Atossa Therapeutics, Inc. (ATOS) Earnings Call Transcript & Summary

Good morning, everyone. This is John Heerdink. I am the Founder and Managing Director of Tribe Public. Thanks so much for joining us today. As many of you know and that have joined us in the past, we are a group that gets together across the world through webinar-based events, and now since we're pushing forward post-COVID, if you will, we have started to do live events on the West Coast again, where we bring forward the CEOs of the companies that the Tribe cares about through our Wishlist process at tribepublic.com. Note that I also run an investment adviser club, Vista Partners. Vista Partners is an investor in Atossa. Please review our full set of disclaimers at both sites as we also work as an adviser to Atossa and have done so over the last couple of years, and we're excited to have our speakers today for our program, which is going to 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, and the event title today is Atossa Therapeutics: Redefining Breast Cancer Prevention and Treatment. Again, this will be posted by the world-renowned scientists 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 and 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, picture in for this event, and he'll be addressing some questions. A 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 5 pharmaceutical products that have been approved by the FDA. Dr. Quay became an MD in 1977 and a PhD in 1975 from the University of Michigan. He 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 as well as the qualifications as physician and a principal researcher overseeing the clinical regulatory development of the company's pharmaceutical programs. Thanks again for coming to this event. And why don't we get started straight away. And we'll start asking some questions from Dr. Quay, but maybe, Dr. Quay, can you give us a little bit of background on how Atossa was started?

Sure. Well, so 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 to atypical to carcinoma in situ, and then the Pap test [indiscernible] took the incidence of cervical cancer from 110,000 a year down to about 15,000 a year. We now know that a virus is involved, there's a vaccination for it. So we're basically looking at the elimination of cervical cancer. So over a decade ago, I said, why can't we do the same thing with breast cancer? And the key process, the 2-step process is, what do you measure before you have cancer in the breast? And can you modulate the changes that are going on, the biology has going on before it crosses the line and becomes cancer. And so 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, so when you do a mammogram, you're really looking for grains of salt, little salt grains, which represent dying cancer. So that's what the mammogram was developed for, is there a cancer or is there not a cancer. And then 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, just with the women that are all white tend to have about 8 to 10x more cancers. So that's exactly the analogy that was done with the cervical Pap smear. So with that backdrop, we're now saying, well, can we modulate those women with high density? Can we make the density lower? And for lots of reasons, we think that is a biologically tunable property. And so the clinical trial we're doing in Sweden, Karolinska Institute, the place where the Nobel Prize is awarded, is looking at exactly that. A woman with high density, if she takes endoxifen or placebo for 6 months, will she see a change with endoxifen, not with placebo. And then if you wait 18 months off of drug to see if it's durable, does the density reduction stay down. So it's probably, as you say, I've invented 5 drugs, they have been used in 80 million people, but this program to 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. And as I've always been very excited about the program [indiscernible] very close to home, as you know, when we originally met, my mom was tripping with the situation in breast cancer and is surviving and still is today, but this unaddressed need here is -- there's still work to be done, and I'm so happy to hear that you're going to continue on this work on this path. So the company, as I understand it, has transitioned from early detection to prevention and treatment. Can you give us an overview of Z-endoxifen, your proprietary Z-endoxifen?

Sure. So 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, then what you want to do is find something that blocks the estrogen. Tamoxifen is the classic example of that. And it's 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, if you will. And so 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, we quantified, probably 95% of the effect. So 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 assay-sensitive, and it gets destroyed by the stomach acid. So we have 2 complementary patents on the white powder as it were and how you would tabulate it to allow us to really push the frontiers of what endoxifen can do. The buzzword in biotech is having a pipeline and a product, and some people have to kind of stretch it. But I think if you see our programs from prevention of breast cancer to neoadjuvant treatment to adjuvant treatment, we really do -- we really are bookending breast cancer. And by the way, there are some other conditions in the body that are estrogen-driven that we may explore.

That's exciting. It's truly a platform to really build an amazing company off of it, and it's exciting that you continue to find ways to carve out a significant IP portfolio as well around endoxifen. If you could continue with -- as you mentioned, as you're investing in using endoxifen in 2 settings, neoadjuvant and mammogram density -- breast density, which is more of a breast cancer prevention plan? Can you explain both again?

