Dyne Therapeutics Raises $115 Million to Advance Therapies for Serious Muscle Diseases
August 11, 2020
Rare Daily Staff
Dyne Therapeutics completed a $115 million equity financing to advance the development of targeted oligonucleotide medicines for serious, genetically driven muscle diseases.
New investors Vida Ventures and Surveyor Capital led the financing with participation by additional new investors Wellington Management, Logos Capital, Franklin Templeton and an undisclosed institutional investor. Existing investors Atlas Venture, which seeded and incubated Dyne, Forbion, and MPM Capital also joined in the financing.
“This capital allows us to leverage our FORCE platform and advance our pipeline of modern oligonucleotide therapeutics aimed at transforming the lives of individuals living with serious muscle diseases,” said Joshua Brumm, president and chief executive officer of Dyne.
Lead programs are designed to knock down gene expression for the treatment of rare, monogenic neuromuscular diseases. Dyne is also developing therapeutics for patients with cardiac and smooth muscle diseases.
Dyne’s platform specifically targets muscle, minimizing systemic exposure. The company has completed preclinical studies indicating that this approach can deliver oligonucleotides that degrade disease-causing RNA, potentially restoring muscle health.
Dyne is developing a broad portfolio of therapeutics for muscle diseases, including programs in the rare genetic wasting diseases myotonic dystrophy type 1 (DM1), Duchenne muscular dystrophy (DMD) and facioscapulohumeral muscular dystrophy (FSHD).
Dyne’s lead program targets DM1, a rare, inherited disorder that causes progressive muscle weakness and other life-limiting complications. DM1 is a monogenic autosomal dominant disease caused by an abnormal expansion in a region of the DMPK gene. There are currently no disease-modifying treatments for DM1, which affects an estimated 40,000 people in the United States.
Dyne’s preclinical therapy consists of a proprietary antibody conjugated with a linker to an antisense oligonucleotide that is designed to reduce the levels of mutant DMPK RNA in the nucleus, releasing splicing proteins, allowing normal mRNA processing and translation of normal proteins, and potentially reversing disease. In preclinical studies the company has observed correction of splicing changes in DM1 patient cells, reversal of myotonia after a single dose in a DM1 model and enhanced muscle distribution as evidenced by reduced levels of cytoplasmic wild type DMPK RNA.
Photo: Joshua Brumm, president and CEO of Dyne.
Sign up for updates straight to your inbox.