Chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL), with or without 17p deletion, with or without prior therapy. Acute myeloid leukemia (AML) in adults 75 years or older, or with comorbidities precluding standard induction chemotherapy, in combination with azacitidine, decitabine, or low-dose cytarabine.
CLL: 20 mg orally once daily (week 1), escalating to 400 mg daily. AML: 100 mg (day 1), 200 mg (day 2), then 400 mg daily in combination with hypomethylating agent.
Tumor Lysis Syndrome (TLS): Potentially fatal. Ramp-up dosing required. Neutropenia: Most common Grade 3-4 laboratory abnormality. Immunization: Do not administer live attenuated vaccines.
Neutropenia (50%), diarrhea (35%), nausea (33%), anemia (26%), upper respiratory tract infection (22%), thrombocytopenia (21%), fatigue (21%), hypokalemia (18%)
Consult the complete prescribing information for a comprehensive list of adverse reactions and their frequencies.
Venetoclax is a selective inhibitor of BCL-2, an anti-apoptotic protein overexpressed in many hematologic malignancies. By blocking BCL-2, venetoclax restores the apoptotic process and triggers programmed cell death in BCL-2-dependent cancer cells. It works independently of p53 status, making it active in TP53-mutated and 17p-deleted CLL.
Half-life: ~26 hrs. Route: Oral. Refer to the full prescribing information for complete pharmacokinetic data.
Clinical efficacy and safety data are available in the full prescribing information and referenced publications.
Chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL), with or without 17p deletion, with or without prior therapy. Acute myeloid leukemia (AML) in adults 75 years or older, or with comorbidities precluding standard induction chemotherapy, in combination with azacitidine, decitabine, or low-dose cytarabine.
Venetoclax is a selective inhibitor of BCL-2, an anti-apoptotic protein overexpressed in many hematologic malignancies. By blocking BCL-2, venetoclax restores the apoptotic process and triggers programmed cell death in BCL-2-dependent cancer cells. It works independently of p53 status, making it active in TP53-mutated and 17p-deleted CLL.
Neutropenia (50%), diarrhea (35%), nausea (33%), anemia (26%), upper respiratory tract infection (22%), thrombocytopenia (21%), fatigue (21%), hypokalemia (18%)