Navidea Biopharmaceuticals, Inc.
Q3 2020 Earnings Call Transcript

Published: 12 Nov 2020

[Operator:]

Greeting and thank you for standing by, welcome to Navidea Biopharmaceuticals' Q3 2020 Earnings and Business Call. During the presentation, all participants will be in a listen-only mode. Afterwards we'll conduct a question-and-answer session. This conference is being recorded, Thursday, November 12th, 2020. And now I'd like to turn the conference over to Jed Latkin, CEO, COO, and CFO. Please go ahead.

[Jed Latkin:]

Thank you, Scott. This call -- first off, I just want to say that this call is being webcast live on our website ir.navidea.com and a replay will be made available. Following prepared remarks, we're just going to do a Q&A as well as always. During the course of the 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 currently running Phase 2b trial in RA. As you know from earlier updates, the trial is completely enrolled, with only the latter half of subjects in arm three continuing to have their longitudinal imaging and clinical assessments as outlined in the study protocol. As a reminder, this 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 healthy subjects and patients with active RA. And in the third arm, we are mirroring the upcoming Phase 3 study in order to enable us to obtain data to help with sample sizing for the Phase 3 as well as to have a look ability of tilmanocept imaging to serve as an earlier predictor -- an early predictor of treatment efficacy and the monitoring tool. As we have discussed and presented in the past, the interim results to-date on all three arms have been very positive. We have data demonstrating that technetium 99m tilmanocept, can provide robust quantitative imaging and healthy controls and in patients with active RA that this imaging is reproducible and can define joints with and without RA involved inflammation, and that tilmanocept imaging can provide an early prediction of treatment efficacy of anti-TNF alpha therapy. This month, we presented the positive interim analysis results of arm three at the American College of Rheumatology's annual meeting. The last couple of months, we have focused quite a bit on the due diligence process with Jubilant. This has been a large effort and taken a great deal of time, but this has also allowed us to continue to analyze the full six month longitudinal data on the first half of subjects in arm three. We believe these data will make an even stronger data set to bring to the FDA in order to support our design and objectives for the upcoming Phase 3.

[Jed Latkin:]

You know, it's more important that my remarks be brief, since I don't have much to say. Dr. Rosol, thankfully has a lot to say because of the tireless efforts of his team, which we'll get to at the end of Joel's part. So, Joel, why don't you give us the financial rundown, please?

[Joel Kaufman:]

Thank you, Jed. Total revenues for the third quarter of 2020 were $268,000 compared to $237,000 for the same period in 2019. Total revenues for the first nine months of 2020 are $696,000 compared to $539,000 for the same period in 2019. The increases in revenue were primarily due to increased grant revenue related to SBIR grants from the National Institute of Health supporting the Manocept development. Research and development expenses for the third quarter of 2020 were $1.4 million compared to $1.8 million in the same period in 2019. As third quarter decrease was primarily due to net decreases in drug product expenses, including decreased Manocept diagnostic and technetium 99 tilmanocept development costs coupled with decreased employee compensation. R&D expense for the first nine months of 2020 were $3.7 million compared to $3.6 million in the same period in 2019. The year-to-date increase was primarily due to net increases in drug product expenses, including increased Manocept diagnostic development costs, offset by decreased Manocept therapeutic and technetium 99 tilmanocept development costs, coupled with increased employee compensation. SG&A expense for the third quarter of 2020 was $1.8 million, compared to $1.5 million in the same period in 2019. The third quarter increase was primarily due to increased legal and professional services and employee compensation, offset site decreased travel, insurance and depreciation costs. SG&A expense for the first nine months of 2020 were $4.9 million compared to $5.1 million in the same period in 2019. The year-to-date decrease was primarily due to decreased travel, legal and professional services, insurance, depreciation and Investor Relations related costs offset by increased employee compensation and franchise taxes. Navidea's net loss attributable to common stockholders for the third quarter of 2020 was $3.3 million, or $0.13 per share compared to $3.1 million or $0.17 per share for the same period in 2019. Navidea's net loss attributable to common stockholders for the first nine months of 2020 was $8.4 million, or $0.37 per share, compared to $8.2 million or $0.62 per share in the same period in 2019. Navidea ended the third quarter of 2020 with $3.7 million in cash and cash equivalents. Since September 30, 2020 the company has received $700,000 of cash related to the August 2020 funding transactions. And I will now turn it back to Jed for closing remarks.

