Merck Completes Acquisition of EyeBio
Acquisition strengthens and diversifies Merck’s pipeline with the addition of Restoret™, a novel late-phase candidate for diabetic macular edema and neovascular age-related macular degeneration, as well as preclinical candidates
“The EyeBio acquisition further diversifies our late-stage pipeline with the addition of a promising candidate based on novel biology and genetics for the treatment of certain retinal diseases,” said Dr. Dean Y. Li, president, Merck Research Laboratories. “We are excited to welcome the EyeBio team and look forward to working together to advance Restoret for the patients that need it.”
EyeBio’s lead candidate, Restoret™ (EYE103), is an investigational, potentially first-in-class tetravalent, tri-specific antibody that acts as an agonist of the Wingless-related integration site (Wnt) signaling pathway. Based on positive results from the open-label Phase 1b/2a AMARONE study in patients with diabetic macular edema (DME) and neovascular age-related macular degeneration (NVAMD), Restoret is scheduled to advance into a pivotal Phase 2b/3 trial to evaluate its potential for the treatment of patients with DME in the second half of 2024.
Additional pipeline candidates include clinical and preclinical assets being developed for the prevention and treatment of vision loss associated with retinal vascular leakage, a known risk factor for retinal diseases.
Transaction details
Under the terms of the agreement, Merck, through a subsidiary, has acquired all outstanding shares of EyeBio. As previously disclosed, this transaction is being accounted for as an asset acquisition. Merck will record a charge of approximately
About Restoret
Restoret is an investigational, potentially first-in-class tetravalent, tri-specific Wnt antibody designed to address unmet medical need in patients with retinal diseases, including diabetic macular edema (DME) and neovascular age-related macular degeneration (NVAMD). Restoret is administered as an intravitreal injection seeking to eliminate vascular leakage in retinal diseases by agonizing the Wnt pathway with the goal of restoring and maintaining the blood-retinal barrier. Preclinical evidence indicates that agonizing the Wnt pathway in the retina may reduce vascular leakage.
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