1 therapy, bevemipretide, was shown to ease brain inflammation in mice
Written by Andrea Lobo | July 16, 2026
- Massachusetts-based biotech Mighty Therapeutics has raised $150 million to advance treatments for Parkinson's and other diseases.
- One drug in its pipeline is bevemipretide, which was shown to reduce brain inflammation in mice.
- The company's work targets the dysfunction of mitochondria, which are energy-producing structures in cells.
Mighty Therapeutics, a Massachusetts-based biotech company, announced that it has raised $150 million to support the clinical development of its treatment candidates for Parkinson’s disease and other neurodegenerative conditions.
The new funding is expected to expedite pipeline initiatives in Parkinson’s as well as ongoing late-stage drug development programs in other diseases, according to a company press release detailing the financing.
The biotech’s work focuses on mitochondria, small energy-producing structures inside cells that serve as their powerhouses, whose dysfunction has been linked to a number of conditions marked by nerve cell loss, including Parkinson’s and amyotrophic lateral sclerosis (ALS).
In Mighty’s pipeline is bevemipretide (SBT-272), a small molecule designed to improve mitochondrial function. In a mouse model of Parkinson’s, the treatment candidate was found to reduce markers of brain inflammation.
The developer says it will use the new funding to “progress commercial and clinical development of [a] new class of mitochondrial targeted medicines.”
“These financings … [support] our continued leadership of the burgeoning field of mitochondrial medicine across a broad range of therapeutic areas,” said Reenie McCarthy, Mighty’s CEO. “With our strong commercial momentum and promising pipeline, we are poised for long-term growth and continued patient impact.”
Parkinson’s is caused by the progressive loss of dopaminergic neurons, which are nerve cells that produce dopamine, a signaling molecule that plays a role in voluntary movement. Several mechanisms are thought to contribute to neuronal damage and loss in Parkinson’s, including the accumulation of toxic clumps, or aggregates, of misfolded alpha-synuclein protein and mitochondrial dysfunction.
Misfolded alpha-synuclein can bind to cardiolipin, a fatty molecule found in the inner membrane of mitochondria, reducing their ability to produce energy.
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