Earnings Transcript for NAVB - Q1 Fiscal Year 2021

Operator: Greetings, and welcome to the Navidea First Quarter 2021 Earnings Call. At this time, all participants are in a listen only mode. A question-and-answer session will follow the formal presentation . As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Jed Latkin, CEO.

Jed Latkin: Thank you. This call is being webcast live on our Website and a replay will be made available. Following prepared remarks, we will be conducting a question-and-answer segment. Navidea’s Chief Medical Officer, Dr. Mike Rosol and the company’s Vice President of Finance, Erika Eves, will be joining me on the call today as well. During the course of this conference call, we will be making forward-looking statements regarding future events and the future performance of the company. These events relate to our business plans to develop Navidea’s molecular diagnostics and immunotherapeutics, which include clinical and regulatory developments and timing of clinical data readouts along with capital resources and strategic matters, as well as the impact of the COVID-19 pandemic on Navidea’s business operations.

Mike Rosol: Thank you, Jed and hello everyone. As always, I'm happy to participate in today's call and provide you with updates from the clinical side. So I'll begin with the progress on our Phase 2b trial NAV3-31 in RA. As I announced on the call two months ago, all patients and all visits have occurred in this study, and we are in the midst of the analysis of the full data set in trial close out. As you know, this trial and the data we have analyzed from it thus far were critical to moving us forward in RA. As a reminder, that Phase 2B is a three arm trial. In arms one and two, we are evaluating the repeatability, reproducibility and stability of our tilmanocept imaging readout in both healthy subjects and in patients with active RA. And in the third arm, we are mirroring the upcoming Phase 3 study to obtain data to help with sample sizing for the Phase 3, and to have a first look at the ability of tilmanocept imaging to serve as an early predictor of treatment efficacy.

Jed Latkin: Thank you, Mike. As you can see, we have a lot going on in all the different areas of the company. So now let's move on to the financial updates with Erika Eves. Erika.

Erika Eves: Thanks, Jed. Total net revenues for the first quarter of 2021 were $124,000 compared to $156,000 for the same period in 2020. The decrease was primarily due to decreased grant revenue related to Small Business Innovation Research grants from the National Institutes of Health and supporting manifest development. That decrease was offset by partial recovery in the first quarter of 2021 of deaths that were previously written off in 2015. Research and development expenses for the first quarter of 2021 were $1.2 million compared to $999,000 in the same period in 2020. The increase was primarily due to net increases in project expenses, including increased tilmanocept diagnostic and therapeutic development costs and increased Tc99m tilmanocept development costs, and will also be offset by decreased employee compensation. Selling, general and administrative expenses for the first quarter of 2021 were $2.2 million compared to $1.8 million in the same period in 2020. The net increase was primarily due to increased legal and professional services, insurance, investor relations services and employee compensation, offset by decreased franchise taxes. Finally, Navidea’s net loss attributable to common stockholders for the first quarter of 2021 was $3 million or $0.11 per share compared to $2.7 million or $0.13 per share for the same period in 2020. Navidea ended the first quarter of 2021 with $7.5 million in cash and cash equivalents. I will now turn the call back over to Jed for closing remarks.

Jed Latkin: Thank you, Erika. As you can see, things are really progressing very well. We finally have a substantial amount of cash on the balance sheet that will help us as we move forward into the Phase 3 and the 3-32 trial, and we remain very excited about what's to come over the next couple quarters. With that, Joe, I'd like you to open up the line for Q&A.

Operator: Our first question is from Jason McCarthy with Maxim Group.

Michael Okunewitch: Michael Okunewitch on the line for Jason. So I'd like to see if you could give just a little bit more granularity on what kind of timelines we should be looking at for some of the upcoming events like the Phase 2B meeting, the full data from the Phase 2B and then the results in atherosclerosis?

