As we also work as an advisor to Atossa and have done so over the last couple of years. We're excited to have our speakers today for our program, which is gonna be about 30 minutes. If for any reason you want to review what we speak with Dr. Quay and Kyle Guse, the CEO and CFO of Atossa, after the event, we'll be publishing the video of this event at the Tribe Public YouTube channel for all to view as early as possible after we get the recording set. I'd like to again thank all of you for joining us today, the event title today is Atossa Therapeutics: Redefining Breast Cancer Prevention and Treatment. Again, this will be co-hosted by the world-renowned scientist in the picture there, author, entrepreneur, Steven Quay, MD, PhD, founder and CEO of the Seattle-based Atossa Therapeutics. The symbol again is Nasdaq, on the Nasdaq, ATOS. Atossa is a clinical stage biopharmaceutical company developing innovative proprietary medicines to address significant unmet needs in cancer. We also have esteemed colleague, Kyle Guse, the CFO of Atossa, pictured in for this event, and he'll be addressing some questions. Little bit of background about Dr. Quay. He's had an amazing career and is a named inventor on 87 U.S. patents, 130 pending U.S. patent applications, named inventor on patents covering five pharmaceutical products approved by the FDA. Dr. Quay, an MD in 1977 and a PhD in 1975 from the University of Michigan. Received his BA degree in biology, chemistry, and mathematics from Western Michigan University in 1971. He was selected to serve the company's board of directors at Atossa because of his role as a founder of the company and as well as his qualifications as a physician and a principal researcher overseeing the clinical and regulatory development of the company's pharmaceutical programs. Thanks again for coming to this event. Why don't we get started straight away, and we'll start asking some questions for Dr. Quay. Maybe, Dr. Quay, can you give us a little bit of background on how Atossa was started? Sure. Well, John, I mean, it was started in the context of looking at the amazing success that was achieved in cervical cancer when there was a test that could see the progress from normal to Hyperplasia, atypical to Carcinoma in situ. That Pap test, it was just called, took the incidence of cervical cancer from 110,000 a year down to about 15,000 a year. We now know that it's a virus is involved. There's a vaccination for it. We're basically looking at the elimination of cervical cancer. But over a decade ago, I said, "Why can't we do the same thing with breast cancer?" The key process, the two-step process is, what do you measure before you have cancer in the breast? Can you modulate the changes that are going on, the biology that's going on before it crosses the line and becomes cancerous? The answer to that is yes and yes. The first issue is that by looking at the density of the breast, that is the background parenchyma. When you do a mammogram, you're really looking for grains of salt, little salt grains, which represent dying cancer. That's what the mammogram was developed for. Is there cancer or is there not cancer? After about 20 years, someone looked at it and said, "Hey, if I look at just the background, is the background mostly black or is the background mostly white?" These are all women with no cancer. If I follow them for 10 years, guess what? The women that are all white tend to have about eight to 10 times more cancers. That's exactly the analogy that was done with the cervical Pap test. With that backdrop, we're now saying, well, can we modulate those women with high density? Can we make the density lower? For lots of reasons, we think that is a biologically tunable property. The clinical trial we're doing in Sweden at the Karolinska Institutet, the place where the Nobel Prize is awarded, is looking at exactly that. A woman with high density, she takes Endoxifen or placebo for six months. Will she see a change with Endoxifen? Not with placebo. If you wait 18 months off of drug to see if it's durable, does the density reduction stay down? It's probably, as you say, I've invented five drugs that have been used in 80 million people. This program to prevent perhaps prevent upwards of 200,000 breast cancers a year would be the capstone of all the things I've done in my career. That's fantastic. Thanks for your continued research in this area. As I've always been very excited about the program, it's hit home very close to home. As you know, when we originally met, my mom was stricken with the situation in breast cancer and is surviving and still is today. It's this unaddressed need here is there's still work to be done, and I'm so happy to hear that you're gonna continue on this work, on this path. The company, as I understand it, has transitioned from early detection to prevention and treatment. Can you give us an overview of, you know, of the (Z)-Endoxifen, that your proprietary (Z)-Endoxifen? Once you know that you can measure density and once you know that the density is under control of the estrogen that a woman produces in her ovaries, what you wanna do is find something that blocks the estrogen. Tamoxifen is the classic example of that, and is really the first hormone modulation therapy that was brought into the cancer field. Tamoxifen, however, in the body, makes about 21 different chemicals. It's really quite a pleomorphic drug as you will. By teasing out which of the 21 had the greatest activity, we and others were able to show that (Z)-Endoxifen was the real agent