Today, I would like to introduce our presenter, Ron Bentsur, who is the President and CEO of Nuvectis, which is advancing its small molecule therapeutics for the treatment of serious conditions of unmet medical need in oncology. The floor is yours.
Thank you very much. Thank you, Josh, and I want to thank H.C. Wainwright for inviting us to present at the conference. It's a pleasure to be here. My name is Ron Bentsur, and I will be introducing you to the Nuvectis Pharma story. I will be making some forward-looking statements, so I do encourage anyone who's interested in the Nuvectis story to please read our public disclosures, including the risk factors, the latest set of which was published in the Q2 10-Q. So please read those if you're interested in the story. By way of some key investment highlights, we are focused on precision medicine or targeted therapy for oncology. We have two drugs in the pipeline, which I'll talk about obviously in more detail, NXP-800 and NXP-900.
Both are very different in terms of mechanism of action, addressing different diseases, but we believe that each represents a very interesting opportunities in their own right. In terms of the management team, so there are three co-founders of the company, myself, Enrique, who's also here in the room, and a third individual by the name of Shay. And collectively, over the last. We've been working together on and off for the last twenty years or so, but, if you look at our track record over the last ten years or so, we were involved in with three different companies before founding Nuvectis four years ago: Keryx, UroGen, and Stemline. And at each one of these companies, we're able to get a drug approved.
I was CEO of both Keryx and UroGen, and the latter two drugs, Jelmyto and Elzonris, that you see there on the screen, are actually for unmet medical needs in oncology. Very similar in terms of scale and scope, to what we're trying to achieve at Nuvectis. So we do have fairly recent experience on not only getting drugs approved, which obviously ultimately is the most important goal, but also, interacting with the FDA and kind of navigating those waters. So hopefully, we can, emulate and replicate, that same level of, success, at Nuvectis. So by way of, the pipeline, where we stand today, so, as I mentioned before, we've got, two drugs in the pipeline, NXP-800 and NXP-900. NXP-800 is currently in a phase I-B, study.
The disease cohort, which is the furthest along, is in a disease called platinum-resistant ARID1A-mutated ovarian cancer, which in essence means patients that fall into two subsets within ovarian cancer. One is called ovarian clear cell carcinoma, and the second one is called ovarian endometrioid carcinoma. These are two subsets where you find patients with the ARID1A mutation, and also, these happen to be patients with a very, very poor prognosis, absolutely horrible. Once they kind of make it into our study, in essence, third-line patients, because the standard of care there is first-line chemotherapy, typically platinum-based chemotherapy, and then second line is also chemotherapy, also platinum, sometimes with another chemotherapy, or with Avastin or something like that.
The patients that come into our study, by and large, are third-line patients, and their prognosis at that stage is very poor, far less than one year in terms of life expectancy, and just overall, you know, not a good condition. That's the study that is furthest along. We do expect to report an update from the study, both efficacy and safety, this fall. We presented some early data, which I'll talk about in a couple of slides, in late March, and this is a follow-up to that. This particular data update, which we expect in the near term, will be on 12 to 15 patients.
And then another disease cohort that we have as part of this phase I-B umbrella is technically run as an investigator-initiated program that's being done in collaboration with the Mayo Clinic, and that's in the area of cholangiocarcinoma, which is cancer of the bile duct. Down below, you see where we are with NXP-900. That's our second drug in development, and this is in a phase I-A dose escalation. Obviously, that's something that's mandatory by the FDA, where you start at a low dose, and you go up and up and up until you find a dose that you feel comfortable taking forward. And right now, we're probably be about two-thirds of the way through. We finished already the 20mg, 40mg, and 80mg dose groups. We're in the 150mg dose group as we speak.
That'll be done in a few weeks, and then, obviously, we expect probably one or two dose groups after that. At some point, we will start hitting toxicities, as one would expect, and that's where we're going to stop. And I'll talk about, obviously, the vision of the phase I-B program for that drug as well. The mechanism of action for NXP-800 is GCN2 kinase activation. I'm not going to go into too much detail, but we think that obviously there's a very elegant and distinct crosstalk with each GCN2 activation mechanism and the susceptibility of the cancer cells that have the ARID1A mutation. This is some of the preclinical data that was generated.
This happens to be a specific ovarian clear cell model in platinum-resistant ARID1A-mutated tumors that were implanted into these mice, and you can see very elegant data there. These were head-to-head models against this platinum, which is the primary form of arsenal that's used in the front-line setting. That's a platinum-based chemotherapy. And you can see that, whether irrespective of whether you're talking about the left one or the right one, the left one happens to be a platinum-resistant model. You can see the green graph there on the left kind of going up, so platinum doesn't do much, or the right model, where the platinum does do a fair amount.
You can see that the green graph there does a lot better than the one on the left, 'cause platinum is much more effective in that model on the right side. But irrespective of whether you're looking at the left one or the right one, NXP-800 in red does appear to outperform platinum, which obviously is very encouraging. And this was actually the basis for the Fast Track designation that we were able to achieve with the FDA for this compound in platinum-resistant ARID1A mutated ovarian cancer about a year ago or something like that. More recently, we're able to achieve orphan drug designation as well for this disease. And on the right side, you can see the patient numbers there.
This is kind of a classic orphan type of an indication in oncology. There are not a whole lot of patients, but it's a fair amount relative to a condition that is as severe as what we're talking about here. You're talking about several thousand patients who suffer from this disease, who are in desperate need of novel medications to help their situation. As I mentioned before, the prognosis is absolutely horrible. This is some of the data that was generated in cholangiocarcinoma. This is a very busy slide, but down below, you can see the graphs, and the graphs are all very consistent. ARID1A, NXP-800 in red appears to be extremely potent in these types of models.
These are models that are called PDX models, so patient-derived xenografts. So, tumors are actually extracted from the patients, from specific patients, and implanted into the mice, and then the mice get tested, and the data looks very impressive. This was all done by the Mayo Clinic, all this preclinical work, and obviously, that prompted the next step, which was to start the investigator-initiated program with the Mayo Clinic in cholangiocarcinoma, which is being run as we speak. Another area that we wanna go into, hopefully very soon, is endometrial. This is different from ovarian endometriosis. This is a different disease, but very much related. Obviously, it's another women's oncology type of an indication.
And just in terms of logistics and efficiency, these would be the same centers, the same physicians that we're using right now in ovarian, that I think we could tap into to start this particular disease cohort, once we choose to do so. And you can see again, very elegant preclinical data that was generated with the ARID1A mutation. Again, very consistent story there, and we think the drug can have an effect in this disease area as well. That's kind of the marketing slide.
You can see the patient numbers for all these different diseases, some of which I mentioned, some of which I didn't mention, but the ARID1A mutation is prevalent, across a number of tumor types, not all, but a number of tumor types, and you can see some of the numbers there and the ones that stand out a little bit more. There's really no shortage of opportunities, but as you know, in the real world, and also with the FDA, you have to kind of crawl before you walk. You have to establish a beachhead in one or two of these, first, and then hopefully, you can have a real dialogue about having a tumor-agnostic type of an approach, which would, in essence, mean patients that have the ARID1A mutation could be treated with a drug.
We're not there yet, but hopefully, we'll get there, in due course. In terms of the data that's been presented so far, for NXP-800, so we did a phase I-A, classic dose escalation. I'm not gonna talk too much about that. I'm gonna spend a minute talking about the preliminary data readout that we had back in March from the ongoing phase I-B program in ovarian. This was a very small data set. It was four patients for safety and three patients for efficacy. But, well, first of all, what was interesting on the efficacy side, again, three patients, so obviously, not a huge data set, but we did have one PR, one partial response, and two stable disease.
So obviously, that's very encouraging to see that right out of the gate in the first three patients. And in terms of the four patients that were included in the safety evaluation for this press release, we did see three cases of Grade 4 thrombocytopenia, which is a low platelet count. Obviously, that's something that you need to monitor very carefully. So what we did after we saw this was to implement a few provisions into the existing protocol to help us better manage the thrombocytopenia and mitigate it.
Things like being able to move to intermittent dosing instead of every day, to dose five, five days on, two days off, and to be able to monitor and surveil, basically, what's going on with the patient much sooner, to be able to intervene much sooner, which is something we could not do before we put in these provisions. And I can tell you that so far, it's helped out a lot. When I look at all the incremental patients that have come on board since this press release came out, so the fifth patient and beyond, we haven't seen any further cases of Grade 4 and even Grade 3 thrombocytopenia. That doesn't mean we're not gonna see it in the future.
Of course, if we treat enough patients, we're gonna see it, but I think to a large extent, we've been able to mitigate it, so we're very encouraged by that, and obviously, that helps going forward. And it also helps when you think about, things like potential combination strategies, trying to move upstream to second-line or first-line, 'cause there, we would have to combine with platinum-based chemotherapy, and one of the DLTs for platinum is thrombocytopenia. So obviously, you can't double down on the thrombocytopenia. No one would ever do that. So we need to make sure that at least we can better control for the thrombocytopenia to be able to talk about the potential for a combination with platinum-based chemotherapy. So hopefully, with the data that we've seen so far, that's a good kind of bellwether for what to expect in the future.
Now I'm gonna switch gears and talk a little bit about NXP-900, which is the second compound that we have in development. This is a compound that was in-licensed from the University of Edinburgh in Scotland. By the way, the first compound, NXP-800, was in-licensed from the ICR, Institute of Cancer Research, in the U.K. They're kind of similar to the NIH or the NCI here in the U.S., and NXP-800 is a very potent and selective Src inhibitor. Now, there are other Src inhibitors that have been developed in the past. You may be familiar with drugs such as dasatinib and bosutinib, which technically are called multi-kinase inhibitors that also inhibit Src. These are drugs that are approved....
But when you look at the history of their development, they're only approved for hematological tumors, for blood cancers, CML and AML. But they were tested extensively way back when for solid tumors as well, and in fact, actually showed some pretty interesting activity in some tumor types. But they always ran into major systemic side effects that prevented them from getting an approval in a solid tumor setting. That was their problem, and the reason they encountered these side effects, we believe, is what you see here on this slide on the right side, so this is the kinome heat map for dasatinib to see what kind of kinases and other targets dasatinib hits, and you can see that it hits. It's very promiscuous.
It hits a whole bunch of kinases, whereas NXP-900 is much more selective, much more specific. In fact, was designed from day one, from the get-go, to be a selective Src inhibitor, because at the University of Edinburgh, they knew about the systemic side effects that dasatinib and bosutinib encountered. Then, obviously, they tried to overcome that by trying to come up with a very selective and specific Src inhibitor, and you can see that NXP-900 certainly fits that category. Another thing that we believe NXP-900 has going for it is a more potent way of inhibiting the Src kinase, so really in the mechanism of action. What you see here in the middle is basically a fully functioning Src kinase.
And just like most kinases, not all, but most kinases have both a catalytic domain and a scaffolding domain. The catalytic domain is where the signal transduction takes place. The scaffolding domain is kind of the docking station, really kind of the communication hub for the kinase. Ideally, you want to be able to shut down both the catalytic and the scaffolding domains, and on the right side, you see what dasatinib is able to do. Dasatinib is able to shut down the catalytic domain, so it shuts down the signal transduction, which is great, but it's unable to shut down the scaffolding domain, so you still remain with a partially active kinase.
Whereas if you go to the far left of the slide, you see that NXP-900 is able to shut down both the catalytic and the scaffolding domains, in essence, rendering this kinase completely incapacitated. And when you look at the three-dimensional crystallography pictures of the binding of dasatinib with the Src kinase, and the binding of NXP-900 with the Src kinase, you see a really stark difference. Because when you look at dasatinib, the kinase remains in an upright position. It's in an open conformation. It's still active. Whereas when you look at the binding of NXP-900 to the Src kinase, you see that the Src kinase is basically collapsed. It's in a close conformation. We know it's completely incapacitated.
So we do believe that there could be a mechanistic advantage that can also play favorably when, you know, when it comes time to treating target patient populations. In terms of potential single-agent types of trajectories that we wanna pursue, we're thinking about obviously different indications where targeting Yes1, which is kind of the main culprit within the Src family, it's kind of the Al Capone of the Src family, is really believed to be an important target to be able to to inhibit, and I'm not gonna go into the slide here, but mechanistically, we think that there's a tremendous amount of rationale to try to target cancers of squamous cell origin, and here are some different indications that come to mind.
So, for example, esophageal, which is about 30%-40% squamous origin, or head and neck, which is over two-thirds squamous origins. So as you can see, there's really no shortage of these types of potential indications for us to pursue. So those would be, we believe, reasonable single-agent types of approaches. But we also believe that there are very exciting potential combination strategies here with NXP-900, namely in non-small cell lung cancer, going after EGFR resistance and ALK resistance. And let me just talk a little bit about that. So on the left side, what you see here is kind of the highlight from a publication that was done by the AstraZeneca R&D group.
