Ethos Technologies Inc.

Good afternoon, ladies and gentlemen, and welcome to the Atire Pharma fourth quarter and full year 2023 conference call. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session, and instructions will be given at that time. To ask a question during the session, please press star 1-1 on your telephone and wait for your name to be announced. To withdraw your question, please press star 1-1 again. As a reminder, this conference is being recorded for replay purposes. It is now my pleasure to hand the conference call over to Ashley Dunstan, ATAR's Director of Investor Relations and Public Affairs. Ms. Dunstan, you may begin.

Thank you, and good afternoon, everyone. Thank you for joining us today to discuss ATAR's fourth quarter and full year 2023 operating results and corporate update. We are joined today by Dr. Sanjay Shukla, our President and CEO, and Ms. Jill Broadfoot, our CFO. On the call, Sanjay will provide an update on our corporate strategy, including our clinical program for ExoFitimod and research and discovery programs. Jill will review our financial results and our current financial position before handing it back to Sanjay to open the call up for any questions. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provision of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer in the company's press release issued this afternoon, as well as the risk factors in the company's SEC filings and included in our most recent annual report on Form 10-K, subsequently filed quarterly reports on Form 10-Q, and in our other SEC filings. Undue reliance should not be placed on forward-looking statements which speak only as of the day they are made as facts and circumstances underlying these forward-looking statements may change. Except as required by law, Atire Pharma disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. I will now turn the call over to Sanjay.