Mike Rosol: The analysis of the full Phase 2B is ongoing. What we're projecting is that we should have those fully analyzed. And in parallel, we're working on the clinical study report that was submitted to the FDA. Over the next maybe end of June or early July is what we're hoping for to get this done and get it done well. I think that's reasonable. Then what we'll do at some point in that interval is you then make the meeting request with the FDA. And then of course there's a process there for when they get back to you and set up the meeting. So we'll be a little bit at the mercy of the FDA as well as the guidance, and they've been very good about following their guidances, even as the country emerges from the COVID stuff. So I would anticipate that that would happen, ideally that'll happen in the summer sometime, in the formal summer. So we're going to be working on these things day and night as we are, and we'll try to push these timelines and shorten them as much as possible, but those are probably reasonable. There's quite a bit of data and actually we're learning in a very good way some things and doing some further analysis of the full dataset now from the Phase 2B and there is lots of encouraging stuff coming out of it. And for the FDA briefing that we submitted before, that work of course is very important to getting us to this point and much of that work that we've done, we would have had to do at the end of the road anyway. So preparing that giant 800 plus page document is something that -- it's nice that the bulk of that is behind us and that we can just go out in the final data analysis and discussions from the full data set. So, I think we're in a good place. The FDA feedback was very positive overall. I was really pleased to see that they understood. All the nuances of what we're doing and we seem to be in good alignment with them. And so that's the RA side of things. In terms of the atherosclerosis, I think to be fair, I don't know if they're on the phone. They're probably not, but the MGH folks are probably getting tired of me bugging them, but they're doing a great job. They had one or two subjects, not to get too much into the weeds here, but they've got one or two subjects they've needed to recruit and they just had a number of circumstances happened that those folks haven't been able to make their scheduled appointments. So really they're at the very end of the road in terms of acquiring the full set of healthies, as well as AIDS patients for the trial by interest rate they’ve got almost any day now. And then what they're been doing in parallel was analyzing the data as they collected, both for the SPEC/CT side of things, as well as the CT component, to look at the comparisons of the CT, with the uptake of tilmanocept. And what we've seen so far is it has been very promising. But that should happen soon. I don't want to promise for them. We're not running that study. It's an investigator initiated one, so I can't hold them to task. But they're interested in finishing this up and moving to the next thing as soon as possible, as well as we are. So it should happen pretty soon and we will let you know.

Michael Okunewitch: And I have another one that you might actually be particularly qualified to answer here. I wanted to ask you a bit about the news you put out this morning. How does the unmet need in diabetic nephropathy compare to something like RA, and what's the target market for something like this? Is there similar phenotyping in treatment response angle as you have with RA or is it just more traditional disease monitoring?

Mike Rosol: Well, in terms of the population, I think the number of folks with diabetes, unfortunately, is large and never growing. So I think, there is a wide, large market for kidney monitoring in patients with diabetes, as well as, you saw if you read the quotes and you probably did from the UCFC investigators, there are potential applications in renal cancers as well. And so I think the market, this opportunity is large, the medical need is large, and there's nothing really out there these days to monitor these patients, in particular, the diabetics and in early stage that this potentially could do. In terms of the mechanism. I mean, we are -- I’m not sure you actually asked that, but I'll just say it anyway. It turns out that an important group of cells in the kidney has actually expressed CD206 with so called the mesangial cells. And so tilmanocept, it turns out is taken up by the cells. And we have seen -- it's taken up at quite a good level. And in some of the preliminary work to get to this phase, there's been some promising already in patients who have kidney disease that there's a differential uptake in normals versus patients with kidney disease. So we think it shows a lot of promise and I think it's a very large market. And I'm not sure I answered your last question, if you want to -- if I didn't ask it again and I'll see if I can answer.

Michael Okunewitch: I just wanted to know if there's like a phenotyping and treatment response angle you have with RA or is it just for monitoring?

Mike Rosol: I mean, I think that's a great question, I think the applications will evolve. Initially, the first pass is just to be kind of look to see if the imaging readout can be a predictor of kidney disease, of disease status at a given time point that then would buy you potentially the ability to look early on to see when somebody is crossing over into a type of disease that you're monitoring, so chronic kidney disease in this case. So it'd be maybe an initial kind of surveillance tool for screening and then monitoring these folks over time as they evolve. And then potentially for treatment response, indeed. So if there are therapies out there for either chronic kidney disease or even in renal cancers that may alleviate some of these, then in theory, we should be able to monitor the treatment response as well. But that's further down the road.

