Eli Lilly Acquires Disarm and Its SARM1 Inhibitors for Preventing Axonal Degeneration
Eli Lilly and Company has acquired Disarm Therapeutics and its emerging therapies designed to prevent axonal degeneration in neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), multiple sclerosis, and peripheral neuropathy.
Disarm’s new class of disease-modifying treatments, called SARM1 inhibitors, target the central driver of axonal degeneration, or loss of nerve fibers, in these diseases.
Under the agreement, Eli Lilly will acquire Disarm for $135 million. Equity holders at Disarm may be eligible for an additional $1.225 billion should Lilly successfully develop and commercialize new medicines that result from the acquisition.
“The scientific team at Disarm discovered an important and highly promising approach to combat axonal degeneration. We will move quickly to develop their SARM1 inhibitors into potential medicines for peripheral neuropathy and neurological diseases, such as ALS and multiple sclerosis,” Mark Mintun, MD, vice president of pain and neurodegeneration research at Lilly, said in a press release.
Nerve cells have a long projection, called a nerve fiber or axon, that transmits signals throughout the nervous system. Damage or degeneration of this structure underlines a broad range of neurological diseases, and causes severe sensory, motor, and cognitive symptoms.
There is currently no treatment that effectively inhibits axon degeneration, but preclinical studies have shown that Disarm’s SARM1 inhibitors directly prevent the loss of axons in mice and cell models of disease, making SARM1 inhibition a potential approach for neurodegenerative treatments.
Investigators at Disarm Therapeutic in 2018 presented work demonstrating that inhibiting SARM1 activity prevented damage in axons in neurons grown in a lab dish.
The following year, the researchers presented additional data showing that blocking SARM1 activity protects human and mouse axons from multiple damage sources, including mechanical (such as crushing or severing the axon) and chemical (from exposure to chemotherapy drugs).
SARM1 inhibition also reduced neurofilament light chain, an axon-specific protein released when axons are damaged.
“Disarm’s innovative approach to treating axonal degeneration holds tremendous promise for addressing a wide spectrum of neurological diseases, and we have made significant strides toward enabling potentially transformative therapies,” said Disarm CEO Alvin Shih, MD.
“Lilly is ideally suited to advance this exciting new approach to treating axonal degeneration, and we look forward to seeing patients benefit from the work that Disarm initiated,” Shih said.
Disarm was founded by Atlas Venture, Jeffrey Milbrandt, MD, PhD, and Aaron DiAntonio, MD, PhD, of Washington University School of Medicine in St. Louis, Missouri, and Atlas entrepreneurs Rajesh Devraj, PhD, and Raul Krauss, PhD.