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Enasidenib

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDDRUG-ENASIDENIB
TypeDrug
Aliases
IdhifaЕнасиденіб
Statusreviewed 2026-04-30 | pending_clinical_signoff
DiseasesDIS-AML
SourcesSRC-ELN-AML-2022 SRC-NCCN-AML-2025

Drug Facts

ClassSelective IDH2 (mutant) enzyme inhibitor
MechanismSmall-molecule allosteric inhibitor of mutant IDH2 enzyme (R140Q, R172K hotspots). Mutant IDH2 catalyzes neomorphic conversion of α-ketoglutarate to 2-hydroxyglutarate (2-HG), an oncometabolite that drives DNA + histone hypermethylation and blocks myeloid differentiation. Enasidenib reduces 2-HG, restoring TET2-dependent demethylation and inducing terminal differentiation of leukemic blasts. FDA-approved Aug 2017 on the basis of phase 1/2 single-arm data in R/R AML (AG221-AML-001).
Typical dosing100 mg PO once daily, continuous, until disease progression or unacceptable toxicity. Take with or without food at the same time each day. Median time to first response ~1.9 months; continue ≥6 months before declaring non-response.
Ukraine registeredFalse
NSZU reimbursedFalse
Ukraine last verified2026-04-30

Warnings

Notes

Pivotal trials: AG221-AML-001 (Stein et al., Blood 2017) — phase 1/2 monotherapy in R/R IDH2-mut AML: ORR 38%, CR 19%, median OS 9.3 mo. IDHENTIFY (NCT02577406) — phase 3 enasidenib mono vs conventional care in R/R AML; did not show OS benefit overall but enriched benefit in IDH2-mut HMA-naive subgroup. AG221-AML-005 — combination with azacitidine in 1L unfit IDH2-mut AML: ORR 71%, CR 53% — basis for emerging 1L combination use. Differentiation syndrome (~14%) is the signature AE — same monitoring + dexamethasone protocol as ivosidenib. Hyperbilirubinemia (~80% any grade) is biochemical UGT1A1 inhibition — usually asymptomatic, no dose adjustment unless symptomatic. Ukraine: NOT registered, NOT reimbursed; EU access also limited (CHMP negative). Trial source SRC-IDHENTIFY pending — citing umbrella SRC-NCCN-AML-2025 + SRC-ELN-AML-2022.

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