[Jed Latkin:]

Thank you, Joel. Before we turn to Q&A, I just want to once again thank the clinical team for the tireless work in these very trying times. They are in the office every day wearing their masks, and driving the trials forward. They also take the time to hit the road constantly to do their site visits regardless of the risk to their health. And words can express my continued appreciation of all of them from Bonnie, Dave and Rachel all the way down to our interns. With that, I would like to turn it over to Scott to open up the Q&A.

[Michael Okunewitch:]

Hey, guys. Thanks for taking the question. This is Michael Okunewitch on the call for Jason.

[Jed Latkin:]

Hey, Michael, how you doing?

[Michael Okunewitch:]

Good. How are you doing, Jed?

[Jed Latkin:]

Good. So we're thankfully we're chugging along here. It's good.

[Michael Okunewitch:]

Yeah, no, as I said, it's a good result. Congratulation. I like to see in the quarter, a bit more about the subset of patients where the baseline result can be predictive of the non-responsiveness. What are the characteristics of these patients? And how does the tilmanocept signaling vary between patients who respond versus those who want a baseline?

[Mike Rosol:]

Sure. Great question. So, this is Mike Rosol for the record. Hey, nice to speak to you. So there are thought to be three general subtypes of rheumatoid arthritis, right, at least according to one classification scheme. Those subtypes are the myeloid, the lympho-myeloid and the fibroid pauci-immune. One of the main distinguishing characteristics between those different subtypes is the amount of macrophage involvement in the rheumatoid arthritis pathophysiology for each of them. With the lympho-myeloid, and the myeloid being macrophage rich rheumatoid arthritis and the fibroid pauci-immune having a much lower level of macrophage involvement. So, our molecule or radiopharmaceutical, tilmanocept, of course, targets with very high affinity, the activated macrophage. So you might say to yourself, oh, my golly, those fibroid pauci-immune maybe you're not going to build image to them. And that'd be bad for you, right? Because you're looking at the macrophage, and you just told me there aren't that many? Well, it actually turns out that this could be tremendously important for rheumatologists and their patients in a good way. And so, the thing is, right now, there's no way to distinguish those different subtypes what type you as an RA person might have, no way at all, unless you do a synovial tissue biopsy. This is something that it’s not done everywhere. It's only done at research institutions. There's no way it's going to be standard-of-care. And it has its own deficiencies in terms of accuracy and sensitivity. So what we think is our hypothesis is this. Since we are measuring our radiopharmaceutical is imaging the macrophage, we would expect that RA subjects who have RA as diagnosed by all the other hallmarks of RA, those who have the fibroid or the pauci-immune subtypes, those scans with tilmanocept will likely look more like a healthy subject or a normal person than the other two that have a lot of macrophage involvement and likely would have a lot of localization of tilmanocept, right. So, it turns out that the fibroid subtype, there's a growing body of literature suggesting that that subtype in particular does not respond well to anti-TNF alpha therapies at all. And that makes sense, because really in the main pathway of the anti-TNF alpha therapies is the macrophage. So it makes sense that those fibroid subtypes are likely going to be enriched or full of the non-responders. And so our hypothesis, as I mentioned has been that our first scan, the baseline scan, before there's any changes of a patient with the fibroid pauci-immune subtype will look much more like a healthy person. And we would then predict based on that scan alone, that they are much less likely to receive a benefit of an anti-TNF alpha therapy. Now, in the small numbers that we've looked at so far, 16, and we actually have others kind of accumulating along the way, I can tell you that we do see a different -- at least a couple of maybe three different populations of localization accumulation in these patients that we're imaging. And for sure, we think we can divide them at least into the very little macrophage activity and those who have much more macrophage activity, right, because we see roughly a third or so a little bit more of the patients look more like normal, and then maybe two thirds or a half look like they have significant localization in certain joints, right. And I should mention that the distribution of those different subtypes across the populations is roughly across the population of RA subjects is roughly thought to be about a third, a third, a third, maybe more, maybe 40% of the fibroids, it depends on what paper you read and who you ask. So we're seeing about that number of patients in our scans who look more like the normal. And guess what we followed them to 12 and 24 weeks after they were put on their anti-TNF alphas, and most of them don't respond. And so that is accumulating evidence that our hypothesis is going to hold to be true. That just at that baseline scan, if you look more like a normal, you're likely to be a fibroid pauci-immune, and you're less likely to respond to the anti-TNF alphas. So our data are accumulating that support that. Now the NAV3-32 Phase 2b study where we're doing synovial tissue biopsy, as well as imaging will help establish that with ground truth, where we will not only be looking at the number and the density of the macrophages in the joints by sampling those joints with a needle, but we'll also have the rheumatologists then classify those cases as one of those three subtypes. To me, it's much more important to look at the correlation with the actual number and density macrophages than it is to worry about the subtype naming. What I think we're going to be able to do is say, look, your scans show you look -- you've got all the signs and symptoms of RA, you’ve been diagnosed, the scan at baseline looks pretty normal, you're probably a fibroid type, or at least you're a subtype, whatever we call it, we could call it out. You're a subtype that doesn't have a lot of macrophages. You're less likely to respond to an entire class of drugs. And so we don't have to go through all of those where you might be, you're going to be wasting money; the insurer is going to be paying for drugs that aren't likely to be benefit to you -- of benefit to you. You might have side effects because these are serious potent drugs. We're going to forget all those. And we're going to put you on something else which has a higher likelihood of success. I talked a lot. Did I answer your question? Maybe I missed some things.

