Good morning, everyone. My name is Meir Lightman from the Jefferies Healthcare Investment Banking team. It is my true honor and pleasure, I met a little bit of the Atossa team a couple of minutes ago, but my true honor and pleasure to introduce Dr. Quay here, Chairman and CEO of Atossa. Atossa's focus specifically on the breast cancer and the oncology sector. We will learn a little bit about it during the presentation. Thank you. And good morning, everyone. Welcome to the Atossa Therapeutics Corporate presentation. Whoops, let me back up. We are a public company on NASDAQ under the symbol ATOS. And so you should review all of our SEC filings before making any investment decisions. I will be making forward-looking statements today. Atossa is addressing a multi-billion dollar opportunity in estrogen receptor-positive breast cancer. This is with our lead molecule, (Z)-endoxifen, which has many unique properties, which I'll go through today. It's demonstrated broad utility from the earliest stage, which we consider the prevention of breast cancer, through the early diagnostic phase called neoadjuvant to then the stable adjuvant treatment. And now with our focus with FDA approval in the metastatic space, y ou can see that it covers the mets and bounds of the entire space. We have a robust and growing IP portfolio. I've invented seven drugs that are FDA- approved. I have 92 patents. I'm very proud of the patent estate we've built at Atossa because it'll add great value for shareholders in the future. We also have a very experienced leadership team. Some of them are here today with us. Finally, we have a strong financial position. We are one of probably only 20% of biotech companies in the space that have over two years of cash and are trading well above our cash position. This is the leadership team here. In the room with me today is our CFO, Heather Reese, as well as Michael Parks, our VP of Investor and Public Relations. We also have two experienced executives, one who's just returning from the ASCO meeting in Chicago, Dr. Claudia Lopez, and Delly Behen, our VP of Operations. As I indicated, we are guided by a world-class leadership advisory group that includes Dr. Per Hall on the left from the Karolinska Institutet, where he has been deeply involved in breast cancer prevention. We've been supporting and working with him for many years. In addition, Laura Esserman, who is a professor at the University of California, San Francisco, literally the architect of the iSPY adaptive clinical trial process, is doing some very exciting work for us with (Z)-endoxifen, which I'll get into. Dr. Matthew Getz, an MD from the Mayo Clinic, who probably has the most clinical experience with (Z)-endoxifen and is our principal investigator for the Evangeline trial. Finally, Dr. David Lyden here in New York City, who is deep in the research in our triple-negative breast cancer programs. The problem is that there are unmet needs in estrogen receptor-positive breast cancer. About 40%-50% of patients stop taking the treatment at some point during its timeframe. This is principally driven by the adverse events. Many of the drugs have minor but significant frequency adverse events that lead women to simply stop taking the drug. Of course, there's no benefit when a woman is not taking her drug. That's one of the things we focus on, is crafting a profile for (Z)-endoxifen that is tolerated and very well attractive in that perspective. There's another population of patients, almost half of the patients, who don't respond to first-line aromatase inhibitors plus CDK4/6 inhibitors. This is a class of drugs that is commonly used, but again, almost half of the patients don't have a proper response to it. Finally, the gold standard, if you could call it, before (Z)-endoxifen came along, the fulvestrant monotherapy also has a high level of failure in the settings here. Despite all of the endocrine therapy that's been around for a very long time, and which is addressing the most common kind of breast cancer, there are significant unmet needs that we believe (Z)-endoxifen will address. These include improved efficacy, a reduced resistance, induced apoptosis. This is an important kind of scientificy thing, but nonetheless, most endocrine therapies are static. That is, they stop the cell from growing. They put the brakes on it. When you stop taking it, the brake comes off and the cancer continues. (Z)-endoxifen is quite unique in having a pathway that, again, I'll go into the science a little bit more, a little bit later, but a pathway which actually triggers what's called apoptosis. Our cells are programmed to commit suicide effectively to kill themselves. At certain levels in certain kinds of cancer, (Z)-endoxifen triggers that. That is quite unique. Finally, improved adherence. Again, this gets down to those frequent, not necessarily medically important, but for the patient, very important side effects that if you can get around, if you do not have them with your drug, the adherence, which is the definition of people taking the medicine long term according to the prescription their doctor has given them, improves greatly. You do not get any benefit if someone is not taking your drug. A little bit