Eight years after Atlas Venture began probing a group of nervous system cells and their effects in Alzheimer’s and other neurological disorders, the venture creation firm launched a new startup in the field this week.
Vigil Neuroscience launched Tuesday with $50 million in financing from Northpond Ventures, Alexandria Venture Investments and others. Drug giant Amgen Inc. (Nasdaq: AMGN) also has a stake in the company after licensing multiple nervous system drug candidates to the Cambridge startup. Thanks to the Amgen licensing deal, Vigil anticipates asking the FDA for permission to begin its first clinical trial in the second half of 2021.
Vigil’s work revolves around immune cells in the brain and spine called microglia.
Atlas began its interest in these cells back in 2012, when scientists were noticing the link between them, the TREM2 gene and Alzheimer’s disease, according to Vigil CEO Ivana Magovčević-Liebisch. The following year, Amgen subsidiary deCODE Genetics reported that patients with a mutation were three times more likely to develop Alzheimer’s.
After years of Atlas looking for the right investment in this part of the field, the opportunity popped up last year to acquire Amgen’s drug candidates.
Amgen did not respond to questions about the divestment to Vigil. That same year, it and partner Novartis AG (NYSE: NVS) shut down two clinical trials last year of an Alzheimer’s drug that used a different approach.
They weren’t the only ones interested in microglia — Biogen (Nasdaq: BIIB) and development partner Eisai Inc. are also exploring the role of microglia in diseases like Alzheimer’s. Earlier this year, Biogen enlisted Cambridge startup Camp4 Therapeutics’ help in mapping microglia in order to better understand the role they play in the brain.
San Francisco’s Alector Inc. (Nasdaq: ALEC) has found in preclinical testing that activating the TREM2 gene may enhance protective microglia in Alzheimer’s patients.
“Our strategy involves initially developing VGL101 for a rare neurodegenerative disease for which microglia dysfunction is the causative driver,” Magovčević-Liebisch said. “For common neurodegenerative diseases such as Alzheimer’s disease, our approach would involve identifying and targeting genetically stratified patient populations with clear evidence of microglial dysfunction.”
