Positive Preclinical Data for IPF Drug

Thykamine demonstrated anti-fibrotic effects in the lungs during a bleomycin pulmonary fibrosis mouse model in vivo study.

RT’s Three Key Takeaways:

1. Demonstrated Antifibrotic Efficacy: Thykamine showed statistically significant reductions in lung fibrosis, inflammation, and collagen-related gene expression in a bleomycin-induced pulmonary fibrosis mouse model.
2. Dose-Responsive, Low-Dose Activity: At doses as low as 0.5 mg/kg, Thykamine improved lung pathology and molecular markers, outperforming pirfenidone in key physiological endpoints within the study.
3. Expanded Therapeutic Potential: These findings position Thykamine as a promising disease-modifying candidate for pulmonary fibrosis and other fibro-inflammatory conditions, addressing a major unmet medical need.

Devonian Health Group Inc revealed a potential expanded therapeutic application for Thykamine, with compelling preclinical data results demonstrating proof of concept efficacy in a well-established animal model of pulmonary fibrosis.

The study investigated the effects of Thykamine in bleomycin-induced pulmonary fibrosis (IPF) mouse model, a widely used preclinical tool for studying idiopathic pulmonary fibrosis (IPF) pathophysiology and testing antifibrotic therapies. Pulmonary fibrosis was induced in mice using intranasal bleomycin, a gold-standard and clinically relevant model that closely mirrors key pathological features of human idiopathic pulmonary fibrosis.

Thykamine was administered orally at doses of 0.05, 0.1, 0.25, 0.5, and 1 mg/kg, and benchmarked against pirfenidone dosed at 220 mg/kg. Over a 21-day period, animals were monitored for body weight and survival, followed by comprehensive lung assessment. Fibrotic burden was evaluated through lung weight, collagen content, fibrosis-related gene expression, and histopathological scoring.     

In this bleomycin-induced pulmonary fibrosis model, Thykamine demonstrated statistically significant antifibrotic activity, while pirfenidone did not reach statistical significance in physiological endpoints. Treatment with Thykamine at 0.5 mg/kg significantly reduced lung wet weight and lung tissue index compared with the bleomycin/vehicle group.

Bleomycin exposure led to marked increases in fibrosis (Ashcroft score) and inflammation compared with sham controls. Thykamine treatment significantly reversed these pathological changes, reducing both fibrosis and inflammation scores and indicating meaningful improvement in lung morphology.

Consistent with its effects on lung pathology, Thykamine at 0.5 mg/kg produced a statistically significant down-regulation of key fibrosis- and inflammation-associated genes, including Fn1 (fibronectin), Col1a1, Col3a1, Col6a1, and Col6a3 (collagen isoforms involved in extracellular matrix deposition), Birc5, and the chemokines Ccl2 and Cxcl2 (inflammatory cell recruitment). In parallel, Thykamine significantly increased Mmp9, a matrix metalloproteinase associated with extracellular matrix turnover, while reducing Mmp13, a collagenase often linked to progressive tissue injury and inflammation. Together, this gene expression profile is consistent with controlled matrix remodeling and attenuation of fibrotic progression. 

This well-validated model delivers a strong, dose-responsive demonstration of antifibrotic efficacy across multiple translational endpoints, clearly positioning Thykamine as a differentiated, next-generation therapeutic candidate in pulmonary fibrosis. The Company plans to present data in an upcoming scientific publication.

“These results represent a major inflection point for Thykamine,” said Dr. Andre P. Boulet, PhD, Chief Executive Officer. “The pulmonary fibrosis data not only confirm and extend the antifibrotic effects we previously observed in mouse MASH model, but also significantly broaden Thykamine’s mechanism of action. By combining potent anti-inflammatory and anti-fibrotic activity at low doses, Thykamine demonstrates clear potential to address the underlying biology of fibro-inflammatory diseases and to serve as a scalable, multi-indication platform with disease-modifying potential.”

References from Devonian Health Group Inc