Pz-1

Research use only, not for human use.

Pz-1 is an inhibitor of VEGFR2 and RET (rearranged during transfection) tyrosine kinase that blocks the blood supply required for RET-stimulated growth.

Pz-1 is an inhibitor of VEGFR2 and RET (rearranged during transfection) tyrosine kinase that blocks the blood supply required for RET-stimulated growth.(In Vitro):Pz-1(1.0 nM) strongly inhibited phosphorylation of all tested RET oncoproteins in cell-based assays with IC50s of less than 1 nM for both VEGFR2 and RET wild type kinases.(In Vivo):Pz-1 (1.0 mg/kg) abrogated the formation of tumors induced by RET-mutant fibroblasts and blocked the phosphorylation of both RET and VEGFR2 in tumor tissue. Pz-1 featured no detectable toxicity at concentrations of up to 100.0 mg/kg.

Pz-1 is a Type-II tyrosine kinase inhibitor, able to bind the DFG-out conformation of the kinase. In cell-based assays, 1.0 nM of Pz-1 strongly inhibits tyrosine phosphorylation of VEGFR2 and clinically relevant RET mutants, including those refractory to vandetanib and cabozantinib (RETV804M and RETV804L).

Pz-1 is shown active on VEGFR2, which can block blood supply required for RET-stimulated growth. At 1.0 mg/kg/day per os, Pz-1 abrogates formation of tumors induced by RET-mutant fibroblasts and blocks phosphorylation of both RET and VEGFR2 in tumor tissue. Pz-1 features no detectable toxicity up to 100.0 mg/kg, which indicates a large therapeutic window.

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Angiogenesis

VEGFR

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1800505-64-9

454.534

C26H26N6O2

>98% (HPLC)

In Vitro:?DMSO : 50 mg/mL (110.01 mM)

Cn1cc(cn1)-c1ccc2n(cnc2c1)-c1ccc(CC(=O)Nc2cc(on2)C(C)(C)C)cc1

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(-20℃)

With Ice Pack

≥ 2 years