216163-53-0
Chemical Structure
PD 174265
- CAS No.: 216163-53-0
- Formula:C17H15BrN4O
- Molecular Weight:371.23
IUPAC Name: N-(4-((3-bromophenyl)amino)quinazolin-6-yl)propionamide
InChIKey: WUPUZEMRHDROEO-UHFFFAOYSA-N
SMILES: CCC(NC1=CC2=C(NC3=CC=CC(Br)=C3)N=CN=C2C=C1)=O
Biological Activity: PD 174265 is a highly selective, reversible EGFR/ErbB2 tyrosine kinase inhibitor (IC50=0.45 nM) and cell differentiation inducer. By blocking receptor autophosphorylation and the downstream ERK signaling pathway (with an IC50 of 0.45 μM for full-length ERK), PD 174265 effectively inhibits tumor growth and exhibits antitumor activity without obvious toxicity in in vivo models. PD 174265 drives oligodendrocyte precursor cells to switch from a proliferative state to a differentiated state, significantly upregulates the expression of myelin proteins such as CNP, PLP and MBP, and induces neurite branching. PD 174265 shows no inhibitory effect on other kinases including insulin, PDGF and basic FGF receptors, and serves as a crucial tool molecule for investigating the treatment of human epidermoid carcinoma and the mechanism of myelin repair in multiple sclerosis[1][2][3][4].
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PD 174265 | 98.35% | PD 174265 is a highly selective, reversible EGFR/ErbB2 tyrosine kinase inhibitor (IC50=0.45 nM) and cell differentiation inducer. By blocking receptor autophosphorylation and the downstream ERK signaling pathway (with an IC50 of 0.45 μM for full-length ERK), PD 174265 effectively inhibits tumor growth and exhibits antitumor activity without obvious toxicity in in vivo models. PD 174265 drives oligodendrocyte precursor cells to switch from a proliferative state to a differentiated state, significantly upregulates the expression of myelin proteins such as CNP, PLP and MBP, and induces neurite branching. PD 174265 shows no inhibitory effect on other kinases including insulin, PDGF and basic FGF receptors, and serves as a crucial tool molecule for investigating the treatment of human epidermoid carcinoma and the mechanism of myelin repair in multiple sclerosis. | ||||||||||||||||||||
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- [1]. Joubert L, et al. Chemical inducers and transcriptional markers of oligodendrocyte differentiation. J Neurosci Res. 2010;88(12):2546-2557. [Content Brief]
- [2]. Fry DW, et al. Specific, irreversible inactivation of the epidermal growth factor receptor and erbB2, by a new class of tyrosine kinase inhibitor. Proc Natl Acad Sci U S A. 1998;95(20):12022-12027. [Content Brief]
- [3]. Wang S, et al. Cellular uptake mediated by epidermal growth factor receptor facilitates the intracellular activity of phosphorothioate-modified antisense oligonucleotides. Nucleic Acids Res. 2018;46(7):3579-3594. [Content Brief]
- [4]. Krieg T, et al. Mitochondrial ROS generation following acetylcholine-induced EGF receptor transactivation requires metalloproteinase cleavage of proHB-EGF. J Mol Cell Cardiol. 2004;36(3):435-443. [Content Brief]
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