Tevard Biosciences has presented new preclinical data demonstrating the potential of its suppressor tRNA (suptRNA) platform to restore full-length functional proteins in models of Duchenne muscular dystrophy (DMD) and dilated cardiomyopathy caused by titin truncations (DCM-TTNtv). The findings were showcased during an invited oral presentation and poster session at the 2025 Federation of European Biochemical Societies (FEBS) Special Meeting “Expanding Frontiers in Aminoacyl-tRNA Synthetase Research” in Dubrovnik, Croatia.

The data show that AAV-delivered suptRNAs targeting nonsense mutations can restore, on average, 70% of wild-type dystrophin protein in DMD models, correlating with improvements in motor function and proteomic biomarkers. In the DCM-TTNtv program, suptRNA treatment produced full-length titin protein in iPSC-derived human cardiomyocytes within four days and restored cardiac proteomic homeostasis in mouse models within six weeks. Both programs reported dose-dependent effects and durable protein rescue, sustained up to 12 weeks after a single intravenous dose, with no observed toxicity or off-target effects.

“These results show that our engineered suppressor tRNAs are capable of restoring full-length, native protein expression at levels that are not only biologically meaningful but clinically promising,” said Elisabeth Gardiner, chief scientific officer of Tevard Biosciences. “When dealing with structural proteins like dystrophin and titin, where proper folding, localization, and protein-protein interactions are essential, restoring a full-length protein makes all the difference. Our platform uses native cellular machinery to produce natural proteins that function the way the body expects.”

Daniel Fischer, co-founder, president and CEO of Tevard Biosciences, added: “Being selected for a featured oral presentation and poster session at this world-class conference highlights the impact of our suppressor tRNA platform. Recent breakthroughs in suppressor tRNA and vector design have achieved the levels of protein rescue needed to confidently advance our DMD and DCM-TTNtv programs into the clinic at safe, efficacious doses.”

Tevard’s platform has evolved from first-generation molecules with a single anticodon edit to third-generation candidates optimized through high-throughput screening of over 80,000 variants. The engineered suptRNAs enable codon-specific readthrough of premature stop codons, which are responsible for 10–40% of all genetic diseases, positioning the company’s lead candidates to restore up to 70% of wild-type protein levels in preclinical models. Both the DMD and DCM programs are advancing toward development candidate nomination in Q1 2026.