Sorry, I didn't hear that. You broke up technically.

Yes, I'm sorry. I said -- basically, what I'm looking for is can you explain in the 2 settings, neoadjuvant treatment and mammographic breast density, which is more of a breast cancer prevention plan? Can you explain both?

Yes. So treatment of density, because high density is a condition that is not cancer, but women that haven't have a very high incidence of 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 there's -- if it's needed, for local disease. So that window can be as short as about 3 weeks or as long as 6 months in some settings. And it's kind of ironic that the 2/3 to 3/4 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 in tamoxifen, 6 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 4 hours, you have blood levels and within 24 hours, you have therapeutic blood levels. So basically, a woman can go from a needle biopsy of a lesion. The bad news is it's cancer. The good news is, here's a prescription, go to your pharmacists and start taking endoxifen because we think, based on what we hope, what Atossa's clinical trials will show, we think that this will stop, slow down the tumor, maybe shrink it before we even get to surgery. So 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. And so that's kind of our focus. Now there's a corollary focus, which is that breast cancer can occur in women in 2 stages of their life, premenopausal, postmenopausal. So in the postmenopausal case, the ovaries have stopped making estrogen, there's a little bit of estrogen made in the breast itself, and so 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. So if you go in with a modest suppressor of estrogen, what happens is the ovaries overpower that and you get ovarian activity. So there's a protocol called ovarian suppression, which is common in premenopausal women in the neoadjuvant setting, and it's pretty harsh in terms of quality-of-life issues. It's really -- the women really don't like it. Sometimes they will actually risk getting cancer rather than stay in compliance in that particular protocol. So the other setting we're trying endoxifen is because it is such a strong suppressor of estrogen activity itself, we believe that it will work in a premenopausal women without ovarian suppression, which would be [indiscernible] for these women in terms of their quality of life.

Yes, that would be fantastic. Could you also speak to the sort of "market size" or the patient population size in the U.S. for -- in both of these settings?

Yes, well, sure. So they're big numbers. So in terms of density reduction, we start with a number that there are 39 million to 40 million mammograms each year done in women. And that's about 80% of what we think should be the right number. So women are much better than men, frankly, and that's a whole separate conversation on their own health. And so we're getting about 80% of women who should be getting mammogram, are getting it. And that's because there's a lot of financial support and programs and education around getting your annual mammogram. So 40 million is your total number there. And upwards of 10 million have high density. And so when you combine that with maybe a couple other risk factors, you get millions of women who would be candidates for a 6-month treatment to reduce their density, which then we believe will help downturn effects on incidence of cancer. In the cancer setting itself, about 0.25 million women in the U.S. are getting cancer each year, 2/3 to 3/4 of those are estrogen receptor-positive. So that's 200,000 is a good number to imagine, is the treatment. So those women are going to go through neoadjuvant, they are going to have surgery, they are going to have radiation and then they're going to have 5 years of follow-up adjuvant therapy. So the ER-positive population is roughly 200,000 plus 5 years of 200,000 or about 1 million women in the U.S.

Great. 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 II trials. Can you tell us about the studies that you're currently conducting, EVANGELINE?

Yes, sure, sure. I mean the study in Sweden is a placebo-controlled trial. It involves 240 women in groups [indiscernible]. The treatment is 6 months, and they either get a sugar pill or endoxifen, Nobody knows what they get. One of the surprise, 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. So 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. And so in a population that doesn't have breast cancer, you're trying to reduce your incidence in the future, your tolerance for sort of quality of life or side effects is not very high. And so one of the things that we thought we would have an issue with endoxifen was a similar pattern of side effects. And knock on wood, we don't see the same incidence of what we call vasomotor symptoms, which are night sweats [indiscernible] basically. We will see those with endoxifen at nearly the level you do with tamoxifen, and it's a remarkable difference. So again, at this point in time, early days in our clinical trials, but that's a really beneficial process. The process is a baseline mammogram, mammogram at 6 months, mammogram at 24 months. And the 3 of those are used to look at the trajectory in these women of whether there's a dramatic drop between the first and the 6-month one and whether a drop, if it occurs, is maintained out for 24 months. There really is -- we do have some preliminary data in like 20 or 30 women, where if you do see a reduction with tamoxifen or other drugs like that, it seems to be pretty durable in about 85% of women. So we're expecting that to be successful, but science is science, and that's why you have to do it before you can opine on it completely. But looking at the durability will be an important factor. From a business point of view, a lot of companies want to have a drug that they give alone for their entire life or patients for their entire life. And that's a business model, money-making business model. We think here the best care, maybe as 6-month process. And that's exciting from a physician's point of view because women shouldn't think about their breast health unless she has a family history and until she is 40, she has her first mammogram and she has high density, not great, not the best day of our life. But with a 6-month prescription, if it goes down and if it stays down, we can really change their whole future and perhaps give them a 20-year window of reduce the risk on breast cancer. I work 20 or 18 out of the hours in the day, and this is -- these concepts and this opportunity is what gets me out of bed [indiscernible].