[Michael Okunewitch:]

Yeah, no, thanks. It's kind of my hunch is that it was going to be really what we find out in that 3-32 study, but you're seeing some initial signals from this.

[Mike Rosol:]

Yeah. You got it.

[Michael Okunewitch:]

So I'm just like to see if you could give it a highlight what you're seeing in the patients who don't get a predictive result at week five. Are these patients not demonstrating a reduction in tilmanocept update value at week five, but then they are responding in week 12 or 24? Is really that a question of the test not detecting patients who are responding or is it that the patients taking longer to display a response?

[Mike Rosol:]

Yeah, that's a good question. So here's my view, which is somewhat biased, but I tried to base it in fundamental facts. So the way it is determined that somebody is responding to or not to any therapeutic an RA, these are done with composite assessments and these consist of a variety of semi objective to subjective things. For example, the rheumatologist will look at a patient's hand joints, the wrists, their elbows, their shoulders, and say, are they swollen or not and they will do a count of those, the ones that are swollen. There are 28 joints in particular that they look at. They will also then squeeze those joints and say, Does that hurt? Does that hurt? Does that hurt? So there you can see immediately that there are going to be subject, there's a subject of nature to those. The other kind of two main components that are used in these assessments are a global assessment of the patient him or herself of how they're doing, which obviously has value. And then the physician also contributes in overall global assessment. You put all of those into the meat grinder, and you come up with a number that says the patient, is this, this is the status of the patient. But because each one of those is subjective in its nature, there's a lot of variability in those composite scores. So they're pretty noisy. One of the reasons that trials, one of the main reasons, it's not the main reason that trials and rheumatoid arthritis require lots of patients, typically for new therapies, and they need to be followed over usually significant chunks of time are because of that fact that these are subjective measurements that are very noisy, so to see a true signal across the noise takes big numbers or time. So if you ask me, I think what we're doing is measuring a fundamental unit of biology, the macrophage. I think in the end, biology wins. Eventually, we're going to know if the patient is getting better or not, because we're measuring that biology. But on any given day, there's going to be influence in those composite scores from how the patient or even the doctor is doing. Maybe they're really happy. Maybe they feel like they switched to a new drug by golly, it has to be working. Maybe it's in their nature to be happy or pessimistic with times of year. There are all sorts of variables. I think as we accumulate more subjects, our accuracy is potentially going to go up and as you look over time, I'm pretty sure it will, meaning that we'll be able to make the right call. And it just might take a while for those clinical assessments to catch up. Doesn't mean that's always going to be the case though. There are some that -- so specific to your question, the ones that we've seen that our prediction has been not correct, at least not yet. I really do think a lot of it has to do with the target itself. So we're hitting an amorphous, target the clinical assessments. And I actually would be a little bit scared if we hit 16 out of 16 of an amorphous target, because that might mean we're equally amorphous. So again, I think the biology will win out. In some of these, though and all of these three that we haven't met, there's borderline things going on with the macrophages that I would expect would eventually be borne out in the clinical assessments. We're not going to keep following them beyond six months. So we may not learn that, maybe we can follow up with some of these. But I wouldn't -- I'm not surprised we're not hitting 100% in terms of these clinical assessments as the outcome. That makes sense.

