GT Biopharma, Inc. (GTBP) Q2 2021 Earnings Report, Transcript and Summary

Greetings and welcome to the GT Biopharma Second Quarter 2021 Conference Call. All participants are currently in a listen-only mode. Following the formal presentation, we'll open the call up for a question-and-answer session. At this time, I'd like to turn the conference call over to David Castaneda, Investor Relations for the company. Thank you. You may proceed.

Thank you, operator. Good morning, everyone and welcome to GT Biopharma’s second quarter 2021 conference call. Earlier this morning, we issued a press release, summarizing the company's second quarter 2021 corporate updates that management will discuss on the call today. You can access the press release by going to the News & Media section and then the Press Releases page on our website and gtbiopharma.com. GT Biopharma’s following presentation and ensuing question-and-answer session will include statements that are or may be deemed forward-looking statements. In some cases, you can identify forward-looking statements by terminology including anticipates, believes, can, continue, could, estimates, expects, intend, may, plan, potential, predicts, should, will, would or negative thereof, other variations there on or other comparable terminology. We operate in a very competitive and rapidly changing environment and new risks emerge from time to time. As a result, it is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor or combination of factors may cause actual results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed in this presentation may not occur and actual results could differ -- to differ materially and adversely from those anticipated or implied in the forward-looking statements. You are cautioned not to place undue reliance upon such forward-looking statements as predictions of future events. Although, we believe that the expectations reflected in the forward-looking statements are reasonable, we cannot guarantee that the future results, levels of activity, performance or events and circumstances reflected in the forward-looking statements will be achieved or occur. We drafted our Annual Report on Form 10-K for the year ended December 31, 2020, our subsequent current reports on Form 8-K, our quarterly report on Form 10-Q for the quarter ended March 31, 2021, and our other filings with the Securities and Exchange Commission. Any forward-looking statement included in this presentation speaks only as of the date here of. Except as required by law, we do not undertake any obligation to update or revise or to publicly announce any update or revision to any of the forward-looking statements, whether as a result of new information, future events, or any other reason after the date of this presentation. For all forward-looking statements, we claim the protection of the Safe Harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995. Nothing in this presentation or discussion shall be deemed an offer to purchase or sell the company's securities. Now, I'd like to turn the call over to Tony Cataldo, Chairman and CEO of GT Biopharma. Tony?

Yes. Thank you, David. Good morning, everyone, and thank you for joining us, as this is GT Biopharma first scheduled conference call. I want to thank the investment community for paying attention to the progress that GT Biopharma has demonstrated in the first half of this year. Additionally, I want to thank my entire staff for their due diligence, hard work and the contribution they have made for an amazing first half of the year. The last fiscal quarter has been marked with numerous events and milestones, reflecting tremendous success for the company. We were added into the Russell 2000, the Chicago Options Exchange, and now have enough money to execute the company's business plans for the next couple of years, approximately $40 million. We also completed our new sponsored research agreement with the University of Minnesota, headed by the TriKE creator, Dr. Jeffrey Miller and his team at the University of Minnesota. This will further enhance our advancement of the TriKE platform, adding more value to GT’s expanding portfolio. Our GTB-3550 TriKE clinical trial continues to show safety and clinical results and remains well-tolerated with patients who have for all intents and purpose has been written off. The TriKE clinical data has shown that it is remarkably effective at activating patient's own NK cells creating persistence of NK cells, proliferation of NK cells and making NK cells serial killers of cancer cells. Unlike our competitors, we don't need ex-vivo outside manufacturing of NK cells or a combination drug therapies to supplement our product. Everything that TriKE does is inside the body. The TriKE stands alone in the field of NK cell technology companies as a true monotherapy. Additionally, the TriKE is a toolkit for other NK cell therapies. We had data that shows that GT will continue to update the investment community as events unfold as well as significant corporate development milestones. I often indicate to existing and prospective investors and analysts that I believe that it is the data and not the CEO that speaks most meaningfully to the merit and potential in GT Biopharma. As such, I will now turn the call over to Martin Schroeder, our Chief Technical Technology Officer; and Dr. Greg Berk, our Chief Medical Officer who will recap the impressive and encouraging data we observed and reported in recent months. We will close out the call with the Q&A session. To reiterate, I'm exceedingly pleased with our advancement over the last quarter has clearly evidenced by our continued share price appreciation. And with that, I'll gladly pass this call over to Martin Schroeder. Martin, take it away.

