We are a clinical-stage biotechnology company focused on developing therapeutics that harness the body’s natural regulatory mechanisms to modulate the immune response in patients with chronic inflammatory diseases. We are currently evaluating our lead drug candidate, obefazimod, in Phase 3 clinical trials for the treatment of adults with moderately to severely active ulcerative colitis (“UC”). We are also in the planning stages of initiating a Phase 2a clinical trial of obefazimod in patients with Crohn’s disease (“CD”), as well as evaluating other potential inflammatory indications. We focus on indications where existing treatments have left patients with significant unmet needs, and where we believe our investigational agents have the potential to be meaningfully differentiated from currently available therapies. The indications we target have substantial populations and represent large commercial opportunities, pending regulatory approvals and successful commercialization. Our initial focus is on inflammatory bowel diseases (“IBD”), chronic conditions involving inflammation of the gastrointestinal (“GI”) tract, of which the two most common forms are UC and CD. As of 2022, an aggregate of approximately 2.9 million patients across the United States, EU4 (France, Germany, Italy and Spain), the United Kingdom and Japan suffered from IBD, with 1.5 million of these patients in the United States alone. One of the primary goals of IBD therapy is to achieve durable clinical remission while simultaneously taking into consideration a patient’s quality of life and concerns regarding potential side effects. Despite a number of different therapies approved for UC and CD, the vast majority of these therapies require chronic administration via injections or intravenous infusions, and may come with serious and concerning warnings, including, but not limited to, risks of serious infections leading to hospitalizations or death and increased risks of various malignancies. A vast majority of IBD patients do not achieve clinical remission with existing therapies, and a significant number of patients will lose response over time, especially those patients on TNF-a inhibitor therapy where anti-drug antibodies are very common. Further, despite the increased number of biosimilars, such as TNF-a inhibitor therapies, becoming available for the treatment of IBD, biosimilars unfortunately do not alleviate any of the potential side effect concerns that often cause patients to delay, or avoid altogether, stepping up to more advanced therapies. In addition, although a small number of oral therapies have more recently been approved for the treatment of IBD, these therapies also come with concerning potential side effects, which can discourage patients from initiating treatment with advanced therapies. Therefore, there continues to be significant unmet need for novel oral therapies with durable efficacy, improved safety profiles and minimal preinitiation requirements for patients with moderately to severely active IBD. Moreover, we believe the IBD market has significant growth potential driven by growing diagnosis of these diseases and increased penetration of oral treatments with improved benefit/risk profiles. We believe our lead drug candidate, obefazimod, is differentiated from competing approaches for the treatment of IBD via its novel mechanism of action. Obefazimod was demonstrated to specifically enhance the expression of a single micro-RNA, miR-124, which plays a critical role in the regulation of the inflammatory response. In the context of inflammation, miR-124 is a natural regulator of the inflammatory response, controlling progression of inflammation and restoring homeostasis of the immune system, without causing broader immunosuppression. In contrast to currently available advanced therapies, prescribed post-conventional therapies, some of which target only a single cytokine or pathway, miR-124 modulates the expression of several key cytokines and pathways. Modulating multiple inflammatory pathways simultaneously may lead to more durability of efficacy results over the long-term, which is critical in lifelong conditions such as IBD, potentially differentiating obefazimod from currently available IBD treatments. In our Phase 2 clinical trials for the treatment of moderately to severely active UC, consistent with the pharmacological effects observed in our preclinical studies, obefazimod demonstrated an onset of symptom relief by day 8 of dosing, with meaningful reductions in rectal bleeding and stool frequency scores. In our induction Phase 2b clinical trial, which included 252 patients, obefazimod met the primary endpoint of a statistically significant reduction in Modified Mayo Score, a measure of disease activity relative to placebo. In addition, we observed high rates of sustained and newly achieved clinical remission in the subsequent open-label maintenance extension trial of up to two years of treatment, of which approximately 45% of patients were previously exposed to biologics or Janus kinase (“JAK”) inhibitors. Greater than 90% of patients previously