Additionally, it mitigated the hepatotoxic effects of flutamide. Therefore, this combination may represent a new treatment strategy for PCa.

(IC₅₀ 1.83-6.43µg/mL), with additional activity against Schistosoma mansoni (IC₅₀ 114.83-247.0µg/mL) and Plasmodium falciparum 3D7 (IC₅₀ 5438.27ng/mL). Antibacterial MICs ranged 16-512µg/mL and antifungal MICs 16-256µg/mL, consistent with bacteriostatic/fungistatic effects.

P=N/A, N=74799, Completed, University of Pecs

P3, N=180, Recruiting, Beni-Suef University

The combination therapy demonstrated excellent tolerability without observable systemic toxicity. Moreover, Integrating GEPIA3 database and clinical specimen analyses, we find that BTN3A1 and BTN2A1 are highly but heterogeneously expressed in esophageal cancer tissues, and that metformin‑mediated upregulation may restore sensitivity to Vγ9Vδ2 T cell immunotherapy particularly in patients with low baseline expression-uncovering a novel immunomodulatory function of metformin that provides a compelling rationale for its repurposing as a combinatorial agent against immunologically cold tumors such as esophageal carcinoma.

P1/2, N=55, Active, not recruiting, National Eye Institute (NEI) | Recruiting --> Active, not recruiting | Trial completion date: Sep 2028 --> Feb 2029 | Trial primary completion date: Sep 2028 --> Feb 2028

To address the parallel needs for high QOL and disease control, we developed an alternative therapeutic approach termed"Coexistence Therapy for Cancer,"employing the combination of a carbohydrate-restricted ketogenic diet, metformin, vitamin-D, eicosapentaenoic acid (EPA) and additional complementary therapies, with S-1 (tegafur/gimeracil/oteracil potassium) at doses low enough to avoid side effects. These findings suggest that this therapeutic strategy may serve as a complementary treatment option for patients who are unable to tolerate standard chemotherapy. Further accumulation of clinical cases is required to validate the effectiveness of this approach.

In zebrafish MASLD-HCC, PRS-OPT-nominated dosing reduced hepatic macrophage accumulation and improved disease-relevant transcriptional and morphological readouts. PRS-OPT enables interpretable, multi-objective dose nomination for MASLD-relevant HCC contexts, and establishes PRS-OPT as an interpretable, multi-objective framework for regimen nomination that is directly extensible to additional phenotypic endpoints for preclinical evaluation.

Ten high-priority targets of brain-penetrating compounds included ACE and NISCH (cardiovascular drugs), NDUFA2, NDUFB6, and NDUFS1 (metformin), CDK4, NTRK3, and MET (oncology inhibitors), and GLS and NOS2 (enzyme inhibitors). We found genetic evidence for established and novel MD targets across the drug development pipeline. Novel targets point to mechanisms beyond monoaminergic systems, most with approved drugs for other conditions, offering immediate repurposing opportunities.

Moreover, both alogliptin and metformin exhibited dose-dependent effects, and the 1:8 alogliptin-metformin ratio demonstrated strong synergism (CI 0.04388). These findings suggest that alogliptin-metformin co-therapy ameliorates diabetes-associated skeletal complications through modulation of DPP-4 activity and OPG/RANKL signaling.

Metformin as an adjuvant to febuxostat provides superior improvement in pain, inflammatory markers, uric acid levels, and metabolic parameters in gout patients, without increasing adverse effects.

In vivo intervention via ATF3 knockdown, anti-PD-L1 treatment, or pharmacological perturbation of ChREBP-related metabolism with metformin or an ACSS2 inhibitor significantly suppressed ESCC progression and restored intratumoral CD8+ T-cell infiltration. These findings establish ChREBP as an alcohol-sensitive metabolic-epitranscriptomic switch that integrates genetic susceptibility with immune evasion to drive esophageal carcinogenesis.