Articles related to ACUTE MYELOID LEUKEMIA (AML)

Menin inhibitors, targeting the menin-KMT2A interaction, have demonstrated significant response rates in treating specific genotypes of AML and ALL, offering a new avenue for personalized leukemia therapy.

Explore the latest findings on vibecotamab’s potential in R/R AML treatment, revealing promising results with an optimized dosing regimen that mitigates cytokine response syndrome while improving patient outcomes.

In light of recent findings, CD24Fc emerges as a potential game-changer in preventing acute GVHD in HSCT patients, with a notable survival rate improvement to 96.2% for severe cases.

The findings of this randomized clinical trial support the notion that, despite improved DFS, patients 60 years or younger with intermediate-risk AML, as defined by Medical Research Council cytogenetic criteria, do not benefit from allo-HCT during first CR in terms of OS. Early identification of a suitable donor allows for the timely rescue of patients who have relapsed following conventional consolidation chemotherapy. Future research that uses longitudinal monitoring of residual disease dynamics will aid in personalizing the optimal time point for allo-HCT in the majority of patients.

Data from Study 2102-HEM-101, an open-label, single-arm, multicenter phase 1/2 trial, were used to support the approval. The Abbott RealTime IDH1 Assay was used to identify 147 adults with relapsed or refractory AML who had an IHD1 mutation. Olutasidenib treatment resulted in a 35% complete remission (CR) or complete remission with partial hematologic recovery in patients (CRh).

Gilteritinib is standard therapy for relapsed/refractory FLT3-mutated (FLT3mut) AML but seldom reduces FLT3mut burden or induces sustained efficacy. This phase Ib open-label, dose-escalation/dose-expansion study enrolled 61 patients (63% having received prior FLT3 therapy) to receive 400 mg oral venetoclax once daily and 80 mg or 120 mg oral gilteritinib once daily. The combination of venetoclax and gilteritinib was associated with high mCRc and FLT3 molecular response rates regardless of prior FLT3 inhibitor exposure, but did require dose interruptions for myelosuppression.