Atossa Therapeutics, Inc.

Good morning, ladies and gentlemen. Thank you for standing by, and welcome to the Atosa Therapeutics Q2 2023 conference call. Please be advised, today's conference is being recorded. I would now like to hand the conference over to your first speaker today, Eric Van Setten, Vice President of Investor and Public Relations. Mr. Van Setten, you may begin.

Thank you, Kevin. Good morning, everyone, and welcome to Atosa's second quarter 2023 Corporate and Financial Update conference call. Earlier this morning, we issued a press release providing an overview of our recent corporate highlights and financial results for the quarter ended June 30th, 2023. The press release can be accessed on the investor portion of our website at investors.atosatherapeutics.com. Joining me on the call today are Dr. Stephen Quagg, Atosa's President and Chief Executive Officer, and Greg Weaver, our Executive Vice President and Chief Financial Officer. During today's call, we will be making certain forward-looking statements. which are subject to risks and uncertainties that may cause actual results to differ materially from the anticipated or estimated future results. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change. The description of potential risks can be found in our latest SEC disclosure documents and our press release. You're cautioned not to place undue reliance on these forward-looking statements, and ATOSA disclaims any obligation to update these statements. I will now turn the call over to Dr. Quay.

Thank you, Eric, and thank you to everyone who joined the call today. I'm very proud of the progress we've made in Q2. From a clinical perspective, each of the three ongoing Phase II trials investigating our proprietary Z-endoxifen reached important milestones. I'll start with the CARISMA-endoxifen trial, which is a randomized, double-blind, placebo-controlled efficacy study of oral endoxifen in premenopausal women with measurable breast density. This is a single site trial at the Karolinski Institute in Stockholm, led by Dr. Per Hall, one of the world's foremost authorities in breast cancer epidemiology. Participants in the study are randomized into one of three cohorts to receive placebo, one milligram or two milligrams of endoxifen daily. Participants will take endoxifen for six months, over the course of which mammograms are conducted to measure reduction in breast density. Patients will also have a mammogram at 24 months to assess the durability of density changes. Last month, we announced that 70% or 170 out of the anticipated 240 patients have been enrolled in the trial. We expect the study to fully enroll in the fourth quarter of this year and data to be available in mid-2024. Mammographic breast density is a growing health crisis. Between 40 and 50% of all women are estimated to have mammographically dense breasts, and there are currently no approved treatments. Cancer and dense breast tissue both appear white on a mammogram, which makes mammography less sensitive and more difficult to interpret. As a result, cancers are often larger, more advanced, and more difficult to treat when found in women with dense breast tissue. Additionally, mammographic breast density is a strong independent predictor of breast cancer risk, and women with the highest density are four to six times more likely to develop breast cancer compared to women with the least dense breasts. Our vision for endoxifen in the mammographic breast density setting is to both make mammograms more reliable and decrease the risk that women with dense breast tissue will develop cancer in their lifetimes. In addition to our MBD trial, there are two additional ongoing phase two trials investigating endoxifen in the neoadjuvant setting, which is the window of time between the diagnosis and the primary treatment. which with estrogen-sensitive breast cancer is almost always surgery plus radiation and or chemotherapy. The intent of neoadjuvant therapy is to slow the cancer growth or even shrink the cancer prior to surgery. Doing this makes surgery more effective and with breast cancer, it may alter the surgical approach, meaning some patients could have a lumpectomy instead of a mastectomy. Neoadjuvant therapy has also been shown to to reduce the likelihood that the cancer returns. The first of the two neoadjuvant trials investigating endoxifen is being conducted through the iSPI network, which is a collaborative effort among academic investigators from major cancer research centers across the United States. The iSPI trial is enrolling newly diagnosed pre- and post-menopausal women with estrogen receptor positive breast cancer. As a reminder, about 80% of all breast cancers are ER positive. Patients in the study received daily treatment with 10 milligrams of endoxin for up to 24 weeks prior to surgery. This is a smaller trial with only 20 subjects expected to participate, and we announced in June that the trial was already 30% enrolled. Given the size of the I-SPY network, which includes 41 of the largest cancer centers in the United States, We expect full enrollment either later this year or in early 2024. The third phase two trial is the Evangeline study, which was profiled at the American Society of Clinical Oncology meeting in Chicago in June. This is also a neoadjuvant study, although it differs from the I-SPY trial as only premenopausal women are being enrolled. The Evangeline trial will enroll up to 175 women. The primary objective is to evaluate the endocrine-sensitive disease rate measured by KI-67 after four weeks of treatment with endoxifen compared to treatment with current standard of care, which consists of an aromatase inhibitor plus ovarian function suppression. KI-67 is a measure of tumor cell proliferation, or how fast the tumor is growing. The importance of this is that studies have shown that KI67 above 10% at the time of surgery confers a higher risk of recurrence and a worse survival rate in patients with early breast cancer. The Evangeline trial started with a six-patient pharmacokinetic run-in cohort, which was designed to determine if the 40 milligram dose delivers steady-state plasma levels of between 500 and 1,000 nanograms per milliliter, which is the optimal to target protein kinase C beta inhibition and enhance endoxfin's anti-tumor mechanism of action. We already know that endoxfin binds to estrogen receptors in breast cells and stops the body's own natural estrogen from attaching to them. This cuts off the cancer's fuel source and prevents it from growing and spreading. By further targeting PKC beta, we expect endoxin to have an even greater anti-tumor effect by both blocking the estrogen receptor and by inducing apoptosis, which is a cellular equivalent of a self-destruct button. This is where we could see not only slower progression, but also a reduction in the size of the tumor. We recently received data from the initial 40 milligrams per day PK run-in cohort. As with our previous trials, no treatment related safety or tolerability issues were identified. While the 40 milligram per day dose was well tolerated, it did not achieve optimal plasma concentrations, which means per the protocol, we are in the process of initiating a second dose level at 80 milligrams. Based on concentration levels achieved at 40 milligrams per day, we expect the 80 milligram per day dose will deliver the desired steady-state plasma concentrations. Efficacy data was also captured as part of the PK run-in, including Ki67 at baseline and at four weeks, and MRIs taken at diagnosis and again after 12 weeks of treatment. We are extremely encouraged by these results, and we hope to share them in detail at an upcoming medical conference. Before I turn things over to Greg for a financial update, I wanted to touch on one additional project that we have recently announced, which is our research partnership with Weill Cornell Medicine in New York City to study the potential of inducing estrogen receptor expression in triple negative breast cancer. The term triple negative breast cancer refers to the fact that the cancer cells don't have either estrogen or progesterone receptors and also don't make any of the other receptors, including the human epidermal growth factor receptor 2, or HER2 protein. The tumor cells thus test negative on all three tests. Triple negative breast cancer, or TNBC, accounts for about 10 to 15% of all breast cancers, and it differs from other types of invasive breast cancer in that it tends to grow and spread faster, has fewer treatment options, has a higher risk of recurrence, and tends to have a worse prognosis. The goal of the research we are doing with Weill Cornell is to determine if treating TNBC with extracellular vesicles carrying the estrogen receptor will change the cancer phenotype and turn on the estrogen receptor. Converting the tumor to ER positive would make it sensitive to hormone therapy, including treatment with Z and oxfam. this was fundamentally transformed the treatment approach and outlook for these patients. With that, I'll turn things over to Greg. Greg recently joined us as CFO, but he knows the company extremely well, having served on the board for over 10 years. He is a seasoned financial executive with over 30 years of experience leading finance, operations, and business development at several publicly traded biotech companies. I am thrilled to have him as part of our executive team, and we'll turn things over to him for our financial update. Greg, take it away.