Cambridge biotech raises £25M for mitophagy Mission more than a decade in the making
2024-03-14
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Mission Therapeutics’ strategy of boosting a natural cellular recycling process, called mitophagy, to treat neurodegenerative and mitochondria-related diseases has attracted £25.2 million ($32.1 million) in fresh funding. The biotech, which also boasts a pair of pharma partnerships, is focused on developing small molecule inhibitors of de-ubiquitylating enzymes (DUBs) – the brakes on the garbage disposal system.
Since its founding in 2011, Mission has raised a total of £117 million. Thursday’s series D financing was jointly led by a syndicate of existing investors, including Pfizer Venture Investments. The pharma giant’s first investment in Mission was over a decade ago, and in 2020, Pfizer led a £12 million financing and also staked a claim on its DUB platform. Under the deal, Pfizer has the option to negotiate target exclusivity for certain, prespecified DUB inhibitors.
The Cambridge-based biotech also has a 2018 tie-up with AbbVie for two DUB programmes to treat Alzheimer’s disease.
Other backers of the round include Sofinnova Partners, Roche Venture Fund, SR One, IP Group, and Rosetta Capital.
DUB development
While DUBs’ role in mitophagy-associated diseases is well established, they have been historically difficult to selectively and specifically target with small molecules, as they comprise a large family of proteins.
Mission’s lead candidate, MTX652, is in Phase II testing for acute kidney injury (AKI) associated with cardiac surgery. Thursday’s round will help progress the company’s second candidate, MTX325, which has been cleared to start a Phase I trial for Parkinson’s disease (PD) in the UK.
If cells don’t routinely recycle their mitochondria, an accumulation of the dysfunctional organelles can lead to cellular degeneration, particularly of neurons. Mitochondrial dysfunction is a key driver of PD mechanisms, Mission CEO Anker Lundemose told FirstWord.
Inhibiting USP30 to promote mitophagy is “likely to have a positive impact on dopaminergic neurons undergoing chronic degenerative processes, as such degeneration results in functional impairment,” Lundermose added.
Mission has shown that, in a mouse model of PD, USP30 inhibition can help protect against loss of dopamine and dopaminergic neurons induced by alpha-synuclein.
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