Acumen Pharmaceuticals Inc.

• US
• Acumen Pharmaceuticals Inc.
• Health-Care

ABOS

We are a clinical-stage biopharmaceutical company developing a novel disease-modifying approach to target what we believe to be a key underlying cause of Alzheimer’s disease, or AD. Alzheimer’s disease is a progressive neurodegenerative disease of the brain that leads to loss of memory and cognitive functions and ultimately results in death. Our scientific founders pioneered research on soluble amyloid-beta oligomers, or AbOs, which are globular assemblies of the amyloid-beta, or Ab, peptide that are distinct from Ab monomers and amyloid plaques. Based on decades of research and supporting evidence, AbOs have gained increasing scientific acceptance as a primary toxin involved in the initiation and propagation of AD pathology. We are currently focused on advancing a targeted immunotherapy drug candidate, ACU193, through clinical proof of mechanism trials in early AD patients.

ACU193 is a humanized monoclonal antibody, or mAb, that selectively targets AbOs, has demonstrated functional and protective effects in in vitro assays, and has demonstrated in vivo safety and pharmacologic activity in multiple animal species, including transgenic models for AD. We initiated our Phase 1 clinical trial of ACU193 in the second quarter of 2021 with the objective to evaluate its safety and tolerability and explore its pharmacokinetics and target engagement. This trial is enrolling patients with mild dementia or mild cognitive impairment, or MCI, due to AD, conditions referred to as “early AD.” Data from this trial are expected by the fourth quarter of 2022.

ACU193 is the result of over a decade of research and development undertaken by the company, which included a drug discovery partnership with Merck & Co., Inc., or Merck, from 2003 to 2011. ACU193’s mechanism of action is intended to slow disease progression and potentially preserve or improve memory function in early AD patients by binding to AbOs. AbOs are known to bind to neurons, leading to synaptic malfunction, memory deficits, cognitive impairment and, ultimately, neurodegeneration and cell death.

As such, we believe AbOs are the most toxic and pathogenic form of Ab in the brains of AD patients relative to other forms of amyloid, including Ab monomers and amyloid plaques. We believe the development and commercialization of a drug that reduces toxicity of AbOs is one of the most promising approaches for the potential treatment and prevention of the progression of AD.

In our nonclinical studies, we observed that ACU193 has over 500-fold greater selectivity for AbOs over Ab monomers and has limited or no binding to amyloid plaques. Also, ACU193 potently prevents binding of AbOs to hippocampal neurons. Recent laboratory studies conducted by us and others suggest that inhibiting AbOs may enable damaged brain circuits to regain some function and prevent further degeneration from occurring. ACU193 has demonstrated in vivo biochemical and behavioral activity in several AD mouse models, including crossing the blood-brain barrier and forming complexes with AbOs in a dose-dependent manner. ACU193 has shown consistent pharmacokinetics and brain penetration properties in four animal species. Safety toxicology studies in rats and monkeys provide acceptable margins for dosing in the clinic. Additionally, studies in transgenic mice indicate low potential for microhemorrhage.

Based in part on its binding affinity for AbOs rather than amyloid plaques, ACU193 has the potential to have a lower rate of amyloid-related imaging abnormalities, or ARIA, than the plaque-clearing anti-amyloid antibody therapies currently in development. ARIA is a common adverse event for antibodies targeting amyloid plaque and can be a dose-limiting safety liability for those antibodies.

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