EA ameliorated myocardial IR in a rat model of T2DM and positively impacted TNNT2 and BNP levels, as well as phosphorylation status and mRNA expression of several genes involved in the insulin signaling pathway. Our findings underscore the potential of EA to modulate multiple therapeutic targets in the treatment of myocardial IR. If these effects can be replicated clinically, EA may represent a promising non-pharmacological option for the management of cardiometabolic risks associated with diabetes.

Cytotoxicity varied by compound, while the PPARγ agonist pioglitazone and the PPARα agonist fenofibrate were preferentially active in CTC lines, DG172 hydrochloride was selective for pleural effusion-derived lines, while rosiglitazone maleate, cloxiquine, and agrimol B showed no selectivity. These findings support PPARs as clinically relevant targets in SCLC, with PPAR-directed agents showing cytotoxic effects comparable to those reported in other malignancies. Such agents may aid SCLC treatment and help delineate biological differences between CTCs and resident tumor cells.

We demonstrated that pioglitazone and minocycline protected against glutamate-induced axonal injury, rotenone-induced neuronal death and promoted oligodendrocyte differentiation. In summary, our findings demonstrate that human preclinical IPSC platforms can be used to characterize the neuroprotective properties of compounds and thus may aid the selection of drugs for clinical trials. Moreover, the platform's flexibility allows for the easy incorporation of additional disease-specific phenotypic assays.

P3, N=582, Active, not recruiting, Celltrion | Recruiting --> Active, not recruiting

P3, N=24, Not yet recruiting, The University of Texas Health Science Center at San Antonio | Initiation date: Oct 2025 --> Jan 2026

P2, N=189, Completed, Zydus Therapeutics Inc. | Active, not recruiting --> Completed

P1, N=6, Recruiting, Zydus Therapeutics Inc. | Trial completion date: Aug 2025 --> Dec 2025 | Trial primary completion date: Aug 2025 --> Dec 2025 | Not yet recruiting --> Recruiting

In addition, XFC partially reversed the effects of the PPARγ antagonist GW9662, activated the PPARγ signaling pathway, inhibited oxidative stress and inflammatory responses, and exerted anti-fibrotic effects similar to those of the PPARγ agonist rosiglitazone. XFC inhibits inflammation and oxidative stress by regulating the PPARγ/HMGCS2 pathway, thereby attenuating fibrosis and alleviating lung injury.

The current study demonstrates that PPARγ activation exerts anti-H. pylori effects during gastric ulcer progression by inhibiting the TLR/NF-κB signaling pathway.

P3, N=386, Not yet recruiting, Zydus Therapeutics Inc.

Furthermore, renal Nrf2, HO-1, Bcl-2 expression while lowering NF-κB, KIM-1, Bax and caspase-3 levels. In conclusion, PIO demonstrated significant nephroprotective effects against TAM-induced renal damage by inhibiting apoptosis, reducing inflammation, and counteracting oxidative stress.

P1/2, N=60, Suspended, Ability Pharmaceuticals SL | Trial completion date: Dec 2024 --> Dec 2025