IGF-1R Inhibitor II, PQ401

A cell-permeable phenylquinolinyl-urea compound that inhibits IGF-1R autophosphorylation (IC₅₀ = 12 µM in inhibiting ligand-induced autophosphorylation in MCF-7 cells and <1 µM in a cell-free kinase assay). Reduces IGF-1R-dependent tumor cell growth both in vitro (IC₅₀ = 8 and 15 µM for MCF-7 and MCNeuA, respectively) and in mice in vivo (80% reduction, 100 mg/kg thrice a week per i.p.). The mechanism of inhibition probably involves indirect blocking of ATP binding.

A cell-permeable phenylquinolinyl-urea compound that inhibits IGF-1R autophosphorylation (IC₅₀ = 12 µM in inhibiting ligand-induced autophosphorylation in MCF-7 cells and <1 µM in a cell-free kinase assay). Reduces IGF-1R-dependent tumor cell growth both in vitro (IC₅₀ = 8 and 15 µM for MCF-7 and MCNeuA, respectively) and in mice in vivo (80% reduction, 100 mg/kg thrice a week, i.p.). The mechanism of inhibition probably involves indirect blocking of ATP binding.

Cell permeable: yes

Primary Target
IGF-1R

Product does not compete with ATP.

Reversible: no

Target IC₅₀: 12 µM in inhibiting ligand-induced IGF-1R autophosphorylation in MCF-7 cells and <1 µM in a cell-free kinase assay; 8 and 15 µM in reducing IGF-1R-dependent tumor cell growth both in vitro for MCF-7 and MCNeuA, respectively

Packaged under inert gas

Toxicity: Standard Handling (A)

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Gable, K.L., et al. 2006. Mol. Cancer Ther.5, 1079.

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany