Intensity Therapeutics, Inc. (INTS) September 2026 Conference Transcript

Good morning, everyone, and thank you for joining the HC Wingright 28th Annual Global Investment Conference. We're confident we're going to be able to provide value to you with over 500 companies presenting across multiple sectors devoted to the life sciences, cryptocurrency, technology, media, and telecommunications.

Please join us for one-on-one meetings, corporate presentations, and expert panels. with that said have a productive and enjoyable day and i'd like to introduce our first presenter i'd like to welcome mr lewis bender who is the ceo of intensity therapeutics well uh good morning uh good afternoon and good evening depending on when you're looking at this and thank you very much to the wainwright people and sean for the introduction the opportunity to present i'm going to talk about our new technology for cancer we are a late stage biotech company, and we're developing really a new way to kill cancer, one that causes immunological cell death and developed based on the technology that's used in the Wagovi pill to transport molecules safely through tissue. So my first slide is, please be aware there's forward-looking statements and you should read our filings with the SAC. So this is a technology that has created a potent cancer killing agent. It is injected directly into tumors that you can see. You do not have to inject every tumor. It leads to a diffusion throughout the tumor and a cell penetration of these potent agents that cause a anti-cancer immune response. So we both debulk the tumor and then stimulate a systemic immune response. It is applicable to many solid tumors, not just the ones we're working on, but even cold tumors are applicable. We have over treated over 200 patients in two completed clinical trials, one in metastatic disease, one in presurgical. And we have ongoing phase three study in metastatic sarcoma, a phase two and presurgical breast cancer. And those studies are now back in operation and active and enrolling. We have been very excited about some of the early results we've seen in both studies. Everybody on the team is experienced with public companies in Phase III development. We have a robust patent portfolio of 18 issued patents, four in the U.S., and protection in 42 countries, and are very cash efficient. The technology makes use of a molecular transport molecule. We call it SHAO. It has a fat-loving component, a water-loving component. And after a two-year screening process in mice, we identified this formulation of these two very potent cytotoxic agents, but each have direct killing and immune activating mechanisms that are all different, two direct killing and two immune activating. And we simply mix these three ingredients in a vessel, and they form a very unique supramolecular complex. And remember, these are the same, this is the same similar structure to what is being used commercially in the Wagovi pill. So it's a delivery technology that has a huge opportunity for not only the oral delivery of proteins, but also we believe for intratumoral administration. So this drug is stored frozen. It is stable for up to four years. we have scaled up the batch multiple times. So we're in a phase three study, a randomized controlled study testing our drug alone, a local therapy treating metastatic disease in sarcoma, three different types. Sarcoma is a deadly cancer. The median survival for second line, third line sarcoma is about 14 months. Three-year survival is less than 10%. Our endpoint is overall survival. We are keeping our, hopefully, the patients on our arm alive longer than the patients on the standard of care. I'll go through the study in a second. The second study is a phase two. It is in pre-surgical triple negative breast cancer. It is for women who are seeking to have no live cancer at the time of surgery, so they go on this very harsh chemotherapy regimen. The endpoint is pathological complete response, the absent of all live cancer in the nodes, tumor, or breast. We are randomizing one dose of our drug up front, and then the women will get six months of the standard of care, chemoimmunotherapy, and compared to the standard of care alone. We have orphan drug status in sarcoma, and we have fast track in metastatic breast cancer from the FDA. This gives you a lot of benefits on both of these regulatory achievements. So I'm going to explain a little bit about how we thought about cancer when we set this up. So cancer is obviously a highly deadly and the reason for their deadliness is because they're basically like a foreign alien from the movie with Sigourney Weaver, they eat your organs, they kill you, and they are very highly fat, dense, very poor vascular. They don't have a lot of blood vessels. And you can see here in a sarcoma patient that there isn't a lot of blood vessels here. And you can see that this patient whose sarcoma was in the peritoneum migrated to the liver and started eating the liver. And effectively, you die from organ failure. Again, high pressure, high fat, high density, not a lot of amenability for IV because you don't get a lot of drug into these large sarcoma tumors. And you see the ability for metastases to even have fewer blood vessels. So how do you stop something like this? Well, what we're doing is we are injecting directly into the tumor. And here's some data from our first breast cancer study. And what you can see here is this is a woman who had two injections of our drug. She had a very large invasive ductal carcinoma, almost four centimeters. And this is the resected tumor after two doses of our drug. And you can see that the dotted line here is the live tumor, black line, and red is what we've killed. And we looked at this and we said, well, we should really dose more one time or dose less in different places. And what we did was we showed that we can now kill a larger tumor. The black, the red line is the necrotic area. The black line is the tumor. Again, you don't see a lot of vascular. These tumors now for the first time can be injected with a therapeutic agent that will diffuse through the tumor and cause immunological cell death. If you go on our website, you can see some of the data that supports the fact that there's immunological cell death going on, and a number of our papers will talk about that. So in the pre-surgical setting, in triple negative breast cancer, we have a high risk pre- or post-menopausal women. Majority of tumors are very highly proliferative. There's not a lot of drugs because they're triple negative, they don't have the cell receptors to really give some of the most potent drugs in this type of disease. Majority of women are diagnosed at late stage, stage two or stage three, that's about 62% of the patients. And if you don't get rid of the cancer prior to the surgery with chemo immunotherapy, the risk of the cancer coming back in five years is 50%. But if you can eliminate through a treatment process, a systemic treatment process, or in our case, an injectable plus the systemic treatment, and you can increase the percentage of women who have a PATH-CR, the risk of those women goes down. And unfortunately, in larger tumors, most of the women do not achieve a PATH-CR. So our study is taking women with larger tumors than was done in Merck's Keynote 522 study. With these inclusion criteria, we will provide one injection of our drug, and then the women will go for the standard of care chemotherapy, the endpoint being a pathological complete response, which is, as I said, no live cancer in the nodes, breast, or tumor. And we will do an analysis comparing the standard of care with our drug cohort A to cohort B, which is just the standard of care. That will be for safety purposes. We are actually doing a non-comparative analysis with a hypothesis of achieving a 60% pathological complete response rate. Results so far are very encouraging, even though these are at a higher dose than we are currently running. But five out of seven patients achieved the PATH-CR in the study that is now ongoing. Three out of the seven in the standard of care. Remember, these are patients with larger tumors, so 42% versus 71. That is a major trend to improvement. And we had a significant reduction in the higher-grade adverse events observed using our drug up front. Now, you're going to say, how do you get better safety when you're adding something to the standard of care and that's because our drug targets the immune system to the cancer when you kill the cancer in situ as we do you get an immune response that is precise to the cancer and so what we're seeing because a lot of the the therapy immunotherapy and the chemotherapy are immune activating and by not down-regulating the immune system and getting it to go to the right place with our drug, we see fewer both systemic immune-related and chemotherapy-related adverse events. In fact, 44% less chemotherapy and immunotherapy. And this is important because a half a percent of women will die from the chemotherapy. We're operating in Switzerland where we've started dosing. We've treated patients in Switzerland now, additional new patients with an amended protocol, and we've opened sites in France. And we hope to complete enrollment by the end of 27, but we hope to accelerate that if the data starts to come in pretty exciting. It's both randomized controlled studies, but the doctors know that this is not a blinded study. So I'm going to talk about metastatic disease for a second. We completed a 110 patient study in metastatic cancer that's led to our phase three in sarcoma. We did 64 patients with our drug alone, 30 with our drug plus Merck's Keytruda, and 18 patients with our drug and Yervoy. 95% of the drug stays in the tumor. The drug retention is independent of the cancer type, and only 7 out of 64 patients had a grade 3, generally very mild. There were no grade 4, grade 5s, mostly pain at the injection site, fatigue, and brief nausea. I think the most important thing about any kind of local therapy trying to treat metastatic disease is how you do on the tumors you don't see or you don't inject. And this is data from a paper we published where we see tumors that we don't inject shrinking and going down. In fact, almost 20% of patients had a reported shrunk tumor that we did not inject. And the little tumors, the tumors that aren't reported under a centimeter, and many tumors weren't followed. So we believe that we have at least a 20% abscopal rate in patients that are getting a right concentration of our drug into their tumor burden. And we have published this information. I'll talk about that in a second. So what happens if you kill and de-bolt tumors? You get an abscopal effect, an uninjected tumor shrink. Well, the benefit is that you have the potential to live longer. And so what we've seen in our study where we did the refractory metastatic cancer patients, we saw early on when we were not treating the tumors appropriately, we saw a lot of patients dying quickly, as you would have expected for this population. It's a population of patients who've failed three lines of prior therapy. But as we could dose more and more, we could see that the patients were living longer and longer, more and more meaning treating more, a higher percentage of their tumor burden. And you can see here, overall in these 64 patients, they had a median survival of almost 12 months, which for this population is way above the four to seven that's typically seen. And when we were able to really debulk 40% of the tumor burden, only 40% needed to be treated. We started seeing the patients live a lot longer than you would have expected. And it went from three months to 18.7 months. So we published this information in a very high impact journal, the Lancet Discovery Group's journal, e-biomedicine. The paper was very well received. If you're following the stock, you'll know that we were trading. We traded a billion and a half shares up from our two million that at the time. We also were able to raise capital with that money with that with this announcement. It's the first study ever, we believe, for a local therapy controlling metastatic disease, especially with a high rate at 75 percent. We have the potential for survival benefit, as you saw, and we had a high percentage of patients with uninjected tumors shrinking. Typically, for a local therapy, the best and nearly the only one is radiation that ever shrinks anything local, non-injected, not treated, and that's only less than 1%. So we really had some very unique features in this paper. And if you look, you'll see a lot of immune response data. So we are in phase three in soft tissue sarcoma. We're going to do three types, undifferentiated pleomorphic sarcoma, lyomyosarcoma, liposarcoma. These are 70% of sarcomas. We're going to treat second and third line where, as I said, the median survival is typically 14 months. We were showing much longer in the paper that we published where could show a median survival of 21 months. Our endpoint is overall survival. We'll be doing exploratory quality of life evaluations. We'll be taking interim looks at 20, 40, and 60 percent, and final data readout will be at 80 percent. There'll be no crossover, and we're using a metric for disease progression by CHOI criteria, which is different because the tumors absorb the drug, they get bigger. The immune attacks, it gets bigger. And then the cancer becomes a cyst and it gets bigger. So we're using a density change metric for progression. The end point is overall survival in this randomized controlled study where the patients will get five doses of our drug versus the standard of care, pazopinib, trabectin, and aribulin. They are also eligible, depending on the scans, to continue dosing our drug for two years as well. You can stay on the standard of care two years as well. So we have a lot of news events. A lot of investors are interested in what's your news flow. Our news flow is going to be the enrollments of patients. Our news flow will be hopefully two new publications this year. Our news flow will be start of our study, not only in the US, which is where we're going to go. This study speed in the first top line study here is dependent on capital. We are in discussions with a number of companies following the bio on business development, where we're looking at global or potentially regional players taking a part in helping us enroll patients and taking license rights. That could be non-dilutive capital. We're also looking for an at-the-market transactions. We have a $60 million vehicle that we can continue to tap and use for funding. So between partnerships, potentially pipes, potentially registered direct financings, we need about $30 million to get through 2028 to get to the data points, which if we had capital earlier, we could potentially enroll somewhere in the 2027 timeframe. So that's the milestones, papers, publications, enrollment rates, some data on safety, and possibly data on the percentage of patients getting PRS or stable disease in the phase three. Financially, we've done very well in the last 15 months, we've raised over $23 million. As of the second quarter and June 30th, we had almost $9.5 million in the bank. We have the ability to raise capital. As you saw from our 10Q, we raised the subsequent, I think, $1.2 million in the third quarter so far through the ATM vehicle. So a very exciting time. We have a very clean balance sheet, a very clean cap table, 3.5 million fully diluted shares is a low number. As I said, when we had our paper come out in 2025 in October 30th, we traded a lot more. We went up 670%. So hopefully, the market will react positively. We can raise the capital that we need and go forward. If anybody would like to talk to me, I'm very happy to introduce you to our management team to talk about what we're doing. So this is a target of our first lead programs in very, very deadly cancers for which there's very poor drugs today. We have a novel diffusion-based mechanism which we can kill cancer in a new way, two big ongoing trials, favorable safety for our drug compared to the standard of care in a metastatic disease. And we can treat both metastatic setting and local settings, which can be a very large opportunity should we show effectiveness in either one in the first two studies. And with that, I will say I have completed my presentation.

Thank you, Louis, and I want to thank all of our presenters for taking part in what has been a very productive and informative series of presentations. We appreciate the time and effort that went into preparing them, and we're very grateful for your flexibility and your presence at our conference this year. Thank you again from the HC Wainwright team.