Trial reportBlood advances2026
CPX-351 selectively benefits patients with AML and myelodysplasia-related mutations in the pivotal randomized trial.
Trial report in Blood advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01696084 (Phase III, Multicenter, Randomized, Trial of CPX-351), which is not on this map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phase III, Multicenter, Randomized, Trial of CPX-351 (Cytarabine:Daunorubicin) Liposome Injection Versus Cytarabine and Daunorubicin in Patients 60-75 Years of Age With Untreated High Risk (Secondary) AML
Who cites it
7 citing papers in PubMed.
- CPX-351 plus gemtuzumab ozogamicin in relapsed or refractory acute myeloid leukemia and high-risk myelodysplastic syndrome.Blood neoplasia · 2026Article
- Current and future therapies for acute myeloblastic leukemia.Journal of hematology & oncology · 2026Review
- Article
- Intensive Induction in AML in the Era of Venetoclax: A Standing Count for "7 + 3"?American journal of hematology · 2026Article
- Evolving Management Approaches Toward Personalized Therapy in Acute Myeloid Leukemia: A Narrative Review.Journal of personalized medicine · 2026Review
- Finding the genes that fit CPX-351.Blood advances · 2026Article
- AML, Myelodysplasia-Related: Beyond Classification-Toward Precision Decision-Making.Mediterranean journal of hematology and infectious diseases · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractCPX-351 was approved for the treatment of acute myeloid leukemia (AML) using now-outdated definitions of AML with myelodysplasia-related changes (AML-MRC) and therapy-related AML. We evaluated whether the overall survival (OS) benefit of CPX-351 over standard cytarabine plus anthracycline (7+3) therapy is confined to molecularly defined AML subgroups by performing DNA sequencing in 184 patients enrolled in the pivotal phase 3 randomized trial. Patients were categorized hierarchically based on gene mutations: (1) TP53-AML, (2) DDX41-AML, (3) myelodysplasia-related AML (AML-MR) defined by the World Health Organization fifth edition criteria, or (4) other-AML. TP53-AML was subclassified as single (TP53single) or multihit (TP53multi) based on the number of alleles altered via mutation, deletion, or copy neutral loss of heterozygosity. Two-year OS differed significantly across molecular subgroups: TP53-AML (7%), AML-MR (19%), other-AML (37%), and DDX41-AML (70%) (P< .001). CPX-351 improved survival in patients with AML-MR compared with 7+3 (median, 9.7 vs 6.8 months; P = .037), with no benefit in TP53-AML or other-AML. For patients undergoing transplantation, CPX-351 improved 2-year survival (76% vs 27%; P< .01), an effect primarily observed in AML-MR. Multivariable analysis confirmed the independent association with survival of both CPX-351 and hematopoietic cell transplantation in AML-MR. TP53multi demonstrated significantly worse survival than TP53single (median, 3.8 vs 7.0 months; P = .004). The OS benefit of CPX-351 observed in the trial was driven by AML-MR with no benefit of CPX-351 in TP53-AML, in which the primary prognostic factor was allelic state. This trial was registered at www.clinicaltrials.gov as #NCT01696084.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.