out of all the 21 that was doing, well, we quantified it, probably 95% of the effect. We now have patents on both the chemical synthesis of (Z)-Endoxifen, and then the way you have to formulate it to get it from an oral tablet into the bloodstream, because it's acid sensitive, it gets destroyed by the stomach acid. We have two complementary patents on the white powder, as it were, and on how you would tabulate it, to allow us to really push the frontiers of what Endoxifen can do. You know, the buzzword in biotech is having a pipeline and a product, and some people have to kind of stretch it. I think if you see our programs from prevention of breast cancer to Neoadjuvant treatment to adjuvant treatment, we really are bookending breast cancer. By the way, there are some other conditions in the body that are estrogen-driven that we may explore. That's, that's exciting. It's, you know, truly a platform to really build a. This meeting is being recorded. Ways to carve out a significant IP portfolio as well around Endoxifen. If you could continue with, you know, as you mentioned, as you're investigating (Z)-Endoxifen in two settings, Neoadjuvant and mammographic breast density, which is more of a breast cancer prevention play? Can you explain both again? Sorry, I didn't hear that. You broke up technically. Yeah, I'm sorry. It says, you know, basically what I'm looking for is can you explain, in the two settings, neoadjuvant treatment and mammographic breast density, which is more of a breast cancer prevention play? Can you explain both? Yeah. Well, no. Treatment of density, because high density is a condition that is not cancer, but women that have it have a very high incidence cancer, is it would be considered a prevention process. Neoadjuvant is by definition a treatment that's given to women from the time of diagnosis to the time of definitive therapy, which still currently is surgery and plus radiation if it's needed for local, for local disease. That window can be as short as about three weeks or as long as six months in some settings. It's kind of ironic that the two-thirds to three-fourths of breast cancers that are the most common, that is, the ER-positive cancers, are really not treated in the neoadjuvant setting. We kind of skip that period because every time someone has tried a drug there, it hasn't worked. My hypothesis was that, in the case of Tamoxifen, for example, it takes so long to get therapeutic levels of the tiny amount of Endoxifen that's being produced from Tamoxifen. six weeks is really the steady-state levels that you've moved on to the surgery and radiation by the time you get there. With our (Z)-Endoxifen, within four hours, you have blood levels, and within, you know, 24 hours, you have therapeutic blood levels. Basically, a woman can go from a needle biopsy of a lesion. You know, the bad news is it's cancer. The good news is, here's a prescription. Go to your pharmacist and start taking Endoxifen because we think based on what we hope, you know, what Atossa clinical trials will show, we think that this will stop, slow down the tumor, maybe shrink it before we even get to surgery. That's a really exciting window. It's an unmet medical need again, because there is no other drug that really works in that space. That, that's kind of our focus. Now, there's a corollary focus, which is that breast cancer can occur in two women in two stages of their life, premenopausal, postmenopausal. In the postmenopausal case, the ovaries have stopped making estrogen. There's a little bit of estrogen made in the breast itself. You don't need to do much other than block that local activity to get the cancers to really respond. Premenopausal woman is a more complicated situation because you have the ovaries willing to make as much estrogen as they need to. If you go in with a modest suppressor of estrogen, what happens is the ovaries overpower that, and you get ovarian activity. There's a protocol called ovarian suppression, which is common in premenopausal women in the neoadjuvant setting. It's pretty harsh in terms of quality-of-life issues. It's the women really don't like it. Sometimes they will actually risk getting cancer rather than stay, you know, in compliance in that particular protocol. The other setting we're trying Endoxifen is because it is such a strong suppressor of the estrogen activity itself, we believe that it'll work in a premenopausal woman without ovarian suppression, which would be a godsend for these women in terms of their quality of life. Yeah, that would be fantastic. Could you also speak to the sort of, if you quote-unquote, "market size" or the patient population size in the US in both of these settings? Yeah. Well, sure. They're big numbers. In terms of breast density reduction, we start with a number that there are 39 million-40 million mammograms each year done in women. That's about 80% of what we think should be the right number. Women are much better than men, frankly, and that's a whole separate conversation on their own health. We're getting about 80% of women who should be getting mammogram are getting it. That's because there's a lot of financial support and programs and education around getting your annual mammogram. 