$14.28 +0.26 (+1.85%) As of 04:00 PM Eastern
We are a clinical-stage biopharmaceutical company focused on developing novel disease-modifying therapies for immunology and inflammatory diseases, with an initial focus on chronic fibrotic indications with high unmet medical need. Our product candidates are designed to target established pathways and utilize validated modalities with the aim of increasing efficacy while avoiding systemic toxicities in order to overcome the limitations of prior therapeutic approaches. Our initial focus for the treatment of fibrosis is through inhibition of one of the key signaling pathways involved in fibrosis, the transforming growth factor ß, or TGFß, pathway. Our mission is to develop disease-modifying therapeutics that aim to resolve fibrosis and restore organ function to enable patients with these disorders to live fuller and healthier lives. We are advancing a pipeline of novel product candidates for chronic fibrotic disorders with well-validated targets, significant unmet medical needs and large commercial potential. Our pipeline includes: • Ontunisertib (AGMB-129): Our lead product candidate, ontunisertib, is a selective and potent oral, gastrointestinal-restricted small molecule inhibitor of ALK5, or TGFßR1, in development for the treatment of Fibrostenosing Crohn’s Disease, or FSCD. FSCD is a severe complication of Crohn’s Disease, or CD, that is associated with significant morbidity. There are approximately 1.4 million patients under treatment for CD in the seven major markets of the United States, France, Germany, Italy, Spain, the United Kingdom and Japan, and approximately 620,000, or 46%, of these patients have FSCD. The emergence of burdensome symptomatic strictures is considered to be an inevitable consequence of long-term inflammation for the large proportion of patients with CD who progress to FSCD and eventually require surgery. There are no approved pharmacologic therapies for FSCD. We believe ontunisertib has the potential to change the paradigm for treating FSCD patients and provide the first pharmacologic treatment for strictures. Ontunisertib is designed to act locally in the gastrointestinal tract, enabling high exposure in the target tissue. Then, following absorption, ontunisertib is rapidly inactivated in the liver to avoid potential toxicities associated with systemic TGFß signaling inhibition. In November 2025, we announced topline results of the global randomized, double-blind, placebo-controlled Phase 2a trial of ontunisertib, or the STENOVA trial, in 103 FSCD symptomatic patients with at least one ileal stricture. Part A of the STENOVA study achieved its primary endpoint of assessing the safety and tolerability of ontunisertib 100mg QD and 200mg BID in FSCD patients. Pharmacokinetic results confirmed the GI-restricted profile of ontunisertib, with high local and low systemic exposure of ontunisertib in FSCD patients. We also observed positive signals on several exploratory clinical endpoints. The 48-week open-label treatment extension of the STENOVA trial with ontunisertib is currently ongoing and we expect to report the results of such open-label treatment extension in the second half of 2026. Based on the positive results observed in the STENOVA study to date, we are preparing to initiate a Phase 2b trial of ontunisertib in patients with symptomatic FSCD in the second half of 2026. • AGMB-447: AGMB-447, our second clinical-stage product candidate, is an inhaled small molecule inhibitor of ALK5, or TGFßR1, in development for the treatment of idiopathic pulmonary fibrosis, or IPF. IPF is a rare progressive fibrotic lung disease that has a poor prognosis for patients with a median life expectancy of less than five years. IPF affects approximately 240,000 people in the United States, Japan, the United Kingdom, and the four largest European markets (France, Germany, Spain, and Italy), with 30,000 to 40,000 new cases being diagnosed each year in the United States alone. AGMB-447 is designed to have a high local exposure in the lung tissue, and then upon absorption into the bloodstream, AGMB-447 is hydrolyzed and substantially inactivated in order to avoid potential toxicities associated with systemic inhibition of ALK5 signaling. Direct delivery to the lung through inhalation and subsequent lung restriction are designed to confer high efficacy and a favorable safety profile for AGMB-447. We believe AGMB-447 also has the potential to demonstrate a low potential for drug-drug interactions that could make it well-suited for use as a single-agent and in combination with current standard of care therapies. We are conducting a Phase 1 trial with AGMB-447 and have enrolled 108 healthy participants in the SAD and MAD B1-B6 portions of the trial, initiated the IPF cohort and enrolled the first patients. We completed an interim analysis of the SAD and MAD B1-6 stages in 108 healthy participants, where we observed positive topline interim results, and expect to report data from IPF patients in the second half of 2026. • Discovery and preclinical portfolio: We have a robust discovery pipeline including several programs in the early stages of development. Fibrosis and the role of TGFß Fibrosis represents an aberrant response of a tissue to injury, leading to progressive tissue scarring that may be triggered by trauma, inflammation, infection, cell injury or cancer, amongst others. As a result, fibrosis can lead to organ dysfunction and failure. The body’s normal response to injury involves the activation of cells that produce collagen and other components of the extracellular matrix, or ECM, that are part of the healing process for the tissue. Under normal physiological circumstances, scarring is self-limited and the resulting scar resolves itself, leaving behind a tissue architecture similar to what was present before the injury. However, in certain chronic disease states, this process of healing becomes both prolonged and excessive, resulting in fibrotic remodeling which interferes with organ function. Fibrosis can occur in many organ systems throughout the body including the lungs, liver, kidneys, gastrointestinal tract, skin and muscles. While the exact pathologies for diseases in these organs differ, fibrosis involves many of the same cell types and signaling pathways across different organs and tissue. Signaling by TGFß has been shown to play a central role in the pathophysiology of fibrosis. The well understood role of the TGFß pathway, including through the ALK5 receptor, in driving multiple aspects of fibrosis, has made it an attractive target for antifibrotic drug development. In healthy tissue, TGFß’s physiological role is to initiate healing after injury. In fibrotic diseases, however, TGFß signaling remains continuously activated in response to prolonged insults such as inflammation, leading the surrounding tissue to deposit excess ECM, which eventually leads to tissue fibrosis. There is strong preclinical evidence and encouraging preliminary clinical evidence that TGFß inhibition could be effective in multiple indications; however, development of previous ALK5 inhibitors has been limited due to safety concerns as systemic inhibition of TGFß causes toxicity in the heart and large vessels. We believe our programs have the potential to overcome these systemic toxicity challenges by acting locally within tissue of interest and avoiding systemic exposure while allowing us to leverage the well-described role of TGFß in fibrosis. We were initially incorporated under the laws of Belgium on April 13, 2017 as a Belgian private limited liability company (besloten vennootschap) and were converted under the laws of Belgium into a Belgian limited liability company (naamloze vennootschap) on March 14, 2019. Our principal executive offices are located in Antwerpen, Belgium.
