docetaxel

P3, N=95, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Mar 2026 --> Sep 2026 | Trial primary completion date: Feb 2026 --> Aug 2026

P2, N=80, Recruiting, Sun Yat-sen University | Not yet recruiting --> Recruiting

Docetaxel and vadimezan (DMXAA), a prototypical STING agonist, were co-loaded into GO-EDM to generate GO-EDM-DTX-Vad. Taken together, GO-EDM-DTX-Vad leverages passive tumor accumulation and mannose receptor-guided dual targeting of TAMs and TIDCs to integrate DTX-based chemotherapy, STING-mediated immune activation and mild NIR photothermal therapy. This integrated chemo-photothermal-immunotherapeutic design couples direct tumor cell killing with myeloid reprogramming and immune activation, offering a unified strategy for metastatic TNBC.

In the murine TNBC model, EMMDs demonstrated remarkable antitumor efficacy, obviously provoking a robust STING-mediated type I interferon response and inhibiting tumor growth. This work presents a promising biomimetic strategy for remodeling the tumor immune microenvironment via efficient STING activation.

More importantly, treatment with OTUB2 inhibitor (OTUB2-IN-1) resensitized resistant CRPC to DTX. Together, our findings establish OTUB2 as a novel driver of DTX resistance in CRPC and highlight the role of CAFs-derived FOXD3-AS1 and OTUB2/ALYREF/ABCG4 axis in modulating DTX resistance of CRPC.

We have identified a small molecule produced by a marine sponge as being able to inhibit PTCH1 efflux activity and increase the efficacy of vemurafenib treatment on BRAF-mutated melanoma cells in vitro and in vivo in mice. We found that inhibiting PTCH1 drug efflux activity significantly increased the cytotoxic effect of chemotherapies such as doxorubicin and docetaxel in three TNBC cell lines. Overall, our findings suggest that PTCH1 plays a role in the resistance of TNBC cells to chemotherapy, and that using a PTCH1 efflux inhibitor during neoadjuvant or adjuvant therapy could enhance the efficacy of treatment against PTCH1-expressing TNBC, while preventing treatment resistance, relapse, and metastasis formation.

P1, N=16, Completed, Weill Medical College of Cornell University | Active, not recruiting --> Completed | Trial completion date: Oct 2026 --> Oct 2025

P2, N=99, Recruiting, Mayo Clinic | Trial completion date: May 2031 --> May 2027 | Trial primary completion date: May 2031 --> May 2027

Notably, vindoline exhibited minimal CYP3A4 inhibition and no detectable acute toxicity in vivo. Collectively, these findings establish vindoline as a safe and effective ABCB1-targeting agent with potential to overcome docetaxel resistance in prostate cancer.

Resistance to taxanes, such as docetaxel (Dtx) and cabazitaxel (Cbz), frequently emerges in castration resistant prostate cancer (CRPC). More importantly, NNMT-high patients were found to be non-responders to taxane-containing chemotherapy regimens. Collectively, our findings suggest that targeting NNMT and the pathways it affects, such as TGFβ, offers a viable approach for addressing taxane-resistant PC.

He achieved an excellent response to androgen deprivation therapy (ADT) combined with abiraterone and prednisone, maintaining an undetectable prostate-specific antigen (PSA) level for over 2 years...The patient transitioned to docetaxel plus ADT, resulting in symptomatic improvement and partial radiologic response...Second, standard markers such as PSA and immunohistochemistry may be misleading in atypical presentations. Finally, the case highlights the decisive role of molecular diagnostics, specifically NGS, in identifying tumor origin and preventing misdiagnosis.

Key advances include: (1) In bladder cancer, perioperative durvalumab (NIAGARA) and enfortumab vedotin plus pembrolizumab (KEYNOTE-905/EV-303) set new standards, while HER2-targeted disitamab vedotin plus toripalimab (RC48-C016) improved metastatic survival...(3) In prostate cancer, enzalutamide plus leuprolide improved survival in high-risk biochemical recurrence (EMBARK). Capivasertib plus abiraterone benefited PTEN-deficient metastatic hormone-sensitive disease (CAPItello-281). The PSMAddition trial demonstrated that adding [177Lu]Lu-PSMA-617 to standard therapy significantly improved radiographic PFS in PSMA-positive mHSPC. Docetaxel scheduling was optimized (ARASAFE), and an AI model (STAMPEDE) identified patients for AR inhibitor benefit. Novel agents like saruparib and pasritamig showed promise...The 2025 evidence establishes multiple new standards of care across GU cancers, emphasizing biomarker-driven strategies, immunotherapy integration, novel resistance mechanisms, and treatment optimization. This synthesis provides an evidence-based framework for updating guidelines and highlights the move toward more personalized management, while noting persistent challenges and future research needs.