40 million is your total number there, and upwards of 10 million have high density. When you combine that with maybe a couple of other risk factors, you get millions of women who would be candidates for a six-month treatment to reduce their density, which then we believe will have down term effects on incidence of cancer. In the cancer setting itself, about a quarter of a million women in the U.S. are getting cancer each year. Two-thirds to three-quarters of those are estrogen receptor positive. That's you know, 200,000 is a good number to imagine is the treatment. Those women are going to go through neoadjuvant. They're going to have surgery, they're going to have radiation, and then they're going to have five years of follow-up adjuvant therapy. The ER-positive population is roughly 200,000 plus five years of 200,000, or about one million women in the U.S. That's great. The I guess carrying on with this discussion, could you also, it's my understanding that you have, you're currently investigating in both settings and ongoing phase 2 trials. Can you tell us about the studies that you're currently conducting, EVANGELINE, and please carry on. Sure. Sure. I mean, the study in Sweden is a placebo-controlled trial. It involves 240 women in groups of, divided up in that. The treatment is six months and they either get a sugar pill or a, or Endoxifen. Nobody knows what they get. One of the extra benefits of Endoxifen, which I will take no credit for because I didn't predict it, I predicted the opposite, is the side effect profile. One of the issues with Tamoxifen in the prevention setting, it is approved for prevention. It's used in 2% of women, is because it has a lot of side effects. In a population that doesn't have breast cancer, you're trying to reduce their incidence in the future, your tolerance for sort of quality of life or side effects is not very high. One of the things that we thought, you know, we would have an issue with Endoxifen was a similar pattern of side effects. You know, knock on wood, we don't see the same incidence of what are called vasomotor symptoms, which are night sweats, flushing, overheating, basically. We don't see those with Endoxifen at nearly the level you do with Tamoxifen, it's a remarkable difference. Again, at this point in time, you know, early days in our clinical trials, that's a really beneficial process. The process is a baseline mammogram at six months, a mammogram at 24 months. The three of those are used to look at the trajectory in these women of whether there's a dramatic drop between the first and the six-month one, and whether the drop, if it occurs, is maintained out through 24 months. There really is we do have some preliminary data in a, you know, like 20 or 30 women where if you do see a reduction with Tamoxifen or other, you know, drugs like that, it seems to be pretty durable in about 85% of women. We're expecting that to be successful, but, you know, science is science, and that's why you have to do it before you can opine on it completely. Looking at the durability will be important factor. From a business point of view, you know, a lot of companies want to have a drug that they give a woman for their entire life or give patient for their entire life. That's, you know, that's a business model, money-making business model. We think here the best care may be a six-month process. That's, that's exciting from a physician's point of view because you know, a woman shouldn't think about her breast health unless she has family history. Until she's 40, she gets her first mammogram. If she has high density, not great, not, you know, not the best day of her life. With a six-month prescription, if it goes down and if it stays down, we can really change their whole future, and perhaps, you know, give them a 20-year window of reduced risk on breast cancer. Just, you know, I work 20 or 18 out of the hours in the day, and this is, these concepts and these, this opportunity is what gets me out of bed in the morning. Thank you. Could you give us a little bit more of the specifics on how you structured your trials here, EVANGELINE and also the MBD, KARISMA-E ndoxifen studies? Yeah. Well, I'm not sure quite what you're saying, but, you know, all placebo controlled trials have a randomization process that dictates which particular pathway the patients go down. Then, you know, you're kind of loathe to ever break the blind. So we've talked about it with one particular patient that had some interesting things. She, you know, she probably needed to go off the trial, but we didn't break the blind in that case, and you usually don't break the blind. In the EVANGELINE trial that Matthew Goetz is conducting in other centers, it again is a randomized process to Endoxifen or to ovarian suppression, which is standard of care right now. There is a what we call a PK run-in. We know what blood levels are most effective for various things with respect to Endoxifen 'cause there's so much experience around that. What we're doing is a PK run-in, where we get three to four weeks of drug in the women, and then we measure their blood levels. If they're too low, we have a protocol where we go up a dose. Too high, we go down a dose. This process is we're making progress on this. This will really define the next stage where we'll just do one dose, placebo versus active for about six months. The hope there is to not only you know, suppress ovarian so that the estrogen is reduced, but perhaps get downstaging of the cancers. The ultimate, you know, home run with the bases loaded in neoadjuvant is to take a clinical stage cancer and lower its clinical staging, which usually means it gets smaller. It makes the surgery more compact, maybe more aesthetically, you know, more plastic surgery-like. That's sort of, again, the ultimate outcome. That, that's the design, John. Yeah. Okay. Thank you. On the EVANGELINE