Life Science

A 3-deoxyanthocyanidin.

An orally available, selective inhibitor of both free and prothrombinase-bound factor Xa (Ki = 0.8 nM) effective anticoagulant in both preclinical and clinical models of venous and arterial thrombosis.

An orally available, selective inhibitor of both free and prothrombinase-bound factor Xa (Ki = 0.8 nM) effective anticoagulant in both preclinical and clinical models of venous and arterial thrombosis.

An orally available, selective inhibitor of both free and prothrombinase-bound factor Xa (Ki = 0.8 nM) effective anticoagulant in both preclinical and clinical models of venous and arterial thrombosis.

An orally available, selective inhibitor of both free and prothrombinase-bound factor Xa (Ki = 0.8 nM) effective anticoagulant in both preclinical and clinical models of venous and arterial thrombosis.

An inhibitor of NADPH-oxidase complex assembly that at 300 &muM is effective in preventing the production of superoxide in human white blood cells or neutrophilic granulocytes widely used as an inhibitor of NADPH oxidase activity in the treatment

An inhibitor of NADPH-oxidase complex assembly that at 300 &muM is effective in preventing the production of superoxide in human white blood cells or neutrophilic granulocytes widely used as an inhibitor of NADPH oxidase activity in the treatment

An inhibitor of NADPH-oxidase complex assembly that at 300 &muM is effective in preventing the production of superoxide in human white blood cells or neutrophilic granulocytes widely used as an inhibitor of NADPH oxidase activity in the treatment

An apoptosis inducer that inhibits the mitochondrial F1FO ATPase (Ki = 4-5 &microM) selectively kills transformed glial cells without significantly affecting untransformed cells.

An apoptosis inducer that inhibits the mitochondrial F1FO ATPase (Ki = 4-5 &microM) selectively kills transformed glial cells without significantly affecting untransformed cells.

Promotes the cytochrome c-dependent oligomerization of Apaf-1 into the mature apoptosome, thus increasing procaspase-9 processing and subsequent caspase-3 activation induces apoptosis in leukemia cells (IC50 = 4-9 &muM)

Promotes the cytochrome c-dependent oligomerization of Apaf-1 into the mature apoptosome, thus increasing procaspase-9 processing and subsequent caspase-3 activation induces apoptosis in leukemia cells (IC50 = 4-9 &muM)