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Harwell, Oxford, September 16, 2025, �Ӱ���Ƶ (�Ӱ���Ƶ), a platform biotech company developing novel mitochondrial-targeted persulfide modifiers in obesity, today announces additional data for its novel small molecule Myo4. The preclinical data demonstrates increased muscle fiber size in diet-induced obesity cohorts treated with �Ӱ���Ƶ’s Myo4, confirming lean mass increases demonstrated with MRI. The data also shows that the modality is anti-hepatosteatotic, clearing fat from the liver.��

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These results are shown in an oral presentation by Xavier Jacq, �Ӱ���Ƶ’s CSO, at the 61^st Annual Meeting of the European Association of the Study of Diabetes in Vienna, Austria. Dr. Jacq will be presenting in the EASD 2025 ‘Promising therapies in type 2 diabetes and obesity’ session on Tuesday, September 16, at 2.45pm CEST. The presentation is entitled ‘Characterisation of Myo4 in the murine diet-induced obesity model: a first-in-class anti-obesogenic muscle-preserving small molecule metabolic modulator’. This specific data was generated by histology analysis of tissues including liver, muscle and adipose tissues) in a 4-week study in the main preclinical model of diet-induced obesity.

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This preclinical data adds liver fat reduction and muscle building to data presented at ECO 2025, which demonstrated that Myo4 monotherapy drives fat loss while preserving both muscle and bone mineral content. �Ӱ���Ƶ also provided additional data demonstrating an accentuation of fat loss with muscle preservation when Myo4 is used in combination with semaglutide. Following this, �Ӱ���Ƶ presented additional data at ADA 2025 restoring insulin sensitivity in an industry-standard murine diet-induced obesity model.

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“�Ӱ���Ƶ is developing an alternative to current obesity-treatments by reducing side effects and toxicity. Addressing the inherent side effects of GLP-1s, �Ӱ���Ƶ has developed an entirely new and orthogonal mechanism of action with its mitochondrial-targeted persulfide modifiers. This data which is presented at EASD 2025 demonstrates that treatment with Myo4 does not lead to any detectable toxicity during the 4-week treatment and improves the quality of tissues in the diet-induced obesity model,” said Xavier Jacq, CSO, �Ӱ���Ƶ. “The extent of the clearance of fat deposition in the liver (steatosis) in its own right would justify the further development of Myo4.”��

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“Despite 890 million people living with obesity worldwide, current GLP-1 treatments are associated with the equivalent of 20-years of age-related muscle loss, and weight bounceback results in two-year follow-up weight loss averaging just 4.7%. Patients need the pharma industry to race to bring forward better approaches facilitating weight loss without muscle loss. By going beyond partially stemming the loss of lean mass due to GLP-1 treatment, �Ӱ���Ƶ’s EASD data release demonstrates our leadership in that race,” said Jon Rees, CEO, �Ӱ���Ƶ.��

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About Myo4 and other platform compounds

Myo4 was developed by �Ӱ���Ƶ as an improved mitochondrial-targeted persulfide modifier. These results enable �Ӱ���Ƶ to move Myo4 toward clinical candidate nomination. �Ӱ���Ƶ’s Candidate Engine is engaged in the development of an oral follower.