Intensity Therapeutics, Inc. (INTS) Earnings Call Transcript & Summary

Welcome to the Intensity Therapeutics Discovery Lancet Discovery Group eBioMedicine Publication Webinar. [Operator Instructions] Please also note today's event is being recorded. I would now like to turn the conference over to Lewis H. Bender, Founder, President, and CEO of Intensity Therapeutics, Inc. Mr. Bender, please go ahead.

Thank you, Rocco. Good afternoon, everyone, and thank you for participating in today's webinar on the recently published eBioMedicine paper part of the Lancet Discovery Group Journals. Yesterday, the company issued a press release discussing the recent contents of the paper. A copy of the press release can be found on the company's website under the News and Events tab. We also put out a press release this morning that we will not discuss because this is about the paper. We may make forward-looking statements during this paper -- during this call. By the way, I am so honored and pleased to be joined by Jacob Thomas, first author and Dr. Anthony El-Khoueiry from USC. We are thrilled with the results of this study, and we are looking forward to a very robust discussion of the day. Let's see. Okay. The call, we may be making forward-looking statements, including statements that address Intensity's expectations, future performance, including, but not limited ability to complete our clinical trials for our drug INT230-6. Forward-looking statements involve risks or factors that may cause actual risks to differ materially from those in the statements. For more information about these risks, please refer to the factors and risks described in our recent annual 10-K and subsequent periodic reports filed with the SEC and Intensity Therapeutics press releases that accompanies this call, particularly the cautionary statements contained therein. The contents, I'll remind everybody, the contents of this call are time-sensitive. The information that is accurate only of today, October 31, 2025. Except as required by law, Intensity disclaims any obligation to publicly update, revise any information reflects events or circumstances that occur after this call. Okay. So I'm going to, first, I'll give an introduction to the authors, and then I'll do a background on the technology and then Dr. Thomas and Dr. El-Khoueiry will present the clinical results. So look, these are the top academic researchers in the country, if not the world. Dr. Thomas is Assistant Professor of Clinical Medicine at the University of California's Keck School of Medicine and an oncologist with the USC's Norris Comprehensive Cancer Center. Dr. El-Khoueiry is an Associate Director of Clinical Research and Chief of Section Development at same hospital, at USC Norris and he is also the senior and corresponding author and the Section Chief for Developmental Phase I unit at USC. So really glad to have them and appreciate their time today. Okay. So background. So look, a little bit about the origin of the technology. I'm the founder of the company, I'm the inventor of the technology. I'm a chemical engineer by training and 15 years ago when immunotherapies will come to play, I thought about cancer. We brought the immunotherapies, there stun the gas or release the brakes. And I felt that if we could somehow get a steering wheel into the play by training the immune system on the cancer itself as it dies, it could kill it, then perhaps we would get better efficacy and see. Recently, we've announced this paper. I'm going to now talk about the molecular transport technology. Could we debulk -- can we debulk and stimulate immune responses with the idea originally, and we're going to see the results of that work in that idea. So the molecule -- the compound we're working with is comprised of three elements: a molecule called sodium hydroxybenzoyl amino octanoate, which we have used -- referred to as SHAO. It is combined with cisplatin and vinblastine, two very potent toxic agents in a fixed ratio. And this formulation of this product -- drug product candidate came out of a 2-year screening program that we did with a number of vendors that contract research. The drugs were showing very potency. And interestingly, both drugs have both direct killing and immune activating effects. These are all referenced here. And what we do is we take these three ingredients. The SHAO actually can make molecules -- amphiphilic molecules of SHAO, and it can make molecules soluble in fat and water at the same time. Now, we mix these together. It's a simple mixture. We add some excipients. We keep it in a vial, stored and it has a 3-year shelf life, and we've scaled it up. This is some kind of information that's in the paper -- is from our paper intensity published. It shows that drugs that are water soluble do not penetrate into tumors. This is human pancreatic cancer in mouse model. On the left here, you're seeing that if you inject water into a high density, high fat, high-pressure stromal tumor such as pancreatic or sarcoma or breast cancer or many others, you're not going to get absorption. So intratumoral technologies have tried to use methods to do retention or miss problem. The problem isn't retention, although that is an issue. Problem is dispersion of the tumor and cell penetration. And that SHAO molecule, when you add that molecule to liquid formulations, you change night and day. As you can see on the left when you inject and we put a dye into formulation, the drug comes out. As you see on the right, when the SHAO molecule is added to the formulation of cisplatin and vinblastine, now the drug will be absorbed. It will disperse through the tumor, diffuse through and follows the natural laws of diffusion. And you can see that now there is little leakage. There is a high amount of absorption to the drug. And we dose based on the size of the tumor because the diffusion may go as a volume. And so there's not a fixed dose. It is dependent on the patient's tumor burden from which we treat and how much a tumor will get in an individual injection. So -- in partnership with the National Cancer Institute, we were awarded a CRADA in 2014. And with that CRADA, we were able to show a mechanism by which this drug as a local therapy can create a systemic potent anticancer protective immunity. Not only do we protect and cause uninjected tumors to shrink as cited in this paper by Dr. [indiscernible] that Intensity co-authored, but we see a global systemic. This is the translational science that we hope to achieve in clinical studies. And as I said, we dose based on the size of the tumors and the tumor burden. That's important. Current systemic therapies do fixed weight -- based on your height and weight or fixed dose, two patients coming in with multiple different tumor burden, one on the left here -- on the left screen. And on the right, you can see that these people have a very different outcome likelihood when they have multiple big burdens of tumors. We have a personalized dose to your personal tumor burden, and we give a personalized immune response based on your cancer mutations. Okay. So now I'd like to turn the microphone over to Dr. Thomas, who will go through some of the data on the study design and safety.

