P2, N=40, Recruiting, Fudan University | Not yet recruiting --> Recruiting

P1/2, N=41, Not yet recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

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.

P3, N=239, Active, not recruiting, Seagen, a wholly owned subsidiary of Pfizer | Trial primary completion date: Dec 2026 --> Jan 2026

P2, N=60, Recruiting, Jonsson Comprehensive Cancer Center | Not yet recruiting --> Recruiting

P3, N=574, Recruiting, RemeGen Co., Ltd. | Not yet recruiting --> Recruiting

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.

In this cN + cohort, approximately one in six patients eligible for AST had residual disease only in the axilla. Less-invasive axillary staging procedures were associated with a low estimated theoretical risk of missed AST eligibility. However, these findings should be interpreted in light of the modest sample size.

HER2 expression in urothelial carcinoma was associated with a distinct immune microenvironmental profile characterized by Treg enrichment and relatively low immune checkpoint expression, as supported by our protein-level validation. These findings provide additional biological context for the potential therapeutic benefit of combining RC48 with ICIs. Given the exploratory nature of the HER2-high definition and the limited sample size of the validation cohorts, further prospective studies are warranted to confirm these observations.