Michael Okunewitch: And just one more follow-up on the financial side if you guys don't mind. I’d like to see if you can give us an update on the talks with the investors, the ones that committed at $5 way back in August 2020. If you have any new news on that?

Jed Latkin: We do not have any new news on that. The commitment remains outstanding, that is a ongoing discussion. The focus has been on the $5 million that Mr. Scott committed as well as the continued funding by Keystone. So that is where we're focused for now. Those dollars alone get us to where we need to be on the completion of the Phase 3. But I assure you, we will be taking actions as it pertains to the $5 million at $5 share at some point in time in the near future.

Operator: Our next question is from Mike , a Private Investor. Please proceed.

Unidentified Analyst: The first question pertains more to the 3-31 and what was your meeting with the FDA. Give us any more on -- you said the FDA understood it?

Mike Rosol: So they understood the process of quantitation that we're doing, the predictive capacity of the imaging and how we're looking at that, as well as our clinical assessment targets. And very nicely I might have mentioned this previously, because the flow of RA is so -- RA clinical assessment is so nebulous and noisy as folks embedded in the field like to say, the FDA has allowed and I think even expanded the allowance in a very positive way, the clinical milestone or the clinical targets that we're mapping to, what the heck am I saying? So what I mean is, there are many different ways to assess if a patient is getting better or not in RA, so over time. They've essentially said to us that, you can use the full armamentarium of those different kind of composite clinical assessments just map to one that standardly used are accepted by the folks out there and go with that. And if you can predict that early, then that's a win. And what we're learning is we fully analyzed the Phase 2B data is that actually we're, and this may not be the end of the story, but it's their current status right now. We're actually mapping to what is known as the ACR 50 response very well, and that ACR 50 response, the American College of Rheumatology 50 is a response criteria that rheumatologist think is a very significant one. Because what it means is that a patient is getting better by 50% or more in a bunch of these individual assessments that are performed by the rheumatologist. And so if a patient is getting better in a handful of these assessments by 50% or more, that's considered a significant response clinically and the patient is in a much better place. And we're mapping to that very, very well. In fact, that looks to be our best map. And so that's really good. And so the nice thing about the FDA response is we've collected a whole series of composite scores in our Phase 2b trial, the NAV3-31. And they said, hey, that's great and you might even add a couple in the Phase 3. So I think that's a very good thing. Overall, like I said, when we look through the response, there was nothing that raised any major flags. I think they, they understood our milestones and what we're projecting to. They just want us to come back with the full data set so that we can be sure that the story remains the same. And right now, it's looking pretty good for that.

Unidentified Analyst: So what you're summarizing is they didn't show any hesitancy as to the quality of the data, the results you were seeing, it was more, give us the rest?

Mike Rosol: Yes, exactly. I think that's a fair statement.

Unidentified Analyst: My next question is on 3-32. Has any patient’s biopsy has been done yet, either at Northwestern -- I mean you said not the UK? Has there been any biopsies done at Northwestern yet?

Mike Rosol: No, unfortunately, not yet. They're actively looking. And you know it's not unsurprising for two reasons. It's not awesome. But one thing, it often take sites a while to get things rolling. We see this all the time in clinical trials, it's really not uncommon at all. This is the first one we've done with Northwestern. So they're getting things rolling. They are screening one to two patients per week. The other part that makes it somewhat unsurprising is they're -- I think, especially with the COVID scenario situation, there are maybe people who are less willing to commit to a trial that has this invasive component and come in and do that. But I think that's probably alleviating. They're doing a good job of identifying patients. And I think it's only a matter of time before the floodgates start to open, or at least I hope so.

Jed Latkin: I think it's interesting to note that as the individuals sitting in the room here with me, most importantly, Bonnie and Mike know that when we were doing arm three, every week, I was quite disappointed in the slow uptake at the beginning, but then you sort of had the hockey stick. I mean, we got, one, two patients, it was very, very slow. But to reiterate, I think once they get their feet under it, they really get the knack of the -- going through the patients and going through and screening correctly, I do think that the enrollment will pick up quite nicely. But more importantly, also, with the UK just having gotten going, that's really where we expect to get the lion's share of our patients, because this is something that they've done, it’s something that is more -- they're more used to out there. But just to reiterate with Mike, also, don't underestimate the fact that it is an invasive procedure. It's small but it is invasive. But we do keep on top of these sites and we're going to continue to open up a few more, and really focus on trying to get the patients in as quickly as we possibly we can.

