Docking studies revealed a high affinity of APG for key proteins regulating antioxidant activity, apoptotic pathways, and inflammatory responses. In conclusion, APG-PCHNPs provided superior protection against DLM-induced liver injury by enhancing antioxidant defenses, suppressing NF-κB-mediated inflammation, and modulating Bcl-2/Bax/Caspase-3 signaling to prevent apoptosis, outperforming crude APG due to improved stability, solubility, and bioavailability.

P2, N=203, Active, not recruiting, BioVie Inc. | Recruiting --> Active, not recruiting

Dynamic changes in serum VEGF levels were associated with treatment response; however, these findings should be interpreted with caution due to the retrospective design and absence of a control group. Further well-designed prospective controlled studies are warranted to validate these observations.

P2, N=210, Not yet recruiting, Merry Life Biomedical Co., Ltd.

Collectively, these results implicated that AOPPs may be related to the pathogenesis of HSPN, AOPPs might induce or aggravate inflammation of HSPN through regulating RAGE-NF-κB signaling pathway. Above all, it has important clinical guiding significance for the prognosis judgment of HSPN, and can also provide new therapeutic targets for the HSPN.

P1/2, N=24, Active, not recruiting, University of Nebraska | Trial primary completion date: Jul 2026 --> Oct 2026

Moreover, we identified ACT001 as a novel USP22 inhibitor, and ACT001 induced substantial ERK1/2 ubiquitination and its subsequent degradation, efficiently suppressing the growth of CRC cells in vitro and in vivo by targeting USP22. Overall, this study revealed the mechanism underlying the role of hyperregulated ERK1/2 in CRC development, providing further insights into the pathology of CRC and the potential applicability of USP22-ERK1/2 as a therapeutic target in CRC.

CAPE mitigates the progression of AAA in mice and counteract the abnormal cell phenotype and inflammatory responses in Ang II-stimulated MOVAS cells. These protective effects might be achieved by inhibiting the NF-κB pathway.

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.