doxorubicin hydrochloride

P2, N=41, Recruiting, Jennifer Crombie, MD | Active, not recruiting --> Recruiting

P3, N=700, Recruiting, AstraZeneca | N=183 --> 700 | Trial completion date: Apr 2028 --> Jul 2029

In conclusion, the dual-targeted OMV system enhances tumor specificity via cooperative GPC3/CD133 recognition, optimizes pH-responsive release, and reduces nonspecific clearance by modulating macrophages. These features improve antitumor efficacy and mitigate toxicity, positioning OMV-based nanocarriers as promising platforms for precision HCC therapy.

NP-mediated delivery of a TLR2 inhibitor and doxorubicin produces synergistic anti-cancer effects in breast cancer models. This approach may help overcome chemoresistance and improve therapeutic outcomes, offering a promising strategy for the treatment of advanced breast cancer.

P2, N=97, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2026 --> Jan 2027

P2, N=55, Active, not recruiting, Chinese University of Hong Kong | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2027

Targeting LHX6 decreases UGT8 expression and GalCer synthesis, thereby sensitizing MDA-MB-231 cells to doxorubicin. Given UGT8's role in cell survival and drug resistance, inhibition of LHX6 may represent a promising therapeutic strategy for drug-resistant BC.

Collectively, these findings demonstrate that ART attenuates DOX cardiotoxicity by activating the HuR-Sirt1 axis through the stabilization of Sirt1 mRNA.

In conclusion, this work validates specific isoxazole derivatives as highly promising candidates for development: MO3 for resistant bacterial infections, MO7 for otherwise untreatable adenovirus infections, and MO10 as a dual-action agent against HSV-1 and an adjunct to melanoma chemotherapy.

Our findings validated the rational design that UA has the potential to mitigate DOX-induced myocardial injury in vitro and in vivo by inhibiting ROS-driven apoptosis, which yields significant insights for combating DOX-mediated myocardial injury.

These insights underscore the novelty of the thyroid as a vulnerable target during DOX-based chemotherapy and emphasize the need for routine thyroid monitoring in clinical practice. This work further supports developing adjunct interventions to mitigate thyroid damage and improve long-term safety in cancer survivors.

Doxorubicin or carboplatin treatment of adipogenic differentiating MSC led to an increased percentage of mature BMA confirmed by increased gene expression of the adipocyte marker, PPARG. As FGF2 is a secreted protein we tested and confirmed that transfer of conditioned media from doxorubicin-treated BMA enhanced proliferation of tumour cells in vitro, a phenotype that was partially abrogated when FGF2 was depleted from adipogenic differentiating MSC. Our findings suggest that chemotherapy actively promotes adipogenesis, in part by alteration of FGF2 in the context of doxorubicin treatment, which directly enhances adipogenesis and in turn leads to enhanced tumour cell growth as a result.