Description
As an non-ATP competitive inhibitor, PD0325901 can inhibit MEK with Ki around 1 nM.
Storage
2 years at -20centigrade Powder
Molecular Formula
C16H14F3IN2O4
Chemical Name
(R)-N-(2,3-dihydroxypropoxy)-3,4-difluoro-2-(2-fluoro-4-iodophenylamino)benzamide
Solubility
DMSO 96 mg/mL Water
In vitro
As an non-ATP competitive inhibitor, PD0325901 can inhibit MEK with Ki around 1 nM. PD0325901 can inhibit the PTC cells with the RET/PTC1 rearrangement with GI50 of 11 nM and also inhibit PTC cells with a BRAF mutation with GI50 of 6.3 nM. PD0325901 markedly inhibited ERK phosphorylation and growth of both BRAF mutant and wild-type melanoma cell lines, with IC50 in the nanomolar range. PD0325901 can cause G(1)-phase cell cycle arrest and subsequent induction of apoptosis by modulating cell cycle (cyclin D1, c-Myc, and p27) and apoptosis (Bcl-2 and survivin) regulators.
In vivo
For SKMEL-28 and HCT116 tumors, tumor volumes were not significantly reduced at day 1 following PD0325901 (25 mg/kg) treatment. In SKMEL-28, tumor volume changed from 168.0 mm3 (pretreatment group) to 181.2 mm3 and 248.0 mm3 at days 1 and 10, respectively, following treatment with vehicle.Tumor shrinkage was observed after daily treatment with PD0325901 (25 mg/kg) to 135.8 and 43.2 mm3 (P = 0.05), at days 1 and 10, respectively. HCT116 tumor volumes showed a rapid increase in the vehicle-treated group from 106.670 mm3 (pretreatment group) to 136.7 mm3 and 542.3 mm3 at days 1 and 10, respectively.
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