P3, N=54, Active, not recruiting, Deciphera Pharmaceuticals, LLC | Recruiting --> Active, not recruiting | Trial completion date: Dec 2027 --> Dec 2028 | Trial primary completion date: Feb 2026 --> Dec 2027

P3, N=480, Active, not recruiting, Merck Sharp & Dohme LLC | Trial primary completion date: Jun 2028 --> Aug 2025 | Trial completion date: Dec 2029 --> Mar 2026

Our results demonstrate that dapagliflozin not only enhances the antitumor efficacy of sunitinib against renal cell carcinoma but also alleviates sunitinib-induced cardiac toxicity in mice via modulation of the AMPKα-PPARα axis.

P3, N=240, Recruiting, Celldex Therapeutics | Not yet recruiting --> Recruiting

P1/2, N=144, Recruiting, Tongji Hospital

Further, we performed a post-hoc exploratory analysis and developed an XGBoost model (scPro-X) using scRNA-seq data from pre-treatment tumor samples to predict 12-week ORR identified CD4_Tfh_CXCL13 and CD8_Tex_CTLA4 as potential biomarkers predictive of response. These findings demonstrate that IBI318 plus lenvatinib exhibit promising clinical activity and a manageable safety profile in patients with advanced NSCLC.

Notably, this is the first report of ArtiSential articulated forceps utilized in TAMIS, demonstrating their innovative potential in enhancing surgical precision and outcomes in challenging pelvic procedures. The online version contains supplementary material available at 10.1007/s13691-025-00786-7.

Silencing CLEC4G could reverse the effect of LiCl on PLC/PRF/5-R. CLEC4G modulates the PD-1 expression of HCC cells through the Wnt/β-catenin pathway, thereby reversing the resistance to Lenva.

Oral melanocytic neoplasms are rare and have distinct clinicopathological features. Despite this, a gap exists in molecular data regarding ODN and AMP. Conversely, OMN and OMM have distinct profiles; in particular, the latter may benefit modestly from tyrosine kinase inhibitor treatment, as KIT and BRAF mutations are sensitive to imatinib and vemurafenib, respectively.

Our multi-layered omics framework provided genetically anchored evidence for the role of THBS3, RORC, and TNFRSF25 as druggable targets in IBD. The identified candidate drugs offered new avenues for therapeutic intervention. Further clinical validation is warranted to harness these targets for the development of effective IBD treatments.

A fragment-assisted screen then delivered a phenalene-dicarbonitrile chemotype, S1g-2, and optimized analogs that displace Bim with sub-micromolar potency, dismantle Hsp70-client hubs, and resensitize resistant xenografts to imatinib or tamoxifen without global proteostasis collapse. Future directions include covalent or macrocyclic wedges, degrader hybrids, and adaptive pulse-dose regimens guided by proximity-ligation assays. Collectively, chemical disarming of the Hsp70-Bim alliance exemplifies how precision targeting of chaperone PPIs can recalibrate apoptotic thresholds and unlock new therapeutic space in oncology.

Advancements in single-cell analysis and spatial transcriptomics are anticipated to unveil actionable molecular patterns and support the development of individualized strategies to interrupt immune evasion and therapeutic resistance in EC. These advances offer promise for personalized immunotherapy approaches that could significantly improve outcomes in endometrial cancer patients.