P3, N=450, Active, not recruiting, University of Sydney | Recruiting --> Active, not recruiting

P3, N=0, Withdrawn, Bausch & Lomb Incorporated | N=150 --> 0 | Not yet recruiting --> Withdrawn

This research aimed to examine the impact of an aqueous extract of Capparis spinosa fruit and the lipid-lowering agent fenofibrate (FENO) on hepatic inflammation and steatosis in rats subjected to a high-fat emulsion...Our findings suggest that C. spinosa has a positive anti-inflammatory effect and may protect the liver against hepatic fibrosis, inflammation, and steatosis. These findings demonstrate the promising therapeutic potential of C. spinosa in the management of NASH.

Wnt/β-catenin signaling could be a potential lymphomagenetic mechanism for extranodal infiltration of T-lymphoblastic lymphoma. Fenofibrate has the potential to be an effective therapeutic strategy against liver infiltration of T-lymphoblastic lymphoma in MASH liver.

P2, N=0, Withdrawn, ZyVersa Therapeutics, Inc. | Recruiting --> Withdrawn

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.

P3, N=408, Completed, HighTide Biopharma Pty Ltd | Active, not recruiting --> Completed

P3, N=551, Completed, HighTide Biopharma Pty Ltd | Active, not recruiting --> Completed | Trial completion date: Dec 2025 --> Aug 2025

P3, N=367, Completed, HighTide Biopharma Pty Ltd | Active, not recruiting --> Completed

Our study reveals a distinct lipid signature in gastric metaplasia characterized by TG and LD accumulation, providing novel therapeutic insights into targeting lipid metabolism to prevent GIM malignant transformation and reduce cancer risk.

Collectively, these findings uncover a novel mechanism whereby Neo disrupts lipid homeostasis and induces oxidative stress via PPARα inhibition, and highlight PPARα activation as a potential strategy to mitigate Neo-associated hepatotoxicity, offering valuable insights for its safer therapeutic application.

P1, N=57, Completed, The First Hospital of Jilin University; The First Hospital of Jilin University