Our Team
Our team is pound for pound one of the best in the world for developing drugs targeting protein aggregation disorders. Featuring multiple senior leaders from renowned organizations including Janssen, Elan, Merck, Prothena, and Jazz Pharmaceuticals, all of whom bring extensive preclinical and clinical experience in anti-AB monoclonal antibodies. Our high transparency culture provides everyone with an opportunity to contribute and challenge ideas, even outside their traditional areas of expertise. This collaborative environment fosters innovation and ensures that our drug development processes benefit from diverse experiences.
Leadership
Frederic Godderis
Co - Founder & Chief Executive Officer
Noah Ullman
Co - Founder & Chief Business Officer
Trebor Lawton
Co - Founder & Chief Technology Officer
Enchi Liu
Chief Development Officer
Eric Yuen MD
Chief Medical Officer
Guriq Basi PhD
Preclinical Development
Saira Ramasastry
Corporate Strategy
Dr. Robert Lawton PhD.
Founding Scientist
Scientific Advisory Board
Guriq Basi PhD
Current: SAB Chair & Preclinical Development @ Abyssinia. Former: CSO/ CTO @ Sarepta & Elan
Dennis Selkoe MD
Current: Co-director, Ann Romney Center for Neurologic Diseases
Vincent and Stella Coates Professor of Neurologic Diseases, Harvard Medical School
Coming Soon
Consultants & Advisors
Erica Pascal PhD
Intellectual Property
Raj Dua PhD
CMC
Paul Treacy PhD
CMC
Brian Rogers PhD
Toxicology
Steve Sazinksy PhD
Protein Engineering
Michael Papile
Corporate Finance
Mark Matijevic
Translational Science & Biomarkers
Peter Hoehn
Biomarkers & Diagnostics
Ira Wallis
Regulatory Affairs
Sam Griffin
R&D Intern
Our Science
Why Oligomers?
Treat
Soluble oligomers of amyloid-beta (Aβ) are believed to be the most neurotoxic forms of Aβ. Unlike insoluble plaques, these soluble oligomers can disrupt synaptic function, impair neuronal communication, and lead to cognitive deficits even at low concentrations. They are thought to play a central role in the early stages of Alzheimer’s, contributing to synaptic loss and neurodegeneration as well as driving downstream pathologies like tau dysregulation.
Prevent
By stimulating the immune system to recognize and neutralize toxic oligomers before they aggregate into plaques, a vaccine could potentially prevent the initial synaptic dysfunction and neuronal damage that leads to cognitive decline. This preemptive action would address the disease at an early stage, ideally halting its progression before significant brain damage occurs. Additionally, targeting oligomers specifically avoids the risks associated with removing amyloid plaques, which may sometimes lead to adverse effects.
Diagnose
Soluble amyloid-beta (Aβ) is a crucial biomarker for Alzheimer’s disease due to its early involvement in disease pathogenesis. Monitoring soluble Aβ levels, particularly oligomers, provides insights into disease onset and progression before symptoms appear. Detecting Aβ in plasma offers minimally invasive, repeatable measurements for large-scale screening and longitudinal studies, while cerebrospinal fluid (CSF) analysis, though more invasive, provides a closer reflection of central nervous system changes with higher sensitivity and specificity.