Yes. Thank you, Lou. Thanks for the overview and the background. So to put things into context, I'm just going to kind of give an overview of the study. So first, to height the novelty of this, as Lou was discussing here, a review of the literature shows that we really only found one prior study using intratumoral chemotherapy that is looking at survival after intratumoral injections. In this study, patients were not metastatic. It was done prior to a surgery. So really, this approach used in this study was very, very novel. All right. So as Lou discussed, this technology has previously been published. And this study that was published is the IT01 study evaluating INT230-6 in metastatic refractory patients with solid tumors. And as Lou alluded to, the dose was based on the tumor diameter volume, so customized for each patient. And on a subsequent slide, I'll go into a little more details about how that is done and how it changed over the course of this study. But we determined, we could give up to 175 milliliters of INT230-6 safely in this study. And as you'll see, INT230-6 does activate an anti-tumor immune response, and there's evidence of abscopal effects in immunologically active or cold tumors, which we predicted preclinically and have shown here in this human study as well, as you'll see. Next. And as we'll discuss -- we're seeing favorable disease control rates and overall survival compared to other sort of historical Phase I and II studies with traditional systemic administration. All right. Next slide. So the study design, the Phase I of this study was based on a plus 3 traditional dose escalation design. The study had 6 monotherapy cohorts, 5 were dose escalation where the dose was increased within each patient, which I'll go over in a subsequent slide. A sixth cohort was added with a limit of 175 milliliters with the goal to provide additional safety and efficacy data. Next slide. So this slide goes over how the dose of the drug was changed over the course of the study. On the top left, you can see we initially dosing in a 1:4 ratio. Again, we're measuring the tumor volume based on CT scans of patients. And based on an estimated tumor volume, we would dose INT230-6 in a ratio of 1:4, but we had cutoffs of the maximum total volume initially. So in the first cohort, only 5 milliliters, very small amount of the drug was the maximum amount given. And through these cohorts, you can see we adjusted the dosing interval from 28 days to every 14 days. We also adjusted the dosing ratio from 1:4 to 1:2 to 1:3 and then also adjusted the maximum volume that could administered at any even dosing session. And you can see in the bottom right in the final and the sixth cohort, we ended with a dosing ratio of 1:3 dosed every 14 days and a maximum volume of 125 milliliters in any given session. Okay. Next slide. Here's the demographics for the study. The takeaways here, this is very representative of a typical Phase I solid tumor study. So we had a range of different tumor types enrolled as you can see on the right, the most common was sarcoma patients of various different histologies, but really a wide range of solid tumors represented in the study, as you can see. Next slide. Now moving on to safety. So first, the idea with this drug, giving intratumoral therapies is that we can spare some of the systemic toxicity. So first, showing our pharmacokinetic data, does the drug actually stay in the tumors? And what you can see here is very, very little of the excipients or the component of INT230-6 did get into systemic circulation. So if we look at vinblastine, for example, the values here compared to IV vinblastine administration are 95% or greater stays with the tumor. The comparative pharmacokinetics to IV, it was very favorable here. So this -- looking at the PK data shows us that what we saw preclinically seems to be playing out in the human data as well. Most of the drug staying within the tumors as they're injected. Next slide. So as we had hoped, this translated into a well-tolerated drug here. So intratumoral dosing of INT230-6 was generally well tolerated. There were no dose-limiting toxicities throughout dose escalation, which notable in a Phase I study. Drug retention seemed to be independent of any cancer type location or size. So we didn't seem to see more adverse events in tumors injected in the liver or soft tissue or other places. It seems to be universal regardless of where the tumors were located. Only 7 patients had Grade 3 treatment emergent adverse events related to the study treatment. Notably, we had no Grade 4 or 5 adverse events. The most common drug-related adverse events were injection siting as would be expected. Fatigue, a brief amount of mild nausea and compared to systemic administration of these drugs in cisplatin and vinblastine, this is a very favorable toxicity. And so our experience with the patients on the study is that it was well tolerated and especially compared to systemic therapies in general. So this study highlights an effective dosing strategy based on total tumor burden and the tumor size. Next slide. And so I think we'll turn this over now to Anthony to describe the efficacy and other results of the study.