of chemistry, I will not have a test after this, although I love chemistry. Tamoxifen, which is the mainstay of breast cancer treatment, probably the most commonly administered drug in the history of cancer treatment, if you go back to the 1950s even, is not a cancer drug itself. It's what's called a prodrug, which means there's two kinds of chemistries that have to happen in the liver before it becomes active. The first chemistry is to put a hydroxyl group on the phenyl ring. So can I point with this or I guess I can't. Yeah, maybe I can here. I'll skip that. In any case, the top middle called 4-hydroxytamoxifen is the product of putting hydroxyl group on the phenyl group. And then the drop- down from that, where you see (Z)-endoxifen, is in fact the active ingredient of tamoxifen. And it involves taking a methyl group off of that amine. It becomes a primary amine as opposed to a secondary amine. All of this metabolism of tamoxifen is required for it to have any effect at all on breast cancer. It also makes other things. It makes about 21 different chemicals, many of which have pharmacological activity that we do not necessarily want. Tamoxifen is, you talk about it as being a dirty bomb as opposed to a laser-guided missile. That is kind of the way to think about it. You can give a drug that gives 21 different chemicals, or you can give the only one that has activity. There it is. Just to be sure you could find it in the chart there. (Z)-endoxifen is the drug that we have, the one that we have our patent portfolio on that we are very excited about. Let's talk about its differentiation in the space of ER-positive breast cancer. First and foremost, it has superior estrogen receptor antagonism. 75% of breast cancers are driven by the estrogen receptor, which is a protein in the cytoplasm. Estrogen will bind to it under normal circumstances. It goes to the nucleus. Within about 15 minutes, it changes 5,000 different protein manufacturing processes in a process that drives normal estrogen activity in women, but also when it's hijacked, drives breast cancer. In order to stop that, you need to get between the estrogen that the woman has in her cell and the receptor itself. (Z)-endoxifen does that better than any other drug. It's that simple. That's its first step of differentiation, which is really, really important. The second step is what I talked about earlier, which is programmed cell death or apoptosis. Dr. Getz was really the primary finder of the fact that (Z)-endoxifen, unlike any other estrogen therapy that we are aware of, is a PKC beta-1 inhibitor. We do not have to say that again. It is complicated. Nonetheless, what it means is that (Z)-endoxifen alone in an ER-positive breast cancer has the potential to cause the cells to commit suicide, effectively killing the cells. One of the challenges with estrogen receptor-positive breast cancer is like the challenges we had with COVID, if you think about it, where you have a vaccine and then the virus escaped the vaccine. Breast cancers can do the same thing. When you put pressure on them with estrogen receptor inhibitors, 40%-50% over six months to two to three years will develop a mutation in the estrogen receptor, which makes those drugs no longer effective. They just simply cannot bind anymore. (Z)-endoxifen in that setting continues to have activity. We are very excited about this potential because, as I've indicated, almost all metastatic patients will have one form of estrogen receptor mutation or another. We have activity in that. At this point in time, after testing hundreds and hundreds of women, we have an improved safety and tolerability profile compared to, for example, tamoxifen, which has about 80% adverse events of the type of vasomotor, night sweats, and flushing and that sort of thing, or aromatase inhibitors, where about 40% have an arthritis that's limiting and causes them to go off the drug. In both of those particular comparisons, (Z)-endoxifen is very, very clean with respect to its adverse events. That is very attractive. In the last year and a half, we've done a great deal of generative artificial intelligence work with a company up in Boston called Ins ilico Medicine. The purpose of this was to basically make computational avatars of breast cancer, of female physiology, and then to look at what drugs have activity in breast cancer in addition to (Z)-endoxifen and where are they synergistic. Where is one plus one, three or four? This work has been very gratifying. It is wonderful to report that, for example, (Z)-endoxifen appears to be the best coupling with a CDK4/6 inhibitor. Right now in the iSPY trial in San Francisco, Lilly has contributed their drug to our trial. We've contributed ours. We are very excited to look at the potential of these two drugs working together. There are other combination opportunities for (Z)-endoxifen that we are exploring. I indicated endoxifen covers the mets and bounds of breast cancer. What I meant by that was if you think of the breast cancer process, (Z)-endoxifen has a role at every one of the points. Let's talk about prevention. There is a group of women who are at very high risk of breast cancer. They can be identified in a number of ways. One