idarubicin hydrochloride

P1, N=24, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

P1/2, N=53, Active, not recruiting, University of Southern California | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Jun 2026 --> Dec 2026

P1, N=2, Terminated, Northwestern University | Active, not recruiting --> Terminated; Low accrual

P1/2, N=30, Not yet recruiting, M.D. Anderson Cancer Center

P2, N=41, Active, not recruiting, Institute of Hematology & Blood Diseases Hospital, China | Recruiting --> Active, not recruiting | N=60 --> 41 | Trial completion date: Jun 2027 --> Jun 2028 | Trial primary completion date: Jun 2026 --> Dec 2027

P2, N=172, Active, not recruiting, Massachusetts General Hospital | Recruiting --> Active, not recruiting

Here, we show that direct physical contact between small cell lung cancer (SCLC) cells and lung fibroblasts induces early resistance to standard-of-care chemotherapeutic agents, etoposide and cisplatin. A high-throughput drug screening identified idarubicin as a compound that retains efficacy despite fibroblast-mediated protection, suggesting it could bypass microenvironment-induced resistance early on. Together, our findings identify direct tumor-fibroblasts contact as an early driver of chemoresistance and highlight a potential therapeutic strategy targeting cell-cell interactions within the tumor microenvironment.

P2, N=47, Active, not recruiting, Shanghai Jiao Tong University School of Medicine | Not yet recruiting --> Active, not recruiting

P3, N=875, Recruiting, Stichting Hemato-Oncologie voor Volwassenen Nederland | N=423 --> 875

P3, N=324, Recruiting, Sunshine Lake Pharma Co., Ltd. | Trial completion date: Jun 2027 --> May 2028 | Trial primary completion date: Mar 2026 --> Nov 2027

The patient was initially treated with a hybrid induction regimen of FLAG-IDA (fludarabine, arabinofuranosyl cytidine, granulocyte colony-stimulating factor (G-CSF)-idarubicin) plus vincristine and prednisone, followed by reinduction with decitabine and venetoclax due to persistent disease. In this case, the delayed introduction of midostaurin was favored to minimize toxicity during induction. Ongoing studies are needed to determine the best treatment strategies and timing for targeted therapies in this rare leukemia subtype.

Finally, AMG PERK 44 did not enhance idarubicin efficacy and caused no major off-target effects. These findings highlight the context-dependent role of PERK in the HCC microenvironment and its implications for targeting UPR pathways in liver cancer. Impact statement This study provides an evaluation of PERK as a therapeutic target in hepatocellular carcinoma by demonstrating that its inhibition does not produce the anticipated anti-tumor effects in advanced disease, but instead exerts nuanced, context-dependent influences on the tumor microenvironment.