BioVie Announces Clinical Data Showing Epigenetic Basis for How Bezisterim May Modulate Inflammation and the Biological Aging Process at the 11th Aging Research and Drug Discovery Meeting

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Bezisterim appears to possess broad homeostatic properties relevant to inflammation and human disorders related to aging Patients treated with bezisterim experienced 2 to 4 years age deceleration advantage compared to placebo Bezisterim modulated DNA methylation of proinflammatory genes and appeared to promote the transition of M1 proinflammatory to M2 anti-inflammatory macrophages Bezisterim was associated with 1.5 to 2.3 “fold enrichment” on gene control for hundreds of genes in pathways associated with neurodegenerative disorders and biological processes CARSON CITY, Nev. , Aug. 27, 2024 (GLOBE NEWSWIRE) -- BioVie Inc. , (NASDAQ: BIVI) (“BioVie” or the “Company”) a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders and advanced liver disease, today announced data from an oral presentation at the 11th Aging Research and Drug Discovery Meeting (ARDD 2024) being held August 26-30, 2024 in Copenhagen, Denmark . The presentation “Bezisterim Effects on Biological Age, Alzheimer’s Epigenetics, and Neurologic Assessments” provided an overview of clinical data to-date on bezisterim, focusing on various analyses and measurements related to longevity and its ability to affect the biological aging process broadly and chronic low-grade inflammation specifically. The presentation was given by Christopher L. Reading , BioVie’s Senior Vice President, Alzheimer’s Disease Program. “The presented clinical data provides the deepest understanding yet of how bezisterim may work at the gene level to reduce inflammation and impact disease,” said Cuong Do, BioVie’s President and CEO. “The data shows that patients treated with bezisterim experienced a two- to four-year age deceleration advantage when compared to placebo as measured by various biological clocks. The DNA methylation data also explain how bezisterim could modulate the function of specific proinflammatory genes and support the transition of M1 proinflammatory macrophages to the M2 anti-inflammatory state. Most importantly, the data shows bezisterim’s potential ability to control the expression of specific genes in pathways associated with diseases ranging from Parkinson’s and Alzheimer’s to ALS and biological processes ranging from TNF signaling to apoptosis.” As people age, a natural process called DNA methylation occurs where methyl groups are added to the surface of DNA. The over- or undermethylation of various genes have been shown to be associated with many diseases and the aging process itself. The presentation at ARDD 2024 detailed how bezisterim modulates DNA methylation and may have an impact in the following areas: The extent of DNA methylation of a person’s genome can be measured by a series of “clocks” that measure a person’s biological age, and the difference between the biological age and the number of years since birth is known as age deceleration or acceleration. In a clinical trial, patients treated with bezisterim saw an age deceleration advantage compared to those on placebo on various clocks: 3.68 years advantage on SkinBlood Clock (p=0.017), 4.77 years advantage on the Inflammation Age Clock (p=0.022), 5.0 years advantage on the Hannum Age Clock (p=0.006), 1.92 years advantage on the GrimAge Clock (p=0.068), and 3.71 years on the PhenoAge Clock (p=0.081). Bezisterim is believed to be the first drug candidate to show in a clinical trial an impact on modulating DNA methylation and age deceleration in a manner that is associated with specific diseases. DNA in blood comes predominantly from 3 cell types: monocytes/macrophages, lymphocytes, and granulocytes, and another set of clocks predicts the level of these immune cells. In the trial, the lymphocyte and granulocyte clocks are strongly and significantly correlated to observed levels of these cells for all patients. Placebo-treated patients saw a similar correlation between the monocyte clock and observed monocyte cell levels while bezisterim-treated patients did not show such correlation. Monocytes/macrophages control innate immunity and inflammation. The observed data suggest that bezisterim may support the transition of macrophages (and microglia in the CNS) from pro-inflammatory M1 state toward the M2 anti-inflammatory M2 state. Inflammatory factors, including TNFα, IL6, and MCP1, are produced when molecules such as ERK, MAP3K8, and NFκB perform their roles in various interrelated pathways, and the disruption of their function would disrupt the production of the inflammatory factors. The clinical data presented shows that bezisterim has the potential to significantly modulate the methylation levels of the genes that code for ERK, MAP3K8, NFκB, TNFα, IL6, and others. The data suggest that modulating the methylation levels for the individual actors in the various pathways could lead to reduced production of the inflammatory factors themselves. The Kyoto Encyclopedia of Genes and Genomes (KEGG) provides a mapping of known genes, molecules and pathways associated with individual diseases and cellular functions. The clinical data shows that bezisterim is associated with 1.5 to 2.3 “fold enrichment” (genes modulated compared to the pathway genes) in the pathways examined (all p

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