Proposed MOA for INQOVI + venetoclax1-3

Mechanism of Action (MOA)

INQOVI is an oral HMA composed of decitabine and cedazuridine1

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Decitabine is a nucleoside analog that incorporates into DNA and inhibits DNA methyltransferase (DNMT), resulting in DNA hypomethylation and reactivation of silenced genes, including those regulating cellular differentiation and apoptosis1

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Cedazuridine inhibits cytidine deaminase (CDA), an enzyme in the liver and gut that rapidly degrades decitabine, thereby increasing systemic exposure and enabling oral delivery1

AML efficacy

INQOVI + venetoclax delivered consistent exposure and meaningful response.1,4

MDS efficacy

INQOVI delivers equivalent systemic exposure to IV decitabine.1,5

References: 1. INQOVI [package insert]. Princeton, NJ: Taiho Oncology, Inc.; 2026. 2. VENCLEXTA [package insert]. North Chicago, IL: AbbVie Inc. and South San Francisco, CA: Genentech, Inc.; 2026. 3. Bouligny IM, Murray G, Doyel M, et al. Venetoclax with decitabine or azacitidine in the first-line treatment of acute myeloid leukemia. eJHaem. 2023;4(2):381-392. 4. Data on file. Taiho Oncology Inc., Princeton, NJ. 5. Garcia-Manero G, McCloskey J, Griffiths EA, et al. Oral decitabine-cedazuridine versus intravenous decitabine for myelodysplastic syndromes and chronic myelomonocytic leukaemia (ASCERTAIN): a registrational, randomised, crossover, pharmacokinetics, phase 3 study. Lancet Haematol. 2024;11(1):e15-e26