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[D-Lys3]-GHRP-6ghrelin receptor antagonist

[D-Lys3]-GHRP-6

Catalog No. BCC5850
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5mg $142.00 Ship Within 7 Days
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Quality Control of [D-Lys3]-GHRP-6

Chemical structure

[D-Lys3]-GHRP-6

Biological Activity of [D-Lys3]-GHRP-6

Antagonist at the ghrelin receptor (GHS-R1a) (IC50 = 0.9 μM). Also weakly binds to melanocortin receptors (Ki = 26-120 μM). Centrally active in vivo.

[D-Lys3]-GHRP-6 Dilution Calculator

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Chemical Properties of [D-Lys3]-GHRP-6

Cas No. 136054-22-3 SDF Download SDF
Sequence HWKWFK

(Modifications: Trp-2 = D-Trp, Lys-3 = D-Lys, Phe-5 = D-Phe, Lys-6 = C-terminal amide)

Chemical Name (2S)-6-amino-2-[[(2R)-2-[[(2S)-2-[[(2R)-6-amino-2-[[(2R)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]hexanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-phenylpropanoyl]amino]hexanamide
SMILES C1=CC=C(C=C1)CC(C(=O)NC(CCCCN)C(=O)N)NC(=O)C(CC2=CNC3=CC=CC=C32)NC(=O)C(CCCCN)NC(=O)C(CC4=CNC5=CC=CC=C54)NC(=O)C(CC6=CN=CN6)N
Standard InChIKey MGSNWNLPMHXGDD-DFWOJPNQSA-N
Standard InChI InChI=1S/C49H63N13O6/c50-20-10-8-18-39(44(53)63)58-47(66)41(22-30-12-2-1-3-13-30)61-49(68)43(24-32-27-56-38-17-7-5-15-35(32)38)62-46(65)40(19-9-11-21-51)59-48(67)42(23-31-26-55-37-16-6-4-14-34(31)37)60-45(64)36(52)25-33-28-54-29-57-33/h1-7,12-17,26-29,36,39-43,55-56H,8-11,18-25,50-52H2,(H2,53,63)(H,54,57)(H,58,66)(H,59,67)(H,60,64)(H,61,68)(H,62,65)/t36-,39-,40+,41+,42+,43-/m0/s1
Formula C49H63N13O6 M.Wt 930.12
Solubility Soluble to 0.50 mg/ml in water
Storage Desiccate at -20°C
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.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of [D-Lys3]-GHRP-6

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.0751 mL 5.3757 mL 10.7513 mL 21.5026 mL 26.8783 mL
5 mM 0.215 mL 1.0751 mL 2.1503 mL 4.3005 mL 5.3757 mL
10 mM 0.1075 mL 0.5376 mL 1.0751 mL 2.1503 mL 2.6878 mL
50 mM 0.0215 mL 0.1075 mL 0.215 mL 0.4301 mL 0.5376 mL
100 mM 0.0108 mL 0.0538 mL 0.1075 mL 0.215 mL 0.2688 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Background on [D-Lys3]-GHRP-6

IC50: 0.9 μM

[D-Lys3]-GHRP-6 is an antagonist at the ghrelin receptor (GHS-R1a) and weakly binds to melanocortin receptors (Ki = 26-120 μM).

In vitro: [D-Lysa]GHRP-6 used similar affinities to bind to all the four MC receptors, to which the structurally related Met-enkephalin and the functionally related GHuRH, together with LHRH and somatostatin-14 did not bind. This (the low affinity of the GH-releasing/enkephalin peptides) may indicate that they do not interact with the MC receptors at pharmacological concentrations. [DLys3] GHRP-6 only used slightly higher affinity than GHRP-6 to bind to the MC1 receptor. [1].

Compared with GHRP-6, [D-Lys3]GHRP-6 has higher affinity for all the MC receptors, especially for the MC3 and MC4 receptors. Interestingly, [D-Lys 3] GHRP-6 binds to the MC1 receptor with only slightly higher affinity compared with GHRP-6, which may indicate that the basic hydrophilic residue in position 8 is not important for the MC 1 receptor (as the same as he other MC receptor subtypes) [1,2]. The peptidic GHS-receptor antagonist (D-Lys3)-GHRP-6 (10-4 M) antagonized ghrelin (10-7 M) weakly, showing a much weaker affinity (IC50, 0.9×10-6 M) to the GHS-receptor than ghrelin (IC50, 0.3×10-9 M). Ghrelin increased the electrical activity in 76% of all cells inhibited by leptin (n=17). These data reveal that ghrelin interacts with the leptin hypothalamic network in the arcuate nucleus. Leptin and ghrelin oppositely effect on neurons in the arcuate nucleus, which may serve as a neurophysiological correlate of the orexigenic and anorectic effects of them [2].

In vivo: The administration of D-Lys3-GHRP-6 (an antagonist of GHS receptors) alone had no significantly influence on GH secretion. Oppositely, pretreatment with this antagonist efficiently inhibited the stimulatory effect of AMPA and NMDA on GH secretion. To confirm this contention, further experiments to evaluate different protocols (doses, times, additional GHS receptor antagonists) of administration of D-Lys3-GHRP-6 are carried out. Nevertheless, it is possible that ghrelin may only intervene in situations of hypo- or hypersecretion of GH but not involved in the control of basal GH secretion [2].

