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&beta-Melanocyte Stimulating Hormone(MSH),human(Beta-MSH(1-22)(human))
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
CAS NO:17908-57-5
包装与价格：
包装价格(元)
1mg电议
5mg电议
10mg电议

产品介绍
β-黑素细胞刺激素 (MSH)，人 (Beta-MSH (1-22) (human))，一种 22 残基肽，作为内源性黑皮质素 4 受体 (MC4-R) 激动剂。
Cas No.17908-57-5
别名Β-促黑激素(人),Beta-MSH (1-22) (human)
Canonical SMILESAla-Glu-Lys-Lys-Asp-Glu-Gly-Pro-Tyr-Arg-Met-Glu-His-Phe-Arg-Trp-Gly-Ser-Pro-Pro-Lys-Asp
分子式C118H174N34O35S
分子量2660.92
溶解度Soluble in DMSO
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

β-Melanocyte Stimulating Hormone (MSH), human is a melanocortin (MC) receptor agonist.

β-Melanocyte Stimulating Hormone is a powerful anti-inflammatory agent which effect is brought by activation of the central MC3/MC4 receptors and thereby inhibits NO production by inhibiting the translocation of transcription factor NF-κB to the nuclei of the brain cells and decreasing iNOS expression[1]. β-Melanocyte Stimulating Hormone has significantly higher at human MC4-R transfected into CHO cells (Ki=11.4±0.4 nM) and MC4-R in rat hypothalamic homogenates (Ki=22.5±2.3 nM)[2].

β-Melanocyte Stimulating Hormone suppresses LPS-induced nuclear translocation of the transcription factor NF-κB, and inhibits the expression of inducible nitric oxide synthase, and the following nitric oxide overproduction in the brain[1].β-Melanocyte Stimulating Hormone is a key ligand at the MC4-R populations that regulate feeding, and that inhibition of tonic release of β-MSH is one mechanism contributing to hunger in under-feeding[2].

[1]. Muceniece R, et al. Beta-MSH inhibits brain inflammation via MC(3)/(4) receptors and impaired NF-kappaB signaling. J Neuroimmunol. 2005 Dec;169(1-2):13-9. [2]. Harrold JA, et al. beta-MSH: a functional ligand that regulated energy homeostasis via hypothalamic MC4-R? Peptides. 2003 Mar;24(3):397-405.