Thank you, Lou, and Jacob for the update. So we've learned so far that the drug mostly retained in the tumor and it is very safe, both providing proof of concept for this technology and why it was developed. Let's see how this translates into outcomes in patients. Here, we show what's called the disease control rate, which was the primary -- not primary, but the main way that we assessed benefit in patients in this study, the secondary endpoint. Disease control rate is a combination of patients who had an objective response, like a complete response or partial response or stable disease lasting 2 months or longer. So the light blue bars reflect -- show the disease control rate in all patients on the left with monotherapy, so 75% disease control rate. And then you see that patients with a partial response are in the dark blue. So 2 of them, this is by the traditional RECIST criteria. And then 72% of patients had stable disease. Only a minority of patients, patients had progression as their main or first outcome on their first scan. It became evident during the conduct of the study that outcomes were looking better if injected more drug into more tumors. So based on this, we did an exploratory analysis to look at disease control rate in patients who had 40% or greater of their total tumor burden injected versus less than 40% of their total tumor burden injected. So these are the two next set of bars. So in the middle, you see patients who had 40% or greater of their total tumor burden injected. You see their disease control rate is at 83%. For patients who had less than 40% of the tumor burden injected, their disease control rate is 50%. The partial responses by RECIST were only in patients who had greater than 40% of their tumor injected. Next slide. Now these are images to highlight some important concepts. This is a patient with sarcoma. In the left panel, you see the baseline images of the tumors with their measurements. So 6 centimeters on the right box and 14 centimeters on the left. And this is in March 2018 at baseline. The third follow-up here are images from October 2018. I see that the tumors are definitely smaller. So the 6 centimeter lesion came 3 centimeters, so 14 came 12. But if you look at the content of the tumors, they a lot more darker areas that are broken up. So darker areas represent necrosis or death of the cancer cells and the pickup also reflects that some of these tumors are becoming cystic rather than solid active cancer tumors. Next slide. Another important concept that we observed during the conduct of this trial. When we are injecting large volumes into these tumors, RECIST -- traditional RECIST measurements become a challenge because with the -- the tumor may increase in size initially due to the volume that we are injecting and due to the recruitment of immune cells so there is an inflammatory reaction that happens in the tumors as well, that is necrosis like we showed you. So the traditional way to look at tumor size change by RECIST criteria really is not the ideal way to assess outcome here. So looking at overall survival became very important. So here, what you see in the blue curve represents median overall survival of all 64 patients that were treated. And here, we see a median overall survival of about 12 months. To provide a frame reference, when you look at published data of outcomes of solid tumors in Phase I studies, the median overall survival, especially with chemotherapy, sits around 4 to 7 months in most reported manuscripts. So compared to historical outcomes, this median overall survival appeared very promising. Then similarly, we did the analysis of survival based on total tumor burden injected. So if 40% or greater of the tumor burden was injected, the median survival was close to 19 months, 18.7. And if it's less than 40% burden injection injected, the median survival was 3 months. Next slide. This benefit that was more evident when we acted higher tumor burden was consistent across different tumor burden quartiles. So whether patients had low tumor burden in Panel A or the highest tumor burden in Panel D and there are other in between. The green bars reflect patients who had greater than 40% of their tumor burden injected, and you see that remained on study longer with longer survival versus the ones in red, which had less than 40% of their tumor burden injected and appear to be towards the bottom of these swimmer plots. So this difference based on tumor burden injected was consistent, independent of tumor burden and size. Next slide. Now you heard earlier that sarcoma patients represent the majority of the patients enrolled in this study. And based on this, we looked at this subpopulation, and it's 15 patients. And the blue curve shows the median survival of all sarcoma patients, a variety of histologies. Median survival here is 21 months. These are heavily pretreated patients, except the chordoma patients. Some of them had -- there is no approved therapy. Some of them had 0 other prior treatments. In green, you see the sarcoma