Therapeutics Lancet Discovery Group, eBioMedicine, publishing webinar. All participants will be in listen-only mode. After today's presentation, there will be an opportunity for analysts to ask questions. To ask a question, please dial 412-317-6060 or click the link to join via webphone. Once connected, please press star one on your telephone keypad. To withdraw your question, please press star then two. 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. 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. They 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 call. By the way, I am so honored and pleased to be joined by Jacob Thomas, a first author, and Dr. Anthony El-Khoueiry from USC. We are thrilled with the result of this study, and we are looking forward to a very robust discussion of it. The call, we may be making forward-looking statements, including statements that address Intensity 's expectations, future performance, including, but not limited to, ability to complete our clinical trials for our drug INT230-6. Forward-looking statements involve risks or factors that may cause actual results 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 accompany this call, particularly the cautionary statements contained therein. I'll remind everybody, the contents of this call are time-sensitive. The information is accurate only as of today, the 31st, 2025. Except as required by law, Intensity disclaims any obligation to publicly update or revise any information that reflects events or circumstances that occur after this call. I'm going to first 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. 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 Southern California Keck School of Medicine, and an oncologist with the USC Norris Comprehensive Cancer Center. Dr. El-Khoueiry is an Associate Director of Clinical Research and Chief of Section Development at the same hospital at USC Norris. He is also the Senior and Corresponding Author and the Section Chief for the Developmental phase I Unit at USC. Really glad to have them and appreciate their time today. Okay. Background. Look, a little bit about the origin of the technology. I'm the founder of the company. I'm the mentor of the technology. I'm a chemical engineer by training, and 15 years ago, when immunotherapies were coming into play, I thought about cancer. We thought about the immunotherapies. They're stopping the gas or releasing the brakes. 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. Perhaps we would get better efficacy and safety. 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 an immune response? It It was the idea originally, and you're going to see the results of that work and that idea. The compound we're working with complies with three elements. A molecule called sodium hydroxybenzoyl amino octanoate, which we have referred to as SHAO. It is combined with Cisplatin and vinblastine, two very potent toxic agents in a fixed ratio. This formulation of this drug candidate came out of a two-year screening program that we did with a number of vendors that contract research. Drugs were showing very potency. Interestingly, both drugs have both direct killing and immune-activating effects. These are all referenced here. What we do is we take these three ingredients. The SHAO actually can make molecules, they're amphiphilic molecules of SHAO, and it can make molecules soluble in fat and water at the same time. Naturally, we mix these together. It's a simple mixture. We add some ingredients. We keep it in a vial stored, and it's a three-year shelf life when we've scaled it up. This is some ground information that's in the paper. It's from our paper, Intensity published. It shows that drugs that are water-soluble do not penetrate into tumors. This is human pancreatic cancer in a 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. Intratumoral technologies have tried to use methods to do retention or miss the problem. The problem isn't retention, although that is an issue. The problem is dispersion throughout the tumor and cell penetration. That SHAO molecule, when you add that SHAO 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 the 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'll disperse through the tumor, diffusing through, follows the natural laws of diffusion. You can see that now there is little leakage. There is a high amount of absorption to the drug. We dose based on the size of the tumor because the diffusion may scope as a volume, and it'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 as an individual injection. In partnership with the National Cancer Institute, we were awarded a CRADA in 2014. With that CRADA, we were able to show a mechanism by which this drug, as a local therapy, can create a systemic potent anti-cancer protective immunity. Not only do we protect and cause uninjected tumors to shrink, as is cited in this paper by Dr. Tanya Bloom that Intensity co-authored, but we do see a global systemic. This is the translational science that we hope to achieve in clinical studies. As I said, we dose based on the size of the tumors and the tumor burden. That's important. Systemic therapies do fixed weight or based on your height and weight or fixed dose. Two patients coming in with multiple different tumor burdens, one on the left here on the left screen and one 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 to your personal tumor burden, and we give a personalized immune response based on your cancer's mutants. Now I'd like to turn the microphone over to Dr. Thomas, who will go through some of the data on the study's design and safety. Dr. Thomas? All right. Thank you. Thanks for the overview of the background. To put things into context, I'm just going to give an overview of the study. First, to highlight the novelty of this, as Lew was discussing here, review of the literature shows that we really only found one prior study using intratumoral chemotherapy. That was looking at survival after intratumoral injections. In this study, patients were not metastatic. It was done prior to a surgery. This approach used in this study was very novel. Next. As Lew discussed, this technology has previously been published. This study that was published is the IT01 study evaluating INT230-6 in metastatic refractory patients with solid tumors. As Lew alluded to, the dose was based on the tumor diameter or volume, so customized for each patient. On a subsequent slide, I'll go into a little more detail about how that is done and how it changed over the course of this study. We