P3, N=430, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Dec 2027 --> Jun 2027

P2, N=46, Active, not recruiting, Beth Israel Deaconess Medical Center | Recruiting --> Active, not recruiting | N=90 --> 46 | Trial completion date: Jun 2026 --> Sep 2026

P3, N=6, Terminated, Eli Lilly and Company | N=24 --> 6 | Recruiting --> Terminated; Study terminated due to an inability to enroll participants.

P2, N=40, Recruiting, Children's Hospital Medical Center, Cincinnati | Trial completion date: Nov 2025 --> Nov 2028 | Trial primary completion date: Nov 2025 --> Nov 2028

P1/2, N=35, Recruiting, First Affiliated Hospital of Zhejiang University

Notwithstanding substantial concerns about thrombotic risk due to positive phospholipid antibodies in the context of ruxolitinib treatment, thrombotic events were avoided with patient compliance to low-dose aspirin therapy. This case highlighted that the male patients aged over 50 years presenting with chondritis, refractory autoinflammatory manifestations, and/or unexplained hematological abnormalities, clinicians should consider bone marrow evaluation and UBA1 gene testing to promptly identify VEXAS syndrome, enabling early personalized treatment and improved outcomes.

P=N/A, N=40, Completed, Mazandaran University of Medical Sciences | Active, not recruiting --> Completed | Trial completion date: Jun 2025 --> Nov 2025

P2, N=60, Recruiting, National Institute of Dental and Craniofacial Research (NIDCR)

P3, N=17, Active, not recruiting, University of Texas Southwestern Medical Center | Trial primary completion date: Jun 2026 --> Jun 2025

Treatment also decreased VEGF secretion in both monocultures and HS-5 stromal co-cultures and induced IL-1β in co-cultures. These findings demonstrate that STK405759 exerts potent cytotoxic activity, disrupts microtubules, modulates STAT1 signaling, reduces VEGF secretion, and induces a distinct cytokine profile, while synergizing with ruxolitinib, supporting its further preclinical development as a potential therapeutic strategy in myeloproliferative neoplasms.

We knocked down THBS1 in rat (BRL, BRL-3A) and human (THLE-2) hepatocytes using siRNA and applied Ruxolitinib to inhibit the JAK2/STAT3 pathway, further clarifying the role of THBS1 in this signaling process...In addition, plasma ELISA revealed that the concentration of THBS1 in plasma increased with increasing radiation dose and degree of RILI, which was consistent with the expression level in the liver tissue. This study provides new insights into the pathogenesis of RILI, and identifies THBS1 as a potential biomarker for RILI diagnosis and monitoring.

P2, N=31, Not yet recruiting, Ruijin Hospital