exposed to advanced therapy prior to enrollment were highly refractory, having failed at least two advanced therapies. In April 2023, we reported the results from the final analysis of our Phase 2b open-label maintenance trial, including 217 patients of which 164 patients (76%) completed the second year of once-daily oral treatment with 50 mg obefazimod. At the conclusion of the second year of treatment, 114 of the 217 patients enrolled (53%) achieved clinical remission and 158 patients (73%) achieved clinical response. Among the 98 bio-refractory patients, 66 patients (67%) had a clinical response, 38 patients (39%) were in clinical remission, 46 patients (47%) had endoscopic improvement and 20 patients (20%) had endoscopic remission at week 96. Among the 124 patients that achieved clinical response at the end of the 8-week induction period of the double-blind study, 82 patients (66%) achieved clinical remission at week 48, mimicking the re-randomization of responders approach typically utilized in Phase 3 maintenance trials. Of the 124 patients in clinical response at week 8, 74 patients (60%) achieved clinical remission, 95 patients (77%) had clinical response, 79 patients (64%) achieved endoscopic improvement and 52 patients (42%) achieved endoscopic remission at week 96. In September 2023, we reported an interim analysis of step-down dosing from 50 mg to 25 mg for the third and fifth year of open-label maintenance treatment with obefazimod in UC patients. These patients were treated with 50 mg of oral, once-daily obefazimod for approximately four years in the Phase 2a clinical trial and approximately two years in the Phase 2b clinical trial. Patients were eligible to enroll in the trial if they had a Mayo endoscopic subscore of 0 or 1. Eligible patients were switched to 25 mg, and an interim analysis was performed at week 48 with a cut-off date of July 31, 2023. Of the 71 eligible patients, 63 completed their 48-week visit. Among these patients, 53 out of 63 patients (84%) demonstrated disease control (stable or improved Modified Mayo Score). No new safety signals were detected in UC patients treated up to five years with oral, once-daily obefazimod. Obefazimod’s tolerability profile indicates potentially important clinical differentiation. As of November 30, 2022 (the last safety data cut-off date), 1,074 patients and volunteers had been treated with obefazimod, of which 209 patients were treated with 50 mg obefazimod for one year or more with no change in the observed tolerability profile underscored by 76% of patients that remained on therapy throughout the two-year open-label maintenance trial period. No new adverse safety signals were observed. We initiated our pivotal Phase 3 clinical trials of obefazimod for the treatment of moderately to severely active UC in October 2022, which consist of two induction trials (ABTECT-1 and ABTECT-2) and one ABTECT maintenance trial. Top-line data from the ABTECT-1 and ABTECT-2 induction trials is expected to be announced in the first quarter of 2025, and top-line data from the ABTECT maintenance trial is expected to be announced in the first quarter of 2026. We intend to (i) file an Investigational New Drug Application (“IND”) in the fourth quarter of 2023, (ii) initiate a Phase 2a clinical trial in patients with CD in the first quarter of 2024 and (iii) announce Phase 2a induction trial top-line results in the second half of 2025 with the objective to demonstrate clinical response and tolerability profile consistent with that already observed in our clinical trials for moderately to severely active UC. Based on the results from this Phase 2a clinical trial, we intend to proceed directly to a Phase 3 clinical trial. Our team is comprised of industry leaders in the fields of biology, data analytics and drug development, as well as scientific experts in chronic inflammatory diseases, including IBD. We are led by Marc de Garidel, our Chief Executive Officer, who has more than 40 years of experience in the pharmaceutical and biotechnology sector. Collectively, our team has decades of experience and a proven track record of advancing compounds into and through clinical development and commercialization, including at the following organizations: Amgen, Arena Pharmaceuticals, AstraZeneca, BioNTech, Boehringer Ingelheim, Eli Lilly, Genentech/Roche, Guerbet, Ipsen Pharmaceuticals, J&J, Pfizer, Sanofi, Sanofi-Pasteur and Shire/Takeda. We were incorporated as a société anonyme (limited liability company) on December 4, 2013 and registered at the Paris Trade and Company Register on December 27, 2013 for a period of 99 years until December 22, 2112, subject to extension or early dissolution, under the number 799 363 718. Our principal executive offices are located at 7-11 boulevard Haussmann 75009 Paris, France, and our telephone number is +33 (0) 1 53 83 08 41. We have one wholly owned subsidiary, Abivax LLC, a Delaware limited liability company, formed on March 20, 2023. Our agent for service of process in the United States is CT Corporation System, 1015 15th Street N.W., Suite 1000, Washington, D.C.