of the simplest ways is the high density that they have on their mammogram and some additional parameters that are found in the mammogram that are identified by software programs and the like. For example, 20% of women who have a particular pattern of high density and other features will have a very high incidence of what's called an interval cancer, a cancer before the next interval, the next two-year mammogram. One of the interesting ideas that we have would be to address that population, screening women for mammograms for cancer, identifying those that are high risk of a cancer in the next two years, and then studying that to show that we had superior activity and we actually could prevent those interval breast cancers. That would be an approach to prevention if we were to go into it. As you know, we have focused on metastatic. I think one of the things you should understand is that we believe the metastatic landscape is a foundation for Atossa to then move into the other perhaps larger markets, more impactful markets. Let's go from prevention to women who have been newly diagnosed and they have a four- to six-month period of time when you can begin to treat the tumor before you do the definitive surgery. Maybe they need radiation. That's called the neoadjuvant phase. The way to measure those, they're very attractive trials for identifying the efficacy of a drug because within 30 days, you can look at something like KI67 to see that the cells have stopped growing. Within three to four months, you can begin to look at MRIs to see that the tumors are shrinking. Between four and six months, you can do the surgery where the pathologist takes it out and looks at it and says, "There's a lot of dead cancer here. I can't find any living cancer cells." We have studies that are looking at each of those three time points with our drugs. We've begun to report them last year in December. We will continue to report ongoing trials in that space, that neoadjuvant space. They're very informative and very predictive of what will happen in longer-term trials. That's frankly why you do these kinds of sciencey studies. The adjuvant setting is what happens after the woman's definitive treatment has been done. You have two goals: preventing local cancer in the breast. If they conserve the breast, you want to prevent a recurrence in that breast, which is at a higher incidence once you've had cancer. Unfortunately, these women have a higher incidence in the contralateral breast. Those are the two targets for the adjuvant treatment. Again, one of the key features for (Z)-endoxifen in this space will be its side effect profile because it's up against drugs that have 80% side effects with respect to tamoxifen, 40% arthritis side effects with respect to AI inhibitors, which are the mainstay of this particular space. We believe that at an appropriate time, we can come into the adjuvant market with a very attractive safety profile. That 50% adherence should go much higher with our drugs. Finally, we spent the first quarter taking the data we generated during 2025, looking at it, packaging it for KOLs, key opinion leaders around the world, international group, to say, "With this scientific protocol and then bringing in regulatory authorities, people from ex-FDA people who are now in industry, and giving the two of them the charter to say, 'With this package of drug, with this profile, and with your knowledge of FDA approval processes and the like, where do you see the fastest opportunity for Atossa Therapeutics to get a drug on the market?'" The end of that process was something we announced in March, which was the metastatic route. The next step from that is to then, "Okay, it's great your KOLs like it. It's great that your regulatory folks say this is going to fly well." The truth is, of course, what happens when you go to the FDA? We took their work and our work and put together what's called a briefing package. You go to the FDA, you send it to the FDA, they make comments about it, you have a meeting, they generate minutes. That is the process we're in over the next three to four months. We're very excited to see what they have to say about it. We think we have a very strong position there. Metastatic will be the target for ATOS's first approval. I want to also set the stage that if you back up to adjuvant and neoadjuvant and prevention, this drug has very broad and deep legs in this entire space. As I've indicated, we are now focused on the metastatic setting. The pharmacodynamic effects there are very, very powerful. There have been studies already in this setting that have been done by other people, National Cancer Institute, the Mayo Clinic, which again will de-risk this path for Atossa Therapeutics and de-risk it for our shareholders as well. This is some preclinical data that we have. These are on our website. You can see in the left-hand panel where you look at an ER-positive breast cancer model in the laboratory, the black circles are the growth of the tumor over time. It grows very quickly, obviously, in this mouse model. The red and blue are what the impact of (Z)-endoxifen on that, where you actually see not only does the tumor stop growing, it actually gets smaller, much