The pre-incubation with BAY 11-7082, IKKα/β reduced the damage induced by IL-1β, and, interestingly, potentiated the properties of LW. Our data demonstrated the ability of LW to regulate apoptosis, oxidative stress and gene expression of main factors implicated in OA pathogenesis through a possible modulation of NF-κB signaling pathway. This study supports the use of balneotherapy with a sulfate-arsenical-ferruginous mineral water in the treatment of OA.

These findings indicate that combined curcumin and doxorubicin induce apoptosis primarily through JNK-dependent MAPK signaling, accompanied by stress-associated cellular responses.

This paper summarizes the current mechanistic insight and disease-specific evidence regarding MCL/ACT001 and further evaluates their therapeutic repositioning potential for age-related diseases, including cardiovascular and cerebrovascular diseases, fibrotic conditions, immune disorders, metabolic diseases, and tumors. Additionally, we discussed key translational challenges.

Moreover, they effectively promote CRT exposure, HMGB1 release, and ATP secretion in 4T1 cells. Furthermore, in a murine breast cancer model, CMCS-D + C/NPs significantly upregulate the expression of proteins such as CD8 and Caspase-3, cytokines (IFN-γ and IL-6), and Granzyme B, demonstrating favorable antitumor efficacy.

P2, N=60, Active, not recruiting, BioVie Inc. | Recruiting --> Active, not recruiting | Trial completion date: Jan 2026 --> May 2026 | Trial primary completion date: Dec 2025 --> May 2026

Additionally, PCDH1 activated the NF-κB pathway by promoting nuclear translocation of P65, and inhibition of NF-κB with SC75741 reversed PCDH1-induced EMT, confirming that PCDH1 promotes pancreatic cancer metastasis via the NF-κB/EMT axis. PCDH1 acts as an oncogene in pancreatic cancer, promoting cell invasion, migration, and EMT progression through the NF-κB signaling pathway, making it a potential therapeutic target.

P2, N=12, Suspended, National Neuroscience Institute | Not yet recruiting --> Suspended

We summarize the clinical translation progress of ACT001, including its safety and pharmacokinetic profiles, discuss emerging delivery systems such as micelles, and review the patent landscape of PTN derivatives. By integrating mechanistic insights with progress in clinical applications and drug delivery, this review provides a foundation for further mechanistic studies and supports the translational development of PTN-based therapies for respiratory disorders.

Furthermore, CDDO-Me did not compromise the antitumor efficacy of DOX/LAP in breast cancer cells. CDDO-Me protects against DOX/LAP-induced cardiotoxicity by stabilizing GPX4 and inhibiting ferroptosis, offering a promising therapeutic strategy that preserves cardiac function without interfering with chemotherapy.

Notably, 8 exhibited significant antitumor efficacy comparable to CDDO-Me (bardoxolone methyl), which had entered clinical trials. Taken together, 8 represents a promising candidate for the treatment of cancer and merits further study.

Molecular docking analyses supported the binding of CUR and DOX to key ferroptosis regulators. This study shows the potential of CUR to sensitize DOX-resistant cancer cells through ferroptosis-linked-oxidative stress targeting.

Molecular docking confirmed that LT4 stably occupied the ATP‑binding pocket of PI3Kγ with a binding energy comparable to wortmannin and a conformation similar to antroquinonol. In conclusion, to the best of our knowledge, the present study is the first to comprehensively demonstrate the multi‑target anti‑CRC effects of LT4, highlighting its potential as a therapeutic agent, especially in KRAS‑mutant CRC.