trial, I believe you had your first patient enrolled in February of this year. Is that correct? I think you're trying to pull from, is it 25 sites in the U.S.? Yeah. Yeah. We continue to add sites. It's, you know, clinical trials are really complicated, having a site say, "Yeah, we'd love to enter your trial," and then doing their first patient, there's 3 ft. of paperwork or 2 ft. of paperwork and, you know, meetings and all sorts of things and teams. We're making good progress on that. We'll give you updates when we feel it's appropriate in the, in the terms of the recruitment process. We're, we're feeling comfortable with where we're at in that trial. Well, it seems like again, the treatment on the EVANGELINE is that you treat for up to six months prior to surgery. Is that correct? That's correct. That's correct. You've looking forward to seeing that progress and all of this revealed as you move forward this year and beyond. We're excited to hear about this. In the essence of time, I know we've we should probably continue to move along our path here. One of the things that's important to many investors is that you have a solid patent protection. Can you speak to that? Sure. Yeah. Wanna just correct you. I have 88, not 87 patents, but who's counting? Oh. Patents are very important for pharmaceuticals, and they're really, I mean, one of the only ways that a tiny company like this could ever you know, expect to compete with the Pfizers of the world is this patent system. It allows us to get value for our shareholders from our inventions. The government stands in the way of people simply you know, being so big, they can just come in and take our stuff, so to speak. I know there's, there may be some, you know, popular movements around patents and that sort of thing, but I think people should really realize that the foundation of America's technological success over 250 years is that we were the first company with a formalized patent system. It's in the Constitution, actually, of the country so. In that context, you want to have patents in kind of three areas in pharmaceuticals. You wanna have the composition, the chemical itself. Just five million chemicals in the world, and Endoxifen is one of them, and we own the Endoxifen patent itself. You have to have methods of making that particular drug. Those are a little more complicated 'cause you have to prove infringement going into the factory, but we have those kind of patents. Once the drug is made, it sometimes can be formulated in a patentable way, and that turned out to be the case for Endoxifen. We had to make it enterically stable so that it didn't convert from Z-Endoxifen to a mixture of Z and E, which it wants to do in acid. And the E form is completely inert. You know, you lose 50% of your drug in 40 minutes if you don't use the patented process. The FTC is not gonna allow you know, to ever not use our patented process there. In many cases, the final stage is that you can get methods of treatment, where basically it's the doctor who's doing the infringement. A method of treating breast cancer, the steps consisting of identifying it as ER-positive and then treating it with (Z)-Endoxifen. That, that's been our strategy. We are, I think among the best in patent strategies. I've had five litigations, all won all five of them. Multimillion-dollar settlements for people that thought they could just steal my stuff. We had to show them that in the court system, that was not the case. Got it. Well, switching gears a little bit, what's just also important to investors is to understand how you're funded. Can you speak to, you know, how the company is capitalized, to date and your current burn? I could speak to it. Kyle Guse can do a better job. I'll let him. Fair enough. Thank you. Thanks, David. Thanks, John. Atossa is very well capitalized for a small biotech company. Around COVID time, we raised about $160 million in the capital markets when the capital markets were very, very active. As a result, at the end of 2022, we had over $100 million in the bank. To put things in perspective, that's multiple years of cash for Atossa. You'll notice our auditors do not have a qualification for going concern for Atossa, which is very common in small biotech companies. That's our funding situation right now. Got you. Can you speak to the historic burn? Yeah, John. We historically have burned $1 million-$2 million in cash per month. You know, that will go up a little bit as we continue to enroll in these phase two clinical studies that Dr. Quay was talking about. That's sort of our historic burn rate. We feel very confident about our cash position. Okay. Yeah. Well, you know, with that significant cash position, are you also continuing to look at any potential acquisitions or investments? The short answer is yes. I mean, we're opportunistic. I mean, we have enough cash that we could invest it in something that looks sufficiently compelling. We did make an investment of $4.7 million in a, you know, a venture capital-backed CAR- T company here in the United States, acquired a 19% interest in them. We're constantly evaluating other opportunities. The challenge is finding something that's as exciting as the things that we're working on. Mm-hmm. We don't wanna dilute. Our pipeline and our programs by acquiring something that's not as compelling as what we have. We've set the benchmark pretty high. Yeah. We are opportunistic. Yeah. I guess another way I'd say that, and, you know, Kyle Guse knows this 'cause we worked with you so tightly, John, is the