like we've seen with our patients. Another different tumor, a different ER-positive breast cancer tumor in the right panel shows the same effect. You can see that against fulvestrant, there's not a statistically significant difference. This does translate into the clinic. If you look at those two MRI images, one before treatment and one after treatment, you can see a significant reduction in tumor size. Again, in a trial up against tamoxifen for progression-free survival, which is the clinician's observation of the patient, you can see a very statistically significant and clinically significant increase in survival for women with (Z)-endoxifen versus tamoxifen. In our own trials that we financed, you can look on the left-hand panel, which is looking at that 30-day KI67 measurement, where you see a drop from the initial numbers to the post-30-day numbers. Typically, 10% is a threshold that clinicians find especially attractive in predicting two and three-year long-term effects. You can see that we have substantially our patients going below 10%. The right-hand panel shows these same patients at three to four months where their MRIs are showing significant decreases in tumor size. As I've indicated, we also have this potential of interacting with partnering with other drugs. The CDK4/6 inhibitors are the mainstay. If you think about ER-positive breast cancer, you have the ordinary proliferation rate breast cancer, which is the majority of the population. Maybe 20%-25% are above that in terms of their reproductive pattern. These women will not—we know now that they need something more than just endocrine therapy. The whole space of CDK4/6 inhibitors was developed for that population. We now can see that we can partner very effectively with the CDK4/6 inhibitors through some of the in vitro work that we've done. This is an incredible opportunity for us because we know now we have enough experience that when an estrogen receptor therapy is coupled with a CDK4/6 inhibitor, the outcome is that you will cause resistance to the estrogen receptor. At that point in time, the estrogen component is no longer working. We believe we'll continue to be active at that point in time. From both a preclinical and a clinical perspective, (Z)-endoxifen is both safe and well-tolerated. In the preclinical studies, the two major parameters that we like to see are that it does not induce bone loss, which is, again, very typical of some of the other estrogen receptor modifiers. It does not change uterine weight. Now, why would that be important? It is important because uterine weight change is a precursor to endometrial proliferation, which is a precursor to cancers in tamoxifen. They are very rare, roughly one in 10,000, one in 15,000. They only occur in postmenopausal women. They only occur in women with more than two years of treatment. Nonetheless, endoxifen seems to have a unique profile compared to tamoxifen, which again makes 21 different molecules to show that at the very first start of that whole process that leads to cancer, uterine weight increase does not happen. That is very gratifying for us. Of course, now in the clinic, (Z)-endoxifen has been tested at a lot of doses. Just the dosing is very important. This drug, again, I've invented seven drugs. This drug has the broadest spectrum of dose that I've ever seen. In prevention, we used one to two milligrams per day. In the clinic where you're trying to prevent breast cancers, 40-80 milligrams per day. In the metastatic setting, it's actually been used up to 300 milligrams per day. Cancer drugs typically have a maximum tolerated dose, which is a dose where you go above that, you're really hurting the patient more than you're helping the cancer treatment. Endoxifen doesn't have one of those. We may be very unique, the only drug or a small handful of drugs that do not have a maximum tolerated dose in the cancer space. In the metastatic setting, we've seen there's, again, other people have done activity to de-risk our clinical programs coming up. The current programs that we have in prevention and neoadjuvant were summarized with abstracts at the San Antonio meeting last December. Just to remind you, in the prevention space, we were looking at women who had a high density and then took a sugar pill, had one milligram or two milligrams in a blinded fashion for only six months. We looked at the density reduction and we looked at the side effects. The density reduction between one and two milligrams was different, but not statistically different. The side effect profile between placebo and one milligram was not different. The two milligram had a few more side effects than placebo. At a point in time when we will go forward with prevention, probably 1 milligram per day will be the dose that we will be using in that space. The Evangeline trial, which looked at four-week KI67 with less than 10%, showed that over 85% of patients across the board had the reduction that, again, that 10% threshold is something clinicians will look at and say, "Okay, I can predict two to three years that this woman is in a good place with respect to potential recurrences and the like." The iSPY trial, which, backing up just for a detail, the