Acumen Pharmaceuticals Presents Sabirnetug (ACU193) Fluid Biomarker and Target Engagement Analyses from Phase 1 INTERCEPT-AD Study in Early Alzheimer’s at the AD/PD 2024 Annual Meeting

- Cerebrospinal fluid (CSF) biomarker results are highly supportive of sabirnetug’s downstream pharmacological effects in the brain in early AD

- Poster presentation showcases method used to develop a first-of-its-kind assay to assess sabirnetug’s binding to amyloid beta oligomers (AβOs) in Alzheimer’s disease

- Company on track to initiate Phase 2 trial evaluating sabirnetug in the first half of 2024 and Phase 1 subcutaneous study in mid-2024

CHARLOTTESVILLE, Va., March 08, 2024 (GLOBE NEWSWIRE) -- Acumen Pharmaceuticals, Inc. (NASDAQ: ABOS), a clinical-stage biopharmaceutical company developing a novel therapeutic that targets soluble amyloid beta oligomers (AβOs) for the treatment of Alzheimer’s disease (AD), today presented cerebrospinal fluid (CSF) biomarker data from the sabirnetug (ACU193) Phase 1 INTERCEPT-AD trial in an oral presentation at the International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders (AD/PD) in Lisbon, Portugal, and online. Acumen also presented a poster showcasing the method used to develop a first-of-its-kind assay to measure target engagement of an AβO-selective antibody.

Acumen’s sabirnetug is the first humanized monoclonal antibody to clinically demonstrate selective target engagement of AβOs, a soluble and highly toxic form of Aβ that accumulates early in AD and triggers synaptic dysfunction and neurodegeneration. Positive topline results from 62 participants dosed in the Phase 1 INTERCEPT-AD trial (NCT04931459) were reported in July 2023, and additional insights from exploratory analyses have further confirmed sabirnetug’s proof-of-mechanism and broad therapeutic potential as a next-generation treatment for early AD.

Sabirnetug (ACU193) Lowers CSF Neurogranin & pTau181 Levels in INTERCEPT-AD Study in Early AD

Several key CSF biomarkers are associated with the pathological changes that occur in AD, and evidence suggests these biomarkers may better reflect the underlying pathology of AD than imaging alone.^i,ii Results from CSF samples collected before and after drug exposure in the INTERCEPT-AD study were presented and assessed for biomarkers indicative of amyloid pathology (Aβ42/40 ratio), tau pathology (pTau181, pTau217), neuronal injury (total tau) and synaptic injury (neurogranin).