating TRH release.