doxorubicin hydrochloride

P3, N=420, Recruiting, AstraZeneca | Not yet recruiting --> Recruiting

P4, N=2, Terminated, Ottawa Hospital Research Institute | Completed --> Terminated; The study did not meet the pilot feasibility endpoints and was formally closed to accrual prematurely on February 8, 2017.

Collectively, this study highlights the critical role of TP53 target genes in the immediate response of TNBC cells to DNA-damaging agents like doxorubicin and etoposide. It also reveals distinct molecular mechanisms regulating their expression in resistant versus sensitive cells, offering potential therapeutic targets to improve treatment strategies for TNBC.

The synergistic effect was attributed to enhanced intracellular DOX release mediated by AuNR photothermal heating and increased membrane permeability upon laser exposure. These findings demonstrate that AuNR-assisted chemo-photothermal therapy can overcome drug resistance and amplify apoptosis, providing a rational, targeted, and effective strategy for advancing lung cancer treatment.

MTT assay showed that 6 and 9b were 4.5 and 2 times more potent than doxorubicin against MCF-7 cells, while 9a and 13b were 10 and 7.5 times more effective against MDA-MB-231 cells, respectively...Compound 13b exhibited comparable EGFRL858R inhibition to lapatinib and outperformed pictilisib against PI3Kα, PI3Kβ, and PI3Kδ. Compound 6 showed greater ARO inhibition than letrozole, while being slightly less potent than pictilisib against PI3Kα and PI3Kβ...Docking studies supported the in vitro enzymatic inhibition assays results. Thus, 9b and 13d are potent anti-breast cancer benzoxazoles with selective ARO and PI3kα inhibition activity, respectively, while 6, 9a, and 13b are multi-target inhibitors exhibiting other anticancer synergistic mechanisms.

P1, N=7, Active, not recruiting, H. Lee Moffitt Cancer Center and Research Institute | Trial completion date: Oct 2025 --> Oct 2026

P3, N=99, Recruiting, The Affiliated People's Hospital of Ningbo University | Trial completion date: Dec 2026 --> Aug 2026 | Trial primary completion date: Dec 2026 --> Aug 2026

Besides, patients in the high-risk group exhibited lower IC50 values for vorinostat, elesclomol, OSI-906, pyrimethamine, thapsigargin, and doxorubicin, but a higher IC50 value for cisplatin, compared to those in the low-risk group, indicating differential drug sensitivities. In summary, we established a robust DRGs signature comprising BTN3A1, CEBPA, KCNAB2, TBX21, and MYC, which showed strong prognostic value and predictive potential for immune status and drug sensitivity in OS. Notably, functional experiments confirmed that BTN3A1 acted as a tumor suppressor in OS, highlighting it as a promising therapeutic target.

Furthermore, cephalochromin enhanced the cytotoxicity of paclitaxel and doxorubicin, showing additive synergistic interactions. In conclusion, our study provides compelling evidence of cephalochromin's antineoplastic activity in breast cancer, highlighting its potential to improve treatment outcomes. Further preclinical studies are warranted to validate their therapeutic efficacy and safety.

CD5+ diffuse large B-cell lymphoma (DLBCL) is aggressive, and Rituximab-Cyclophosphamide Hydroxydaunorubicin Vincristine Prednisone (R-CHOP) combined with radiotherapy is recommended, but prognosis is affected by age, Lactate Dehydrogenase (LDH) levels, and molecular characteristics such as TP53 mutations. Radiotherapy and chemotherapy are the first choice for treatment. It is very important to formulate a reasonable treatment plan according to the results of pathology and molecular analysis.

Here, we reported a doxorubicin (DOX)-Fe complex and RSL3 co-loaded liposomes (DOX-Fe/RSL3@LIPs) for ferroptosis-enhanced chemotherapy on TNBC tumors. The tumor cell ferroptosis was observably enhanced via supplements of the ferrous ions and H2O2, and RSL3-derived GPX4 inhibition to severely destroy the oxidation balance in cells. In this paper, the DOX-Fe/RSL3@LIPs have exerted a synergistic anticancer effect on TNBC by combining ferroptosis and conventional chemotherapy, and made a meaningful exploration of new strategies for TNBC therapy.

These findings establish MCLRP as a dual-purpose predictive-analytical tool that not only enhances drug response forecasting but also uncovers mutation-specific pharmacological vulnerabilities through systems-level pattern recognition.