---
title: "ERG344 ACOD1 inhibition reduces colitis and tumor growth via a shared myeloid mechanism"
id: "biorxiv-19-small-molecule-acod1-inhibition-attenuates-colitis-and-tumor-growth-through-a"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-19-small-molecule-acod1-inhibition-attenuates-colitis-and-tumor-growth-through-a"
content_type: "clinical_feed_article"
specialty: "Gastroenterology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1?rss=1"
published_at: "2026-10-22T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ERG344 ACOD1 inhibition reduces colitis and tumor growth via a shared myeloid mechanism
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-19-small-molecule-acod1-inhibition-attenuates-colitis-and-tumor-growth-through-a
- **Specialty:** [Gastroenterology](https://medichelpline.com/clinical-feed/gastroenterology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1?rss=1)
- **Published At:** 2026-10-22T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study reports a small-molecule ACOD1 inhibitor, **ERG344**, that suppressed synthesis of the immunometabolite **itaconate** in endotoxemic mice and in inflamed colonic mucosa. - Investigators observed that, unlike germline Acod1 deletion, pharmacologic inhibition with ERG344 attenuated acute DSS colitis in an ACOD1-dependent manner. - ERG344 treatment associated with diminished early influx of immature monocytes and with accumulation of more mature neutrophils in inflamed tissue; those shifts paralleled reduced pathology. - In multiple syngeneic tumor models, ERG344 prolonged survival and increased tumor-infiltrating lymphocytes plus antigen-presenting dendritic cells, according to the authors. - Across murine and human colitis single-cell RNA-seq datasets and a ten-model syngeneic tumor atlas, **ACOD1** expression marked interferon-stimulated immature monocytes and maturing neutrophils. - The study team found that ACOD1 tracked with SOD2 and CD274 expression independently of canonical interferon and NF-κB signaling axes. - Authors propose a common myeloid recruitment and maturation mechanism linking colitis and tumor responses to ACOD1 inhibition; pharmacologic blockade diverged from genetic deletion in phenotype. - The preprint notes inventor and company conflicts of interest and has not been peer reviewed; the source did not report detailed dosing parameters or full methodological specifics in the abstract.
## Clinical Analysis & Structured Key Points
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Papathanassiu, Weixing Li, Konstantin Gilbo, Ian L Pegg doi: https://doi.org/10.64898/2026.10.17.759827 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Adonia E. Papathanassiu 1 Ergon Pharmaceuticals LLC; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Adonia%2BE.%2BPapathanassiu%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Papathanassiu%20AE&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAdonia%2BE.%2BPapathanassiu%2B) * [ORCID record for Adonia E. Papathanassiu](http://orcid.org/0000-0001-6055-4871 "Open in new tab") * For correspondence: adoniap@ergonpharma.com Weixing Li 1 Ergon Pharmaceuticals LLC; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Weixing%2BLi%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Li%20W&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AWeixing%2BLi%2B) Konstantin Gilbo 2 Vitreous State Laboratory at The Catholic University of America * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Konstantin%2BGilbo%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Gilbo%20K&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AKonstantin%2BGilbo%2B) Ian L Pegg 2 Vitreous State Laboratory at The Catholic University of America * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ian%2BL%2BPegg%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Pegg%20IL&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AIan%2BL%2BPegg%2B) * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5894253/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5894253/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5894253/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5894253/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.17.759827v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5894253/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Aconitate decarboxylase 1 (ACOD1), the enzyme responsible for synthesis of the immunometabolite itaconate, is widely regarded as an anti-inflammatory brake on tissue damage based on Acod1-deficient mice and itaconate supplementation expermiments. ERG344, a small-molecule ACOD1 inhibitor, suppressed itaconate synthesis in endotoxemic mice and in inflamed colonic mucosa and, contrary to genetic-deletion studies, attenuated acute DSS colitis in an ACOD1-dependent manner. ERG344 treatment was associated with reduced influx of immature monocytes early on and accumulation of mature neutrophils. In syngeneic tumor models, ERG344 prolonged survival and increased tumor-infiltrating lymphocytes and antigen-presenting dendritic cells. Across murine and human colitis scRNA-seq datasets and a ten-model syngeneic tumor atlas, ACOD1 marked interferon-stimulated immature monocytes and maturing neutrophils, and tracked with SOD2 and CD274 independently of interferon and NF-κB signaling. ACOD1 appears to act through a common myeloid recruitment and maturation mechanism, making pharmacological ACOD1 inhibition a viable therapeutic strategy in colitis and cancer. ### Competing Interest Statement Adonia E. Papathanassiu is an inventor of patents covering the ACOD1 inhibitor investigated in this study, including its acidic and pharmaceutically acceptable salts. Adonia E. Papathanassiu and Ergon Pharmaceuticals LLC hold a financial interest in the development and commercialization of this inhibitor. All other authors declare no conflict of interest. Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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