0602K + Tirzepatide Muscle Mass / Function and Adipose Transformation Data to be Presented at ADA Scientific Sessions
GRAND RAPIDS, Mich., June 4, 2025 /PRNewswire/ -- Cirius Therapeutics, Inc., developing innovative therapies for patients suffering from diseases caused by insulin resistance, including obesity/overweight and type 2 diabetes (T2D), today announced that new preclinical data combining lead candidate 0602K and tirzepatide as a late-breaking poster will be presented at the American Diabetes Association's (ADA) 85th Scientific Sessions, taking place June 20–23, 2025, at McCormick Place Convention Center in Chicago, Illinois.
Presentation details:
Title: 1982-LB - MPC-Directed Insulin Sensitizer MSDC-0602K Combines with Tirzepatide to Maintain Muscle Mass/Function and Restructure Adipose Tissue [Board No. 1982]
Authors: M. Abu-Farha, J. Abubaker, F. Almulla, M. Abdul-Ghani, L. Norton, R.A. DeFronzo,J.R. Colca, K.S. McCommis
Date & Time: Sunday, June 22, 2025, at 12:30 AM CT
Location: Poster Hall (Hall F1)
The abstract for this late-breaking poster will be available beginning Friday, June 20, 2025 at 6:30 PM CT.
About CiriusCirius is a clinical-stage pharmaceutical company focusing on mitochondrial pyruvate carrier (MPC), addressing the metabolic dysfunction that causes insulin resistance and the organ pathologies associated with type 2 diabetes (T2D) and obesity/overweight. Its lead product candidate, 0602K (azemiglitazone potassium), is a potential best-in-class small molecule being developed as a once-daily oral therapy designed to selectively inhibit the mitochondrial target MPC, which plays a central role in selecting mitochondrial energy substrates. MPC inhibition reprograms mitochondrial metabolism, reducing insulin resistance in cells and driving metabolic benefits in organs throughout the body. This markedly improves glycemic control in T2D, body composition in obesity, liver function and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), and outcomes in cardiometabolic disorders.
About 0602K0602K has completed 7 US clinical trials including a 52-week placebo-controlled Phase 2b study in 392 subjects with MASH with and without T2D, and a 28-day placebo-controlled Phase 2a study in 129 subjects with T2D. In those clinical studies it markedly lowered HbA1c and insulin levels, and reduced liver injury and MASH – including on top of existing GLP-1 therapy. Preclinical studies also demonstrate increased lean muscle mass and function, together with marked metabolically beneficial shifts in adipose tissue phenotype ("bad fat" to "good fat"), including increased brown adipose tissue ("brown fat"). Selectively targeting MPC – while avoiding PPAR-γ activation – 0602K harnesses the real-world proven efficacy of 1st generation insulin sensitizers, such as pioglitazone, but without their side effect concerns.
Directly correcting a major underlying pathophysiology of chronic metabolic disease, 0602K has the potential to become a cornerstone of therapy. Coupling this potent pharmacology with that of the GLP-1s could particularly benefit patients with T2D, obesity/overweight and other diseases.
www.CiriusTx.com
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