investor should imagine that we probably on any given day have one potential acquisition or program that we're looking at. That's kind of been consistent since probably, you know, maybe July or June of last year. Something comes up, we do some due diligence on it. We spend various amounts of times on any one given program. It kind of is, has been historically, we see something, we don't really like it, we say, "Okay." Then like the next week, someone because we have people, you know, and we find things on our own, but we have a lot of people sending us incomings. We start an... We start the process again. We are always active in that space. Just repeating what Kyle said, Endoxifen is one of the greatest opportunities in breast cancer for patients, and we just wanna get that thing across the goal line. With a follow-on, we've got several questions, additional questions from the tribe as given this access to you today. In building on one of the questions that came in, the Australia (Z)-Endoxifen trial was halted early due to tremendous success, which is likely what garnered the attention of many current shareholders. We eagerly await updates from EVANGELINE. If similar success is out there been early participants, could the trial be halted as well? Can you speak to that? Yeah. The basis for that is when you perform the statistical design part of a clinical trial and set the number of patients, you built into that an expected outcome, which is based on, you know, your previous information. When we did the trial in August in Australia, we used what we expected to be the experience from other drugs in that, and Endoxifen blew it out of the park. What that means is that you can stop the trial early in Australia because you have all the efficacy you're ever going to see. You come to the EVANGELINE trial. Well, guess what we have to do by kind of convention is we have to take that efficacy from Australia and bring it in to the statistical evaluation of the number of patients in EVANGELINE to get the. This meeting is being recorded. That very high level of success. I don't expect to be able to stop the trial early because of that particular finding. The bar effectively gets raised in the trial itself. What it does mean is our data will be extremely robust, should we have the similar results. Okay, great. follow on to (Z)-Endoxifen says, another question is, research into the history of (Z)-Endoxifen shows that previous trials have taken place investigating its effects, not just on breast cancer but desmoid and gynecologic tumors as well. One Phase 1 trial concluded in 2020 was funded by the National Cancer Institute and showed encouraging results. Has Atossa considered seeking funding from the NCI for its (Z)-Endoxifen studies and/or expanding its trials to include other forms of cancer? I think the answer, the short answer is that, yes, the National Cancer Institute is constantly funding both in prevention and in treatment for cancer trials. As all companies in the oncology space do, are looking for opportunities to let them assist in the funding because it's non-dilutive funding. It's not free money, but it's, you know, it's very attractive. As for other cancers, again, if you think about it, when you give estrogen to a cell, 15,000 of the 20,000 transcripts, e-enzyme activities going on in the cell are changed within 15 minutes. Estrogen is perhaps one of the most pleomorphic effectors of cells that we know. We are looking at estrogen-driven mechanisms for other diseases for which blocking that activity, could have a salutary effect like it does in breast cancer. That is probably, that investigation or that thinking is a high priority for us, this year. Okay. Can you also provide us with an enrollment update on the two neoadjuvant trials and an idea of when we expect to see that information? It's kind of the same question, John, so you're not gonna trick me. We can't give you updates on the neoadjuvant trial. We've said when they start, we will give you an update at an appropriate point in time, which is typically a data read. I mean, it's great to know if you've done 20 patients or 15 patients or whatever it is. It's great to know, hey, we're doing a look at the data for the following reasons. Here's the results, you know, what's the next step? As soon as we can, we'll be giving you that information. We understand your interest 'cause it's only a millisecond behind our interest. Got it. Another question is, what is the best-case scenario for a neoadjuvant setting? Is the goal to halt tumor growth or shrink the tumor, or is it more about reducing the risk of a recurrence after surgery? Yeah. No, that's a great question, and it's really quite specific, and I think I gave the answer earlier, which is the home run with the bases loaded for neoadjuvant treatment, is a clinical downstaging of the cancer. The clinicians have numbers and letters associated with the clinical stage of the disease. Sometimes the radiologist can say, "Well, the tumor got smaller, and that's really good." It's the clinician who says, "Yeah, but it didn't change the stage of it." Best case scenario is to downstage cancers, and then that kind of puts them on slightly different pathways for what their ultimate treatment would be. That is every neoadjuvant company's goal for the, you know, the highest level. Okay, thank you. Then lastly, will Atossa pursue the 505(b)(2) pathway for the Endoxifen approval at any point, or is that in the rear view? To understand what that, what that means, just three, there are three, there are three flavors of FDA approvals. 