navitoclax

Navitoclax (ABT-263) is a potent oral Bcl-2 inhibitor that binds to Bcl-xL, Bcl-2, and Bcl-w proteins (Ki<1 nM), demonstrating antitumor activity and inducing apoptosis.

Navitoclax dihydrochloride is a synthetic small-molecule antagonist of a subset of the B-cell leukemia 2 (Bcl-2) family of proteins with potential antineoplastic activity.

Desmorpholinyl Navitoclax-NH-Me (Desmorpholinyl ABT-263-NH-Me) is a Bcl-xL inhibitor, which can be employed alongside a CRBN ligand to synthesize XZ739, a PROTAC BCL-XL degrader [1] [2].

Navitoclax-piperazine (ABT-263-piperazine) is a B-cell lymphoma extra large (BCL-XL) inhibitor.

A-1208746 is an inhibitor of MCL-1 with a Ki value of 0.454 nM. This compound effectively activates caspase-3 -7, induces apoptosis in H929 cells, and reduces mitochondrial membrane potential. Additionally, A-1208746 synergizes with Navitoclax, making it applicable in cancer research.

Glasdegib hydrochloride is a small-molecule inhibitor of the Hedgehog (Hh) signaling pathway with potential antineoplastic activity.

Ch282-5, an orally active inhibitor targeting the Bcl-2 protein, promotes mitochondria-dependent apoptosis (Apoptosis) by disrupting mitophagy and the mTOR pathway. It demonstrates antiproliferative effects on colorectal cancer cells, effective both in vitro and in vivo, while also inhibiting metastasis. Further, Ch282-5 augments Oxaliplatin-induced autophagy (Autophagy) by downregulating Mcl-1 protein and raising platelet count, which helps mitigate the adverse effects of Navitoclax.

BDM19 binds to and activates cytosolic BAX dimers, inducing cell apoptosis alone or when used in combination with the BCL-2 BCL-XL inhibitor, Navitoclax [1].