Life Science

Blocks CYP17A1 by potently inhibiting both the 17&alpha-hydroxylase and the 17,20 lyase activities (IC₅₀ = 18 and 17 nM, respectively) essentially eliminates plasma testosterone while producing a 3- to 4-fold increase in plasma

Blocks CYP17A1 by potently inhibiting both the 17&alpha-hydroxylase and the 17,20 lyase activities (IC₅₀ = 18 and 17 nM, respectively) essentially eliminates plasma testosterone while producing a 3- to 4-fold increase in plasma

BH3 mimetic and Bcl-2 inhibitor. It induces apoptosis in chronic lymphocytic leukemia cells

BH3 mimetic and Bcl-2 inhibitor. It induces apoptosis in chronic lymphocytic leukemia cells

BH3 mimetic and Bcl-2 inhibitor. It induces apoptosis in chronic lymphocytic leukemia cells

A BH3 mimetic that selectively inhibits Bcl-2 (Ki 3-fold less avidly to the related family proteins, Bcl-xL and Bcl-W (Kis = 48 and 245 nM, respectively) inhibits the growth of Bcl-2-dependent cell lines and in vivo tumor xenografts and

A BH3 mimetic that selectively inhibits Bcl-2 (Ki 3-fold less avidly to the related family proteins, Bcl-xL and Bcl-W (Kis = 48 and 245 nM, respectively) inhibits the growth of Bcl-2-dependent cell lines and in vivo tumor xenografts and

BH3 mimetic and inhibitor of Bcl-2, Bcl-?, and Bcl-xl. It enhances the efficacy of co-administered chemotherapeutics and inhibits proliferation of chronic lymphocytic leukemia cells.

BH3 mimetic and inhibitor of Bcl-2, Bcl-?, and Bcl-xl. It enhances the efficacy of co-administered chemotherapeutics and inhibits proliferation of chronic lymphocytic leukemia cells.

BH3 mimetic and inhibitor of Bcl-2, Bcl-?, and Bcl-xl. It enhances the efficacy of co-administered chemotherapeutics and inhibits proliferation of chronic lymphocytic leukemia cells.

A potent, orally bioavailable mimetic of BH3 domains that avidly binds Bcl-2, Bcl-xL, and Bcl-W (Ki death proteins, like Bim, leading to apoptosis induces apoptosis in cancer cell lines expressing mutants of &beta-catenin 1.

A potent, orally bioavailable mimetic of BH3 domains that avidly binds Bcl-2, Bcl-xL, and Bcl-W (Ki death proteins, like Bim, leading to apoptosis induces apoptosis in cancer cell lines expressing mutants of &beta-catenin 1.