Vaccinex announces presentation of findings for pepinemab

Vaccinex reports novel findings for its lead product, pepinemab, in a highlighted podium presentation at the Clinical Trials on Alzheimer’s Disease Conference in Boston, MA. Vaccinex has previously reported results of a phase 2 trial in Huntington’s disease that suggest pepinemab treatment prevents decline in glucose uptake associated with astrocyte activation and significantly slows cognitive decline as measured by the Huntington’s Disease Cognitive Assessment Battery. The company now reports data indicating that pepinemab treatment significantly reduced blood levels of GFAP, a biomarker of reactive astrocytes, providing further evidence of the drug’s potential to reverse harmful astrocyte activation and brain inflammation. Astrocytes are key regulatory cells in the brain that, under conditions of brain injury or disease, switch from their normal supportive physiological functions to inflammatory activity that is believed to aggravate damage to brain tissue. This transition is marked by release of glial fibrillary acidic protein, a characteristic astrocyte protein, into blood. Importantly, results from a highly sensitive S-PLEX GFAP immunoassay demonstrated a significant reduction in plasma GFAP levels in HD patients treated with pepinemab compared to those receiving placebo. Elevated GFAP levels in blood have also been found to correlate with Abeta amyloid deposits in brain and to be associated with higher risk of dementia and faster rates of cognitive decline in AD. A committee convened by the Alzheimer’s Association has recently recommended GFAP as a leading blood-based biomarker of astrocytic activation and brain inflammation in AD. Given the many physiological parallels between neurodegenerative processes in HD and AD, we believe that similar biological effects of pepinemab treatment are likely in the two indications. This is being tested in an ongoing randomized, placebo-controlled trial, SIGNAL-AD, supported by awards from the Alzheimer’s Drug Discovery Foundation and the Alzheimer’s Association, for which it is anticipated that the last patient will complete 12 months of treatment by June 2024. Early evidence of limited benefit to AD patients treated with antibodies to Abeta amyloid has stimulated a search for differentiated treatments that could further improve responses. It has been known for some time that beta amyloid deposits can also be present in the brain of elderly subjects who do not progress to Alzheimer’s.