daunorubicin

P2, N=24, Recruiting, University of California, Davis | Trial primary completion date: Feb 2026 --> Oct 2026

Synergism with doxorubicin (DOX) and other chemotherapeutic agents was quantified by combination index (CI) analysis using the Chou-Talalay method and spheroid culture assays...AAP similarly synergized with daunorubicin but not with etoposide or cytarabine, suggesting selectivity for ROS-inducing anthracyclines. These findings establish AMF-derived peptides as promising human-origin chemosensitizers capable of overcoming multidrug resistance in HMs through multi-targeted mechanisms. The ability to reduce anthracycline dosing while maintaining efficacy offers potential for minimizing cardiotoxicity and other dose-limiting adverse effects, warranting further preclinical development toward clinical translation.

P2, N=148, Not yet recruiting, Shen yang

P1, N=50, Active, not recruiting, Dana-Farber Cancer Institute | Trial completion date: Jun 2026 --> Sep 2026

P2, N=181, Active, not recruiting, PrECOG, LLC. | Trial completion date: Dec 2026 --> Jul 2026

P2, N=43, Not yet recruiting, AIDS Malignancy Consortium

P1/2, N=33, Active, not recruiting, University of Washington | Recruiting --> Active, not recruiting | Trial completion date: Jul 2027 --> Jan 2027

The effect of GDF11 on chemotherapy sensitivity was investigated in HL60 cells treated with 10 μM daunorubicin (DNR)...In addition, CTSS activated the extracellular signal-regulated kinase 1 and 2 signaling pathway and inhibited endoplasmic reticulum stress in AML cells. In conclusion, GDF11 inhibited the growth and increased chemosensitivity through inhibiting CTSS expression in AML cells, providing potential therapeutic targets for AML treatment.

P2/3, N=450, Enrolling by invitation, First Affiliated Hospital of Zhejiang University

P2/3, N=267, Enrolling by invitation, First Affiliated Hospital of Zhejiang University

P2/3, N=140, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Dec 2026 --> Mar 2026

We conclude that KIT mutations, especially exon 17, confer a high-risk phenotype in otherwise favorable pediatric AML1::ETO AML. Our exploratory data suggest this may be associated with a chemoresistant profile, potentially driven by SOCS1-associated JAK-STAT dysregulation. These findings highlight the necessity of refined risk stratification based on KIT exon profiling and support targeting the SOCS1/JAK-STAT axis to overcome therapy resistance.