[Michael Okunewitch:]

Yeah. It does make sense. So then one thing I guess I have one more follow-up on that same point. In the Phase 3, is there any plan to include a tilmanocept assessment as well the clinical assessment at weeks12 and 24?

[Jed Latkin:]

Yeah. So we are doing that in the current trial. And we will do that in the Phase 3 as well. So we're going for three main indications, right or the plan is. One is the week zero to week five change just any in the tilmanocept scan. Is that predictive of clinical outcome of either 12 or 24 weeks? That's our main indication. Another indication is can the baseline scan itself be predictive of clinical outcome based on this kind of pathotype or subtype bucketing? And the third indication is the longitudinal monitoring, and that is imaging a multiple time points over -- or imaging over time, and seeing how the patient's disease status, at least as assessed by macrophage activity is over time. And so the way to -- one way to get that is to look at correlations with the clinical assessments. And like I said, and it may stand out to you, I wouldn't expect us to match up at every time point with the clinical, but I think what we're going to be seeing is in some patients, it'll be more anticipatory, right, so the macrophages might be going down, so our signal will go down. And then long-term, the clinical assessments will catch up to that. So there is a plan though to and we are currently acquiring images at every single time point. So we do have those data, and we're looking into the week 12 and week 24 imaging data as well and aligning those with the clinical assessment. I can tell you something that I haven't said before, it's not -- it's encouraging. And that is when we have looked at the week 12 images and quantified those, the trends are holding. So it's pretty cool, right? So if we see a subject, for example, who has achieved a response, as assessed clinically at week 12 or 24 by the clinical assessments, a positive response to anti-TNF alpha. Our imaging, for example, the localization has been going down, at least in some of these subjects from week zero to week five. And then the ones who are still getting better along the way or continue to get better as measured at every time point by those clinical assessments, we actually see the signal go down at week 12 even further, of tilmanocept. So it looks like that that's something that reassures us that we're measuring something that's showing a real effect, and that the effect is lasting, right. So it's not a transient thing for the drug at least in those subjects. The signal is going down, and it continues going down. So we'll keep looking at those data and quantifying those along the way.

[Michael Okunewitch:]

All right. Thank you, Jed and congratulations on the data.

[Jed Latkin:]

Excellent, guys. Excellent, Michael. Thank you. Next question?

[Operator:]

We have a question from Jacob with -- a Private Investor. Please go ahead.

[Unidentified Analyst:]

Hi, Jed. So I know that you touched on it on the conference call just now, regarding the Jubilant transaction? Can you tell us with more clarity as far as how long the exclusivity period is with them?

[Jed Latkin:]

That's a good question. I mean, we have not disclosed that. But all I can say is that we're within the period. We have constant discussions with them. And I trust that based on our discussions, we will be able to complete it within the time that they've allocated. So we have specific. We've been in discussions with them consistently over how long each subject would take. We gave ourselves enough time to get it done to work in for the COVID delays. Unfortunately, on the clinical side, we've had numerous issues with COVID, and people not being able to do calls and whatever. But we're well within the timeline. So I do anticipate that we will get it completed within the set timeframe. But it's not something that we've disclosed publicly what that timeframe is. I do know that once we do continue to move forward to the FDA, that'll sort of push things forward a little bit faster, and sort of push them to a decision faster. But we are well within the timeline. And we do expect that as more data comes through on the remaining due diligence items and clinical legal and financial, we're going to get this thing completed within the timeframe of the contract. So I'm not worried about it. Nothing has really popped up that would worry me, other than the fact that things have gone a little bit slower based -- just because of COVID. And the fact that we can't get into a room, everything's obviously done remote by zoom. But the one good thing that this has done is one, it has allowed us to have this addendum to the second interim look. It is also the company Jubilant has spent just countless amount of money on the commercialization feasibility, all this other stuff, money that we haven't sent that they did, which further validates everything that we're working on. And so that's something that's been a positive that we had not anticipated, and it's something that we're excited about. But we are very, very confident that we will get this thing done within the timeframe allocated under the MOU.