patients who had greater 40% of their tumor injected and median survival was not reached at the time of this report. And those who had less than 40% of their tumor burden injected had a mean survival of 4 months. Next slide. These are the 15 patients who had 21 or longer survival. And you see on the listing of the different tumor types or malignancies. And you see it's actually a wide variety of epithelial cancers, adenocarcinoma, sarcomas, squamous cell cancers, so a broad variety. But currently, there is a high proportion of different types of sarcoma represented here. And the majority of these patients who had greater than 21 months survival had more than 40% of their tumor burden injected. You also see in columns the total tumor burden, the cumulative total dose that was given and the individual overall survival for each one of these patients. Of note, that these 15 patients had a median of 4 prior therapies. So these are heavily pretreated patients. Next slide. Now you had heard that preclinically, the hypothesis was that injecting this formulation into the tumor is going to also change the tumor microenvironment. It's not only going to kill cancer cells, but it's going to change the tumor microenvironment. So on top, we show H&E sections from one, for example. So to the left an Panel A is the pretreatment biopsy and Panel B is the biopsy after 2 doses of INT230-6. The purple color represents the cancer cells. And you see the left panel has a lot of purple. It's very dense with tumor. And you see that after injections in Panel B, the purple becomes quite scarce, showing the direct effect, direct tumor killing of this drug when injected in the tumor. Now the bottom 2 panels show what happens as far as the immune system and tumor microenvironment as well. So there are different colors here to represent different things. The blue colors and the left panel represent cancer cells. You see in the right panel that they largely disappear. And then you see that after treatment on the right, the right panel, there's a lot more yellow and orange, representing the influx of CD4 and CD8 activated T cells that are coming into the tumor microenvironment and hopefully participating in the antitumor that we are achieving here. Next slide. It was our hypothesis that this change in the immune system is not going to be only local in the tumor, but may have a systemic effect throughout the body. What I'm going to show here certainly support that hypothesis. Here we show reductions in the size of certain tumors in individual patients, but these tumors were not injected. These are uninjected tumors that showed decrease in size. Each bar represents an individual tumor. So some patients had more than one tumor that was not injected that showed shrink. For example, you see 2 bars here in the middle, labeled 8. These are 2 different tumors in an individual patient that were not injected still showed shrinkage. So this occurred in patients, which is roughly 20% of the patients injected with a tumor burden of -- where 40% or of the tumor burden was treated. This may be an underestimate because we were not really capturing tumors that were under 1 centimeter. And certainly, many of the smaller tumors may have disappeared as well, but we did not capture that in this trial. So this may be an underestimate. Next slide. So to summarize, INT230-6 has a favorable safety profile that supports that the majority of the active drugs are leaned in the tumor and there is minimal systemic exposure, which helps with the safety profile. This monotherapy shows promising antitumor efficacy and nearly 12 months median overall survival in all-comers in this trial. This favorably compares to that of systemic therapy for solid tumors with historically reported data of median overall survivals of 4 to 7 months, as I mentioned earlier. INT230-6 dose relative total tumor burden showed high survival in patients as more tumor burden is treated. This is the 40% cutoff that we used. As a proof of concept, INT230-6 did induce infiltration of activated immune cells in the tumor microenvironment in the study when we did biopsies pretreatment and on treatment. INT230-6 dose volume is retained within the tumor. There is also immune cell infiltration that assist formation from a necrotic tumor tissue. And as I said earlier, these effects can confound the interpretation of traditional RECIST measurements. So there are some limitations of this study, one in randomized single-arm trial design as is the case of most Phase I trials. It has a limited number of patients. There is variability in imaging frequency among the different patients and cohorts. There are nonavailability of details regarding specific treatments used post INT230-6, which may have influence outcome. There's also heterogeneity of tumor types, volumes and tumor burden, which limit comparison across subgroups and led to the wide 95% confidence intervals. Further studies are certainly warranted to explore potential benefits of this drug diverse cancer types. Thank you.