Thank you. Could you give us a little bit more of the specifics on how you structured your trials here, EVANGELINE and also [indiscernible] endoxifen studies?

Yes. Well, I guess, I'm not quite sure what you're saying, but all placebo-controlled trials have a randomization process that dictates which particular pathway that the patients go down. And then you're kind of low to ever break the blind. And so we -- we've talked about it with one particular patient who had some interesting things that we wanted to -- should 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 [indiscernible] conducting in other centers, again, is a randomized process to endoxifen or to ovarian suppression, which is standard of care right now. There is what we call a PK run-in. So we know what blood levels are most effective for various things with effect to endoxifen because there's so much experience around them. So what we're doing is a PK run-in where we get 3 to 4 weeks of drug in the women and then we measure their blood levels. And if they're too low, we have a protocol where we go up a dose; too high, we go down a dose. And this process is, we're making progress on this, and this will really define the next stage where we'll just do one dose, placebo versus active for about 6 months. And the hope there is to nominally suppress [indiscernible] the estrogen is reduced, but perhaps get down-staging of the cancers. So the ultimate 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 more plastic surgery-like. And so that's one of the -- that's sort of, again, the ultimate outcome. So that's the design, John.

Okay. Thank you. On EVANGELINE trial, I believe you had your first patient enrolled in February of this year. Is that correct? And I think you're trying to pull from, is it 25 sites in the U.S.?

Yes, yes. And we continue to add sites. It's -- clinical trials are really complicated. So having a site say, yes, we'd love to enter your trial and then doing their first patient. There's 3 feet of paperwork or 2 feet of paperwork and meetings and all sorts of things and teams. So we're making good progress on that. We'll give you updates when we feel it's appropriate and in terms of the recruitment process. So we're feeling comfortable with where we're at in that trial.

Well, we've seen -- I guess, again, the treatment on the EVANGELINE is treated for up to 6 months prior to surgery? Is that correct?

That's correct.

That's correct. So you've been looking forward to seeing that progress and all of this revealed as we move forward this year and beyond. So 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. Can you speak -- one of the things that's important to many investors is that you have a solid patent protection. Can you speak to that?

Sure. Yes. I want to just correct you, I have 88, not 87 patents, but who's counting [indiscernible] very important for pharmaceuticals. And they're really -- I mean, one of the -- I won't get too philosophical, but one of the only ways that a tiny company like this could ever expect to compete with [indiscernible] of the world, is this patent system, and it allows us to get value for our shareholders from our inventions because the government stands in the way of people, simply being so big, they can just come in and take our stuff, so to speak. So I know there may be some 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 3 areas in pharmaceuticals. You want to have the composition, the chemical itself, so just by doing 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, so those are a little more complicated because you have to prove infringement going into the factory, but we have those kind of patents. The -- once the drug is made, it sometimes can be formulated in a patentable way, and that turned out to be the case for endoxifen, so we had to make it enterically stable so that it didn't convert from Z-endoxifen to a mixture of Z&E, which it wants to do [indiscernible] and the E-form is completely inert. So you can get -- you lose 50% of your drug in 40 minutes if you don't use the patented process. And the FDA is not going to allow you to ever not use our patented processes. And in many cases, then the final stage is that you can get methods of treatment where basically it's the doctor who's doing the infringement. So a method of treating breast cancer, the steps consisting of identifying [indiscernible] and then treating with endoxifenn. So that's been our strategy. We are, I think, among the best in patent strategies. I've had 5 litigations [indiscernible] 5 of them, multimillion dollar settlements for people that thought they could just steal my stuff, and we had to show them that in the court system, that was not the case.

