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• W3196329835 abstract "Treatment with immune checkpoint inhibitors (ICIs) targeting CTLA-4 and the PD-1/PD-L1 axis is effective against many cancer types. However, due in part to unresponsiveness or acquired resistance, not all patients experience a durable response to ICIs. HBI-8000 is a novel, orally bioavailable class I selective histone deacetylase inhibitor that directly modifies antitumor activity by inducing apoptosis, cell cycle arrest, and resensitization to apoptotic stimuli in adult T cell lymphoma patients. We hypothesized that HBI-8000 functions as an epigenetic immunomodulator to reprogram the tumor microenvironment from immunologically cold (nonresponsive) to hot (responsive).Mice bearing syngeneic tumors (MC38 and CT26 murine colon carcinoma and A20 B-cell lymphoma were treated daily with HBI-8000 (orally), alone or in combination with PD-1, PD-1 L, or CTLA-4 antibodies. MC38 tumors were also analyzed in nanoString gene expression analysis.HBI-8000 augmented the activity of ICI antibodies targeting either PD-1, PD-L1 or CTLA-4, and significantly increased tumor regression (p < 0.05) in the above models. Gene expression analysis of the treated MC38 tumors revealed significant changes in mRNA expression of immune checkpoints, with enhanced dendritic cell and antigen-presenting cell functions, and modulation of MHC class I and II molecules.These findings suggest that HBI-8000 mediates epigenetic modifications in the tumor microenvironment, leading to improved efficacy of ICIs, and provide strong rationale for combination therapies with ICIs and HBI-8000 in the clinical setting.As an HDACi, HBI-8000 plays an important role in priming the immune system in the tumor microenvironment. The current preclinical data further justifies testing combination of HBI-8000 and ICIs in the clinic." @default.
• W3196329835 created "2021-09-13" @default.
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• W3196329835 date "2021-08-30" @default.
• W3196329835 modified "2023-10-18" @default.
• W3196329835 title "The epigenetic immunomodulator, HBI-8000, enhances the response and reverses resistance to checkpoint inhibitors" @default.
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• W3196329835 doi "https://doi.org/10.1186/s12885-021-08702-x" @default.
• W3196329835 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8404302" @default.
• W3196329835 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34461854" @default.
• W3196329835 hasPublicationYear "2021" @default.
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