Cabazitaxel

CD47 was widely expressed on triple‑negative breast cancer (TNBC) cells and tumor‑associated macrophages were the most abundant immune cells in TNBC tumors. CD47 blockade alone enabled phagocytosis but with limited efficacy. A high‑throughput screen identified cabazitaxel as an agent that enhanced programmed cell removal (PrCR) by activating macrophages toward an M1 phenotype via NF‑κB, independent of its direct cytotoxicity. The combination of CD47 blockade and cabazitaxel synergistically eliminated TNBC cells and inhibited metastasis in preclinical models, offering a promising immunotherapy strategy.

Fig. 1 CD47 is a therapeutic target in triple-negative breast cancer (TNBC). (Cao X, et al., 2021)

This phase 3 randomized trial (196 patients ≥65 years with metastatic castration‑resistant prostate cancer) compared biweekly cabazitaxel 16 mg/m² plus G‑CSF (experimental) versus triweekly cabazitaxel 25 mg/m² plus G‑CSF (standard). The primary endpoint (grade ≥3 neutropenia or neutropenic complications) occurred in 62.5% of the standard arm versus only 5.1% of the experimental arm (OR 0.03, P<0.001). Clinical outcomes were comparable. Biweekly cabazitaxel plus G‑CSF dramatically reduces severe neutropenia and should be offered to older patients for whom the standard regimen is unsuitable.

Fig. 2 Kaplan-Meier Curves of Overall Survival and Radiological Progression-Free Survival in the Control and Experimental Groups. (Oudard S, et al., 2023)