Mike Rosol: The UK -- just to follow up on what Jed said. at the UK is the world leader in this, and he's probably the best at recruiting. So it's very good that he's been able to open up. So sorry, Mike, back to you.

Unidentified Analyst: Can you elaborate further on what the difference is in screening versus the biopsy? In other words, we'll they screen a number of people and bring them back in for biopsy, or those that have been screened are not going to be considered? What does that mean?

Mike Rosol: There's a little bit of both, I mean -- so to meet the criteria, there's an extensive criteria for exclusion or inclusion into this trial like any trial. And in this one, though, identify patients, the rheumatologist will say, I think, this person who's coming in is a possible candidate, they have to meet the inclusion exclusion list. And then additionally, they need to have, for example, specific to this trial but not others, is they need to have what's known as a synovitis score of the certain value and that's basically their -- at least one of their joints has to be inflamed to a certain degree, otherwise, they're not going to be able to participate in the trial. And there's a long and boring story behind that but it's a necessary component for all these biopsy trials. So once they pass the kind of clinical assessment in general, they also then have to do -- if they make it past all those hurdles, they then do an ultrasound to make sure they've got enough inflammation going on in their joint, at least one of their joints, so that we can then biopsy it. So some folks don't even get to that stage, maybe the majority of them. And then there are those who have to make it past that stage. So that -- screening is -- takes more than one visit if the person goes all the way through to maybe a couple of visits for this trial.

Unidentified Analyst: So screening one to two week is a pretty good rate then?

Mike Rosol: Yes, it's actually really good. It is.

Jed Latkin: Remember, also, the patients have to do it for the benefit of science as you can’t just offer them thousands and thousands of dollars. If there's a nominal fee they get, but it's really they're doing it for the good of the overall community. And obviously, once we start getting those patients and things get rolling and they get used to it, as I said, we do expect that enrollments pickup.

Mike Rosol: And we've been working with these investigators in preparation. So none of this is a surprise. So we have planned, as Jed alluded to, we've always had plans to open up multiple sites, both in the UK. We're also looking at a couple of other sites in the United States as well. So we're going to do what it takes to get enrollment happening and rolling as fast as possible. And as Jed mentioned in the NAV3-31 trial, there was a time when we weren't getting patients in and then all the sudden the gates opened up and people got it down and then we, as you might recall, we started actually recruiting at a higher rate than is typical for a pharma company in North America in rheumatoid arthritis. And I imagine we're going to be in the same place again because the team, not me, but the team is including -- led by Bonnie here, is really good at this.

Unidentified Analyst: Well, you do anticipate sometime in the future having an interim assessment of 3-32 if you will be able to share, or you're not that far along here?

Mike Rosol: Well, we're going to. The way we built it, it's an adaptive design in the sense that we're looking at a minimum of four subjects in each of the three subtypes of RA. So once we've recruited those, we'll then look at the data and see how that correlation of the imaging readout to the number and density of the macrophages from the biopsy looks. And based on that look, we will then decide if we're going to enroll more patients or if we have a good enough -- or complete enough story to tell. But because we can't select, so we don't know until we've recruited them. We don't know when we'll hit the four, four and four. We might get lucky and just recruit 12 and all goes great and the data look awesome, or we might have to recruit more than 12 in order to get that four, four, four through the door, pardon the RA, in any event. We will have that interim look, which might be the final look.

Unidentified Analyst: One more last question on the 3-32. From a layman's terminology, what it looks like to me is this biopsy will give you a physical validation, the rheumatologist will then be able to know from when they do the readings and see the quantification data, and there has been a physical test then. So will that give them greater encouragement that what they're seeing on the readings in the images and the quantification has been validated and that kind of the guts of this to give them some certainty?