Thank you, Tony. Hello, everyone. As an introduction for those who may be unfamiliar, GT Biopharma is core technology is centered around our proprietary TriKE platform. And this platform originates from the pioneering work of Dr. Jeffrey Miller at the University of Minnesota. TriKE is designed to harness and enhance the cancer killing abilities of the patient's endogenous or own natural killer cells without the need for the addition of supplemental NK cell therapy. TriKE is administered to the patient by infusion and once bound to the patient's NK cells, TriKE directs the NK cell to target certain tumor specific proteins or tumor antigens that are expressed, present on the surface of cancer cells, leading to the death of the cancer cell. Notably, and distinct to try to relative to other therapies, TriKE activated NK cells target and kill multiple cancer cells in a very powerful and serial fashion. So what is TriKE? TriKE is made up of recombinant -- we call it -- referred to as recombinant fusion proteins. These are proteins that recognize specific antigens as I mentioned on the surface of the cancer cell. And as such, we -- they can be designed and engineered with great flexibility allowing us to target a variety of tumor antigens present on hematologic malignancies, sarcomas and solid tumors. TriKE unlike cell therapies does not require patient specific customization. So in addition to the compelling clinical data, we are seeing with GTB-3550 that's being evaluated in Phase I clinical trial, which my colleague Dr. Greg Berk will discuss momentarily. Our pipeline consists of several additional TriKE products, which target solid tumor cancers. Our clinical development pipeline, includes TriKE product candidates, which target PD-L1 positive solid tumor cancers, B7H3 positive, solid tumor cancers are two positive, solid tumor cancers. And these cancers include lung cancers, breast cancers, ovarian cancers, gastric cancers, and prostate cancers to name just a few. The TriKE product candidates are presently undergoing GMP manufacturing and scale up in preparation for filing an Investigational Drug application with the US FDA for evaluation in humans. We are also working on several additional product, TriKE product candidates that are in various stages of preclinical evaluation. At this point, I'd like to turn the call over to Greg Berk, our Chief Medical Officer and he can proceed to discuss the details of our GTB-3550 clinical program. Greg.

Thanks, Martin. The early preclinical and clinical evidence with our first candidate TriKE GTP-3550 for the treatment of relapsed refractory AML and MDS that was reported in the last fiscal quarter is very encouraging. We observe both a positive safety profile and an indication of biologic activity as measured by blast cell reductions. At the 150 microgram dose level, we have one case of Grade 1 CRS, which was not a dose limiting toxicity. There have been no other clinically significant toxicities observed and in fact, next week we are escalating to the next dose level, the 200 microgram cohort. To date, 12 patients have been treated in the GTB-3550 Phase I trial, patients five, seven, nine and 11, experienced 33%, 61%, 63% and 50% reduction in the CD33 positive bone marrow blast levels respectively. 57% of patients treated between 25 and 150 micrograms, experienced the reduction in the AML or MDS blast. Activation, proliferation and persistence of functionally active NK cells occurred without the addition of supplemental NK cells. NK cell activation has been observed to increase early during treatment and is correlated with a proportional and overall increase of absolute number of NK cells. Targeted delivery vial 15 to NK cells via the 3550 TriKE showed preferential proliferation of NK cells and significantly less effect on CD8 positive and CD4 positive T cells. We also observed no CD16 shedding by patients NK cells and saw enhanced HL60 AML target cell killing ex vivo. This data indicates that GTB-3550 rescues the patient's exhausted and inhibited and endogenous NK cells, resulting in their activation, proliferation and persistence. This early data indicates GTB-3550 therapy demonstrates significant bone marrow level reductions in AML and MDS patients without the need for supplemental Autologous and Allogeneic stem cells – I am sorry, cell therapies. This Phase I trial is expected to conclude later this fall, and updated safety and efficacy data will be presented in an oral session at the ESMO conference in September. With that, I'd like to turn the call over to the operator to open up for Q&A. Thank you.

