Alaunos Therapeutics Reports Preclinical Results For ALN1003 Showing Weight Loss, Improved Insulin Sensitivity, And Better Liver Health In Obese Mouse Studies

• ALN1003 demonstrated consistent, favorable effects across key drivers of metabolic disease, including reductions in body weight and fat mass, improved insulin sensitivity, enhanced adipose function, and improved liver health in diet-induced obese mice
• A non-confidential investor presentation summarizing the preclinical dataset is now available

FORT LAUDERDALE, Fla., May 26, 2026 (GLOBE NEWSWIRE) -- Alaunos Therapeutics, Inc. (NASDAQ:TCRT) today reported an integrated preclinical readout for ALN1003, the Company's investigational oral, non-hormonal, non-incretin small-molecule candidate for obesity and related metabolic disorders. The readout consolidates findings from two non-Good Laboratory Practice (non-GLP) diet-induced obesity (DIO) mouse studies previously reported on March 2, 2026 and May 18, 2026, together with newly assembled cross-study analyses presented in an accompanying non-confidential slide deck published today.

Viewed together, the data show treatment-associated improvements across key biological drivers of metabolic disease:

• Body weight and food intake
• Body composition — preferential reductions in fat mass with proportional gains in lean mass as a percentage of body weight
• Insulin-resistance biology — lower fasting insulin and lower HOMA-IR, after adjustment for adiposity
• Adipose endocrine signaling — significantly higher adiponectin and a higher adiponectin-to-leptin ratio
• Hepatic biology — lower liver weight, lower liver-injury and cholestatic enzymes, and qualitative liver histology findings consistent with lower hepatic steatosis
  
   

Metabolic syndrome involves interconnected dysfunction across multiple organ systems, including insulin resistance, adipose dysfunction, and hepatic lipid accumulation. The Company believes a profile that engages several of these systems may be important for future therapeutic approaches.