determined we could give up to 175 milliliters of INT230-6 safely in this study. As you'll see, INT230-6 does activate an intratumoral 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. As we'll discuss, we're seeing favorable disease control rates and overall survival compared to other similar historical phase I and II studies with traditional systemic administration. Next slide. The study design, the phase I of this study, was based on a + 3 + 3 traditional dose escalation design. The study had six monotherapy cohorts. Five 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. This slide goes over how the dose of the drug was changed over the course of the study. In the top left, you can see we initially were dosing in a one-to-four ratio. We're measuring the tumor volume based on CT scans of patients. Based on an estimated tumor volume, we would dose INT230-6 in a ratio of one to four. We had cutoffs of the maximum total volume initially. In the first cohort, only 5 milliliters, a very small amount of the drug, was the maximum amount given. 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 one to four to one to two to one to three. We also adjusted the maximum total volume that could be administered at any dosing session. You can see in the bottom right, in the final sixth cohort, we ended with a dosing ratio of one to three, dosed every 14 days, and a maximum volume of 175 milliliters in any given session. Next slide. Here's the demographics for the study. The takeaways here, this is very representative of a typical phase I solid tumor study. 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. The idea with this drug, giving intratumoral therapies, is that we can spare some of the systemic toxicity. First, showing our pharmacokinetic data, does the drug actually stay in the tumors? What you can see here is very little of the excipients or the components of INT230-6 did get into systemic circulation. If we look at vinblastine, for example, the values here compared to IV vinblastine administration are 95% or greater, stays within the tumor. The comparative pharmacokinetics to IV was very favorable here. This look 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. As we had hoped, this translated into a well-tolerated drug here. Intratumoral dosing of INT230-6 was generally well tolerated. There were no dose-limiting toxicities throughout dose escalation, which is notable in a phase I study. Drug retention seemed to be independent of any cancer type, location, or size. 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 seven patients had grade B treatment adverse events related to the study treatment. Notably, we had no grade four or five adverse events. The most common drug-related adverse events were injection site pain, as would be expected, fatigue, and a brief amount of mild nausea. Compared to systemic administration of these drugs, since Cisplatin and vinblastine, this is a very favorable toxicity. Our experience with the patients on the study is that it was well tolerated, especially compared to systemic therapies in general. This study highlights an effective dosing strategy based on total tumor burden and the tumor size. Next slide. I think we'll turn this over now to Anthony to describe the efficacy and results of the study. Thank you, Lew and Jacob, for the update. We've learned so far that the drug is mostly retained in the tumor and that 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 main way that we assessed benefit in patients in this study. It was a 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 two months or longer. The light blue bars show the disease control rate in all patients, first on the left with monotherapy, so 75% disease control rate. You see that patients with a partial response are in the dark blue, so two of them. This is by the traditional research criteria. Then 72% of patients had stable disease. Only a minority of 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 we injected more drug into more tumors. 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. These are the two next set of boxes. 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%. Patients who had less than 40% of tumor burden injected, their disease control rate is 50%. The partial responses by researchers 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 buttocks and 14 centimeters on the left. This is in March 2018 at baseline. The third follow-up. Here are images from October 2018. You see that the tumors are definitely smaller. The six centimeter lesion became three centimeters, the 14 became 12. If you look at the content of the tumors, they have a lot more darker areas that are broken up. Darker areas represent necrosis or death of the cancer cells. The makeup also reflects that some of these tumors are becoming stick rather than solid active cancer tumors. Next slide. Oops. Yeah, sorry. Another important concept that we observed during the conduct of this trial, when we're injecting large volumes into these tumors, traditional RECIST measurements become a challenge because the tumor may increase in size initially due to the volume that we are injecting and due to the recruitment of immune cells. There's an inflammatory reaction that happens in the tumors as well. That is necrosis, like we showed you. The traditional way to look at tumor size change by RECIST criteria really is not the ideal way to assess outcome here. Looking at overall survival became very important. 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 of 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 four to seven months in most reported manuscripts. Compared to historical outcomes, this median overall survival appeared very promising. Similarly, we did the analysis of survival based on total tumor burden injected. If 40% or greater of the tumor burden was injected, the median survival was close to 19 months, 18.7. If it's less than 40% tumor burden injected, the median survival was three months. Next slide. This benefit that was more evident when we injected higher tumor burden was consistent across four different tumor burden quartiles. 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. 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 appeared to be towards the bottom of these swimmer plots. This difference based on tumor burden injected was consistent independent of tumor burden and size. Next slide. You heard earlier that sarcoma patients represent the majority of the patients enrolled in this study. Based on this, we looked at this population. 