Ladies and gentlemen, at this time we'll begin the question-and-answer session [Operator Instructions] Our first question comes from Justin Walsh from B. Riley Securities. Please go ahead with your question.

Hi. Thanks for taking the questions. I have a couple. Starting off, can you provide any color on what we can expect to see at ESMO? How many patients, how long the follow-up, any details we can get?

Yes. Greg, you go ahead and answer that. But just to remind everybody, because we are speaking at a major conference, there are certain embargoes that we can't articulate until that conference. Go ahead, Greg.

Sure. Justin, at ESMO, which is on September 20 or around that time, we will present updated safety data, at least through 12 patients. We're literally dosing patient number 13 next week. So, we most likely won't have data for that patient at ESMO. So, it'll be up through 12 patients.

Got it. And maybe related to that. So, you'd mentioned that there was the one case of CRS that didn't seem too severe. Can we get any more details on that, like how long after treatment that is observed? How long does it last? What interventions were required? And anything else you can give on that front?

Yes, sure. It's very simple. It was just -- it was just fever. So, fever that persists a certain amount of time is -- it's fever alone without other symptoms, it's a Grade 1 CRS. So, if infection is ruled out, which it wasn’t in this case, it's assessed as a possible CRS.

Perfect, thanks. And I'll just have one more before jumping -- yes.

By the way, Justin, that's not a dose limiting toxicity of Grade 1 fever CRS.

Got it. All right. So, I think the last one for me. Maybe, just some details on how Dr. Miller's involvement is expected to evolve following the Sponsored Research Agreement, and how that is expected to advance GT’s platform.

Yes. Martin, why don’t you take that one? Martin?

Pardon me. Mic was unmuted. Forgive me. Yes. So Jeff’s involvement with the company will continue to be quite strong. He is one of our Founders, and of course, preeminent key opinion leader in the field. The Sponsored Research Agreement, we have several activities plan to help more fully understand TriKE’s capabilities as well as TriKE’s influence on NK cells biology during the course of therapy. And as you're, I'm sure, aware, as I mentioned, we are in the -- we are developing several new TriKE product candidates. Some of those are quite interesting dual targeting TriKEs that simultaneously target two different tumor antigens, the goal to help better cut-off immune escape, particularly when moving into the solid tumor setting. So yes, so Jeff’s efforts with the company will continue to be strong and he will be quite active engaged for the long-term.

Got it. Thanks for taking the questions. I'll jump back in the queue.

Our next question comes from Ram Selvaraju from H.C. Wainwright. Please go ahead with your question.

Thanks very much for taking my questions. Firstly, I was wondering if you could give us some color on the timing of release of final top-line data from the 3550 trial. And if you have line of sight on, which medical conference you expect to present the final data? I understand the interim data is being presented at ASML, but just wanted to get a sense of timing of the presentation of final data?

Sure. Hi, Ram. It’s Greg, I could take that one. As you know, Ram, as we continue to be in dose escalation, it's always difficult to predict what your recommended Phase II dose in your MTD is going to be when you -- once again when you see such a clean safety profile, that's why we've made the decision to escalate from 150 to 200. So when you think about it, it takes a couple of months to get a cohort enrolled, treated and completed with data. So we won't make a decision until -- on the MTD, which is really the driver of the final data for the Phase I until we establish the recommended Phase II dose in MTD. So we're a few months away from that for sure. That's why we're saying it's later in the fall. And then within a few months of that we'll initiate our Phase II. Regarding with the timing of a conference around the final data, I don't think we'll have final data in time for ASH for sure. So it would be a conference later in the winter or early spring for the final data. But we may release that as a press release even before that, a top level press release.

What I would add just to expand on that is just for those who don't really understand it is -- MTD is an important milestone for the company. And it's a good thing. When you're not hitting MTD, that means your products still working. And you may have more effectiveness as you climb that ladder.

Great. And also I wanted to ask about where in the treatment continuum you see 3550 potentially being most likely to be deployed within the context of AML specifically?

