Restoring mitochondrial health in
Our Approach
MitoRx is developing new treatments to restore healthy mitochondrial metabolism in patients living with high-risk obesity.
Our first-in-class small molecule asset, MTRX31, targets the elimination of ectopic fat from affected organs in people with metabolically unhealthy obesity, by restoring mitochondrial health rather than suppressing appetite.
This approach has the potential to deliver durable and higher quality weight loss, lower the risk of cardiovascular complications and other serious diseases, and improve quality of life.
About Us
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The Problem
30-40% of people living with obesity have insulin resistance involving mitochondrial dysfunction.1,2,3 Metabolically unhealthy obesity (MUO) with insulin resistance often features hypertriglyceridemia and high waist circumference. People living with MUO are at disproportionate risk of serious illnesses such as type 2 diabetes, MAFLD/MASH and acute cardiac events.
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Our differentiated science
MitoRx is focused on restoring mitochondrial health at a cellular level, overcoming metabolic flexibility by rebalancing fat and carbohydrate oxidation toward carbohydrate oxidation to deliver significant and durable quality weight loss and improved health.
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Our Program
MTRX31 is a first-in-class small molecule that has shown superior magnitude, quality and durability of weight loss compared with tirzepatide in an industry-standard preclinical model of obesity.
1. Metwally et al., Nature 2026
2. Tsilingiris et al., Current Obesity Reports 2021
3. Sangwung et al., Endocrinology 2020
What is MTRX31?
MTRX31 is a novel mitochondrial-targeted small molecule in preclinical development for the treatment of obesity. In a preclinical diet-induced obesity (DIO) model at thermoneutrality, intermittent treatment with MTRX31 resulted in more durable and greater body weight loss than tirzepatide (Figure A), 62.2% lower fat mass than DIO vehicle after 8 weeks (Figure B) and demonstrated that MTRX31-mediated weight loss does not involve lean mass loss (Figure C) but that MTRX31-mediated weight loss overcomes insulin resistance (Figure D). MTRX31 therapy significantly regressed liver fattiness and demonstrated an additive effect in combination with tirzepatide (Figure E).
Methods: Thermoneutral DIO model – Six-week-old male C57BL/6J mice were fed HFD (60%) or standard chow (NC) for 15 weeks and then dosed with MTRX31 (5 mg/kg; s.c. TIW), tirzepatide “TZP” (5 nmol/kg, s.c. QD), or combinations for 8 weeks (n=10). Fat and lean mass were determined by MRI. Abbreviations: TIW – Three times per week dosing frequency. QD – Daily dosing frequency. HFD – High-fat diet. DIO – Diet-induced obesity. NC – lean animals fed standard chow.
“By restoring mitochondrial health, we believe we will deliver durable, quality weight loss for people living with high-risk obesity. Rather than suppressing appetite, our approach restores metabolic flexibility and overcomes insulin resistance, reducing the disproportionate risk for these patients of progression into serious and critically serious disease such as MASLD, MASH, type 2 diabetes and atherosclerotic cardiovascular disease.”
Latest News & Events
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BIO-Europe, November 9-11
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Sachs 2nd Annual Obesity and Cardiometabolic Innovation Forum, June 5
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American Diabetes Association Scientific Sessions 2026, June 5-8
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Myo-004 (MTRX31) induces bodyweight loss in DIO at thermoneutrality by switching metabolism from fat to carbohydrate oxidation
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European Association for the Study of Diabetes (EASD), 28 September – 2 October