TNFAIP1 knockout not only decreased CYP3A4 expression but also significantly impaired the ability of rifampicin (RIF), an upstream nuclear receptor-pregnane X receptor (PXR) agonist, to induce CYP3A4, indicating that TNFAIP1 is an essential regulator of PXR/CYP3A4 pathway...In vivo experiments demonstrated that overexpression of Tnfaip1 upregulated the Pxr/Cyp3a11 pathway and inhibited tumor growth, whereas Tnfaip1 knockout suppressed this pathway. This study identified TNFAIP1-PXR-CYP3A4 as a novel tumor-suppressive axis in HCC, providing potential molecular targets for HCC diagnosis and treatment.

Silibinin potentiates paclitaxel cytotoxicity by suppressing H19 transcription, offering a potential strategy to overcome paclitaxel resistance. The combination promotes apoptosis via caspase activation, highlighting a novel synergistic therapeutic approach in breast cancer treatment.

Screening of a compound library using this probe identified four natural products, namely Ginkgetin, Silibinin, Ledebouriellol, and Antcin C (R), as potent UGT1A8 inhibitors. Collectively, these findings position UPro1A8 as a robust molecular tool for advancing UGT1A8 functional studies.

SLBZP alleviated NTM-induced lung damage and enhanced NK cell immune response, which might be linked to CD4+ T cell immunity.

P2, N=30, Recruiting, UNC Lineberger Comprehensive Cancer Center | Trial completion date: Dec 2027 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2026

In conclusion, ABCB1 expression in macrophages differs by the cell model (THP-1 cell line vs. primary PBMC) and the polarization phenotype (M1 vs. M2). Strong rifampicin-mediated enhancements of ABCB1 were only observed in THP-1-derived M1 and M2 cells.

P3, N=674, Active, not recruiting, Queen Mary University of London | Trial completion date: Sep 2027 --> Aug 2026 | Trial primary completion date: Feb 2026 --> Aug 2026

P1/2, N=37, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting | N=120 --> 37 | Trial primary completion date: Aug 2026 --> Dec 2025

P2, N=50, Not yet recruiting, Jazz Pharmaceuticals

P3, N=674, Active, not recruiting, Queen Mary University of London | Recruiting --> Active, not recruiting | N=1266 --> 674 | Trial primary completion date: Jul 2026 --> Feb 2026

Collectively, these findings demonstrate that ONC disrupts redox homeostasis, mitochondrial function, and survival signaling in melanoma cells, exerting particularly potent effects in BRAF inhibitor-resistant populations. This study provides mechanistic insight into the anti-melanoma activity of ONC and supports its potential therapeutic application in drug-resistant melanoma.

P=N/A, N=60, Enrolling by invitation, Shaukat Khanum Memorial Cancer Hospital & Research Centre