Yeah, that's a great question Ram. It's something we think about every day, obviously. So our current study is monotherapy. And that's still our base case plans is to hopefully in Phase II, if we see a compelling efficacy signal, and what I mean by that is a significant number of durable CRs not just blasts or reductions, but durable CRs, we would obviously, pursue an accelerated strategy, because these are patients as you know, that don't have any effective or even approved options. We're talking about relapsed refractory AML and high grade MDS. So that's our monotherapy approach. And by the way, we're including I think, as you know, the minimal residual disease cohort in our Phase II, because that's a population of patients who have a high unmet need, virtually all of them will relapse, and we're essentially treating lower volume leukemia. So the MDR, the MRD cohort is very important to us. Ultimately, I believe that the drug could be moved up in combination with standard of care chemotherapy. And we will, while we're continuing our monotherapy expansion cohorts in Phase II, we will initiate a combination trial most likely with venetoclax [ph], which is the most commonly used regimen in the relapse setting. It's also as you know used in frontline setting. There is a lot of published data that NK cells, and hypomethylating agent including both [indiscernible] are synergistic, and work together in AML models ex vivo, there's also a lot of evidence that venetoclaxas well as the hypomethylating agent are not toxic to NK cells. So it makes a lot of sense to combine, the engager, with a standard of care, chemotherapy, and probably the perfect regimen would be another class decided. So that will be done in the future as well.

Great, very helpful color, wanted to switch gears now to talk about your B7H3 targeted TriKE, and ask if you can provide any additional color around the preclinical data that previously announced as well as give us a sense of when it might be presented at a medical conference. And also if you have any thoughts on the current B7H3 competitive landscape, especially in terms of how that compares to other kind of canonical targets that have emerged as being of interest in the context of ontology. Thank you.

Martin, you want to handle that one or Greg? Greg, why don't you actually go ahead and then I chime in.

No, I was just going say Martin has done all the work on it Ram. So I'll have Martin present it – because it's really been his project. A – Martin Schroeder: Yes, I mean, well, actually, the B7H3. TriKE that we are matriculating through preclinical studies was developed by Jeff Miller and his colleagues at the University of Minnesota and Jeff and colleagues have published on the -- on this product candidate already. B7H3 is ubiquitously expressed on a number of tumor targets. Macro genic has been working on B7H3 targeted compounds for a number of years. We see with our preclinical data for Tri KE we see using NK cells as a viable therapeutic modality to very specifically target and kill B7H3 expressed in cancers. Today, we've looked at ovarian cancer, breast cancer and prostate cancer to name a few. And we've seen a good killing in vitro cell assays in our -- in our animal models. Positioning wise, I think that it does provide an additional therapeutic agent for physicians to consider as they move forward with the comprehensive treatment plan for their -- for their patients. So I think that's sounds great.

Great. And then just lastly, I was wondering if you could comment at all on potential common tutorial regimens that you view as most ideal for any and all of your other earliest stage investigational or try candidates. Thank you. A – Martin Schroeder: Well in when you talk combinational therapies, certainly comes to mind the criteria and not the vote protect T cells. But that being said, we are developing dual targeting TriKEs. And the idea there is to assist in cutting off immune escape. So we have dual targeting TriKEs that's our CD 138, which is present on cancer stem cells. We have once we go EGFR, and that Jeff are three for example, PDL1 combination TriKE, so the platform is very versatile. and that allows us to utilize multiple targeting domains with a single TriKE. We could, for example, we have – for example, a CD19 TriKE, and we could co-administer that with CD33 with our GTB-3550 could be done. But it's, I think, more efficient to make a dual targeting CD19, CD33 TriKeE. So it's really the dual targeting strategy that, I think to a large extent, we're focused on more than trying to determine, which TriKeE we should pair with – which other standard-of-care therapy.

I just want to add to that, Martin that. It's a reasonable question, because generally historically in oncology, it's always been about combination, right. We're obviously going to pursue seeking – seeking a signal as monotherapy, because it's a much less challenging regulatory path, if it's – if it's used as a single agent. However, we're going to go with the science tells us to go. And there's a lot of strong rationale scientifically to combine TriKE’s with, as Martin mentioned, checkpoint inhibitors as well as standard-of-care chemotherapy. I do think, we need to initiate combination studies, very early into development, literally after we have a couple of cohorts of single agent, safety data. So, we're going to start doing this with AML with VenAZA, as I mentioned, because the science is really telling us to go there. And we'll look at every possible solid tumor combination as well with our solid tumor TriKE, and be guided by the science as well as making sure there's a clear registration pathway for that combination.