Mike Rosol: We will have validated it through this study, if all goes according to our hypothesis. We'll have validated that the imaging readout directly relates to the macrophage, which relates to the subtype of RA. So we'll have that linkage from the imaging to the subtype of RA. So optimally, not only will we have kind of a grounding, so little bit of ground truth, just as you're saying that the image represents the pathology. But optimally, we'll be giving them the ability to have a virtual biopsy where they don't necessarily need to do that biopsy, but the image you read out alone can be predictive of the subtype. And from that, there is a growing body of literature that suggests from numerous trials that have happened and are ongoing that different subtypes of RA respond differently to different classes of drugs. So the end goal is to be able to say, from a scan, this is the subtype you're likely to have. These are the classes of drugs that have shown some benefits. These are the classes that don't show benefit. So avoid those. Because the rheumatologists, at the end of the day, they would like some tools that tell them that help guide them for what kind of therapy the patients should be on, because right now it's literally trial and error as amazing as that sounds, because these biopsies are not done routinely, they're never going to be done as part of clinical practice routinely and they're not done at very many centers. So right now, there is no other way to get this information. So if we can give it to them from our scans that would be great for them and for their patients, as well as of course the insurers would like that because they don't want to pay for drugs that are not going to be having an effect. And I can tell you what I've been hinting at is not outright saying is that the data from NAV3-31 are inline with our hypothesis that one of those subtypes of RA, the so called fibroid type, it's known that there aren't many macrophages involved in that subtype. It's also known that those folks don't respond to anti-TNF alphas very well, maybe 80% of them, 75% to 80% receive or achieve a clinical response. What we're seeing in our study matches with our hypothesis that those patients will not have much localization of tilmanocept in their joints. And then therefore, we predict they’re fibroid and if they won't respond without knowing for sure the ground truth, because we don't have the biopsy yet. The ones who look like normals or much like healthies without a lot of localization and NAV3-31, they're not responding 92% of those are not responding to the anti-TNF alphas, that completely matches up with our hypothesis and it's very exciting. When we told our KOLs, our key opinion leaders about this that's what they're jazzed about, the ability to be able to tell early on the subtype, which then gives them information to dive in and what treatment to choose or not to choose.

Unidentified Analyst: But translating this into the next two steps, this one should help also give comfort to minimize any pushback from the therapy providers of anti-TNF alphas. Is that a correct statement or not?

Jed Latkin: That is the correct statement and that's what's important. Because remember, this is going to be at the end of the day provided that this bears out when we get the data this is going to be the key for the insurance companies as the hook to get them to make sure that doctors use this on day zero. Because to be able to eliminate a full class, which is the tier one class, it's very important to have this data and that is something that the KOLs across the board, including those that we've discussed in different areas have said that if this is what it is based on what we've seen in the arm three then that is the real hook that they're looking for. Because something that on day zero eliminates a tier one drug is very important. And if we can do that to the tune of 92% rate that is going to be very, very compelling. And that's why we feel that 32 will be very helpful in guiding how we proceed once we get the approval.

Unidentified Analyst: Will it also translate into giving a higher level of comfort to your marketer, and will be optimistic to say that’s jubilant to move forward with their aggressive marketing plan, because you've mentioned, Jed, that it's going to be a very expensive campaign to get up on the marketing. So it should give them comfort too and give them that the rheumatologist is currently receptive to this?