Thank you, Ashley. Good afternoon, everyone, and thank you for joining us for our fourth quarter and full year 2023 results conference call. At ATAR, we are leveraging evolutionary intelligence to translate tRNA synthetase biology into new therapies for fibrosis and inflammation. Our lead therapeutic candidate, efsofitimod, is a first-in-class biologic immunomodulator based on a naturally occurring lung-enriched splice variant of the tRNA synthetase, HARs. Epsophitamide selectively modulates activated myeloid cells via Neuropilin 2, or NRP2, to resolve inflammation without immune suppression and potentially prevent the progression of fibrosis. We're developing Epsophitamide as a treatment for patients with interstitial lung disease, or ILD, a group of rare immune-mediated disorders that can cause chronic inflammation and fibrosis of the lungs. 2023 was an important year for ATAR as we progressed and expanded our efsofitamide clinical development program, which now includes two ongoing clinical studies. The phase three efsofit study in patients with pulmonary sarcoidosis, a major form of ILD, and the phase two efsoconnect study in patients with ILD related to systemic sclerosis, which is known as SSC or more commonly scleroderma. Throughout the past year, we have also greatly enhanced our mechanistic understanding of the way in which Epsilfitamide is conferring its anti-inflammatory effects. NRP2 is highly expressed on activated immune cells during an inflammatory response, notably myeloid cells, including monocytes and macrophages. By binding NRP2, Epsilfitamide guides the differentiation of monocytes at the site of inflammation into a macrophage subtype that is less pro-inflammatory to resolve aberrant inflammation. Dysregulated inflammation is a hallmark of myeloid-driven diseases such as ILD, where persistent uncontrolled inflammation can lead to the progression of fibrosis. With this new understanding, we now have even greater clarity and confidence as to why F-sulfidamide may represent a breakthrough in treatment for ILD. Our lead indication for esophonamide is pulmonary sarcoidosis, the most prevalent form of ILD, where approximately 70% of patients will have symptomatic disease and nearly 20% will develop lung fibrosis. Current standard of care is primarily oral corticosteroids. A highly toxic treatment that has limited clinical evidence is broadly immunosuppressive and comes with side effects resulting in a high disease burden for patients. Epsilfit is a global pivotal phase three study evaluating Epsilfinamide compared to placebo in the context of a forced steroid taper in patients with pulmonary sarcoidosis. This study is currently enrolling at more than 90 centers in nine countries. We're pleased with the progress we've made thus far with this study, which is expected to be the largest interventional study ever conducted in sarcoidosis. Completing enrollment in Epsilfit is our primary focus. and we anticipate doing so in the second quarter of this year. In the past few months, as patients have completed the 52-week exoFIT study, we've received multiple inquiries from study principals, study principal investigators, or PIs, whose patients are requested to continue treatment once they completed the trial. While ATHER PIs and patients are all blinded to what treatment patients receive as part of the study, either esophitamide or placebo, the feedback we've received has suggested that some patients have performed well and want to continue on study drug rather than returning to the treatment regimen they had prior to the study. For some patients, that may entail resuming or increasing steroid dose, which many patients are reluctant to do. Based on this feedback, we decided to implement an individual patient expanded access program, or EAP, for patients who complete FSOFIT. This individual patient EAP is designed to allow access to FSOFITimod for patients who have or are in the process of completing FSOFIT beyond the duration of the clinical trial. The company, PIs, and patients will remain blinded to the treatment that occurred as part of FSOFIT. Safety is a key component of any EAP. We were able to implement this program based on the existing safety database from prior efsofitamide clinical studies and additional safety and tolerability data from a data safety and monitoring board, or DSMB, review of data from efsofit, which included the evaluation of patients that completed 52 weeks of treatment. The DSMB review recommended the study proceed without modification, suggesting no major safety concerns. And while many types of EAPs are typically implemented after data from a study has been unblinded, we decided to implement this individual patient EAP early, not only based on feedback and demand, but in part to continue to support those patients who have dedicated their time and entrusted us with their health by participating in this important study. This program reflects our ongoing commitment to the sarcoidosis community as we work to develop a safe and effective treatment for those in need. Our second indication for afsofitamide is SSC-ILD. SSC is a form of connective tissue disease where ILD commonly occurs and is the leading cause of mortality. Current treatment options are limited and like sarcoidosis, do not treat the underlying disease or improve quality of life. AfsoConnect is a phase two proof of concept study evaluating afsofitamide compared to placebo in patients with SSC-ILD. This study, which does the first patient last quarter, is currently open for enrollment at multiple centers in the U.S. We're focused on generating data from this study in 2024, and we expect to provide an update on the study later this year. We estimate that the two indications that comprise our current clinical program for afsofitamide Olmosarcoidosis and SSC-ILD collectively represent a potential $2 to $3 billion global market opportunity. This does not include any upside potential in other forms of the more than 200 ILDs, where esophitamide's unique mechanism of action to address complex immune pathology and desirable safety profile may be able to disrupt standard of care. While our primary focus is our clinical program for Epsifidamone, we continue to leverage our intellectual property, or IP at State, covering domains from all 20 human tRNA synthetases and utilize our platform as an engine to generate new pipeline candidates. tRNA synthetases are ancient essential proteins that have evolved novel domains to regulate diverse pathways extracellularly in humans. By identifying extracellular receptors and signaling pathways for these domains, we can elucidate the role these proteins play in cellular response and explore disease areas where they may have therapeutic benefits. Our two most advanced tRNA synthetase candidates in preclinical development are ATYR0101 and ATYR0750, both of which have specific interactions with targets that have implications in fibrosis. These targets include latent transforming growth factor beta-binding protein 1, or LTBP1, and fibroblast growth factor receptor 4, or FGFR4, respectively. AQIRO101, which is derived from a domain of the tRNA synthetase DARS, exerts its anti-fibrotic effects by selectively inducing apoptosis of myofibroblasts, targeting a key hallmark of fibrosis pathology, which is the persistence of activated myofibroblasts. This mechanism may support broad therapeutic application in indications like lung, liver, and kidney fibrosis. The hidden biology that we have been able to unlock from our platform continues to inspire us, including the way in which some of these appended domains, like F-sulfidamide, interact excessively with previously under-the-radar targets, like NRP2, and in particular, its role as an immune regulator, or by more well-known targets in unique ways, like 0101 and 0750. This platform, which is based on signaling pathways that have been have evolved over billions of years to maintain homeostasis is an excellent example of bioinnovation and has the potential to disrupt traditional drug discovery, a process that is increasingly reliant on exploiting existing signaling pathways to generate Me Too therapies. Our conviction as to the potential of tRNA synthetase biology to lead to transformative medicines continues to grow stronger as our research advances. I'll now turn it over to our Chief Financial Officer, Jill Broadfoot, to review our financial results.