BioVie Inc., announced positive analysis of unblinded, topline efficacy data from its Phase 3 clinical trial (NCT04669028) of NE3107 in the treatment of mild to moderate Alzheimer?s Disease (AD). Data from evaluable patients show NE3107?s treatment advantage compared to placebo may be equal to or greater than the benefit from approved AD monoclonal antibodies. NE3107-treated patients also experienced a 4.66-year advantage in age deceleration vs.

placebo as measured by epigenetics/DNA methylation Skin Blood Clock. The trial started during the COVID-19 pandemic when access to clinical sites was limited and enrolled a total of 439 patients through 39 sites. Upon trial completion, the Company found significant deviation from protocol and Good Clinical Practice (GCP) violations at 15 sites (virtually all of which were from one geographic area).

This highly unusual level of suspected improprieties led the Company to exclude all patients from these sites and to refer them to the U.S. Food and Drug Administration (FDA) Office of Scientific Investigations (OSI) for further action. After these exclusions, 81 patients remained in its Modified Intent to Treat (MITT) population, 57 of whom were in the Per-Protocol population which included those who completed the trial and were verified to take study drug from pharmacokinetic (PK) data. Key Findings: Patients treated with NE3107 showed improved performance compared to placebo on all cognitive and functional assessments commonly used in the prior approval of amyloid beta (Aß)-based AD therapies, although the data missed statistically significance due to site exclusions.

Placebo-treated patients significantly worsened on virtually all assessments as expected from natural history of the disease. By contrast, NE3107-treated patients experienced a treatment advantage after 6 months that was equal to or greater than results reported from clinical trials for the approved Aß monoclonal antibody treatments after 18 months. Improvements in Clinical Dementia Rating-Sum of Boxes (CDR-SB) among NE3107-treated patients appear correlated to changes in tumor necrosis factor alpha (TNFa), plasma phosphorylated tau (p-tau), and the ratio of Aß42 to Aß40 NE3107 appeared to decrease neuroinflammatory processes that link Neurofilament Light Chain (Nf-L) and Glial fibrillary acidic protein (GFAP), both considered biomarkers of neurodegeneration and cognitive decline.

Patients treated with NE3107 saw an average of -5.66 years of age deceleration of the DNA methylation advantage compared to those on placebo. Age deceleration is the difference between the patient?s biological age as measured by the Horvath DNA methylation Skin Blood clock less the actual chronological age. NE3107 is believed to be the first drug candidate to demonstrate this impact on DNA methylation and the aging process in a double-blinded, placebo-controlled clinical.