Thank you very much.

Our next question comes from Tony Butler from ROTH Capital. Please go with your question.

Yes, thanks very much. Two questions, if I may. The first is maybe for Greg or Martin, in ClinicalTrials.gov it actually states the Phase I/II study for 3550 is enrolling, obviously, Masonic Cancer Center University, Minnesota. But there's also Wisconsin that is listed as well, but not recruiting. And I'm just curious, will you open that side for 3550 or wait for the Phase II? That's question one. Question two is, you spend a little bit of time Martin and Greg talking about other TriKE’s. But I think – at least what was new to watch is this notion of sort of second generation TriKE’s, which have demonstrated greater potency, greater activity, greater cytotoxicity. And I just wondered if you would just spend a minute on those. And in fact, I think the B7N3 TriKE for example is one that has been created, based upon those second-generation attributes. And while you don't spend a lot of time on it, but I just thought it was important that they -- you may mentioned it because I think these thing -- it's just not a one size fits all platform and seems that there -- the flexibility what you have already used, but also the flexibility actually leads to potentially was greater cytotoxicity, but that may be target dependent? I appreciate any commentary around that? Thanks very much.

Sure. I can quickly answer the question about the sites and then hand it over to Martin for the discussion on the newer generation TriKE. Regarding sites and what's posted on clinical trials.gov is we have pre-initiated and initiated Wisconsin and we've gone through the process also with Oregon. At the time we started the process of initiating sites, frankly, we thought we would be wrapping up Phase I now. We didn't think we would get this high -- to this high of a dose and it made sense for us to put a hold on those sites until we initiate have them come in at Phase II. Therefor sure coming in the Phase II, but they may very well come in at the tail end of Phase I now, but they are ready to go. And we -- by the way are bringing on multiple new sites for the anticipated Phase II. And we'll have up to eight, eight sites, 8 to 10 total sites. And we received a tremendous amount of interest from many of the KOLs and AML who want to participate in Phase II. So those initiations are starting already. I'll hand over to Martin. I’m sorry.

Yeah. So thanks, Tony, for the insightful question. Yes, our platform is very versatile. And our second-generation TriKE, which are -- we're implementing across the -- all of our portfolio. What we've learned about how TriKE interacts with the NK cell and a target cell has led to the second-generation platform. And the key thoughts are we wanted to improve the steric interaction between the various binding domains of the TriKE molecule and the NK cell and the target cell. So in that regard, we've moved away from single chain variable fragments to nanobodies. And in that case, we have seen dramatic improvement in the potency of the drug -- of our drug candidates in some cases tenfold better improvement, just because of improved the steric interaction between TriKE molecule and the NK cell. And we've done the same investigation with respect to how the NK cell binds to the target cell. In there, in the case of the B7H3, TriKE that you mentioned, it's a double nanobody construct with IL-15 in the middle. So we have been optimizing the platform to accentuate very other positive elements of TriKE therapy. And we'll continue to do so, obviously, as we grow and mature the platform.

Thanks, Greg and Martin, appreciate it.

And ladies and gentlemen, at this time, we've exhausted the audio questions. I'd like to turn the floor back over for any offline questions. And we're showing no offline questions. So at this point, I'd like to close the question-and-answer session. And I'd like to turn the floor back over to Tony Cataldo for any closing remarks.

All right. Thank you. And thanks, everybody. I know all of you would like to gearing up -- got an update on patients 10, 11 and 12. And as Greg was articulating, we actually have been selected to do an oral presentation at the ESMO Conference in September. And because of that, we're under an embargo prohibiting us to release this kind of data. This is actually good news for GT results presented at a major conference like this. We see much more coverage than a typical press release. I want to thank everyone for listening to our second quarter of 2021 corporate update call, and for the continued support for our shareholders. We additionally appreciate the courageous participation of the patients in our clinical trials, and the day -- dedication of all of those trial investigators. We look forward to sharing future data readouts from our preclinical and our clinical activities as they progress. Again, thank you everyone and have a great weekend.

Ladies and gentlemen, with that, we’ll conclude today's conference call. We do thank you for attending. You may now disconnect your lines.