Okay. So Rocco, I think we're going to start the question-and-answer session. Do you want to explain that a little bit?

[Operator Instructions] Our first question comes from Kumar Raja with Brookline Capital Markets.

Congratulations on the data. I just had a question with regard to the tumor-specific antigen. What are you seeing in terms of tumor-specific antigen, especially with regard to that tumor burden as well as when you're able to target most of these cancer cells and how that correlates to the systemic effects.

So I don't know that we look for tumor-specific antigen, particularly in this study. We simply did the immunohistochemistry. But the tumor-specific antigen was done on the mouse studies, but we didn't look at it here in this study.

Okay. Great. In terms -- you showed a slide with regard to the T cells. So how does that correlate with regard to the tumor burden as well as the ability to target more of the tumor cells.

Anthony, would you want to address that?

Yes. So the number of patients who had pre- and on-treatment biopsies that were analyzable, it was not 60-40. It was not all patients. So it was a smaller subset. So it became very difficult to make any correlations between the degree of T cell infiltration and outcome, if that's what you're asking. We did not do this analysis. The numbers are too small. But what's interesting to us is that in all patients, except one who have pre- and on-treatment biopsies, we did see this significant increase in T cells within the tumor microenvironment, dependent of their outcome.

[Operator Instructions] Actually, it looks like -- I apologize, sir. It looks like we do have a question now from James Molloy at Alliance Global Partners.

Matt on, for Jim today. Congrats on the publication. First, for Lou. Just wanted to ask about the next steps for the Phase III that's currently on pause due to funding. What is that? What are the next steps there look like? What kind of capital needs to be raised before it gets restarted? And how do these results and then what's gone on in the past day or so affects that plan, if at all?

So just to give a background on what is -- where the status is of the Phase III. So we have acceptance in eight countries. Eight country regulatory authorities have approved the study design. Our drug alone as a local therapy in metastatic disease of 3 subtypes of sarcoma, liposarcoma, undifferentiated pleomorphic sarcoma, UPS and leiomyosarcoma. So patients come in with those tumor burdens and they are randomized either to our drug alone at a 2:1 ratio or the standard of care systemic chemotherapy, which can be anyone depending on the tumor type and the doctor's choice of either trabectedin, eribulin or pazopanib, which are four different routes of administration and intratumoral, a port, an IV, and an oral. So this is not a blinded study. It is randomized, controlled. But the endpoint is overall survival. As Dr. El-Khoueiry said, RECIST confounds our endpoint of trying to determine progression. So we are using overall survival as a primary efficacy endpoint. We'll be taking interim looks during that study. So to go to your question we are maintaining that study, in that we are continuing to treat the patients. The patients are receiving monitoring and care and getting dosed in the maintenance phase. We are doing the pharmacovigilance. We're maintaining contact with the regulatory authorities. We are following SUSARs, if there are any. And so that study could be reenergized with funding which we feel would be about $25 million at this point. To really -- we don't want to start it and then stop it again. So to complete enrollment and to complete getting to the interim looks that we've designed into the study, we really want to have enough money to pay for it. So look, today, we announced some funding. I think this is a very good sign that this was a fundamental institutional investor that's come in, big, well-known name. Hopefully, that will bring in others, and we are excited to be talking with our bankers about getting the capital we need and potentially with partnerships, ideally with a pharmaceutical company that wants to help us pick up a Phase III program, we'd be more than welcome to talk about that. So these are the kinds of things that we're looking at today, funding, we did a very nice movement in the stock yesterday. And hopefully, we will be able to get the funds to allow this very promising, I believe, very promising new product to be fully tested and vetted in a randomized controlled study. Randomized controlled studies are the gold standard of what we do. And until you have that, the regulatory authorities will not obviously approve the drug. So that's what we're trying to complete.

All right. Much appreciated. And specific to this study, the study stated that daily NSAID use was an exclusive criteria, were any patients who experienced tumor pain or any other AEs pain-related lost off study due to starting NSAIDs at all? Was that a concern?

So I can address that. Yes. So NSAIDs are one form of a pain medication, but they can increase the risk of bleeding, which is why those were not allowed. These injections are done by radiologists with needles, sometimes into deep tumors. So we obviously want to avoid any bleeding issues. So some patients did experience pain after injections, but there are plenty of other pain medications that can safely be used that don't cause increased risk of bleeding. So specifically to your question, I don't believe there are any patients that were lost because they could not use NSAIDs. They can use Tylenol or other prescription pain medications to manage the pain, and that generally was not an issue.