[Unidentified Analyst:]

Okay. And on that same front, on the August 10 call, you mentioned about the investor group, that would be paying $5 per share for up to 1 million shares of Navidea. And then they also talked about if the stock were to rise to that $5 range, they'd be making at least or they'd be making another 3 million share investment, which is $15 million. What's the exact latest date of the first investment, of the first $5 million on the 1 million shares? And then what exactly is the last date on the remaining $15 million worth?

[Jed Latkin:]

So the first is approximately the 23rd or 24th because it was it's a 45 business days contingent on the acceptance and of the application. So then there's 45 business days thereafter. And what I want to stress is that the agreement we have is the first $5 million is guaranty that's definitely coming in at $5 a share for the $1 million shares. The remaining and it's actually $20 million is at the company's option, if the stock trades between five and 575 for five consecutive days. Given the financials we have in place, as I've said numerous times, I'm not the -- one of the CEOs of these biotechs that get some good news and look to raise $100 million just to have it on the balance sheet. I know how much it's going to cost to get us to our product, I don't want to needlessly dilute. So we have the option to do that if the stock goes above five. But given the 15 million Series D that we have in place, we have more than enough money. But for those dates we have, it's approximately November 23, and then 45 days thereafter for the expiry of the remaining 20. But that's going to be sort of a wait and see, because I just don't think at this juncture, it's money that we need, given that we have the funding in place. We're moving at a good pace with Jubilant. We have our plans in place for moving forward on cardiovascular and some of the other projects we're working on. So I'm not going to needlessly look to fund. I mean, I'm very happy, we've been working with the auditors on how the Q was going to look in terms of financial disclosure. And given what my budget is over the next two years, we have enough money in the bank allocated to get us from here until approval. So I'm not going to -- I wouldn't 100% rule out using it, because it really depends on what happens. But I would say that it would be highly unlikely that we would use that second tranche, but the $5 million is coming in, and it should be in within the next week or two.

[Unidentified Analyst:]

Right. That's it for me. I'm good. Thanks.

[Jed Latkin:]

Excellent. Thank you, Jacob. Next question?

[Operator:]

We have a question from Mike Rically with Navidea . Please go ahead. Your lines open.

[Unidentified Analyst:]

Yes. This is Mike Rically, independent investor. Question. A couple questions here. Two financial and I appreciate you taking the call. Jed and Mike and Joel. First question is what you were just talking to the prior caller Jacob about? So when you were on the KOL and you said there was a $20 million coming in, is that the $5 million plus the $15 million, Jed?

[Jed Latkin:]

Yeah. Yes, it is. And I think on one hand, that's also as an aside, helps move Jubilant forward faster, because they understand that it would be -- it's great, I do firmly believe we're going to get the deal done. I think that's going to happen. But remember, we now have a lot of financial freedom. This is something that we have not had, in many, many years. And I know a lot of the people on the phone call have been with us for many years and they understand that. I was looking back a lot of the decisions we always made were, well do we want to have milk or bread or something like that. Now we finally have an opportunity to complete the trial, to work on a bunch of other projects in a very focused and directed manner. So we get things to completion and not just scattershot investments here, there and everywhere. But we also have the benefit of moving forward with a great partner. So I'm talking about the five that is guaranteed and the 15 that is guaranteed under the Series D preferred. And then we have the other option, which is for an additional 20. But as I said, with the five and the 15, we're more than covered to take care of all of our financial needs for the next couple years.

[Unidentified Analyst:]

So as the 700 that came in after the third quarter was that from Jubilant, was that from somebody else?

[Jed Latkin:]

No, no, the 700 was from the Series D.

[Unidentified Analyst:]

So, they've already started funding?

[Jed Latkin:]

Yes, they have. Yeah, so they've funded. Well, you know, you'll see the Q tomorrow, but they've already started funding. Yes. We'll see that if you look at the Q tomorrow, the important thing to look down is on the balance sheet, look under the equity section, you'll see the equity receivable as well as the Series D outstanding. So if you put those two together, you'll see what the financing -- what we have planned over the next nine months coming in on a guaranteed basis. So it's nice to have a nice positive receivable on the balance sheet for once.

