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HNMPA
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。
HNMPA图片
CAS NO:132541-52-7
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议

产品介绍

化学性质

Physical AppearanceA crystalline solid
StorageStore at -20°C
M.Wt238.2
Cas No.132541-52-7
FormulaC11H11O4P
SynonymsHydroxy-2-naphthalenylmethyl Phosphonic Acid
Solubility≤20mg/ml in ethanol;1mg/ml in DMSO;15mg/ml in dimethyl formamide
Chemical NameP-(hydroxy-2-naphthalenylmethyl)-phosphonic acid
Canonical SMILESOC(P(O)(O)=O)C1=CC2=CC=CC=C2C=C1
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

HNMPA is a tyrosine kinase inhibitor that inhibited both the receptor serine and tyrosine phosphorylation, including insulin receptor tyrosine kinase activity [1].

Receptor tyrosine kinases (RTKs) are the high-affinity cell surface receptors for growth factors, cytokines, and hormones. The insulin receptor is one of a number of growth factor receptors with intrinsic tyrosine kinase activity that can be activated upon ligands binding [1].

HNMPA (Hydroxy-2-naphthalenylmethyl Phosphonic Acid) is a tyrosine kinase inhibitor that blocks receptor serine and tyrosine phosphorylation. HNMPA does not affect protein kinase C or cyclic AMP-dependent protein kinase activities. HNMPA inhibited tyrosine kinase activity of autophosphorylated insulin receptor towards poly (Glu4, Tyr) or insulin receptor-(1155-1165) peptide by 82% and 81%, respectively. HNMPA also inhibited autophosphorylation of insulin receptors by 13% + 4.6% in the presence of insulin. HNMPA not only inhibited insulin receptor tyrosine phosphorylation but also effectively decreased insulin receptor serine phosphorylation [1]. In β-cells exposed to high glucose, HNMPA was able to further increase the exe-4-induced insulin secretion [2].

References:
[1].  Baltensperger K, Lewis RE, Woon CW, et al. Catalysis of serine and tyrosine autophosphorylation by the human insulin receptor. Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):7885-9.
[2].  Moon MJ, Kim HY, Park S, et al. Insulin contributes to fine-tuning of the pancreatic beta-cell response to glucagon-like peptide-1. Mol Cells. 2011 Oct;32(4):389-95.