Lexicon Highlights Preclinical Studies Showing Biological Effects Of Sotagliflozin In Hypertrophic Cardiomyopathy And Thrombotic Disease Pathways

-- Preclinical study demonstrates positive effects of sotagliflozin on cardiac function and structure in hypertrophic cardiomyopathy --

-- Second preclinical study shows inhibitory effects of sotagliflozin on platelet activity and thrombus formation --

-- Findings underscore differentiated biology associated with dual SGLT1 and SGLT 2 inhibition --


THE WOODLANDS, Texas, Oct. 21, 2026 (GLOBE NEWSWIRE) -- Lexicon Pharmaceuticals, Inc. (NASDAQ:LXRX), a leading cardiometabolic biopharmaceutical company, today highlighted findings from two newly reported preclinical studies that provide additional insight into the biological effects of sotagliflozin, Lexicon's first-in-class dual SGLT1 and SGLT2 inhibitor. The investigator-initiated studies, funded by Lexicon and conducted by independent academic investigators, demonstrated favorable effects of sotagliflozin on key pathways involved in hypertrophic cardiomyopathy (HCM) and thrombotic cardiovascular events.

The first study, published in the Journal of Molecular and Cellular Cardiology Plus1, found that sotagliflozin improved cardiac structure and function in a mouse model of hypertrophic cardiomyopathy, while reducing oxidative stress and upregulating mitochondrial gene sets associated with energy production in myocardial tissues. Investigators reported that sotagliflozin normalized measures of diastolic function, reversed progression of cardiac hypertrophy and reduced cardiac fibrosis, findings that support further evaluation of its potential in HCM.

The second study, published in the Journal of Clinical Investigation2, demonstrated that sotagliflozin, but not the selective SGLT2 inhibitor empagliflozin, reduced platelet activation and thrombus formation in ex vivo human blood and animal models, including an SGLT1 gene murine knockout model, without adversely affecting normal hemostasis. These findings provide additional insight into the differentiated biology of dual SGLT1 and SGLT2 inhibition and may provide support for previously observed reductions in myocardial infarction and stroke risk associated with sotagliflozin in heart failure and Type 2 diabetes clinical studies