Overall, combining anti-CTLA-4 with either proton radiation or OXi4503, but not with hyperthermia, enhanced growth inhibition of C3H mammary carcinoma compared to that seen with each treatment alone, suggesting potential clinical relevance.

P=N/A, N=90, Not yet recruiting, Sohag University

Notably, JX-594 activity was not correlated with TK1 or EGFR expression, suggesting additional determinants of viral susceptibility in GC. These findings provide preclinical evidence that molecular heterogeneity influences the response of GC to oncolytic virotherapy and support further investigation of JX-594 as a potential therapeutic strategy for gastric cancer.

P1, N=12, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Feb 2026 --> Feb 2027

We identify the microtubule targeting agents lexibulin, colchicine, and combretastatin A-4 as three compounds that bind to the colchicine-binding pocket of the a/b tubulin dimer, and which show increased efficacy in a P47S liver cancer cell line compared to parental cells with WT p53. We find evidence for an unusual mechanism underlying this increased efficacy: our data indicate that the P47S variant shows increased ability to bind to the peptidyl-prolyl isomerase PIN1; this leads to decreased PIN1-cyclin D1 complexes in P47S cells, along with increased cell cycle arrest in response to lexibulin. IMPLICATIONS: These findings support the growing literature that particular mutant forms of TP53 may have specific therapeutic vulnerabilities that can be targetable; improved understanding of these unique vulnerabilities can lead to improved understanding of p53 function.

P2, N=14, Terminated, National Cancer Institute (NCI) | Completed --> Terminated; Interim analysis indicated limited efficacy

P3, N=100, Recruiting, Steba Biotech S.A. | Trial primary completion date: Jun 2025 --> Mar 2026

SCHEMBL4796824, a BPR0L075 derivative with antitumor properties, targets tubulin's colchicine binding site and induces DNA damage response in ovarian cancer...Notably, these effects were more pronounced in c-MYC amplified SK-OV-3 cells. In summary, SCHEMBL4796824 disrupts the canonical Wnt/β-catenin signaling, inducing DNA damage, and inhibits the Wnt/β-catenin/c-MYC axis, triggering cellular senescence in a pathway-dependent manner, hinting at a novel therapeutic approach.

P2, N=64, Completed, Benha University

P1, N=13, Completed, Massachusetts General Hospital | Recruiting --> Completed | N=30 --> 13 | Trial completion date: Oct 2024 --> Jul 2025 | Trial primary completion date: Oct 2024 --> Jul 2025

We identified BAP1 as a potential predictive biomarker for JX-594 treatment and explored its underlying mechanisms. However, given that the study used immunodeficient models, the findings reflect tumor-intrinsic interferon responses and require further validation in immunocompetent models to assess immune microenvironment modulation and clinical relevance.

P1, N=30, Completed, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Completed | Trial completion date: Dec 2025 --> Jul 2025 | Trial primary completion date: Dec 2025 --> Jul 2025