[Unidentified Analyst:]

Well, that's great to hear. I'm glad to see it started funding. The rest -- several more questions, but there are on the scientific side. The first one is on the FDA window. You've said that before there's a 60 day window from the time you request the meeting with the FDA till you have that meeting at a minimum. Have you made that request yet with the FDA for the P3 review?

[Mike Rosol:]

Hey, Mike. It's Mike. How are you?

[Unidentified Analyst:]

Fine, Mike, appreciate it. Mr. Rosol.

[Mike Rosol:]

Yeah. Thanks for the question. We have not made that request yet. So what we've been doing, like I said is, while we've been doing the due diligence with Jubilant we've -- it allowed us to accumulate more of this data that I just went over and to have the first half of the subjects actually a little bit more, and on three, completed through their six month follow up. And so if you ask me, and you're asking me, I think that actually puts us in a better position than if we had asked for the FDA meeting before, because this gives us the data that would actually be how we would design and are seeking the thinking of designing the Phase 3, following up the subjects all the way to six months, because that's what is done. Clinically, you look at the patients and see if the drug is working after three and six months. This is -- this has given us the time to get data, where we have imaging, and all of these time points. But most importantly, as I just went over the baseline in the five week, and then we can compare those to the 12 and the 24 week clinical outcome. So it gives us a stronger story to tell. I mean, there was some risk there, maybe things got worse as we followed them for 24 weeks, versus 12. You remember the 12 week data were very powerful. But it turns out the 24 week data are equally powerful. And I think that's very important. But what this does is reinforce our hypotheses and what we're thinking in terms of what to tilmanocept can bring to the table. So I think it's put us in a better position, frankly. But we haven't asked it yet the plan is to, to ask for that meeting in the next, before the end of the year, for sure is the plan. And we're putting all these data together in what is known as a briefing book that also has all sorts of other explanations and descriptors of the prior trials. So that the FDA can have everything in front of their fingertips as they make their -- give us their feedback on our trial design, as well as our proposed end points and objectives and milestones. So, again, a long answer to your short question, we haven't asked for it yet. But we're going to ask for it before too long. Q - So, Michael, does that point to sometime late in the first quarter of 2021? Before starting the P3?

[Mike Rosol:]

Yeah. Most likely, I mean, things could happen sooner, right? So that's the typical response time like that I've said, it's unlikely, it'll be sooner given things that are going on in the world. I mean, the response time, given the COVID scenario. So once we asked for it, we'll have feedback from them in 60 days. And then we're in a good position to go. Now, again, we should, you should know that we're not going to the FDA for our formal approval process to start the Phase 3. But we just want to make sure that they're that they agree with what we're proposing. So that will increase our likelihood of success. If we meet these milestones that, they've agreed upon, and then we deliver those data at the end of the Phase 3, since they've been involved in the decision making, it's much more likely that we're going to be in agreement that the data support the indications are going for. So it's not a requirement to do at this stage, we think it's a smart way of doing it, to make sure that the Phase 3 has the most likelihood of being accepted as a registerable study, assuming it meets our targets. Q - So you just made a very important clarification there that may not have been understood, you do not need for the FDA to start the P3. But all of this effort you're going to in this continual refinement of -- understanding of data will make the P3 more effective. So are you saying you could start the P3 any times, but you're choosing to better refine the data before you start and go to them?

[Mike Rosol:]

Yes, yeah, we could start it at risk sooner than that. But as Jed is -- outlined and due to his efforts, we're in a position where we don't we can make it to the end of the road and do it in the best fashion possible right in the smartest way. Where we have the resources now to do it and set us up set ourselves up for the best chance of success.

[Jed Latkin:]

I think I really want to build on what Dr. Rosol just said, because I think it's important that you know, that refund books are being worked on now. And that's something that is going to be submitted the preponderance of evidence that we're now bringing, having these 16 patients that we 24 really is what I would say like the crucial linchpin for getting the FDA’s buy in, and yes, we don't need to go to them again. We could launch at any point in time, but we have the flexibility. We have the runway to do it. And now that we can provide to them a package that includes this really key week 24 data, we made a decision internally it was obviously a risk, because maybe we didn't have such a positive week 24. But thankfully, we have the data is very, very good, I'm really, really happy with it, I think it couldn't have been better. And now, we can use that as part of our package to the FDA, if you remember the last time we submitted to the FDA, we're actually caught off guard because they responded so quickly. We submitted it was the middle of the summer, and I was like, okay, we're going to submit, we can take off a few weeks, relax, and then have the meeting. And then we heard back within two weeks. And next thing, everybody had to cancel their summer vacations, and we're working on it. So I'm really happy with the fact that, we're going to be presenting such a robust data package to them. And I think that, it'll really lead us to have a nice springboard into the launch of the Phase 3. Q - You know this is excellent information that both of you just passed on. I don't think the general population understood that. I think the general understanding was that you still had to get approval for the Phase 3, but you're actually trying to make the Phase 3, a better -- a better more well understood and accepted trial. And you're not waiting because you can't get approval. So that's a really important piece of information that I --

