SAN DIEGO, Calif. — aTyr Pharma, Inc. (Nasdaq: ATYR) (“aTyr” or the “Company”), a clinical stage biotechnology company engaged in the discovery and development of first-in-class medicines from its proprietary tRNA synthetase platform, today announced a publication demonstrating the anti-fibrotic effects of ATYR0101 in the Journal of Biological Chemistry. The publication, entitled, “Natural Asp-tRNA Synthetase Fragment Targets Myofibroblasts to Abrogate Tissue Fibrosis,” is available on the journal’s website and at: https://www.jbc.org/article/S0021-9258(26)02458-0/fulltext.
ATYR0101 is a fusion protein derived from a proprietary extracellular domain of aspartyl-tRNA synthetase (DARS) that binds to latent transforming growth factor beta binding protein 1 (LTBP-1) to induce myofibroblast apoptosis.
“Fibrosis remains a major global health challenge across multiple organ and tissue systems with limited therapies that only slow disease progression,” said Leslie A. Nangle, Ph.D., Vice President, Research at aTyr Pharma. “This publication highlights the novel mechanism by which ATYR0101 disrupts fibrosis through a unique molecular program that facilitates a transition towards a restorative phenotype thus fundamentally altering the underlying fibrotic cellular landscape. These findings suggest that ATYR0101 does not merely stop disease progression but may also facilitate a reversal of fibrotic pathology, providing a differentiated approach to current anti-fibrotic therapies in conditions such as idiopathic pulmonary fibrosis, where more effective treatment options are greatly needed.”
The publication describes the mechanism by which ATYR0101 selectively triggers apoptosis in myofibroblasts by targeting LTBP-1 on the extracellular matrix, with ATY0101 induced myofibroblast apoptosis shown to be dependent on active transforming growth factor beta (TGF-β), a central player in the pathogenesis of fibrotic diseases. Furthermore, the pharmacologic activity of ATYR0101 was demonstrated in an in vivo bleomycin lung model of fibrosis, where ATYR0101 showed a significant reduction in both collagen content and Ashcroft score leading to a marked decline in pulmonary fibrosis compared to the use of nintedanib, a known anti-fibrotic, as a control.
About ATYR0101
ATYR0101 is a fusion protein derived from a proprietary extracellular domain of aspartyl-tRNA synthetase (DARS) that binds to latent transforming growth factor beta binding protein 1 (LTBP-1) to induce myofibroblast apoptosis. ATYR0101 interacts with LTBP-1 through a unique way that presents a differentiated approach to targeting fibrosis. ATYR0101 has demonstrated anti-fibrotic effects in models of lung and kidney fibrosis suggesting it may have broad therapeutic potential in multiple fibrotic diseases. ATYR0101 is currently undergoing IND-enabling studies.
About aTyr
aTyr is a clinical stage biotechnology company leveraging evolutionary intelligence to translate tRNA synthetase biology into new therapies for fibrosis and inflammation. tRNA synthetases are ancient, essential proteins that have evolved novel domains that regulate diverse pathways extracellularly in humans. aTyr’s discovery platform is focused on unlocking hidden therapeutic intervention points by uncovering signaling pathways driven by its proprietary library of domains derived from all 20 tRNA synthetases. aTyr’s lead therapeutic candidate is efzofitimod, a novel biologic immunomodulator in clinical development for the treatment of interstitial lung disease, a group of immune-mediated disorders that can cause inflammation and progressive fibrosis, or scarring, of the lungs. For more information, please visit www.atyrpharma.com.
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