Jed Latkin: Not to put too fine a point on it. This is it. This is the -- it comes down to this, which is why we've pivoted our discussions for that very reason. Given what we saw in arm three and given the nature of how the data was coming in, we would be foolish to go forward prior to getting this data because the data is something very, very valuable. Remember, the original label, the idea was anti-TNF monitor be able to predict. But if you have that first step where you could knock out 35% to 40%, those with this type of phenotype right off the bat and we can get that on the label right away, well, that's a very, very compelling reason to use it, especially since, as we all know, and as I said, I've given this example a million times, if somebody using the anti-TNF user, I know how these things work. So I do enjoy discussing these with other people. Because if you're aren't in the system and if you're not a product of these biological drugs, you don't understand the hurdles that it takes. And I do and so that's something that's very important. And that's why to have something that can tell you 35% to 40% of the time, on average that it’s just not going to work in those subsets that is a very, very big deal. One of the KOLs we spoke to said right off the bat, well, they weren't a big fan of the whole anti-TNF because the market is definitely changing. The fact is the anti-TNFs though, are the first line. There are biosimilars out there, which are cheaper, the other treatments are more expensive. And if we can eliminate that and allow the insurance companies to have comfort to move on to the next tier, because it's just not going to work that saves the system money that gets people treated better, faster. And it also alleviates other issues because remember, when you start taking an anti-TNF, you put yourself on a time clock, believe me, I know, because I have to get my infusion every eight weeks, if you miss within a few days, your body becomes immune to it. And then you're sort of screwed not to put too fine a point on it. And you don't want to do that. Just like you don't want to start an anti-TNF, if you know it's not going to work, because then that creates other issues in your body, when your body starts producing more TNF to sort of compensate for the changes that the biologics are having on you. And so this is something that is very, very important. And in our discussions with our potential partner, this is something that we have focused on and this is something we remain focused on. And that is why this data will unlock what we feel will be a better overall agreements and that is why we are willing to wait. One, we have the financing in place and two, it’s going to unlock a better, more robust financial package for Navidea.

Operator: Our next question will be from Alan Stone with Wall Street Research.

Alan Stone: Just wanted to -- I was asked by some people just a couple days ago to take a look at your company and put a little bit of reading about over the weekend and yesterday, and sort of to be able to listen to your conference call today. I was wondering, it seems to me like based on the size of the market and unmet medical needs that you have that your share value appears to be probably lower than it should be. And I was wondering if there are other companies in the US, big pharma companies in the US, or Europe that might be doing anything at all similar to the type of discovery that you're looking to create here and the competitive nature of this?

Mike Rosol: I think you're right, the share price doesn't reflect the possible value here that we're bringing to the table, I think possibly -- there are competitive molecules that can target the macrophages. But without being too biased here, there are a few things, a few points to that. One, there's none that I know of that are really being rallied by with a large impetus or large company behind them. But the ones that are being migrated forward in terms of research, again, bias aside, I think this is -- to one of the reasons I'm here, because I did my own due diligence. They have their own deficiencies compared to the tilmanocept molecule that we have. So I think we have some biological advantages that those -- overall, those other molecules that are out there that might be used for assessing disease status, whether it’d be to the macrophage or some of the other cells that are involved in RA. So we have that advantage. We're also way ahead of those folks, even the ones that are being brought up by maybe smaller research groups or with smaller efforts than Navidea has brought to the table. So I don't see -- maybe you will surprise me or somebody else will with something that I haven't, that I’ve missed. But I don't see a large competitor emerging in a short time period. So I think we're going to be good for quite some time in terms of what we're doing. And in terms of other methodologies for assessing this, in the imaging domain where we're the leader, there are those who are looking at different blood borne biomarkers and using machine learning algorithms to predict treatment response either from baseline or overtime. I think from the data that we've seen, we also have advantages over those folks. And I could go into that in some further one on one discussion, whatever I'm allowed to say. But in any of event, there are folks who are looking into it because the market is large but we have advantages over the imaging modality, kind of molecules, as well as I think over these kind of algorithmic based approaches that make us really put us at the forefront of this.

Alan Stone: And just to follow-up on that a little bit. How many potential partners are there for you out there, let's say, in a Phase 3 clinical trials and for licensing types of deals that you could be making out there? How many -- are there -- maybe you could just give us some indication of that?