Evangeline trial is in premenopausal women only. The iSPY trial in the same patient population with respect to disease is both pre and postmenopausal women. You can see we very strategically tried to, again, expand where this drug could have effect by having trials in different spaces to give us unique information. The iSPY trial reached its primary endpoint in 95% of the participants who completed at least 75% of the planned dosing. Again, remember that number of 50% of women who stopped taking drug is an indication here that that did not happen in this particular setting. The mean KI67 reduction was from 10.5%- 5%, about a 65% reduction over there. With respect to imaging, almost a 78% reduction in tumor size. This is important not only for knowing that you're killing the tumor, but it can change the surgeon's treatment. He can go from having to do a mastectomy if it's really large to maybe a lumpectomy to have the same clinical outcome, but a different outcome for the woman in terms of quality of life. This table summarizes the features and the various treatments. Again, I'm starting to repeat myself, and you're starting to hopefully understand the uniqueness of endoxifen. It's superior to tamoxifen, which is its parent drug, but which has 20 other materials that don't have activity on cancers, but can have activity in other spaces. Not all women can make endoxifen because they don't have the liver enzymes to do that two-step chemistry I spoke about. The aromatase inhibitors, which are more effective than tamoxifen in classic trials, but have a 40% arthritis rate that many times can lead a woman to stop taking the drug because of its severity. Final, fulvestrant, which is a monthly injection, it's supposed to be very reasonably painful, but is the gold standard with efficacy and which are, again, one of our KOLs said this drug may be endoxifen may be as good as fulvestrant. One of its challenges is that the week before your next injection, so you get an injection every month, you're going to have trough levels where as the drug decays, you're going to have trough levels where the tumors will escape. Having a tumor that's suppressed for three weeks out of the month, but for one week it's growing again is not a profile that is attractive when you can give a single pill on a daily basis. We have a number of upcoming events. I've indicated what we've done in this first half of the year was to very deliberately focus on what's the fastest path to approval, what is the group that can help advise us on that. We came to the conclusion that the metastatic setting is the best approach. Inside of that small statement, there's 12 or 13 different inclusion/exclusion criteria that can help define the trial. Those are now embedded in a document where we've sent to the FDA to say, "This is our perception of the best trial to get this approved in metastatic. What do you think?" We will take their feedback. We will reincorporate it. In the background, this will be an international trial. It'll be a trial that will be run by some of the standard CROs. We are currently, without even having the results from the briefing meeting, currently vetting CROs for that process because it's very important. They will be the lifeblood of getting us across the finish line with respect to patient recruitment. We will be reporting on these events in the third quarter and then into the fourth quarter. Remember, all of these trials, all the foundational trials in, excuse me, misspoke, in the neoadjuvant setting, will be having reports out as they progress through the rest of this year. We have said publicly that it is our goal to have our first patient in our FDA-approved registration trial by the end of this year. That is New Year's Eve. Key statistics which you can find: our cash position, $65 million as of March 31st. That gives us two years of runway with our current operations. These trials will take more money than that particular conversation. Nonetheless, we will be able to define very clearly, here's the trial, here's the CRO, here's the FDA's opinion, here's the cost to help get that drug FDA approved. Market cap about $112 million. We have some outstanding warrants which are expiring in June, July, and September. We have no debt on our balance sheet. Again, let me summarize here. We have a multi-billion- dollar opportunity in ER-positive breast cancer. We believe that we have the best drug in that case from both a scientific point of view with respect to killing cancers, from a safety and profile and quality of life point of view with respect to patients' experiences with it. It demonstrates broad utility from preventing breast cancer to the metastatic setting and everything in between. We have a robust and expanding IP portfolio. I take great pride in the IP of the companies that I've been involved with. I have 92 patents. So hopefully that speaks to that. Very experienced leadership team inside the company and with respect to advisors and a strong financial position. Again, two years of runway on the balance sheet, no debt. With that, I would thank you very much for your attention and appreciate your participation with Atossa Therapeutics in preventing and treating breast cancer.