Tevard

Tevard Biosciences, Inc., a biotechnology company pioneering tRNA-based therapies to cure a broad range of genetic diseases, will share new preclinical data at the 2026 American Society of Gene & Cell Therapy (ASGCT) Annual Meeting, held from May 11-15 in Boston. Tevard will present data demonstrating that its next-generation suppressor tRNAs (sup-tRNAs) restore full‑length dystrophin protein and achieve wild-type levels of functional rescue in multiple mouse models of nonsense mutation-mediated Duchenne muscular dystrophy (DMD). The company will also present data showing that its novel sup-tRNAs provide durable rescue of full-length titin protein in a mouse model as well as functional rescue in human cardiomyocyte models of dilated cardiomyopathy caused by TTN truncations (DCM‑TTNtv).

“We have made significant progress in the last year optimizing our latest generation of suppressor tRNAs and enhancing manufacturability across our tRNA platform,” said Daniel Fischer, Co-Founder, President and CEO of Tevard Biosciences. “Achieving restoration of full-length protein in DCM-TTNtv models and demonstrating wild-type levels of motor-function rescue in DMD at clinically relevant doses represent a major milestone for the field. We are now preparing to advance to the clinic with transformative and safe tRNA therapies for patients.”

Oral Presentations:

Title: Engineered Suppressor tRNAs Restore Full-Length Dystrophin and Motor Function at Clinically Relevant Doses in a Severe Model of Duchenne Muscular Dystrophy
Presentation ID: 284 Presenter: Julien Oury, PhD, Associate Director Session Date and Time: Thursday, May 14, 2026, 8:00 a.m. – 8:15 a.m. ET Location: MCEC Room 052AB (Exhibit Level) Key Findings: In the DMD program, Tevard’s advanced screening platform revealed potent sup-tRNAs capable of achieving complete (~100%) restoration of full‑length dystrophin in targeted muscles following intramuscular delivery in a TAA PTC D2.mdx model. With systemic delivery, motor function was restored to wild type levels. Full length dystrophin rescue was successfully demonstrated using sup-tRNAs specifically focused on TAA, TGA and TAG premature stop codons. These results support the potential of sup-tRNAs to restore native, full‑length dystrophin in patients across all nonsense mutations (~15% of DMD cases).

Title: Engineered Suppressor tRNAs Restore Full-Length Dystrophin and Motor Function at Clinically Relevant Doses in a Severe Model of Duchenne Muscular Dystrophy

Presentation ID: 284

Presenter: Julien Oury, PhD, Associate Director

Session Date and Time: Thursday, May 14, 2026, 8:00 a.m. – 8:15 a.m. ET

Location: MCEC Room 052AB (Exhibit Level)

Key Findings:

In the DMD program, Tevard’s advanced screening platform revealed potent sup-tRNAs capable of achieving complete (~100%) restoration of full‑length dystrophin in targeted muscles following intramuscular delivery in a TAA PTC D2.mdx model. With systemic delivery, motor function was restored to wild type levels.
Full length dystrophin rescue was successfully demonstrated using sup-tRNAs specifically focused on TAA, TGA and TAG premature stop codons.
These results support the potential of sup-tRNAs to restore native, full‑length dystrophin in patients across all nonsense mutations (~15% of DMD cases).

Title: Suppressor tRNA Gene Therapy Restores Full-length Titin in models of ArgTGA TTN-Truncation Dilated Cardiomyopathy
Presentation ID: 384 Presenter: Alexander Auld, PhD, Principal Research Scientist Session Date and Time: Thursday, May 14, 2026, 4:30 p.m. – 4:45 p.m. ET Location: MCEC Room 206AB (Level 2) Key Findings: In human iPSC‑derived cardiomyocytes engineered with disease‑relevant TTN truncating variants, TAA and TGA‑targeting sup-tRNAs restored full‑length titin and reestablished sarcomere structure. In a complementary Arg‑TGA mouse model, systemic AAV delivery of sup-tRNA produced durable titin rescue and in proteomic indicators of cardiac health. Together, these data support a mutation‑class–targeted therapeutic strategy capable of addressing diverse TTN nonsense variants.

Title: Suppressor tRNA Gene Therapy Restores Full-length Titin in models of ArgTGA TTN-Truncation Dilated Cardiomyopathy

Presentation ID: 384

Presenter: Alexander Auld, PhD, Principal Research Scientist

Session Date and Time: Thursday, May 14, 2026, 4:30 p.m. – 4:45 p.m. ET

Location: MCEC Room 206AB (Level 2)

Key Findings:

In human iPSC‑derived cardiomyocytes engineered with disease‑relevant TTN truncating variants, TAA and TGA‑targeting sup-tRNAs restored full‑length titin and reestablished sarcomere structure.
In a complementary Arg‑TGA mouse model, systemic AAV delivery of sup-tRNA produced durable titin rescue and in proteomic indicators of cardiac health.
Together, these data support a mutation‑class–targeted therapeutic strategy capable of addressing diverse TTN nonsense variants.

“Our compact tRNA architecture enables flexible AAV packaging, precise dose control, and broad applicability for pathogenic nonsense mutations across diverse unmet medical needs,” said Elisabeth Gardiner, PhD, CSO of Tevard Biosciences. “These two programs highlight the versatility of the suppressor tRNA platform and its ability to restore native protein expression in a cell-specific, durable manner.”

About Tevard Biosciences

Tevard Biosciences is pioneering tRNA‑based and other mRNA‑modulating therapies to cure a broad range of genetic diseases. The company’s suppressor tRNA platform is designed to restore endogenous, full‑length protein expression for diseases caused by premature termination codons. Tevard is advancing programs in muscular dystrophies, heart disease, and neurological disorders. For more information, visit www.tevard.com.

SOURCE: Tevard Biosciences

Tevard Biosciences Presents Preclinical Data Showing Complete Dystrophin Restoration and Robust Titin Rescue with Suppressor tRNA Therapy at ASGCT 2026