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 for derma patients, some of them had, there is no approved therapy. Some of them had zero other prior treatments. In green, you see the sarcoma patients who had greater than 40% of their tumor injected, their median survival was not reached at the time of this report. Those who had less than 40% of their tumor burden injected had a median survival of four months. Next slide. These are the 15 patients who had 21 months or longer survival. You see on the list a listing of the different tumor types or malignancies. You see there's actually a wide variety of epithelial cancers, adenocarcinomas, sarcomas, squamous cell cancers, so a broad variety. There is a high proportion of different types of sarcoma represented here. 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 these 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, these 15 patients had a median of four prior therapies. These are heavily pretreated patients. Next slide. 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. On top, we show H&E sections from one, for example. To the left, panel A is the pretreatment biopsy. Panel B is the biopsy after two doses of INT230-6. The purple color represents the cancer cells. You see the left panel has a lot of purple. It's very dense with tumor. You see that after injections in panel B, the purple becomes quite scarce, showing the direct effect, the direct tumor killing of this drug when injected into the tumor. The bottom two panels show what happens as far as the immune system and tumor microenvironment as well. There are different colors here that represent different things. The blue colors in the left panel represent cancer cells. You see in the right panel that they largely disappear. 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 anti-tumor act 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 also have a systemic effect throughout the body. What I'm going to show you here certainly supports 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. Some patients had more than one tumor that was not injected that showed shrinkage. For example, you see two bars here in the middle, labeled eight. These are two different tumors in an individual patient that were not injected and still showed shrinkage. This occurred in 10 patients, which is roughly 20% of the patients injected with a tumor burden of where 40% or more of their tumor burden was treated. This may be an underestimate because we were not really capturing tumors that were under one centimeter. Certainly, many of the smaller tumors may have disappeared as well, but we did not capture that in this trial. This may be an underestimate. Next slide. To summarize, INT230-6 has a favorable safety profile that supports that the majority of the active drugs are retained in the tumor, and there is minimal systemic exposure, which helps with the safety profile. This monotherapy shows promising anti-tumor efficacy and nearly 12 months of 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 four to seven months, as we mentioned earlier. INT230-6 dosed 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. There is cyst formation from necrotic tumor tissue. As I said earlier, these effects can confound the interpretation of traditional resist measurements. There are some limitations to this study. One, it's not a 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 is non-availability of details regarding specific treatments used post INT230-6, which may have influenced outcome. There's also heterogeneity of tumor types, volumes, and tumor burden, which limits comparisons across subgroups and led to the wide 95% confidence intervals. Further studies are certainly warranted to explore the potential benefits of this drug in diverse cancer types. Thank you. Okay. Rocco, I think we're going to start the question and answer session. You want to explain that a little bit? Yeah, of course, sir. To ask a question, put down 412-317-6060 or click on the link in your webcast window. Once again, the number is 412-317-6060 or click on the link in your webcast window. Once you're on the call, you may press star then one on your telephone keypad, and that will join you to the screen queue. If you're on a speakerphone, we ask that you please pick up your handset before pressing the keys. To withdraw your question, please press star two. Once again, ladies and gentlemen, once you are connected to the call, please press star then one to join the question queue. Our first question today comes from Okay, go ahead. I thought we had to, yeah, go ahead, Rocco, please. Absolutely. Our first question comes from Kumaraguru Raja with Brookline Capital Markets. Please go ahead. Thanks for taking my questions and 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 the tumor burden, as well as when you are able to target most of these cancer cells, and how that correlates with the systemic effects? I don't know that we looked at tumor-specific antigen, particularly in this study. We simply did the immunohistochemistry. Tumor-specific antigen was in the mouse studies, but we didn't look at it here in this study. Let me know. Okay. In terms of your short slide with regard to the T cells, 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? Yeah. The number of patients who had pre and on-treatment biopsies that were analyzable was not 64. It was not all patients. It was a smaller subset. 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 the analysis. The numbers are small. What's interesting to us is that in all patients except one who had pre and on-treatment biopsies, we did see this significant increase in T cells within the tumor microenvironment, independent of their outcome. Okay, great. Thanks so much. Yeah, so— Okay, go ahead, Rocco. I was just going to read here a little bit. Go ahead. Just wanted to remind everyone, if you had a question, to dial 412-317-6060 and then press star when you get into the call. Please go ahead, sir. Actually, it looks like I apologize. It looks like we do have a question now from James Molloy at Alliance Global Partners. Please go ahead. Hey, it's Matt on for Jim today. Thanks for taking our questions and congrats on the publication. First, for Lew, just wanted to ask about the next steps for the phase III that's currently on pause due to funding. What are the next steps there look like? What kind of capital needs to be raised before it gets restarted? How do these results and what's gone on the past day or so affect that, if at all? Just to give a background on what the status is of the phase III. We have acceptance in eight countries. Eight regulatory authorities have approved the study design. The study is our drug alone, a local therapy, in metastatic disease of three subtypes of sarcoma: liposarcoma, undifferentiated pleomorphic sarcoma (UPS), and leiomyosarcoma. Patients come in with those tumor burdens, and they're randomized either to our drug alone at a two-to-one ratio, or the standard of care systemic chemotherapy, which can be any one depending on the tumor type and the doctor's choice of either trabectedin, eribulin, or pazopanib, which are four different routes of administration: an intramuscular, a port, an IV, and an oral. This is not a blinded study. It is randomized controlled. 