Okay. Great. And then finally, just on the end number. I know in the Lancet pub, it was 64. I think you guys said at some point, mentioned 110, but I don't know if that was a different study. Could you just comment on in the Phase I, how many patients there were and how many patients were added in the Phase II, I guess, in the full intent-to-treat population?

So the 110 number is because there were two cohorts in combination with immunotherapy. I'll let Anthony or Jacob describe those cohorts, If they had the additional patients in either cohort with immunotherapy or -- and I'll let Anthony or Jacob describe those cohorts.

Sure. Just to be clear, those 2 cohorts were not reported in this paper. We did not report on the patient characteristics or their outcomes or the safety of these cohorts. One cohort combined INT230-6 with an anti-PD-1 antibody, the other cohort combined it with an anti-CTLA-4 antibody. These were naturally smaller cohorts. But again, that are not shown in this publication.

Yes. Just to add to that, those cohorts we received from Merck, the pembrolizumab that we received from Bristol, the CTLA-4. We plan to draft the manuscript and submit that for publication. Now this first cohort -- first manuscript is published with our drug alone, which is the key to what we wanted to look at, but we would like to submit another manuscript at an appropriate time.

[Operator Instructions] Please proceed, sir.

Yes. Me? There's no question. Okay. No question in the queue. Yes. So look, the -- this study, as Dr. El-Khoueiry and Dr. Jacob Thomas reported with the data is really a, I believe, good translation of what we saw in the mice, which is why the Lancet when they decided which publication they felt that this would be best in was in their eBioMedicine Journal, which is a translational science specific not just for cancer, but for multiple other medical translations going from one species to another. And so I think it was the right choice by the editors when they were reviewing. Their questions and their comments caused us to do a lot of additional analysis. It was the reviewers that suggested we look at the quartile to make sure that all the benefit wasn't just in small tumors, that the -- for or a good assessment. We listened to a lot of what the reviewers said, and we were able to I think, address all their concerns. It was a good process because they asked for a lot of background data, background information, which increased the word count substantially. We had written it for 3,000 words and the additional questions from the reviewers moved it to 5,500 words. So there was clearly -- this is really a new way to kill diffusion-based intratumoral technology is new. And there were a lot of background questions as to why we chose the parameters that you see in the slide that Dr. Thomas presented earlier in this talk with the different cohorts and the different ratios and the different volumes and the escalation in the patient. This was all part of the discovery process to determine the proper doses for the -- for this new technology. So we're coming up on the time limit. Actually, we're a little bit past what we've planned. Are there any other questions, Rocco?

Not at this time, sir.

Okay. Well, I would like to thank everybody who's been on the call or who will be listening in the future to this call. I'd like to thank the patients, their families, the investigators who participated, and the authors, other authors on this paper. It was a team effort by a lot of people, they're coordinators, the nurses, and the doctors, the administrators, the regulatory people at the hospitals, what goes into a clinical trial, even one of this size, with 8 or 9 sites, is enormous -- an enormous effort and our CRO management, catalyst did a wonderful job of coordinating it. And thanks to Dr. El-Khoueiry and Dr. Thomas for today. And Dr. El-Khoueiry and Dr. Thomas were instrumental in telling us to be more aggressive about dosing at a more greater frequency. And I remember the call we had where we needed to move to once every 2 weeks. As Dr. El-Khoueiry said, let's go to every 2 weeks and that showed to be safe and effective in a much better way than what we were using at the time. And so with that, I will again sign off and thank you, Dr. El-Khoueiry, you, Dr. Thomas, for your time today early in the morning where you are in L.A. and now you have to get to work. So I appreciate all of your time and effort to help with this presentation, with the paper, with the editing, with the submissions to the editors, there's an enormous amount of work in running a study, but it's almost as much to try to get a paper over the finish line in -- on a first new novel technology. And without Dr. El-Khoueiry, he's a senior author, and Jacob, who took the first -- Dr. Thomas, who took the first draft, it would not have gotten done. And so thank you for all the work that you've done on this new technology. Very much appreciated, certainly by our staff and our Board and the patients that I think benefited from the trial. Thank you.

Thank you, sir. Today's conference has now concluded, and we thank you all for attending today's presentation. You may now disconnect your lines, and have a wonderful day.