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Cellagen Technology
IGF-1R/IR/ALK inhibitor
GSK1838705A is a pyrrolopyrimidine-based inhibitor of IGF-1R, IR, and ALK with IC50s of 2.0, 1.6, and 0.5 nM, respectively. Despite its potency against the insulin receptor, no major effect on glucose homeostasis was observed at efficacious doses. [1] In NIH-3T3/USN and NIH-3T3-hIR cell lines GSK1838705A inhibits ligand-induced phosphorylation of IGF1R and IR in a concentration-dependent manner, with concomitant decrease in phosphorylated AKT, IRS-1, and ERK. Antiproflierative EC50s ranged from 20 nM to 8 uM, with most values
In IGF-1-induced mice xenografts, a single oral dose of GSK1838705A at 0.1 and 0.3 mg/kg resulted in 35% and 65% inhibition sof IGF-1R phosphorylation; doses >1 mg/kg completely inhibited phosphorylation. [1]
In ALCL tumor cells bearing ALK fusion genes, proliferation was inhibited in a concentration-dependent manner with EC50s ranging from 24 to 88 nM. [1]
Cellagen Technology
IGF-1R/IR/ALK inhibitor
GSK1838705A is a pyrrolopyrimidine-based inhibitor of IGF-1R, IR, and ALK with IC50s of 2.0, 1.6, and 0.5 nM, respectively. Despite its potency against the insulin receptor, no major effect on glucose homeostasis was observed at efficacious doses. [1] In NIH-3T3/USN and NIH-3T3-hIR cell lines GSK1838705A inhibits ligand-induced phosphorylation of IGF1R and IR in a concentration-dependent manner, with concomitant decrease in phosphorylated AKT, IRS-1, and ERK. Antiproflierative EC50s ranged from 20 nM to 8 uM, with most values
In IGF-1-induced mice xenografts, a single oral dose of GSK1838705A at 0.1 and 0.3 mg/kg resulted in 35% and 65% inhibition sof IGF-1R phosphorylation; doses >1 mg/kg completely inhibited phosphorylation. [1]
In ALCL tumor cells bearing ALK fusion genes, proliferation was inhibited in a concentration-dependent manner with EC50s ranging from 24 to 88 nM. [1]
