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Vaccinex (NASDAQ:VCNX) today provided an update on new clinical findings from its SIGNAL-AD Phase 1b/2 trial of pepinemab antibody in Alzheimer's disease.
Vaccinex recently announced positive results of the phase 1b/2 study of its lead product, pepinemab, in early stages of Alzheimer's disease (AD). The purpose of this report is to share additional data demonstrating stage-specific biomarker and cognitive effects starting with Mild Cognitive Impairment (MCI), the very earliest diagnostic stage of AD, and following through to progression to later stages of mild dementia. Currently approved treatments for AD are designed to reduce expression of Abeta amyloid and appear to modestly slow cognitive decline. The Vaccinex strategy is to intervene early to block astrocyte activation and associated inflammation with pepinemab so as to potentially achieve greater reduction in overall disease activity.
We report today that expression of plasma GFAP and p-tau 217 biomarkers appears to increase predominantly during MCI and that this is inhibited by pepinemab treatment. Glial Fibrillary Acidic Protein (GFAP) is a well-characterized marker of increasing astrocyte reactivity, and p-tau 217 is a peptide fragment of toxic "tau tangles" that accumulate in neurons during disease progression. In the absence of effective treatment, patients typically progress to mild dementia, which approximately corresponds to Mini-Mental State Examination (MMSE) scores of 22-26 . We report that pepinemab treatment at this stage may slow further cognitive decline as evidenced by strong treatment trends for multiple different cognitive measures.
In further support of potential treatment benefit, we performed a proteomic analysis of Cerebrospinal Fluid (CSF) from patients treated with pepinemab or placebo. The results identified several proteins that have been previously reported to increase during normal AD progression but are here shown to be inhibited by pepinemab treatment. These constitute additional disease-associated biomarkers whose inhibition, we believe, further supports the benefit of pepinemab treatment.
Finally, investors will be aware of concerns regarding damage to vascular integrity of brain tissue and the risk of inflammation and hemorrhage due to treatment with antibodies to Abeta amyloid. We have not seen evidence of such effects for treatment with pepinemab antibody. On the contrary, employing a human Brain-Chip model, we were able to demonstrate that damage caused by toxic aggregates of alpha synuclein can be inhibited or reversed by treatment with pepinemab. The results of similar analysis of damage caused by Abeta amyloid in the presence or absence of anti-Abeta antibody will be reported soon.
Posted In: VCNX
