P2, N=95, Recruiting, Fudan University | Not yet recruiting --> Recruiting | Phase classification: PN/A --> P2 | N=66 --> 95 | Trial completion date: May 2028 --> Dec 2028 | Initiation date: Apr 2025 --> Nov 2025 | Trial primary completion date: Jul 2026 --> Dec 2027

P2, N=180, Recruiting, Seoul National University Hospital | Trial completion date: Dec 2026 --> Jun 2028 | Trial primary completion date: Dec 2026 --> Jun 2028

Altered E-cadherin and/or vimentin expression was more frequently observed in responders (p = 0.013) and associated with longer progression-free survival (p = 0.048). These results suggest that eribulin efficacy may be predicted by altered E-cadherin and vimentin expression before treatment.

P1, N=48, Recruiting, M.D. Anderson Cancer Center | Phase classification: P1/2 --> P1

These findings suggest that IL-6 contributes to eribulin resistance in breast cancer and that IL-6 receptor inhibition is a promising therapeutic strategy to overcome this resistance.

P4, N=49, Not yet recruiting, Yantai Yuhuangding Hospital; Yantai Yuhuangding Hospital

P1, N=18, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

In nonclinical evaluations, Eribulin-loaded dtNDC demonstrated potent antitumor efficacy across three xenograft models...These findings position dtNDC as a promising therapeutic combining durable tumor regression with exceptional tolerability. Moreover, its simplified structure and cost-effective manufacturing process make this dtNDC a compelling next-generation therapeutic for cancers.

By selectively targeting EP300, CCS1477 orchestrates a dual pro-death mechanism involving both intrinsic apoptosis execution and PINK1-driven mitochondrial clearance, resulting in significant inhibition of diffuse large B-cell lymphoma pathogenesis.

This phase II study of eribulin for patients with BRAF V600E mutant mCRC did not meet the primary endpoint. Although BM2 on gene expression analysis of BM subtype may be a predictive marker of eribulin efficacy, further studies are required to validate this hypothesis.

To further dissect its mechanism, Wnt signalling was perturbed using siRNA against GSK3β, β-catenin and ICG-001 (a CBP/β-catenin interaction inhibitor), and their combination...This study identifies miR-195-5p as a potent regulator of CSCs and proliferation, and modulator of the Wnt signalling cascade. Co-inhibition of GSK3β and CBP/β-catenin through miR-195-5p highlights its therapeutic potential in combating stemness and proliferation in breast cancer.

P2, N=46, Not yet recruiting, Fudan University