AstraZeneca obviously is the marketer of Tagrisso, osimertinib, which is kind of the main EGFR drug that's out there. And basically, what they did here was they took Tagrisso-resistant cell lines, and they tried to resensitize these cell lines to Tagrisso treatment by taking Tagrisso with a bunch of other drugs to try to combine Tagrisso with these other drugs to see what could basically flip-flop these curves and basically resensitize these cell lines to Tagrisso treatment. And in fact, our drug, NXP-900, won this dog and pony show. You can see that in those tables on the left side. It's very hard to see in terms of the fine detail, but that combination of osimertinib or Tagrisso, together with NXP-900, was able to reverse the resistance, the only one within the scope of what they did.
One thing I'll add is that we have full commercial rights to the compound. This was basically done through a research type of a collaboration that they had with the university. AstraZeneca does not have the rights to the compound. We do. On the right side, you see kind of a similar story, but this time with ALK. So many of the non-small cell lung cancer patients eventually get treated with EGFR inhibitors or ALK inhibitors, and some of these drugs are absolutely terrific. They can put the patient in maintenance or even remission for a very long time, but eventually, all patients will become resistant to either EGFR or ALK, and obviously, once that happens, their prognosis, you know, becomes a slippery slope, so that's when you want to intervene.
And these are the specific combination strategies that we're thinking about based on, obviously, mechanistic rationale, but even more so, based on preclinical data that was generated, not just by us, but in the case of the EGFR, by AstraZeneca. And also, as a follow-up, by some of the in vivo data that's being generated as we speak that hopefully will be published soon to support this particular notion that our drug NXP-900, in combination with an EGFR on one hand, and but also with an ALK on the other hand, can have a real effect in being able to provide a benefit to these patients. And, of course, here, you know, you don't have to convince people that this is a very big market. Everyone knows that.
You look at a company like Nuvalent, who's coming up with kind of a third-generation ALK, and you can see their valuation. So, obviously, we think that that's gonna be a very short explanation in terms of, you know, being able to convince people that there's a market out there. So these are some of the. Again, this is the market slide in terms of the addressable patient population and what we're thinking about. So these are kind of the key cancers that come to mind of squamous cell origin. And we talked about esophageal, we talked about head and neck. There are some other ones as well. Some of them are bigger, some of them are smaller, but again, there's no shortage of opportunities. But again, you need to be very modular in your approach.
You can't just jump into this pool and try to grab whatever is out there. You have to be very careful and very thoughtful about how you proceed, and the phase I-A, as I mentioned, is ongoing. We're in the fourth dose group right now, which will end in about two weeks, and then we move up to either two hundred or two fifty, to be determined based on discussions that we're gonna have with the physicians. And this is kind of the housekeeping slide. So we finished the Q2 of this year with about $18.1 million of cash. As we speak right now, we've got about $16.8, maybe $17, $17 million. Our burn rate is very controlled. Currently, it's running at about just under $3 million per quarter, something like that, which is extremely low.
I think we run a very tight ship. Another thing that's important to mention is the insider ownership. So when you look at the three co-founders and also the five or six biggest shareholders, who were there for us, really from day one, collectively, we own about 65% of the stock, so the stock is fairly tightly held. You can see the research coverage there. And finally, just to go back to the investment highlights slide, I think we're in a very good position, having two drugs in the pipeline, targeted therapies, each one of which I think can generate a tremendous amount of excitement, if they're successful. NXP-800, we're pursuing currently the ovarian opportunity and also cholangiocarcinoma.
With NXP-900, we hope to start the phase I-B in the early part of 2025, depending on when we finish the phase I-A, obviously. And the highlight there, I think, will be to start these combinations, which could be very exciting. And in terms of the management team, again, without, you know, pounding on our own chests, and you know, this is-- we've done this before. Obviously, it's not a guarantee that we're gonna succeed again, but at a minimum, I think we would like to believe that you believe that we know that, you know, that we know what we're doing. So I'll end the formal part of the presentation, and thank you all very much. And if there are any questions, I guess. Thank you.
Yep, so thank you so much, Ron, and if anyone would like to-