Clinical trial: So far, no clinical study has been conducted.

References:
[1].  Schith HB, Muceniece R, Wikberg JE. Characterization of the binding of MSH-B, HB-228, GHRP-6 and 153N-6 to the human melanocortin receptor subtypes. Neuropeptides. 1997 Dec;31(6):565-71.
[2].  Traebert M, Riediger T, Whitebread S, Scharrer E, Schmid HA. Ghrelin acts on leptin-responsive neurones in the rat arcuate nucleus. J Neuroendocrinol. 2002 Jul;14(7):580-6.
[3].  Pinilla L, Barreiro ML, Tena-Sempere M, Aguilar E.Role of ghrelin in the control of growth hormone secretion in prepubertal rats: interactions with excitatory amino acids. Neuroendocrinology. 2003 Feb;77(2):83-90.

References on [D-Lys3]-GHRP-6

[D-Lys3]-GHRP-6 exhibits pro-autophagic effects on skeletal muscle.[Pubmed: 25450862]


[D-Lys3]-GHRP-6 is regarded as a highly selective growth-hormone secretagogue receptor (GHSR) antagonist and has been widely used to investigate the dependency of GHSR-1a signalling mediated by acylated ghrelin. However, [D-Lys3]-GHRP-6 has been reported to influence other cellular processes which are unrelated to GHSR-1a. This study aimed to examine the effects of [D-Lys3]-GHRP-6 on autophagic and apoptotic cellular signalling in skeletal muscle. [D-Lys3]-GHRP-6 enhanced the autophagic signalling demonstrated by the increases in protein abundances of beclin-1 and LC3 II-to-LC3 1 ratio in both normal muscle and doxorubicin-injured muscle. [D-Lys3]-GHRP-6 reduced the activation of muscle apoptosis induced by doxorubicin. No histological abnormalities were observed in the [D-Lys3]-GHRP-6-treated muscle. Intriguingly, the doxorubicin-induced increase in centronucleated muscle fibres was not observed in muscle treated with [D-Lys3]-GHRP-6, suggesting the myoprotective effects of [D-Lys3]-GHRP-6 against doxorubicin injury. The [D-Lys3]-GHRP-6-induced activation of autophagy was found to be abolished by the co-treatment of CXCR4 antagonist, suggesting that the pro-autophagic effects of [D-Lys3]-GHRP-6 might be mediated through CXCR4. In conclusion, [D-Lys3]-GHRP-6 exhibits pro-autophagic effects on skeletal muscle under both normal and doxorubicin-injured conditions.

The effect of ghrelin antagonist (D-Lys3) GHRP-6 on ovariectomy-induced obesity in adult female albino rats.[Pubmed: 25110211]


We aimed to investigate the effect of ghrelin antagonist (D-Lys3) GHRP-6 on the treatment of ovariectomy-induced obesity as compared to hormone replacement therapy with estradiol.

Identification of ghrelin receptor blocker, D-[Lys3] GHRP-6 as a CXCR4 receptor antagonist.[Pubmed: 22211109]


[D-Lys3]-Growth Hormone Releasing Peptide-6 (DLS) is widely utilized in vivo and in vitro as a selective ghrelin receptor (GHS-R) antagonist. Unexpectedly, we identified that DLS also has the ability to block CXCL12 binding and activity through CXCR4 on T cells and peripheral blood mononuclear cells (PBMCs). Moreover, as CXCR4 has been shown to act as a major co-receptor for HIV-1 entry into CD4 positive host cells, we have also found that DLS partially blocks CXCR4-mediated HIV-1 entry and propagation in activated human PBMCs. These data demonstrate that DLS is not the specific and selective antagonist as thought for GHS-R1a and appears to have additional effects on the CXCR4 chemokine receptor. Our findings also suggest that structural analogues that mimic DLS binding properties may also have properties of blocking HIV infectivity, CXCR4 dependent cancer cell migration and attenuating chemokine-mediated immune cell trafficking in inflammatory disorders.

The GHS-R blocker D-[Lys3] GHRP-6 serves as CCR5 chemokine receptor antagonist.[Pubmed: 22211090]


[D-Lys3]-Growth Hormone Releasing Peptide-6 (DLS) is widely utilized in vivo and in vitro as a selective ghrelin receptor (GHS-R) antagonist. This antagonist is one of the most common antagonists utilized in vivo to block GHS-R function and activity. Here, we found that DLS also has the ability to modestly block chemokine function and ligand binding to the chemokine receptor CCR5. The DLS effects on RANTES binding and Erk signaling as well as calcium mobilization appears to be much stronger than its effects on MIP-1α and MIP-1β. CCR5 have been shown to act as major co-receptor for HIV-1 entry into the CD4 positive host cells. To this end, we also found that DLS blocks M-tropic HIV-1 propagation in activated human PBMCs. These data demonstrate that DLS may not be a highly selective GHS-R1a inhibitor and may also effects on other G-protein coupled receptor (GPCR) family members. Moreover, DLS may have some potential clinical applications in blocking HIV infectivity and CCR5-mediated migration and function in various inflammatory disease states.

Kewords:

[D-Lys3]-GHRP-6,136054-22-3,GPCR/G protein,Ghrelin Receptors, supplier, inhibitor,Antagonist,Blocker,Modulator,Agonist, activators, activates, potent, BioCrick

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