leflunomide

P2, N=53, Not yet recruiting, The Third Affiliated Hospital of Naval Medical University (Shanghai Eastern Hepatobiliary Surgery Hospital); The Third Affiliated Hospital of Naval Me

P=N/A, N=3, Terminated, University Hospital, Basel, Switzerland | N=15 --> 3 | Active, not recruiting --> Terminated; The study was prematurely terminated due to significant difficulties in recruiting participants, arising from the extremely rare nature of the targeted gene mutation.

P4, N=100, Recruiting, Tongji Hospital | Enrolling by invitation --> Recruiting | Trial completion date: Dec 2025 --> Mar 2027 | Trial primary completion date: Dec 2025 --> Oct 2026

We demonstrate that BCOR-deficient cells have a heightened sensitivity to DHODH inhibitors such as brequinar and leflunomide, that are already in clinical use. Rather, DHODH's role in the electron transport chain, essential for mitigating reactive oxygen species, may be the physiological vulnerability that pushes BCOR-mutant cells toward cell death when DHODH is inhibited. DHODH inhibitors could be repurposed as targeted therapies for BCOR-mutant tumors, offering a promising strategy for precision medicine in AML and other cancers.

It is a pyrimidine synthesis inhibitor that has an inhibiting effect of tumor necrosis factor alpha (TNF α) signaling. We present a case of with generalized pustular skin lesions after intake of leflunomide, which resemble a pustular exacerbation of a pre-existing psoriasis as well as a generalized pustular psoriasis.

P1, N=1, Active, not recruiting, City of Hope Medical Center | Trial completion date: Dec 2025 --> Nov 2026 | Trial primary completion date: Dec 2025 --> Nov 2026

P2/3, N=70, Completed, Ain Shams University | Active, not recruiting --> Completed

P=N/A, N=50, Recruiting, King Chulalongkorn Memorial Hospital | Trial completion date: Jan 2026 --> Jul 2026 | Trial primary completion date: Sep 2025 --> Dec 2025

Collectively, our findings demonstrate that ARS improves LEF responsiveness in RA by activating the cGMP-PKG pathway and suppressing TRAF6/NFATc1-mediated osteoclastogenesis. These mechanistic insights may provide a theoretical basis and experimental foundation for future clinical studies exploring combination strategies for patients with RA with a poor therapeutic response to LEF.

The mice were assigned to 6 groups, including the normal group, the model (CIA) group, the model + CSJBD-L (8.1 g/kg) group, the model + CSJBD-M (16.2 g/kg) group, the model + CSJBD-H (32.4 g/kg) group, and the model + leflunomide (LEF) (0.05 mg/10 g) group, with 10 mice in each group...Wnt7b overexpression reversed the inhibitory effect of CSJBD on the Wnt/β-catenin signaling pathway and the proliferation of RA FLSs, indicating that Wnt7b is the direct target of CSJBD. CSJBD inhibits RA pathology by blocking the WTAP-Wnt7b-Wnt/β-catenin signaling axis, with Wnt7b identified as a direct therapeutic target of CSJBD.

P=N/A, N=15, Active, not recruiting, University Hospital, Basel, Switzerland | Recruiting --> Active, not recruiting

Emerging biologics have significantly advanced the management of PsA, offering greater efficacy and safety compared to conventional DMARDs. IL-17 and IL-23 inhibitors, along with newer agents like bimekizumab, present promising treatment options for patients with inadequate responses to TNF inhibitors. Personalized treatment strategies, based on disease phenotype and individual patient needs, are essential for optimizing outcomes in PsA management. Further research into long-term efficacy and safety is required to refine treatment protocols and improve patient outcomes.