idarubicin hydrochloride

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.

P1, N=30, Active, not recruiting, Fred Hutchinson Cancer Center | Recruiting --> Active, not recruiting | Trial completion date: Dec 2029 --> May 2029 | Trial primary completion date: Dec 2026 --> May 2026

Fludarabine, cytarabine, and G-CSF-based therapy (FLAG) yields approximately 60% 5-year overall survival (OS) in core-binding factor (CBF) AML, with potential added benefit with gemtuzumab ozogamicin (GO)...We interrogated these factors in 219 frontline patients with CBF-AML (median age 52 years; range 19-80) treated on a phase 2 trial (NCT00801489); 51% received FLAG-GO and 49% FLAG-idarubicin...On multivariate analysis, baseline mutations did not affect OPR or survival, while FLAG-GO favored both. In CBF-AML, FLAG-based therapy possibly attenuates the prognostic impact of concurrent baseline genomics.

P3, N=106, Completed, Arog Pharmaceuticals, Inc. | Recruiting --> Completed | N=322 --> 106 | Trial completion date: Oct 2024 --> Apr 2026 | Trial primary completion date: Oct 2024 --> Apr 2026

P2, N=48, Recruiting, Beijing 302 Hospital

P3, N=875, Recruiting, Stichting Hemato-Oncologie voor Volwassenen Nederland | Not yet recruiting --> Recruiting | N=328 --> 875

Molecular docking revealed higher binding affinities for both Idarubicin (- 9.98 kcal/mol) and Larotrectinib (- 9.42 kcal/mol) compared to the reference drug Erlotinib (-8.91 kcal/mol). Additionally, they demonstrated favorable predicted cytotoxicity against NSCLC cell lines. In conclusion, our integrated bioinformatics analysis identifies idarubicin and larotrectinib as putative candidates for drug repurposing targeting EGFR in NSCLC, providing a rational foundation for future experimental validation and further preclinical and clinical investigations.