Exciting. Well, switching gears a little bit. What's also important to investors is to understand how you're funded? Can you speak to how the company is capitalized to date and your current burn?

I could speak to it, but Kyle Guse can do a better job. So I'll let him.

Fair enough.

Thanks, Steven. Thanks, John. Yes, Atossa is, I'll say, 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. And as a result, at the end of 2022, we had over $100 million in the bank. To put things in perspective, that's multiple-year of cash for Atossa. So you'll notice our auditors do not have a qualification for [indiscernible] concern for Atossa, which is very common in small biotech companies. So that's our funding situation right now.

Okay. And can you speak to the historic burn?

Yes. Yes, John. We historically have burned $1 million to $2 million in cash per month. Yes, that would go up a little bit as we continue to enroll in these Phase II clinical studies that Dr. Quay was talking about, but that's sort of our historic burn rate. So we feel very confident about our cash position.

Okay. Well, with that significant cash position, what -- 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 venture capital backed CAR-T company here in the United States, acquired a 19% interest in them. And so we're constantly evaluating other opportunities. The challenge is finding something that's as exciting as the things that we're working on. We don't want to dilute our pipeline and our programs by acquiring something that's not as compelling as what we have. So we've set the benchmark pretty high, but we are opportunistic.

Yes. I guess [indiscernible] Kyle knows this because [indiscernible] the investors should imagine that we probably on any given day, have one potential acquisition or a program that we're looking at. And that's kind of in system since probably maybe July or June of last year. So something comes up, we do some due diligence on it, we spend various amounts of time on any one given program [indiscernible] historically, we see something, we don't really like it, we say, okay, and then like the next week, someone -- because we have people and we find things on our own, but we have a lot of people sending us incomings, we start the process again. So we are always active in that space. But just repeating what Kyle said, endoxifen is one of the greatest opportunities in breast cancer for patients, and we just want to get that thing across the [indiscernible].

Just with a follow-on. We've got several questions -- additional questions from the Tribe that has given this access to you today. Building on one of the questions that came in is, says the Australia Z-endoxifen trial was halted early due to tremendous [indiscernible], which is likely what garnered the attention of many current shareholders. As we eagerly await updates from EVANGELINE, if similar success is out there with the early participants, could the trial be halted as well? Or can you speak to that?

Yes. So the basis for that is when you perform the statistical design part of the clinical trial and set the number of patients, you built into that an expected outcome, which is based on your previous information. So when we did the trial in Australia, we used what we expected to be the experience from other drugs in that and endoxifen blew it out of the park. So 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. Now 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 into the statistical evaluation of the number of patients in EVANGELINE to get the results. So the number of patients is baked in to that very high level of success. So 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. But what it does mean is our data will be extremely robust, should we have the similar results.

Okay. Great. Follow-on to Z-endoxifen. Another question is, research in the history of Z-endoxifen shows that previous trials have taken place, investigating its effects not just on breast cancer [indiscernible] gynecologic tumors as well. [indiscernible] trial completed in 2020 was funded by the National Cancer Institute and showed encouraging results. Has Atossa considered seeking funding for the NCI for its Z-endoxifen studies and/or expanding its trials to include other forms of cancer?

Yes. So 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. And 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 very attractive. As for other cancers. So again, if you think about it, when you give estrogen to a cell, 15,000 of the 20,000 transcripts, enzyme activities going on in the cell are changed within 15 minutes. So estrogen is perhaps one of the most pleomorphic effectors of cells that we know. So 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. And 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 2 neoadjuvant trials and an idea of when we expect to see that information?

Yes. It's kind of the same question, John, so you're not going to trick me. We can't give you updates on the neoadjuvant trial. We said when they start, and we will give you an update at an appropriate point in time, which is typically a data read. So I mean, it's great to know if you've done 20 patients or 50 patients or whatever, but it's great to know, hey, we're doing a look at the data for the following reasons, here's the results and what's the next step. So as soon as we can, we'll be giving you that information. We understand your interest because it's only a millisecond behind our interest.

