doxorubicin hydrochloride

P2, N=115, Active, not recruiting, St. Jude Children's Research Hospital | Trial primary completion date: Dec 2025 --> Dec 2026

P2, N=18, Recruiting, University of Washington | Not yet recruiting --> Recruiting

P3, N=468, Recruiting, Hansoh BioMedical R&D Company | Not yet recruiting --> Recruiting

Doxorubicin (DOX) forms stable π-π stacking complexes with PDA, creating a versatile chemotherapeutic delivery platform...We hypothesize that this integrated approach will demonstrate enhanced antitumor efficacy while promoting functional bone reconstruction. Comprehensive in vitro evaluations will elucidate the underlying mechanisms and provide preclinical validation for this precision oncology strategy.

P3, N=600, Not yet recruiting, GlaxoSmithKline

Conversely, inhibition of CPT1 by etomoxir caused increased intracellular Dox retention, leading to Dox-induced cytotoxicity and attenuating the invasiveness of TNBC cells. Taken together, Dox-resistance reprograms cellular metabolism towards FAO regulatory circuit sustaining the mitochondrial bioenergetics, promoting drug efflux, and accentuating breast cancer progression. Based on these findings, it is possible that FAO inhibitors effectively combat drug-induced TNBC chemoresistance.

These values reflect a potency at least fourfold greater than that of the reference drug Doxorubicin (IC₅₀ = 33 µM)...Conversely, compound 7b, with an IC₅₀ value of 85 µM against MCF-7 cells, was the least active, underscoring the critical role of the phenyl moiety in antiproliferative activity. Furthermore, a molecular docking study was conducted to investigate the binding interactions of 6a within the active sites of EGFR and HER-2, providing insight into its potential mechanism of action.

Dormancy was induced with low-dose FAC (5-Fluorouracil, Adriamycin, Cyclophosphamide). Notably, disseminated cell frequency inversely correlated with primary tumor size during neoadjuvant chemotherapy, underscoring the need for systemic therapies targeting distant dormant cells. These findings identify Bcl-xL as a central survival factor in chemotherapy-induced dormancy, and suggest that tumor-targeted systemic delivery of A-1331852 may eradicate disseminated dormant cells and prevent metastatic relapse in high-risk TNBC.

Elevated IC₅₀ values and reduced efficacy of doxorubicin, paclitaxel, and cyclophosphamide were observed. These organoids enable efficient testing of chemotherapy responses, supporting more personalized and effective treatment selection. The scalability and adaptability of SOAR also broaden its impact beyond oncology, offering a versatile platform for high-throughput drug screening, toxicology assessments, and applications in regenerative medicine.

Following confirmation of multiple lung metastases, the patient was treated with doxorubicin monotherapy. Subsequent next-generation sequencing (NGS) revealed a RET fusion, leading to the diagnosis of an RET-rearranged spindle cell neoplasm. This case highlights the importance of genomic testing for certain spindle cell sarcomas and the potential benefit of RET-specific inhibitors against RET-altered sarcomas.

Drug sensitivity analysis revealed that high DDR1 expression was associated with reduced sensitivity to methotrexate but increased sensitivity to vinblastine, doxorubicin, cisplatin, and docetaxel, with no significant difference observed for gefitinib. IHC of clinical samples confirmed DDR1 overexpression in 55.88% of NSCLC patients. Our study demonstrated that DDR1 promotes tumor progression and immune evasion and is frequently overexpressed in NSCLC patients, suggesting that DDR1 is a potential prognostic biomarker and therapeutic target.

Hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (Hyper-CVAD) induction achieved morphological complete remission, but measurable residual disease (MRD) persisted. Consolidation with mini-cyclophosphamide, vincristine, and dexamethasone (mini-CVD) and prednisone, vincristine, methotrexate, and 6-mercaptopurine (POMP) maintenance failed to eradicate MRD, and overt relapse occurred at month 7. Nelarabine salvage was initiated...Early molecular risk stratification and deployment of targeted agents, venetoclax-based combinations, or timely allogeneic transplantation should be considered before irreversible genomic complexity emerges. Prospective studies tailored to high-risk cytogenetic subsets of MPAL are urgently needed.