Zolinza (vorinostat)

Single-agent activity favored vorinostat, followed by phenformin and 6-diazo-5-oxo-L-norleucine. Combinations favored gemcitabine plus oxaliplatin (GEMOX) and 5-FU plus interferon... The present findings are exploratory, and hypothesis-generating and should not be interpreted as evidence of clinical efficacy. Prospective clinical validation and mechanistic studies will be required to further define the therapeutic relevance of these observations in fibrolamellar carcinoma.

These results were further validated by the effective reduction in tumour growth in the xenograft mouse model. Collectively, RM-3-22 could be a promising alternative inhibitor for TNBC by targeting the autophagy-ferroptosis mechanism(s).

Glioblastoma (GBM) frequently develops resistance to temozolomide (TMZ), a process critically mediated by pro-survival autophagy. Preclinically, the HDAC inhibitor Vorinostat targets ELFN2, restores PP1 activity, and synergizes with TMZ to overcome resistance in vitro and in vivo. Our study reveals a novel PP1-centered phospho-splicing circuit governing pro-survival autophagy in GBM and provides a mechanistically grounded, immediately translatable combination therapy to combat TMZ resistance.

Furthermore, the blockade of pericyte differentiation by SAHA synergizes with propranolol, which inhibits endothelial differentiation of HemSCs, in a complementary manner. Additionally, SAHA promotes adipogenic differentiation of HemSCs and accelerates IH involution. Collectively, our work highlights the clinical significance of cell fate determination during IH progression, and establishes HDAC inhibition as a novel therapeutic option for IH through targeting pericyte differentiation of HemSCs, which provides a promising enhancement to current treatment strategies of refractory IH.

Based on the number of enriched model genes, butyrate, dimethyl sulfoxide, and vorinostat were identified as potential target drugs. EXOSC4, MMP9, ABCB1, and SOX2 are important exosome-related biomarkers for the diagnosis of CRC, and butyrate, dimethyl sulfoxide, and vorinostat have the potential to serve as targeted therapeutic drugs for CRC.

This triple combination strategy synergistically enhances HCC immunotherapy. Vorinostat induces MAEL expression to "unmask" tumors, while TIGIT blockade overcomes T cell exhaustion, amplifying antigen-specific CTL activity. This approach shows promise for HCC treatment.

P2, N=0, Withdrawn, Virogen Biotechnology Inc. | N=162 --> 0 | Trial completion date: May 2020 --> May 2026 | Unknown status --> Withdrawn | Trial primary completion date: Dec 2018 --> May 2026

Multi-omic analysis of the NRG/RTOG-0539 cohort shows that updated WHO grading criteria, incorporating molecular and cytogenetic features, improve risk stratification. However, molecular classification, particularly the Proliferative group, remains an independent and stronger predictor of RT response. These findings support integrating molecular biomarkers alongside modern grading frameworks to guide treatment and trial design in meningioma.

HGLRGs are aberrantly upregulated and actively contribute to LF progression through metabolic dysregulation and immune remodeling. FABP5 and ISG20 represents promising biomarkers and therapeutic target. This study providing novel diagnostic markers, drug repurposing opportunities, and strategies for improved clinical management of liver cirrhosis.

We investigated the effect of the HDACi suberoylanilide hydroxamic acid (SAHA) on cell viability and immunogenic cell death (ICD), as well as its combinatory potential with a SOCS3 peptidomimetic (KIRCONG chim PEG), designed to inhibit STAT3 phosphorylation (pSTAT3), in TNBC cell lines...Conditioned media from co-treated MDA-MB-231 cells promoted CD4+T cell activation, as shown by increased HLA-DR and CD69 expression. Overall, these findings indicate that SOCS3 functional replacement enhances SAHA anti-cancer and immunogenic effects in IL-6 high TNBC cells, supporting a context-dependent combinatory strategy targeting the IL-6/STAT3 axis.

P1, N=83, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Apr 2026 --> Apr 2027

P1/2, N=35, Recruiting, National Institute of Allergy and Infectious Diseases (NIAID) | Trial completion date: Jun 2026 --> Jun 2035 | Trial primary completion date: Jun 2026 --> Jun 2035