Gosselies, Belgium – May 18th, 2026
EPICS Therapeutics announces the publication of a peer-reviewed article in the journal Diabetes describing how EP282 (referred to in the publication as Compound 1, or Cpd1), its first-in-class FFAR2 agonist, improved disease outcomes in preclinical models of type 1 diabetes.
The study, titled “Activation of Intestinal Type 3 Innate Lymphoid Cells and Regulatory T Cells Through Free Fatty Acid Receptor 2 Ameliorates Type 1 Diabetes in Mice,” was conducted by EPICS’ academic partners at the University of Belgrade.
The research demonstrated that EP282, EPICS’ first-in-class FFAR2 agonist, alters the course of autoimmune disease, providing therapeutic benefit in preclinical models of Type 1 diabetes.
These findings provide insight on the role of FFAR2, a receptor that links microbial signals to immune regulation, in modulating autoimmune disease in organs distal to the intestinal microbiome, such as in the pancreas. They also provide new evidence supporting the therapeutic rationale for EP282 in the treatment of autoimmune disease.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks insulin-producing β-cells in the pancreas. While current treatments replace the insulin that is lost, they do not address the underlying immune dysfunction driving disease progression.
The newly published research explores a different approach. Rather than broadly suppressing immunity, EP282 activates FFAR2 (Free Fatty Acid Receptor 2), a receptor that normally senses short-chain fatty acids produced by beneficial gut microbes. Through this pathway, EP282 amplifies natural immune signals that help maintain intestinal and immune homeostasis -the balanced state that allows the immune system to protect the body without causing excessive inflammation.
Treatment with EP282 increased the activity of type 3 innate lymphoid cells (ILC3) and regulatory T cells (Treg), two immune cell populations that play a critical role in controlling inflammation and maintaining immune tolerance. These effects are associated with reduced pancreatic inflammation, preservation of insulin-producing cells, and improved blood glucose control in diabetic mice.
Highlights from the publication
- Reduced immune-cell infiltration of pancreatic islets (clusters of insulin-producing cells) and preserved insulin-producing β-cells
- Improved blood glucose control and circulating insulin levels in preclinical models of type 1 diabetes
- Increased protective type 3 innate lymphoid cells (ILC3) and regulatory T cells (Treg), key mediators of immune tolerance
- Strengthened intestinal barrier integrity and immune homeostasis
- Identified IL-22, a signaling molecule involved in maintaining intestinal barrier integrity and immune regulation, as an important mediator of the therapeutic response
- Demonstrated that activation of FFAR2 can modulate immune pathways linking the gut and pancreas
- Provides new preclinical evidence supporting FFAR2 activation and the therapeutic rationale underlying EPICS’ EP282
Commenting on the findings, Graeme Fraser, PhD, Chief Executive Officer and Chief Scientific Officer, said:
“Our original thinking on FFAR2 was really focused on intestinal autoimmune disorders, such as ulcerative colitis, as we learned about the link to the intestinal microbiome and the activation of gut-origin ILC3s. This publication expands our knowledge to include autoimmune disease in organs beyond the intestines. Type 1 diabetes is a validated, pharmaceutical market following the unprecedented approval of teplizumab. EP102 has completed a Ph1 trial and is on-track for clinical entry into Ph2 trials in autoimmune disease.”
The study builds upon previous work demonstrating that FFAR2 plays a central role in maintaining intestinal immune balance. By activating this pathway with a potent and selective small molecule, EP282 offers a scalable and controllable alternative to microbiome-based interventions such as fecal microbiota transplantation or live bacterial therapies.
About EP282
EP282 is a first-in-class, orally available FFAR2 agonist designed to restore immune homeostasis by activating a natural signaling pathway that links the gut microbiome to the immune system.
Unlike microbiome-based therapies that seek to alter microbial composition directly, EP282 provides a precise and highly selective stimulus to FFAR2, reproducing beneficial microbial signals through a small-molecule approach.
A completed Phase I clinical study demonstrated that EP282 is safe and well tolerated and identified biomarkers consistent with clinically active target engagement. EP282 is currently being advanced toward Phase II clinical development for diseases characterized by disrupted microbiome-immune signaling.
About EPICS Therapeutics
Epics Therapeutics is a clinical-stage Belgian, private, drug discovery and development company that invents and develops small molecule drugs targeting RNA epigenetics¹ and G-Protein Coupled Receptor² mechanisms involved in cancer development. By targeting these mechanisms, Epics Therapeutics aims to translate science into life-changing therapies for patients.
¹RNA epigenetics refers to the post-genomic changes in protein synthesis directed by chemical marks added to RNA molecules, such as N6-methyladenosine (m6A). These marks do not change the genetic code itself, but they influence how the instructions in RNA are read and used to make proteins. In healthy cells, this helps regulate growth and differentiation. In cancer, these marks are applied in an aberrant manner, tipping the balance toward uncontrolled cell proliferation.
²G-protein coupled receptors are a large family of receptors expressed on the cell surface that respond to signals like hormones, neurotransmitters, or metabolites. When activated, they trigger G-proteins in the cell membrane to transduce signals inside the cell that affect how the cell behaves with application to a broad range of physiological outputs, including in the field of cancer.
For more information, visit www.epicstherapeutics.com
Contact: EPICS Therapeutics Media Relations Desk at media_relations@epicstx.com