[Mike Rosol:]

Yeah. Thanks Mike. I am glad you highlighted that. I'm sorry to over talk you, but I think we've noticed that in our conversations and readings. And so I wanted to make that clear. And I know Jed did as well. So thanks for also emphasizing that point. Q - That's excellent. On your remaining participants in the arm three, based on what it's taken to get these done. Are you seeing those being done by the first quarter of next year also?

[Mike Rosol:]

Oh, yeah. So we've got, they will have their imaging events and the last clinical assessments, I think there's only one subject who's lagging, because they it took them a while and maybe, maybe a couple that are lagging, because it took them a while to get their anti-TNF. But in terms of the analysis, we're doing it in a rolling fashion. So with those, lagging one or two aside, we'll have all the data analyzed at some level in the first quarter. How this is or maybe you don't, and maybe I should tell the folks out there, it formally done and analyzed with statistical input and analysis and tables, figures and legends that that need to be done. And a final clinical study report done that takes some months after. But the way we're looking analyzing the data internally in a rolling fashion, so we're going to know a lot about those in the first quarter. So even before the Phase 3 starts, we're going to have more information, even that I've discussed today, and more detailed analysis will have been done on those cases as well. So that will help us. I don't foresee it changing the design, as Jed mentioned, and as I've tried to relate today, things are going along according to hypotheses exceedingly well. And so I think this is all supportive for our, even our current design of the Phase 3 and now we're also using these data to help us in the sample size estimation, we already have estimations of that. But we're able to use these data to help us refine that even more. So we can really hit the ground running with a very targeted phase three, not, not larger than it needs to be and not too small so that we can’t achieve success.

[Jed Latkin:]

And the other thing to build on that, this arm three, has really shown to me, I don't know about, our clinical guys are obviously very experienced in all of this. But you know, I'm more of the outsider, I would say, but the arm three has really shown to me why there's such a need for this product. The fact that, it takes some of these patients forever, who aren't on great health care plans to get the anti-TNF is because you know what? They know that once they get it, it's a six month authorization. And there's you know, they don't -- they get there -- they get their medicine and maybe it works, maybe it doesn't. The fact that we're going to have something that can tell you at week five, whether or not it works, is going to invite the insurance companies to be more apt to say what, we'll take the chance because instead of authorizing for six months, and paying for six months of a drug, we're going to pay for five weeks of a drug, and which is essentially, two or three injections. And we'll know whether or not it's going to work. So it's sort of money well spent, how the insurance company, they view all of us as positives and negatives, where we're just dollars and cents to them. I think the patient care doesn't really care. But thank god, they're companies like us, who do care about the patients and are putting forward a product that will allow these insurance companies to make the decisions in a timely manner, because they know that their commitments not going to go beyond that five week, because we're going to be accurately able to predict it. And at five weeks, we predicted working, the insurance companies more than willing to pay for it, we've had issues with patients who just can't get the drug, insurance companies more and more are tightening their belts, and they don't want to have to pay. And this is why our diagnostic is so greatly needed. Because this is something that's going to open up patients who need the drug and be able to get access to it faster. And that's why we have several patients that will go past this quarter, because they just couldn't get the truck. I mean, that's the it's the lunacy of this whole thing, that sometimes you really need it, if you're going to get it, because there's, well we know, it's working, we now know it's working. Do I want to have to pay for six months of a drug? The insurance companies don't, for them, it's all about the dollars and cents, and we're going to make that decision so much easier for them. And that's something that has really given us a moment of pause and really encouraged us to how good of a product this will be and how successful it will be long-term. Q - Well, you and Mike just lead into something and this was from your KOL with Graf, he did a really good job in explaining from his viewpoint, what was going on it within the in the medical community. But one thing he brought up that was really important was the acceptance of this after it gets approved, which we're all hoping for positive outcome. And will the people who make the TNF -- anti-TNF, excuse me, try to do anything negative to it. And what he said was, basically there's 30 other types of drugs out there just chomping at the bit to get out into the market. So the big companies that are making the anti-TNFs may not be receptive to this. But there's plenty of others that also. So I took away from that that -- that have mitigated the risk, a lot of non-acceptance. Is that a fair assessment from the KOL?

