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2025.10.15

META Nominates MP-5342 as First Pre-clinical Candidate for Inflammatory Bowel Disease 2025/10/15

The first candidate molecule derived from the innovative immunometabolism platform has completed preclinical development and is approaching the IND-enabling study stage.

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  • The first candidate molecule derived from the innovative immunometabolism platform has completed preclinical development and is approaching the IND-enabling study stage.
  • The preclinical data package validates lactate dehydrogenase (LDH) as a novel therapeutic target with potential across multiple inflammatory diseases, including IBD, MS, and PBC.
  • Based on robust human translational data, the lead indication has been identified as inflammatory bowel disease (IBD).
  • Preparations for the Investigational New Drug (IND) application are underway, with first-in-human clinical trials expected in H2 2026.

Shenzhen, CHINA – 15 October 2025– META Pharmaceuticals Inc., an innovative biopharmaceutical company focuses on autoimmune and metabolic diseases, has nominated MP-5342 as its first pre-clinical candidate for inflammatory bowel disease (IBD). This follows the successful completion of key testing for the IBD pipeline clinical candidate (PCC). MP-5342 will now advance into regulatory-required preclinical studies to support an Investigational New Drug (IND) application.

MP-5342 is an oral, targeted, disease-modifying anti-inflammatory therapy with first-in-class potential. It targets lactate dehydrogenase (LDH), a key enzyme regulating glucose metabolism in immune cells. By inhibiting LDH, MP-5342 can modulate T cell and B cell function, offering a novel therapeutic strategy for inflammatory diseases. This mechanism may restore immune balance and normalize dysfunctional immune cells, providing durable relief for patients with limited treatment options.

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As the world’s first highly selective oral LDH small-molecule inhibitor with favorable in vivo drug-like properties, MP-5342 has demonstrated broad potential in autoimmune diseases, including IBD, multiple sclerosis (MS), and primary biliary cholangitis (PBC). LDH plays a key role in immune cell energy metabolism during autoimmune inflammation, making its selective inhibition an innovative approach to disease intervention.

Dr. Ke Xu, CEO of META Pharmaceuticals, commented: “Nominating MP-5342 as our first clinical candidate for IBD represents an extremely exciting milestone for META Pharmaceuticals and an important step in our transformation into a clinical-stage company. Our scientific team has built a robust preclinical data package based on a deep understanding of LDH’s role in IBD pathogenesis. These data give us strong confidence to advance this program into the clinic, and we look forward to its future progress.”

Dr. Anjin Xianyu, CTO of META Pharmaceuticals, added: “IBD is a chronic and debilitating disease with a high unmet need for therapies that can modify disease progression. Current treatments remain limited in efficacy and safety. We have made significant progress with our lead candidate, MP-5342, an oral targeted therapy that has the potential to deliver meaningful benefits to patients.”

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Preparations for the IND application are underway, and clinical trials are expected to commence in the second half of 2026.

As the first project in META Pharmaceuticals’ pipeline to advance into clinical development, MP-5342 not only underscores the company’s R&D strength in immunometabolism innovation, but also marks a key step in translating metabolic modulation therapies into clinical application.

References

[1].Peng M, Yin N, Chhangawala S, et al. Aerobic glycolysis promotes T helper 1 cell differentiation through an epigenetic mechanism. Science. 2016;354(6311):481–484. DOI: 10.1126/science.aaf6284.

[2].Xu K, Yin N, Peng M, et al. Glycolysis fuels phosphoinositide 3-kinase signaling to bolster T cell immunity. Science. 2021;371(6527):405–410. DOI: 10.1126/science.abb2683.

[3].Xu K, Yin N, Peng M, et al. Glycolytic ATP fuels phosphoinositide 3-kinase signaling to support effector T helper 17 cell responses. Immunity. 2021;54(5):976–987. DOI: 10.1016/j.immuni.2021.04.008.