Got it. And another question is what is the best-case scenario for neoadjuvant setting? Is the goal to halt tumor growth or shrink the tumor? Or is it more about reducing the risk of recurrence after surgery?

Yes, 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 down-staging of the cancer. So the clinicians have numbers and letters associated with the clinical stage of the disease. And so sometimes the radiologist can say, well, the tumor got smaller, and that's really good, but a clinician says, yes, but you didn't say it didn't change the stage of it. So best-case scenario is to down-stage cancers. And then that kind of puts them on slightly different pathways for what their ultimate treatment would be. So that is every neoadjuvant company's goal for the highest level.

Okay. Thank you. And then lastly, will Atossa pursue the 505(b)(2) pathway for Z-endoxifen approval at any point [indiscernible]?

Yes. To understand what that means, just there are 3 flavors of FDA approvals, 505(b)(1), 505(b)(2) and 505(j). 505(j) is generics. 505(b)(1) is a brand-new drug that the FDA has 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. So one of the categories for 505(b)(2) allowance is to be a metabolite of an already approved drug. We checked that box. And the advantage is we do get credit for the work that's already been done on endoxifen and/or tamoxifen and we don't know about that inside the FDA. And there's some market exclusivity issues. We have patents, so that's less important for us. But -- it still is a nice [indiscernible] if we were to sell the endoxifen program to a big pharmaceutical company. I make a lot of that of the value of that market exclusivity and the overall transaction, those kind of things. So yes, we would definitely pursue 505(b)(2).

Okay. [indiscernible]. 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?

Yes, sure, John. So 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, 1/3 of the shares. And the purpose is simply to make it easier to establish a quorum so that we can have stockholder meetings. And so it's to facilitate meetings of our stockholders. It's effective now, it was effective for today's meeting, and it will be effective going forward. And so it's simply to facilitate in establishing a quorum for our stockholder meetings.

Yes. 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. So many companies have some of these challenges. Because in the last, say, 5 years, there have been differences in what shares get voted by the brokers versus the owners and whether if you loan your shares, you don't vote then and those kind of real technical things.

I see. Thank you. The stock currently is under $1. Can -- is there a possibility we can expect a reverse split at any point in order to comply with NASDAQ?

Yes. 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 drive stock price movement with strong results and the things we're working on. So 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. But we prefer not to. We prefer to drive out of this $1 stock threshold through fundamental work here at the company.

Yes. Thank you. Well, gentlemen, we're right at the edge, probably need to be cutting yourself, but I want to give you one more chance to sort of sum up, Dr. Quay, anything that you would like to leave with us at this point before we sign off today?

Yes. So 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 just further strengthens our position there. Our activities, both at the Mayo Clinic and at the Karolinska Institute in Sweden, are beginning to generate, how can I say, a buzz in the oncology community. So one of the very gratifying things for me is to begin to think about working with some of the true, top of the pyramid KOLs with respect to developing this drug. Seeing it's increased potential within treatment pathways in breast cancer, is truly exciting and really justifies a portfolio on a product proposal. And 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 late last year, this year, more into the year of the future. So I'll just reiterate, I mean I really don't want to reverse the stock. We think we have so much value in what we have that you know about and what we have that we'll be enrolling out as in a staggered process and appropriate process over the next year or two, that I think the true value that when people can see what we have will be expressed in a stock price that's much higher than 60 cents a share.

Thank you. It's exciting to be 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, an exciting platform with a very significant markets that are unmet. It's truly exciting to be in front of you today. Again, a reminder to you folks. This -- again, Atossa trades on the NASDAQ symbol, ATOS. We want to thank Dr. Quay and Kyle Guse, the CFO of Atossa, today for sharing their insights and addressing many of our questions. And 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 want to thank you. And if you have any questions, you can also fire those back at me. And if you want to see Dr. Quay and Kyle back on Tribe at some point, please submit your interest through the Wishlist process at the Tribe Public YouTube Channel -- I'm sorry, website, which is www.tribepublic.com, and look forward to hearing from you and thanks for being the best part of the Tribe. And thank you again, Dr. Quay and Kyle for joining us today. Have a great rest of the day.

Thanks, John.

Thanks, John. Thanks, everybody.