P1, N=24, Recruiting, Novartis Pharmaceuticals | Not yet recruiting --> Recruiting

P1, N=24, Not yet recruiting, Novartis Pharmaceuticals

Specifically, the c-Myc inhibitor JQ1 and bovine serum albumin (BSA)-decorated nanoparticles loaded with the actin cytoskeleton inhibitor NP-G2-044 (BPG) were encapsulated into a reactive oxygen species (ROS)-sensitive hydrogel (JQ1 + BPG@gel). This hydrogel system improved the anti-recurrence efficacy of CAR-T therapy by 9-fold compared with monotherapy while establishing durable immune surveillance via memory T-cell differentiation within lymphoid organs. This research offers an innovative strategy to improve postoperative tumor cure rates and potentiate CAR-T immunotherapy.

P1/2, N=216, Active, not recruiting, Bristol-Myers Squibb | Trial completion date: May 2026 --> Aug 2028 | Trial primary completion date: May 2026 --> Aug 2028

P1, N=30, Suspended, National Cancer Institute (NCI) | Recruiting --> Suspended

P2, N=200, Recruiting, Zenith Epigenetics | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

P1/2, N=40, Enrolling by invitation, Zenith Epigenetics | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2026 --> Dec 2027

Scirrhous CAFs had heavily acetylated super-enhancers, and therapeutic targeting of super-enhancers by a BET bromodomain inhibitor, mivebresib and JQ-1, markedly decreased their migration-promoting activity. Notably, in scirrhous gastric cancer patients, normal fibroblasts in non-cancerous tissues also had a strong migration-promoting effect. It was suggested that fibroblasts in the non-cancerous tissue of scirrhous gastric patients have already acquired tumor-promoting capacity, forming a stromal field for scirrhous gastric cancer although its spatial extent remains to be solved.

Bromodomain and extraterminal motif (BET) inhibitors, such as JQ1, are promising cancer therapeutics that target epigenetic regulators, particularly BRD4...Collectively, our findings establish BRD2 as a critical mediator of pan-cancer adaptive resistance to BETi and identify NFYA as a novel transcriptional regulator of this process. Co-targeting BRD2 or its regulatory network offers a rational strategy to enhance the durability and efficacy of BET-based therapies.

The BRD4 inhibitor JQ1 reduces eccDNA production, while the HDAC inhibitor TSA induces an increase of eccDNAs...Furthermore, large eccDNA breakpoints are found to be coordinated with TAD boundaries and inclined to align at enhancers and promoters. Our study suggests that eccDNAs are more frequently detected from regulatory regions in the genome, consistent with their generation being associated with enhancer-promoter dynamics.

P1/2, N=216, Active, not recruiting, Bristol-Myers Squibb | N=108 --> 216

Preliminary results using JQ1-treated melanoma cells in a mixed lymphocyte-tumor cell culture (MLTC) markedly enhanced TIL proliferation and resulted in a T cell product enriched for CD8+ T cells. These findings reveal how the pleiotropic effects of BETi on melanoma cells broadly boost their immunogenicity towards CD8+ T cells and uncover novel pathways that might be therapeutically exploited to enhance CD8+ T cell-mediated anti-tumor immunity in ex vivo and in vivo approaches to cancer immunotherapy.