Publications, Posters and Presentations

Below is a list of relevant publications, posters and presentations related to our programs. Articles with starred (*) titles are available free of charge through the third party link. Within each section, articles are listed most recent first.

Efzofitimod (ATYR1923)

Therapeutic Doses of Efzofitimod Demonstrate Efficacy in Pulmonary Sarcoidosis

Efzofitimod is an Immunomodulator of Myeloid Cell Function and Novel Therapeutic Candidate for Interstitial Lung Diseases

Efzofitimod Promotes Macrophages with Anti-inflammatory Profile via Neuropilin-2 Receptor

Efzofitimod, a First-in-Class NRP2-Targeting Immunomodulator, Ameliorates Rheumatoid Arthritis and Associated Lung Fibrosis in Preclinical Models

Exposure-Response Analyses of Efzofitimod in Patients With Pulmonary Sarcoidosis

Therapeutic Doses of Efzofitimod Significantly Improve Multiple Pulmonary Sarcoidosis Efficacy Measures

Efzofitimod: A Novel Therapeutic Candidate for SSc-ILD

EFZO-FIT™: A Phase 3 Study of Efzofitimod, a Novel Immunomodulator for the Treatment of Pulmonary Sarcoidosis

Exposure-Efficacy Analysis Supports Proof of Concept for Efzofitimod in Pulmonary Sarcoidosis

Efzofitimod, a Novel Immunomodulator for Pulmonary Sarcoidosis, Modulates Patient Inflammatory Responses Through Myeloid Cells

Efzofitimod: A Novel Anti-Inflammatory Agent for Sarcoidosis

Efzofitimod for the Treatment of Pulmonary Sarcoidosis

A Novel Neuropilin-2 (NRP2) Antibody for Immunohistochemical Staining of Patient Tissue Samples

Efzofitimod (ATYR1923) Treatment Reduces Pro-inflammatory Serum Biomarkers in Pulmonary Sarcoidosis Patients

Safety and Efficacy of Efzofitimod (ATYR1923), a Novel Immunomodulator for Pulmonary Sarcoidosis: Results of a Phase 1b/2a Randomized Placebo-Controlled Trial

Immunomodulatory Protein ATYR1923 Disrupts an In-Vitro Model of Sarcoid Granuloma Formation

Treatment with ATYR1923 Reduces Biomarkers in COVID-19 Pneumonia

Neuropilin-2, the Specific Binding Partner to ATYR1923, Is Expressed in Sarcoid Granulomas and Key Immune Cells

ATYR1923 Specifically Binds to Neuropilin-2, a Novel Therapeutic Target for the Treatment of Immune-Mediated Diseases

ATYR1923 Modulates the Inflammatory Response in Experimental Models of Interstitial Lung Disease

ATYR1923 Reduces Neutrophil Infiltration in an Acute Lipopolysaccharide (LPS) Lung Injury Model

ATYR1923 Ameliorates Dermal and Pulmonary Fibrosis in a Murine Model of Sclerodermatous Chronic Graft vs. Host Disease

Preclinical Characterization of ATYR1923 (iMod.Fc), an Immune-Modulatory Therapeutic With Potentially Broad Application in Interstitial Lung Diseases

Identification of a T Cell Immunomodulatory Domain in Histidyl-tRNA Synthetase

Resokine Modulates Immune Cell Infiltration Into the Lung and Provides Therapeutic Activity in a Bleomycin-induced Lung Fibrosis Model

The Resokine Pathway is Implicated in the Pathology of Interstitial Lung Disease

ATYR2810 and other NRP2 Antibodies

Demonstration of an Isoform-Specific Anti-inflammatory Role for Neuropilin-2 Through a Novel Interaction with the Chemokine Ligand 21

Inhibition of VEGF Binding to Neuropilin-2 Enhances Chemosensitivity and Inhibits Metastasis in Triple-Negative Breast Cancer

Therapeutic Blocking of VEGF Binding to Neuropilin-2 Diminishes PD-L1 Expression to Activate Antitumor Immunity in Prostate Cancer

Resistance to Cancer Therapy via Upregulation of the NRP2/VEGF-C Axis Can Be Neutralized By ATYR2810

ATYR2810, a Fully Humanized Monoclonal Antibody Targeting the VEGF-NRP2 Pathway Sensitizes Highly Aggressive and Chemoresistant TNBC Subtypes to Chemotherapy

ATYR2810 an Anti-NRP2 Monoclonal Antibody Targets Tumor Associated Macrophages

Engineering an Anti-Neuropilin-2 (NRP2) Antibody that Selectively Blocks NRP2 Interactions with Semaphorin and Plexin

ATYR2810, a Neuropilin-2 antibody, selectively blocks the NRP2/VEGFR signaling axis and sensitizes aggressive cancers to chemotherapy

The Neuropilin-2 Targeting Antibody ATYR2810 Inhibits Non-Small Cell Lung Cancer Tumor Growth in Monotherapy and Combination Therapy

A Domain-Specific Antibody to NRP2 Down-Regulated Epithelial-Mesenchymal Transition Genes and Enhanced Efficacy of Standard-of-Care Therapeutics for Aggressive Breast Cancer

Neuropilin-2 is Expressed on Immune Cells Present in the Tumor Microenvironment, and May Contribute to the Suppression of Immune Regulation Leading to Progression and Metastasis of Cancer

Domain-Specific Antibodies to Neuropilin 2 Implicate VEGF-C and not Semaphorin 3F in Breast Cancer Stem Cell Function

The N-terminal domain of HARS is a novel NRP2 ligand and can regulate NRP2-dependent macrophage function

TRNA Synthetase Pipeline

Alanyl-tRNA synthetase fragment binds to FGFR4 and induces morphological changes and downstream signaling in liver cells with functional similarities to FGF2

Identification of Key Fibrotic Extracellular Targets for Alanyl- and Aspartyl-tRNA Synthetases

Identification of Latent Transforming Growth Factor Beta Binding Protein 1 (LTBP1) as a Binding Partner of Aspartyl-tRNA Synthetase

Identification of Key Extracellular Binding Proteins Implicate Role in Inflammation and Fibrosis for Alanyl- and Aspartyl-tRNA Synthetases

A Mass Spectrometry Proteomics-Based Approach to Identify Target Receptors for Novel Extracellular tRNA Synthetase Fragments

Foundational Science

Circulating His-tRNA Synthetase is Reduced in Patients Harboring the Usher Syndrome Type 3B-Linked Mutation Y454S

Serum-circulating His-tRNA synthetase inhibits organ-targeted immune responses

Human tRNA synthetase catalytic nulls with diverse functions.

Essential nontranslational functions of tRNA synthetases.

New functions of aminoacyl-tRNA synthetases beyond translation.

Two distinct cytokines released from a human aminoacyl-tRNA synthetase.

Associated Research

Isolation of monoclonal antibodies from anti-synthetase syndrome patients and affinity maturation by recombination of independent somatic variants

Bi-allelic Mutations in the Phe-tRNA Synthetase Associated with Multi-system Pulmonary Disease Supports Non-Translation Function.

CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase.

Secreted histidyl-tRNA synthetase splice variants elaborate major epitopes for autoantibodies in inflammatory myositis.

Internally deleted human tRNA synthetase suggests evolutionary pressure for repurposing.

Functional expansion of human tRNA synthetases achieved by structural inventions.*

Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase.*