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 the primary efficacy endpoint. We'll be taking interim looks during that study. 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 regulatory authorities. We are following suicides or if there are any. That study could be re-energized with funding, which we feel would be about $25 million at this point. We don't want to start it and then stop it again. 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. Today we announced some funding. I think this is a very good sign that this was a fundamental institution 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, 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. These 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. That's what we're trying to complete. All right. Thank you for the color, much appreciated. Specific to this study, the study stated that daily NSAID use was an exclusion criteria. Were any patients who experienced tumor pain or any other AEs related lost off study due to starting NSAIDs at all? Was that a concern? I can answer that. 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. We obviously want to avoid any bleeding issues. 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. Specifically to your question, I don't believe there were any patients that 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. Thank you. Finally, just on the end number, I know in the Lancet pub of 64, I think you guys had 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, and I guess in full intent to treat population? The 110 number is because there were two cohorts in combination with immunotherapy. I'll let Anthony or Jacob describe those cohorts. They had the additional patients in either a cohort with immunotherapy, and I'll let Anthony or Jacob describe those cohorts. Sure. Just to be clear, those two 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 anti-PD-1 antibody. The other cohort combined it with an anti-CTLA4 antibody. These were naturally smaller cohorts, but again, they are not shown in this publication. Yeah, just to add to that, those cohorts, we received from Merck the pembrolizumab, and we received from Bristol the CTLA4. We plan to draft a manuscript and submit that for publication. Now, this first cohort, this first manuscript is published with our drug alone, which is the key to what we wanted to look at. We would like to submit another manuscript at an appropriate time. Great. Okay. Thank you guys for the color and the clarification, and congrats again on the publication. Thank you. As a reminder, please go ahead, sir. No, go ahead, Rocco. You're going to have a course of. Sorry about that. Let me know when you want me to wait. Hopefully, you're finding that. Okay. I just wanted to give everyone a reminder that to join the question queue, please dial 412-317-6060 or click the link on your webcast window. Once you do join the call, please star one to join the question queue so we know we have a question. Once again, that's 412-317-6060, or you can click the link on your webcast window. Please proceed, sir. There's no question. No question. No, nothing as of now. Yes. No question in the queue. Yeah. This study, as Dr. Anthony El-Khoueiry and Dr. Jacob Thomas reported with the data, is really, I believe, a 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. I think it was the right choice by the editors when we were reviewing. Their questions and their comments caused us to do a lot of additional analysis. The reviewers suggested we look at the quartile to make sure that all the benefit wasn't just in small tumors, that for 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 to 5,500 words. There was clearly, this is a real new way to kill. DfuseRx -based intratumoral technology is new. 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 patient. This was all part of the discovery process to determine the upper doses for this new technology. We're coming up on the time it. Actually, we're a little bit past what we've planned. Are there any other questions, Rocco? Not at this time, sir. Okay. I'd like to thank everybody who's been on the call or who will be listening in the future to the call. I'd like to thank the patients, their families, the investigators who participated, and the other authors on this paper. It was a team effort by a lot of people, their coordinators, the nurses, the doctors, the administrators, the regulatory people at the hospital. What goes into a clinical trial, even one of this size with eight or nine sites, is enormous, an enormous effort. Our CRO, the management catalyst, did a wonderful job of coordinating it. Thanks to Dr. El-Khoueiry and Dr. Thomas for today. Dr. El-Khoueiry and Dr. Thomas were instrumental in telling us to be more aggressive about dosing at a greater frequency. I remember the call we had where we needed to move to one every two weeks. It was Dr. El-Khoueiry, let's go to every two weeks and show it to be safe and effective in a much better way than what we were using at the time. 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 LA, and now you have to get to work. I appreciate all your time and effort to help with this presentation, with the paper, with the editing, with the submits to the editors. There's an enormous amount of work in running a study. It's almost as much to try to get a paper to the finish line on a first novel technology. Without Dr. El-Khoueiry as a senior author and Jacob, who took the first—Dr. Thomas, who took those drafts, it would not have gotten done. Thank you for all the work that you've done on this new technology. Very much appreciated 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 concluded, and we thank you all for attending this presentation. You may now disconnect your lines and have a wonderful day.