HNMPAcell impermeable tyrosine kinase inhibitor |
Sample solution is provided at 25 µL, 10mM.
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- Purity ≥ 95.00%
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Chemical structure
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Cas No. | 132541-52-7 | SDF | Download SDF |
Synonyms | Hydroxy-2-naphthalenylmethyl Phosphonic Acid | ||
Chemical Name | P-(hydroxy-2-naphthalenylmethyl)-phosphonic acid | ||
Canonical SMILES | OC(P(O)(O)=O)C1=CC2=CC=CC=C2C=C1 | ||
Formula | C11H11O4P | M.Wt | 238.2 |
Solubility | ≤20mg/ml in ethanol;1mg/ml in DMSO;15mg/ml in dimethyl formamide | Storage | Store at -20°C |
Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
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. |
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.
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