Jingzhuda (entinostat)

P1/2, N=47, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Feb 2026 --> Feb 2027

Nine compounds significantly activated Wnt signaling, including antivirals (imidocarb, proflavine, aminoacridine), anticancer agents (entinostat, enzastaurin, abemaciclib), and GSK-3β inhibitors (BIO, CP21R7). In mice, aminoacridine-especially combined with minoxidil-showed the strongest hair regrowth, while proflavine and imidocarb enhanced nail elongation. These results reveal new therapeutic candidates for hair and nail regeneration.

Combination regimens such as retinoic acid with entinostat and doxorubicin achieve potent antitumor synergy in preclinical models. Notably, emerging methylation-based classifiers that identify retinoid-responsive triple-negative breast cancer subsets, together with the paradoxical pro-tumorigenic effects of stromal RARβ, underscore the novelty and translational significance of integrating tumor-intrinsic and microenvironmental determinants of retinoid sensitivity. Together, these approaches may help re-establish functional retinoid signaling and realize the therapeutic potential of retinoic acid in breast cancer.

Aggregated CMap analysis nominated histone deacetylase (HDAC) inhibition, with entinostat (MS-275) ranking highest as a candidate to reverse the high-risk transcriptomic program. An Arg-axis-anchored approach resolves biologically coherent NB subtypes and yields a parsimonious, fixed-coefficient four-gene signature that generalizes across cohorts, aligns with immune contexture, and proposes testable therapeutic hypotheses. These results support metabolism-informed risk stratification in NB and motivate prospective validation with standardized processing, mechanistic flux assays, and rational combination studies.

Entinostat, an inhibitor of class I HDAC, synergizes with cisplatin by preventing ARHGDIB delactylation. Collectively, our findings unveil a unique paradigm in which delactylation of tumor suppressors drives metastasis and chemoresistance. Targeting lactylation dynamics with HDAC inhibitors presents an avenue for intervention of bladder cancer.

P=N/A, N=50, Not yet recruiting, Sun Yat-sen University Cancer Center; Sun Yat-sen University Cancer Center

These findings offer preliminary clues for future risankizumab-based combination strategies in psoriasis.

In conclusion, our work elucidates a coherent epigenetic pathway wherein entinostat activates AZGP1 to inhibit HCC metastasis. These findings nominate AZGP1 as both a critical mediator and a potential biomarker for entinostat-based therapy in advanced HCC.

P2, N=118, Recruiting, Zhejiang Cancer Hospital

Entinostat demonstrates strong anti-NSCLC activity by suppressing EGFR expression and downstream signaling, highlighting its potential as a therapeutic agent.

The short-term in vitro effects of 5d were modulated by a compensatory upregulation of autophagy. However, in long-term, this protective mechanism becomes insufficient to sustain tumor survival, resulting in strong antitumor efficacy in vivo in the CAM assay for both compounds even outperforming entinostat.

P1/2, N=49, Recruiting, National Cancer Institute (NCI) | N=30 --> 49