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Bioisosteric Discovery of NPA101.3, a Second-Generation RET/VEGFR2 Inhibitor Optimized for Single-Agent Polypharmacology

Marialuisa Moccia, Brendan Frett, Lingtian Zhang, Naga Rajiv Lakkaniga, David C. Briggs, Rakhee Chauhan, Annalisa Brescia, Giorgia Federico, Wei Yan, Massimo Santoro, Neil Q. McDonald, Hongyu Li, Francesca Carlomagno

2020Journal of Medicinal Chemistry27 citationsDOIOpen Access PDF

Abstract

) of <0.003 μM for both RET and VEGFR2. NPA101.3 inhibited phosphorylation of all tested RET oncoproteins as well as VEGFR2 and proliferation of cells transformed by RET. Oral administration of NPA101.3 (10 mg/kg/day) completely prevented formation of tumors induced by RET/C634Y-transformed cells, while it weakened, but did not abrogate, formation of tumors induced by a control oncogene (HRAS/G12V). The balanced synchronous inhibition of both RET and VEGFR2, as well the resistance to demethylation, renders NPA101.3 a potential clinical candidate for RET-driven cancers.

Topics & Concepts

ChemistryPharmacologyCancer researchVandetanibDrug discoveryIn vivoKinase insert domain receptorTyrosine kinaseReceptorVEGF receptorsBiochemistryBiologyVascular endothelial growth factorVascular endothelial growth factor ABiotechnologyLung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCytokine Signaling Pathways and Interactions
Bioisosteric Discovery of NPA101.3, a Second-Generation RET/VEGFR2 Inhibitor Optimized for Single-Agent Polypharmacology | Litcius