Biologically Active Small Molecules

An orally bioavailable inhibitor of Smo blocks binding of BODIPY cyclopamine (IC₅₀ = 21 nM) and inhibits Gli activation in cell lines that express wild-type Smo or activated mutant forms of Smo (IC₅₀s = 6-35 nM) inhibits Shh

An orally bioavailable inhibitor of Smo blocks binding of BODIPY cyclopamine (IC₅₀ = 21 nM) and inhibits Gli activation in cell lines that express wild-type Smo or activated mutant forms of Smo (IC₅₀s = 6-35 nM) inhibits Shh

A cell-permeable inhibitor of Cdk1/cyclin B and Cdk2/cyclin E (IC₅₀s = 6 and 9 nM, respectively) blocks the cycling of HCT116 cells (EC₅₀ = 0.29-0.49 &microM).

A cell-permeable inhibitor of Cdk1/cyclin B and Cdk2/cyclin E (IC₅₀s = 6 and 9 nM, respectively) blocks the cycling of HCT116 cells (EC₅₀ = 0.29-0.49 &microM).

BMS-3 is a potent inhibitor of activated LIM domain kinases LIMK1 and LIMK2 (IC₅₀s = 5 and 6 nM, respectively). It is used to study the role of activated LIMK isoforms in the signaling of Rho family GTPases to cytoskeletal proteins,

BMS-3 is a potent inhibitor of activated LIM domain kinases LIMK1 and LIMK2 (IC₅₀s = 5 and 6 nM, respectively). It is used to study the role of activated LIMK isoforms in the signaling of Rho family GTPases to cytoskeletal proteins,

BMS-3 is a potent inhibitor of activated LIM domain kinases LIMK1 and LIMK2 (IC₅₀s = 5 and 6 nM, respectively). It is used to study the role of activated LIMK isoforms in the signaling of Rho family GTPases to cytoskeletal proteins,

BMS-3 is a potent inhibitor of activated LIM domain kinases LIMK1 and LIMK2 (IC₅₀s = 5 and 6 nM, respectively). It is used to study the role of activated LIMK isoforms in the signaling of Rho family GTPases to cytoskeletal proteins,

A dual inhibitor of IGF1R kinase and IR (IC₅₀s = 100 and 73 nM, respectively) blocks IFG1R autophosphorylation and signaling through MEK1/2 and Akt, leading to G1 arrest and apoptosis in ML-1 cells reverses EMT in MCF10A cells

A dual inhibitor of IGF1R kinase and IR (IC₅₀s = 100 and 73 nM, respectively) blocks IFG1R autophosphorylation and signaling through MEK1/2 and Akt, leading to G1 arrest and apoptosis in ML-1 cells reverses EMT in MCF10A cells

A dual inhibitor of IGF1R kinase and IR (IC₅₀s = 100 and 73 nM, respectively) blocks IFG1R autophosphorylation and signaling through MEK1/2 and Akt, leading to G1 arrest and apoptosis in ML-1 cells reverses EMT in MCF10A cells

A dual inhibitor of IGF1R kinase and IR (IC₅₀s = 100 and 73 nM, respectively) blocks IFG1R autophosphorylation and signaling through MEK1/2 and Akt, leading to G1 arrest and apoptosis in ML-1 cells reverses EMT in MCF10A cells