cyclosporin A microemulsion

P=N/A, N=200, Recruiting, Masonic Cancer Center, University of Minnesota | Trial completion date: Oct 2026 --> Feb 2027 | Trial primary completion date: Oct 2025 --> Feb 2026

P3, N=102, Recruiting, Bristol-Myers Squibb | Trial completion date: Dec 2033 --> Jun 2034

Here, cyclophilin A (CypA) is identified as a critical mediator of cisplatin (DDP)/paclitaxel (DTX) resistance in NSCLC by suppressing ferroptosis, an iron-dependent form of regulated cell death...knockout of CypA or pharmacological inhibition with cyclosporine A (CsA) reverse resistant NSCLC cells to DDP/DTX both in vitro and in vivo by restoring ferroptosis...The study uncovers a CypA/SLC7A11/TRIM3 axis governing ferroptosis evasion in NSCLC chemoresistance and highlights CypA as a promising therapeutic target. Repurposing CsA to inhibit CypA represents a translatable strategy to overcome chemotherapy resistance, offering preclinical validation for improving outcomes in NSCLC patients.

P3, N=62, Completed, Zambon SpA | N=220 --> 62

P3, N=102, Recruiting, Bristol-Myers Squibb | Trial completion date: Dec 2031 --> Dec 2033 | Trial primary completion date: Dec 2030 --> Dec 2032

P3, N=150, Recruiting, University of California, San Francisco | Not yet recruiting --> Recruiting | Trial completion date: Jun 2027 --> Sep 2027 | Initiation date: Jun 2025 --> Sep 2025 | Trial primary completion date: Jun 2027 --> Sep 2027

Overall, 8173 biologics users (TNF-α, IL-12/23, IL-23, or IL-17 inhibitors) were compared to 41,598 patients treated exclusively with cyclosporine A or methotrexate. Biologics appear relatively safe with respect to cardiovascular disease and may reduce the risk of certain comorbidities such as mood disorders and solid tumors in patients with psoriasis or psoriatic arthritis. Clinicians should consider comorbidity profiles when selecting biologic agents for individual patients.

This review highlights multiple methodologies used to establish S-LCLs, including the use of cyclosporin A, CpG DNA, checkpoint kinase inhibitors, and cytokine modulation, and presents findings from diverse clinical contexts such as autoimmune diseases, post-transplant lymphoproliferative disorders, and cancer...Additionally, we explore how cytokines, particularly IL-10, support S-LCL survival, and how sodium butyrate and antiviral agents like acyclovir can influence EBV reactivation and replication. The review also considers the diagnostic and therapeutic relevance of LCLs, including their potential as antigen-presenting cells, vaccine platforms, and models for cellular immunotherapies such as CAR T-cells and virus-specific cytotoxic T lymphocytes. By evaluating the generation, molecular features, and immunological significance of S-LCLs, this review underscores their value in modelling EBV-driven disease and advancing novel therapeutic strategies.

Here, we investigated the mechanistic role of eRNA and its interplay with TNF-α signaling in cardiac I/R injury, and evaluated the therapeutic potential of RNase1 and cyclosporine-A (CsA)...These findings identify eRNA as both a biomarker and pathogenic mediator of myocardial I/R injury, and support a dual-targeted strategy using RNase1 and CsA to interrupt the TNF-α/TNFR1-driven inflammatory and mitochondrial death pathways. Targeting both upstream inflammatory and downstream mitochondrial mechanisms represents a promising cardioprotective intervention for acute myocardial infarction.

P=N/A, N=30, Enrolling by invitation, Tianjin Eye Hospital

Notably, the anti-malignant effects of DUSP6 knockdown were partially reversed by the mitophagy inhibitor cyclosporin A. Mechanistically, DUSP6 modulates mitophagy by increasing the phosphorylation status of mTOR, a central autophagy regulator, and DUSP6 knockdown-induced mitophagy was partially restored after treatment with mTOR activator MHY1485. Our findings indicate that high DUSP6 expression promotes BC progression by inhibiting mTOR-mediated mitophagy, leading to a poor prognosis for BC patients. These insights suggest DUSP6 as a potential therapeutic target in the treatment of BC.

The inhibition of mPTP opening through the application of cyclosporin A (CsA) led to a decrease in the cytoplasmic release of mtDNA and a subsequent reduction in cellular PANoptosis...The presence of mtDNA enhances the intranuclear transcription of IRF1, which in turn upregulates ZBP1 expression. ZBP1 recognizes mtDNA and contributes to cellular PANoptosis.