Safety
cardiac failure, death, coronary spastic angina, renal failure, MDS, TEAEs, hypercalcemia, Drug-induced renal injury, AKI, hypertension, acute kidney injury, TLS
CARDIAC FAILURE, ACUTE MYELOID LEUKEMIA, RENAL FAILURE, AML, DIABETIC NEPHROPATHY, HYPERCALCEMIA, ACUTE RENAL FAILURE, ADVERSE EVENT, HYPERTENSION, TUMOR LYSIS SYNDROME
TEAEs reported in ≥20% of patients, regardless of severity or relationship to the study drug, are listed in Common TEAEsAE, adverse event; VEN, venetoclax; LDAC, low-dose cytarabine; TEAE, treatment-emergent AE; WBC, white blood cell.SAEs were reported in six patients (42.9%) (SAEs of venetoclax and LDACNo patients reported tumor lysis syndrome (TLS) in this study, where all patients received either TLS-prophylactic agents or hydration. SAE, serious adverse event; SOC/PT, MedDRA system organ class and preferred term; AKI, acute kidney injury.
TEAEs of venetoclax leading to death and action takenAE, adverse event; AML, acute myeloid leukemia; PT, MedDRA preferred term; TEAE, treatment-emergent AE; WBC, white blood cell.


A Grade 3 AKI was observed in an 80-year-old man with hypertension and diabetic nephropathy. He also used nifedipine and furosemide for coronary spastic angina and cardiac failure during study treatment. On Day 24, the antifungal prophylaxis was changed from caspofungin to fluconazole, and the dose of venetoclax was reduced to 300 mg accordingly. Subsequently, elevation of serum creatinine, hypercalcemia and decreased blood pressure were observed. Venetoclax was discontinued on Day 26 owing to persistently elevated creatinine level. Nifedipine and furosemide were also discontinued. On Day 45, renal failure improved. Drug-induced renal injury, decreased blood pressure and hypercalcemia were suspected to be the causes of acute renal failure. The causality of the study drugs could not be ruled out.Fatal Grade 5 cardiac failure was reported in a 61-year-old male patient during post-treatment. He was previously diagnosed with MDS 75 days before initial dosing of the study drug and was not reported to have received AZA. After his diagnosis of AML, he consented to participate in this study and the Study Cycle 1 was started. On Day 24, bone marrow aspiration showed no therapeutic effect. The study drug was discontinued at the end of Cycle 1 on Day 28. Post-treatment was started on Day 31 with reduced-dose 7 + 3 AraC (67 mg/m