doxorubicin hydrochloride

Overall, liposomal co-delivery maintains DOX cytotoxicity while strengthening G₁/S checkpoint blockade and increasing programmed cell death, with partial moderation of DNA fragmentation. These in-vitro data motivate stability optimization and in-vivo evaluation in CRC models.

P2, N=39, Active, not recruiting, University of Rochester | Recruiting --> Active, not recruiting

P3, N=559, Completed, Sun Yat-sen University | Recruiting --> Completed

Taken together, endothelial TFEB protects against EC damage and cardiac dysfunction, constituting a potential target for treating cardiotoxicity induced by DOX. Our study provides new mechanistic insights into cardiotoxicity associated with chemotherapy.

Besides, according to in vivo studies, the combination of RSL3 and Dox further suppressed BC tumor growth without inducing significant adverse effects. On these accounts, RSL3 makes BC cells more sensitive to Dox by inducing glycolytic dysfunction, implying that RSL3/Dox co-treatment could be a viable therapeutic approach for BC patients.

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.