Acute Myeloid Leukemia — IDH1/2-Mutant
Sequencing for IDH1/2-mutant acute myeloid leukemia: frontline therapy split by fitness for intensive induction (intensive 7+3, or an IDH1-targeted ivosidenib + azacitidine vs venetoclax-based lower-intensity regimen), then relapsed/refractory therapy targeted to the IDH subtype (ivosidenib for IDH1, enasidenib for IDH2) with a non-cross-resistant salvage for prior ivosidenib exposure, then clinical trial or allogeneic transplant.
Fitness for intensive induction chemotherapy?
- Fit for intensive induction → Intensive induction (cytarabine + daunorubicin, "7+3")
- Unfit for intensive induction → Lower-intensity regimen selection (unfit for intensive induction)
1L: Intensive induction (cytarabine + daunorubicin, "7+3")
For fit patients (younger, good performance status, acceptable organ function). Standard 7+3 induction followed by consolidation; proceed to allogeneic transplant based on risk. IDH inhibitors may be incorporated in trials or maintenance settings.
- Relapsed / refractory → IDH mutation subtype at relapse/refractory (no prior IDH inhibitor)
Lower-intensity regimen selection (unfit for intensive induction)
- IDH1-targeted (ivosidenib + azacitidine) → Ivosidenib + azacitidine (IDH1-targeted)
- Venetoclax-based → Venetoclax + azacitidine
1L: Ivosidenib + azacitidine (IDH1-targeted)
For newly diagnosed IDH1-mutant AML in patients unfit for intensive chemotherapy; AGILE showed superior event-free and overall survival versus azacitidine alone. Monitor for differentiation syndrome, QTc prolongation, and tumor lysis.
Evidence: AGILE
- Relapsed / refractory (prior IDH1 inhibitor) → Non-cross-resistant salvage (venetoclax + azacitidine) after frontline ivosidenib
1L: Venetoclax + azacitidine
Active regardless of IDH status and a standard lower-intensity option for unfit patients. Requires tumor-lysis prophylaxis and a venetoclax ramp-up; manage prolonged cytopenias with dose/schedule adjustments.
- Relapsed / refractory → IDH mutation subtype at relapse/refractory (no prior IDH inhibitor)
IDH mutation subtype at relapse/refractory (no prior IDH inhibitor)
- IDH1 mutation → Ivosidenib (IDH1-mutant, no prior IDH1 inhibitor)
- IDH2 mutation → Enasidenib (IDH2-mutant)
2L: Ivosidenib (IDH1-mutant, no prior IDH1 inhibitor)
Single-agent ivosidenib for relapsed/refractory IDH1-mutant AML in patients not previously exposed to an IDH1 inhibitor. Watch for differentiation syndrome, QTc prolongation, and leukocytosis.
- Progression → Clinical trial or allogeneic hematopoietic cell transplant
2L: Enasidenib (IDH2-mutant)
Single-agent enasidenib for relapsed/refractory IDH2-mutant AML. Watch for differentiation syndrome and indirect hyperbilirubinemia.
- Progression → Clinical trial or allogeneic hematopoietic cell transplant
2L: Non-cross-resistant salvage (venetoclax + azacitidine) after frontline ivosidenib
For IDH1-mutant patients who already received frontline ivosidenib + azacitidine: switch to a non-cross-resistant regimen (venetoclax-based, if not already used) or a clinical trial rather than repeating the same IDH1 inhibitor.
- Progression → Clinical trial or allogeneic hematopoietic cell transplant
3L+: Clinical trial or allogeneic hematopoietic cell transplant
Consolidate responders with allogeneic transplant where feasible; otherwise prioritize a clinical trial. Best supportive care for patients ineligible for further therapy.