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Positive results from a follow-up preclinical study of Thykamine show dose-dependent effects on key pathological hallmarks of MASH.
Devonian Health Group has announced positive results from a follow-up preclinical study evaluating Thykamine™ in a human metabolic-associated steatohepatitis (MASH) model using PhysioMimix® Liver-on-a-Chip platform. The study was conducted by CN Bio Innovations, Cambridge, UK.
As described in a February 19, 2026, release from the Company, the study demonstrates that Thykamine™ exerts dose-dependent effects on key pathological hallmarks of MASH, including fibrosis and inflammation, in a physiologically relevant human liver system, representing a notable translational bridge between Devonian’s previously disclosed efficacy in the mouse STAM® MASH model and a predictive human microphysiological model.
“These findings show that Thykamine™ does more than modulate individual biomarkers—it impacts the core biological processes that define MASH, including fibrosis and inflammation,” André Boulet, PhD, Chief Executive Officer of Devonian, said in a statement. “Together with our previously reported mouse STAM® data, this study strengthens the translational rationale for Thykamine™ as a potential disease-modifying therapeutic candidate.”
Currently, the MASH treatment landscape comprises 2 US Food and Drug Administration approved therapies, resmetirom (Rezdiffra) and semaglutide (Wegovy), with several other agents currently in the pipeline.2,3
Thykamine™, the first pharmaceutical product issued from Devonian’s SUPREX™ platform, aims to prevent and treat health conditions related to inflammation and oxidative stress, including ulcerative colitis, atopic dermatitis, psoriasis, rheumatoid arthritis, and other autoimmune disorders. The anti-inflammatory, anti-oxidative and immunomodulatory properties of Thykamine™ have been demonstrated by multiple in vitro and in vivo studies as well as in a phase 2a clinical study in patients with mild-to-moderate distal ulcerative colitis and in a large phase 2 study in adult patients with mild-to-moderate atopic dermatitis.
Thykamine™ was evaluated at 4 low concentrations of 0.025, 0.05, 0.1, and 0.2 mg/mL over a 14-day treatment period in a dynamic, triple-cell liver model incorporating primary human hepatocytes, Kupffer cells, and hepatic stellate cells under continuous microfluidic flow to induce a MASH phenotype. Elafibranor, a clinically advanced compound previously evaluated in MASH clinical trials, was included as a reference positive control (20 uM), alongside a vehicle control.
Results showed Thykamine™ produced a clear, dose-dependent reduction in fibrosis-associated biomarkers, including pro-collagen and TIMP-1, with the strongest effects observed at 0.1 and 0.2 mg/mL. Confocal imaging additionally confirmed a significant decrease in Type I collagen deposition, indicating attenuation of one of the core structural features of fibrotic MASH. At higher doses, the magnitude of collagen reduction was greater than that observed with elafibranor under identical experimental conditions.
Thykamine™ also induced a dose-dependent reduction in pro-inflammatory cytokines IL-6 and IL-8 at later time points, reflecting an effect on inflammatory pathways known to contribute to hepatocellular injury and disease progression in MASH. Of note, LDH levels remained low throughout the study, with no evidence of drug-induced liver injury. Observed changes in albumin production were not associated with cytotoxicity and will be further investigated.
In the release, Devonian described plans to advance additional preclinical studies to further characterize Thykamine™’s disease-modifying potential and support continued development in MASH and other fibrotic diseases.