Zolinza (vorinostat)

Besides, patients in the high-risk group exhibited lower IC50 values for vorinostat, elesclomol, OSI-906, pyrimethamine, thapsigargin, and doxorubicin, but a higher IC50 value for cisplatin, compared to those in the low-risk group, indicating differential drug sensitivities. In summary, we established a robust DRGs signature comprising BTN3A1, CEBPA, KCNAB2, TBX21, and MYC, which showed strong prognostic value and predictive potential for immune status and drug sensitivity in OS. Notably, functional experiments confirmed that BTN3A1 acted as a tumor suppressor in OS, highlighting it as a promising therapeutic target.

P2, N=118, Not yet recruiting, New Approaches to Neuroblastoma Therapy Consortium

These findings contribute to the understanding of PIAS family genes in HNSC pathogenesis, diagnosis, prognosis, and potential therapeutic targeting.

Here, we report the development of H93, a hybrid small molecule integrating functional groups derived from NSC232003 and vorinostat, respectively...In vivo, H93 demonstrates significant antitumor efficacy. Overall, this study elucidates the structural and mechanistic basis of H93, establishing it as a promising UHRF1-targeted therapy for PCa.

Our findings suggest that TFEB promotes the chemoresistance of GBM tumors and GSCs by suppressing apoptosis. Co-treatment with etoposide and SAHA inhibits TFEB activity and enhances apoptotic cell death, representing a promising therapeutic strategy for treating malignant brain tumors.

Genetic or pharmacological degradation of RBM39 (using the clinically explored molecular glue indisulam) potently reactivates latent HIV-1 in J-Lat cell models, primary CD4⁺ T cells from people living with HIV-1 (PLWH), and synergizes with established LRAs (Bryostatin-1, JQ-1, SAHA) to broadly activate proviral reservoirs...In addition to establishing RBM39 as a promising therapeutic target for addressing the limitations of current "shock and kill" strategies, our findings establish a novel mechanistic framework for m⁶A-dependent regulation of viral gene expression. This framework may serve as a valuable reference for investigating similar regulatory mechanisms in other latent viral infections or oncogenic processes where RNA methylation plays a pivotal role.

Histone deacetylase inhibitors, such as vorinostat, show promise as treatment for T-cell lymphomas including cutaneous T-cell lymphoma...Histone deacetylase inhibitor-resistant cell lines displayed heightened sensitivity to inhibition of the NF-κB pathway by bortezomib and dimethyl fumarate. These findings implicate aberrant NF-κB activation as a central driver of the emergence of histone deacetylase inhibitor resistance in cutaneous T-cell lymphoma. Ultimately, our results provide a strong rationale for exploring NF-κB inhibition as a therapeutic strategy to restore or enhance the efficacy of histone deacetylase inhibitor-based therapies, overcome histone deacetylase inhibitor resistance, and improve outcomes for patients with cutaneous T-cell lymphoma.

Additionally, a microbial prognostic-predictive signature was established comprising Succinimonas, Collimonas, and Marichromatium, which also exhibited potential for indicating immunotherapeutic benefit and predicting drug sensitivity to cisplatin, cytarabine, pyrimethamine, olaparib, bicalutamide and vorinostat in LUAD treatment. This study identified intratumoral microbes associated with metabolism, revealed distinct subtypes and their roles in LUAD, and established a predictive signature for the prognosis and therapeutic responsiveness of LUAD.

P1, N=50, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed | Trial completion date: Jun 2028 --> Nov 2025 | Trial primary completion date: Jun 2028 --> Nov 2025

PFN2 is an oncogenic driver that promotes OSCC progression through HDAC1-dependent transcriptional reprogramming. PFN2 may serve as a prognostic biomarker and predictor of response to HDAC-targeted therapy.

Among the ERGs, PAX3 showed the strongest correlation with the risk score and was overexpressed in glioma, where it promoted proliferation, migration, epithelial-mesenchymal transition, and resistance to vorinostat through regulation of HDAC1/2/3 targets, as confirmed by functional assays showing that PAX3 knockdown suppressed proliferation and migration, while overexpression enhanced these effects. In conclusion, this study developed and validated a four-gene ERG-based prognostic model with high clinical utility and identified PAX3 as a potential therapeutic target that drives glioma cell migration and vorinostat sensitivity.

In this study, 14 HDAC degraders featuring a polyamine linker are designed and synthesized by conjugating HDAC inhibitors (HDACi, Vorinostat) with Cereblon (CRBN, an E3 ubiquitin ligase ligand)...Additionally, compound N exhibited the highest cellular uptake efficiency in a dose- and time-dependent manner. The findings presented in our manuscript provided valuable insights for the development of a proteolysis targeting chimera with high cellular uptake efficiency.