Mike Rosol: I think that on the RA side, as I guess, we've signed an MOU with one partner who we feel could be a very good long term partner on the RA side. We're very excited by the prospect, especially given the marketing muscle that they could put behind the molecule. But you actually hit on a great point for the overarching theme of what Navidea hopes to become over the next several years. And I think it gets back to where the stock price is, it is not right to discuss that in a call, so we won't. But what I will say is that there have been many years of potential. And it is -- similar to what the usage of the Walter Mondale was the potential for -- the hope, the future of the Democratic Party, and he always will be. But with this, there were a certain key steps that needed to be taken on certain sides of the business that have now been taken, be they formulation, basic chemistry, basic testing, things that were never done in the past but now have been done that will allow us to partner. First off, 3-32 will give us the biomarker support that we need that will allow us to potentially partner in trials with all of the companies that are out there developing new RA treatments. And if you look on trials.gov is that who's who of every single major pharmaceutical is looking at new methods of action, new molecules, be they non-injectables, oral, biologics, different pathways for RA that is very important. But more importantly, the molecule as it will be done in the future as we have made certain key changes that we have not discussed, nor will we at this juncture will make it more compatible to get us to what the original idea was for Navidea, which is to be able to take other products, take other therapeutics and make them better by making them more targeted and delivering them in a better way. The idea of the targeted payload delivery only works when you have the right chemistry, the molecule that is what it says it is. And we are finally at a point, where we have that molecule. This is stuff we have not discussed nor will we discuss. But there's a lot of things going on behind the scenes and we've made a lot of changes and a lot of improvements that will bear out we feel over the next several years that will make this a very compelling and very interesting company, which is why we think we are so fundamentally undervalued. Because for many years there was promise, but there was no delivery. For many years, there were discussions about certain parts, but no poster presentations. As we've discussed, we'll have one this week and it is something that we are very, very excited about. Because we finally have taken the key steps to really get us in the right place, things that hadn't been done in the past. So we do feel that on that side of the business, there are very many potential partnerships, but that will come in time. And I am not going to tell you today, I'd be lying if I did, that you can expect something tomorrow or even in the next several quarters. But we are taking the right steps. We are finally going step by step as we're supposed to and as you are supposed to develop a product. And now that we've done that, without discussing and this is stuff we've done over the last several years, we are really, really excited to start putting that into action over the next several quarters and years to come.

Operator: We have another question from Mike , a Private Investor.

Unidentified Analyst: I have one last question. Can you highlight anything that we will see as investors in the Frontiers Symposium abstract that will be very encouraging, or do we have to wait to see abstract?

Mike Rosol: I think, I mean, I've touched on it in my little preamble to the abstract today. So I think it's okay. I think, what you'll see is that we have accumulated evidence of our mechanism of action, which I think is obviously very important for therapeutic. And we've shown that, we can change the phenotype of macrophages with our construct, drive them from one type to kind of the so called force field type that is protective in the cases of cancers, for example, to more inflammatory type that actually rallies the body’s immune system against the cancer. So that's something you'll see some fundamental data on. And you'll also see data from one of the tumor models that we've run in rodents where we've shown that our drug actually in a type of tumor that is moderately responsive to an approved therapy. So an already approved checkpoint inhibitor therapy, generally as it’s class of humans, we actually show that we can make that therapy better, at least from the data showing that the tumor growth reduction is increased when our drug is used in concert with that approved drug. I want to emphasize that and that's why I'm emphasizing it, that it's an already approved drug that we actually appear to make perform better in terms of it’s tumor response in a number of animal models. And you're going to see that in one of those. And what we're doing now, as I also mentioned on the call is, we're engaging with a contract research organization, the one where we ran some of the studies in rodents, to look at different dosing, both amounts of our construct as well as delivery time points related to that other approved drug and in other cancer type, just so that we can hone in on this and perhaps maximize the efficacy of this synergistic response. So in a nutshell, you're going to see some fundamental mechanism of action, as well as some proof of concept in a relevant rodent model, all of which is critical to moving forward into possible first in inhuman.

Unidentified Analyst: Was the improvement in the rodent model significant in your view?

Mike Rosol: I wouldn't mention it if it wasn't statistically significant. So it is indeed statistically significant. And again, I want to emphasize that that model was chosen specifically because even the approved therapy is not super duper responsive, we wanted to give ourselves some dynamic range to show that we're actually having an synergistic effect and we indeed saw that. So it's very encouraging.

Jed Latkin: I think that's all we have time for. So I just want to thank everybody for dialing in today. We look forward to hopefully some news over the next couple of months as certain key items for the company come to fruition, we are expecting over the next several months. And I look forward to speaking to all of you guys soon in near future.

Operator: Ladies and gentlemen, this ends today's conference. You may disconnect your lines at this time. Thank you very much for your participation, and have a great day.