Vigil Neuroscience Enters into Definitive Merger Agreement to be Acquired by Sanofi

In This Article:

Vigil Neuroscience, Inc.
Vigil Neuroscience, Inc.

- Vigil’s shareholders to receive up to $10.00 per share in cash, comprised of $8.00 per share in cash at closing and a non-tradeable contingent value right of $2.00 per share in cash following the first commercial sale of VG-3927 -

- Acquisition expected to strengthen development path for the oral small molecule TREM2 agonist program, including VG-3927, a Phase 2-ready clinical candidate for potential treatment of Alzheimer’s disease –

- Companies expect transaction to close in third quarter of 2025 -

WATERTOWN, Mass., May 21, 2025 (GLOBE NEWSWIRE) -- Vigil Neuroscience, Inc. (Nasdaq: VIGL), a clinical-stage biotechnology company committed to harnessing the power of microglia for the treatment of neurodegenerative diseases and Sanofi (NASDAQ: SNY), today announced that it has entered into a definitive merger agreement pursuant to which Sanofi will acquire Vigil for an upfront payment of $8.00 per share of common stock in cash. Vigil shareholders will also receive a non-tradeable contingent value right (CVR) entitling the holder to potentially receive an additional $2.00 per share in cash payable following the first commercial sale of VG-3927 if achieved within a specific period. The total equity value of the transaction, including the potential CVR payment, represents approximately $600 million on a fully diluted basis.

"We are incredibly proud of the legacy we have built at Vigil and today’s announcement is a testament to the value of our TREM2 agonist pipeline,” said Ivana Magovčević-Liebisch, Ph.D., J.D., President and Chief Executive Officer of Vigil. “Sanofi’s development capabilities, therapeutic expertise, global footprint, and financial strength provide the greatest opportunity to further the development of VG-3927 for the potential treatment of Alzheimer’s disease and potentially bring this important and differentiated therapy to those struggling with the immense burden of this disease.”

Activating TREM2 is expected to enhance the neuroprotective function of microglia in Alzheimer’s disease. In neurodegenerative diseases such as Alzheimer’s disease, microglial activation is dysregulated, leading to debris accumulation, chronic inflammation and neurodegeneration in the central nervous system. Activation of TREM2 has shown to promote the migration of microglial cells to sites of injury, enhance their capability for phagocytosis, proliferation, and survival. Consequently, this facilitates the prevention of neural degeneration that is frequently associated with adult-onset neurodegenerative diseases.