[Mike Rosol:]

Yeah. And there's another point, great point. This is my Mike Rosol. I agree, did a great job, Jonathan Graf. He is now -- we've had a number of discussions with a minute, they've all been really informative. And in fact, he was one of the KOLs, who helped us design the currently running trial, as well as the Phase 3. And so he's been instrumental. His insight has been instrumental all along the way. And he's a -- he's an influencer in the field of Rheumatology. And in addition to what you said, there, Mike, I want to emphasize that something Jed has said multiple times. We think is holding true at least in our limited data so far. So when I mentioned to you the positive predictive value is 100% for imaging readout for predicting clinical outcome at 12 weeks and 24 weeks, I don't know that that number is going to hold. But what that means is in subjects where we see an beneficial effect in our tilmanocept imaging readout. All of those subjects, where we said, you're getting better by tilmanocept, every one of them got better clinically. So that's something where a payer or a company that's making an anti-TNF alpha, I think we'll see that information is valuable, because that would then be usable to reinforce that their anti-TNF alpha treatment is working. So they can keep, the patient will then need to stay on it, the doctor will advocate that the patient stay on it, because they have something in hand that says objectively it is working. And as Jed is, using it as an example of himself over time, the payers are going to want some concrete information to say this drug we're paying, $5,000 a month for is working, right. So this will be something, we can give that says indeed it is working.

[Jed Latkin:]

And we've seen it firsthand with patients who look like they're great for the trial. And I'm always getting on in Bonnie about that. She’s been working her butt-off on this thing for years. And I always yell at her what happened to that patient, why they couldn't get drug? We have patients that screen and look great, and they can't get the drug because the insurance company just doesn't want to pay. And this is I mean, and yes, Mike made the point is maybe I'm a bit selfish, because this will help me long-term with my Crohn's disease. And in my in my situation, getting my anti-TNF, but it's going to help so many people and it's something that we're really, really excited about. Q - Well, you guys have done a great job here. I got one more an easier your question for the end. You said several times that you've been doing some preclinical studies on therapeutics. Can we -- can you leave us with a teaser of some of those been looking at cancers or CV therapeutics? What? Can you tease us a little bit what some of those preclinical that you got out there? You're working on now?

[Mike Rosol:]

Sure. So the main one is the main is -- the main domain is oncology. So cancer, yes, we've looked at a number of tumor models. And I think this part has been publicly discussed in general, the theory is that and the evidence is supportive in general, that our therapeutic in concert with existing immunotherapies can have then added synergistic effect. And we're seeing that in our preclinical models, and we have some compelling data demonstrating that that we've been talking about and are likely to write up for abstract and a publication before too long. These are -- these are, we think, very strong data that showed that we can impact the macrophages associated with tumors in such a way that not only have a clinical benefit themselves, but also can kind of release the body's immune system as encouraged by other immunotherapies and increase the effect of those immunotherapies. So we think this is a very powerful story, potentially, in the cancer space. I'll leave it at that. Q - Okay. Well, I appreciate you sharing that little bit. I'm very -- I'm a long-term shareholder. I'm very encouraged by what you guys are doing and what you've done. And I appreciate it, and applaud you and say thank you.

[Jed Latkin:]

Excellent. Thank you, Mike. And I think I think that was it for the questions.

[Jed Latkin:]

And so I know it's already late. So I just want to thank everybody once again for calling in. And I look forward to speaking with you guys all again in the near term, we're going to be trying to set up some more of these virtual fireside chats as well as appearances at some of these other virtual investor conferences so that way we can get out in front of investors as much as possible. So everybody, have a great day and thank you so much for tuning in.

[Operator:]

That concludes the call for today. We thank you for your participation. And I say please disconnect your line.