505(b)(1), (b)(2), and J. J is generics. (b)(1) is a brand new drug that the that the FDA's never seen before, and the company owns all of the safety and all of the efficacy data by their ownership. They submit that, and they get approval. 505(b)(2) is a very interesting hybrid where we will own our data, but we're asking the FDA to reference data they may have that we don't even know about with respect to Endoxifen because it's a metabolite of tamoxifen. One of the categories for 505(b)(2) allowance is to be a metabolite of an already approved drug. We check that box. The advantage is we do get credit for the work that's already been done on Endoxifen and/or Tamoxifen that we don't know about that's inside the FDA. There's some market exclusivity issues. We have patents, so that's less important for us, but it still is a nice, you know, have, if we were to, you know, sell the Endoxifen program to a big pharmaceutical company, I'd make a lot of that, of the value of that market exclusivity and the overall transaction, those kind of things. Yeah, we would definitely pursue 505(b)(2). Okay, thank you. This is probably directed more towards Kyle. The question is, what was the rationale for change in bylaws to lower the quorum requirement to 33%, and how does this impact shareholder voting moving forward? Yeah, sure, John. Historically, to achieve a quorum at our stockholder meetings, we needed a majority of the shares represented in voting. We recently reduced that to a lower amount, one-third of the shares. And the purpose is simply to make it easier to establish a quorum so that we can have stockholder meetings. It's to facilitate meetings of our stockholders. It's effective now. It was effective for today's meeting, and it'll be effective going forward. It's simply to facilitate establishing a quorum for our stockholder meetings. Okay. I mean, I think, John, it's actually a response to some of the changes in the way brokerage firms decide how to vote shares and those sorts of things. You know, many companies have some of these challenges because in the last, say, five years, there have been differences in what shares get voted by the brokers versus the owners. Whether if you loan your shares, you don't vote them, and those kind of real technical things. I see. Thank you. The stock currently is under $1. Is there a possibility we could expect a reverse split at any point in order to comply with Nasdaq? Yeah. I'll address that one, John. I mean, our plan to address the stock price is to drive stockholder value with the programs that we're talking about and to, you know, drive stock price movement with, you know, strong results on the things we're working on. That's really what we're focused on. The stock, if it continues to trade under $1 and we get close to the Nasdaq deadline, we'll evaluate doing a reverse stock split then. You know, we'd prefer not to. We'd prefer to drive out of this $1 stock threshold, through, you know, fundamental work here at the company. Got it. Thank you. Well, gentlemen, we're right at the edge. Probably need to be cutting us off, but I want to give you one more chance to sort of, sum up. Dr. Steven Quay, anything that you would like to leave with us at this point, before we sign off today? Yeah. I mean, I think that we've been working on Endoxifen for a number of years. Our patents are starting to be issued. You may see more patents in the area which not just further strengthens our position there. Our activities, both at the Mayo Clinic and at the Karolinska Institutet in Sweden, are beginning to generate, how can I say it, a buzz in the oncology community. One of the very gratifying things for me is to begin to think about working with some of the true, you know, top of the pyramid KOLs with respect to developing this drug. Seeing its increased potential within treatment pathways in breast cancer is truly exciting, and really, you know, justifies a portfolio on a product proposal. Again, I'm a science guy probably at the end of the day, so seeing new opportunities for other estrogen-related processes that Endoxifen may have a role in has been an important part of my time. This meeting is being recorded. Thank you. It's exciting to be, you know, in front of you two today at this point, a company that has significant cash in this market, as we all know, is in a runway for several years. With that, is in a certain power position to look at acquisitions, as we spoke about, to look at developing their respective programs and exciting platform with a very significant with very significant markets that are unmet. It's truly exciting to be in front of you today. Reminders here, folks. This Atossa trades on the Nasdaq symbol ATOS. We wanna thank Dr. Quay and Kyle Guse, the CFO of Atossa today for sharing their insights and addressing many of our questions. Note that the video of this event will be up soon this week at the Tribe Public YouTube channel if you'd like to review any of the comments that they've made in the presentation today. We wanna thank you and, if you have any questions, you can also fire those back at me. If you wanna see Dr. Quay and Kyle back on Tribe at some point, please submit your interest through the wish list process at the Tribe Public YouTube channel. I'm sorry, website, which is www.tribepublic. com. Look forward to hearing from you, and thanks for being the best part of the Tribe. Thank you again, Dr. Quay and Kyle for joining us today. Have a great rest of the week. Thanks, John. Thanks, everybody.