Our research revealed comprehensive metabolic alterations in gastric cancer, including upregulated lactate metabolism that promotes tumorigenesis via the lactate shuttle. Niclosamide targets the m6A methylation regulatory protein YTHDF2, which influences genes related to metabolism, indicating its potential as a prospective treatment for GC.

Tyrosine kinase inhibitors (TKIs), such as sunitinib and sorafenib, are standard treatments for renal cell carcinoma (RCC). RNA sequencing (RNA-seq) and bioinformatic analyses showed that niclosamide modulated critical pathways, including BRIP1- and FANCA-mediated DNA repair and E2F2-regulated cell cycle progression. These findings provide proof-of-concept that niclosamide enhances TKI efficacy through modulation of DNA repair and cell cycle pathways, supporting the rationale for DNA damage response (DDR)-targeted combination strategies in RCC.

P2, N=176, Not yet recruiting, Jiangsu HengRui Medicine Co., Ltd.

Given the reduced ATP-generating capacity of SDHB -KO cells, we hypothesized they would be uniquely sensitive to futile cycle induction with mitochondrial ionophores (2,4-Dinitrophenol (2-DNP), BAM15, Niclosamide, Nitazoxanide). Thus, the accumulation of succinate in SDH-deficient tumors inhibits KDM4 activity, impairs DNA repair and yields enhanced susceptibility to Ym155-induced reactive oxygen species (ROS) generation. The identified intrinsic susceptibilities of SDHB -deficient cancers has the potential to be therapeutically leveraged.

P1, N=0, Withdrawn, M.D. Anderson Cancer Center | N=33 --> 0 | Trial completion date: Jun 2028 --> Nov 2025 | Active, not recruiting --> Withdrawn | Trial primary completion date: Jun 2026 --> Nov 2025

The STAT3 agonist Colivelin reverses the anti-proliferative effects of allicin, while the inhibitor WP1066 enhances these effects. These findings collectively suggest that allicin exerts its anti-inflammatory and anti-remodeling effects in asthma by targeting the STAT3/PIM1 pathway, providing a new therapeutic strategy for asthma treatment.

P1, N=33, Active, not recruiting, M.D. Anderson Cancer Center | Not yet recruiting --> Active, not recruiting

This study investigates the characterization and biological effects of Dual Drug-Loaded Nanoparticles on HepG2/doxorubicin (DOX) cells, focusing on the anti-cancer ability of Doxorubicin/Curcumin-Polyethylene Glycol-Polycaprolactone Nanoparticles (DOX/Cur-PEG-PCL-NPs)...These results demonstrate that DOX/Cur-PEG-PCL-NPs effectively reverse chemoresistance and suppress tumor progression through modulation of the Nrf2 pathway and apoptosis induction, offering a promising strategy for targeted liver cancer therapy. The online version contains supplementary material available at 10.1007/s10616-025-00855-y.

P1/2, N=340, Completed, AstraZeneca | Active, not recruiting --> Completed

P1, N=38, Recruiting, Montefiore Medical Center | N=24 --> 38 | Trial completion date: Jul 2028 --> Mar 2030 | Trial primary completion date: Oct 2025 --> Jun 2027

Four immune metabolism-associated diagnostic genes were identified, including TRAF3IP2, RIPK1, KEAP1, and DPP4 for OMAS.

Furthermore, CHL reduced p-p65 expression by 5-fold, indicating its effective inhibition of NF-κB transcriptional activity and thereby alleviating inflammatory responses. Therefore, the LAP-activable co-prodrug CHL holds promising potential as a candidate for the synergistic treatment of liver injury.