Because of systemic side effects that they encountered, namely, immunosuppression and cardiovascular risk and things like that. The reason for that was because they weren't very specific. In fact, they were the polar opposite of that. They were very dirty compounds. They hit many different targets, and when you have too much of a good thing, you can start running into these types of issues, and that's in fact what happened to them. The first thing was to try to come up with a drug that was very specific.
From, from day one at The University of Edinburgh in Scotland, which is where this compound was in licensed from, by us, this drug was rationally designed to be a much more specific, a much cleaner selective SRC inhibitor. That's the first thing. The second thing is the mechanism of action by way this compound shuts down the SRC kinase. The SRC kinase, just like most kinases, not all, but most of them, has two active domains, what's called the catalytic domain. That's where the signal transduction process takes place, the passing of the phosphate molecule.
But there's also the scaffolding domain, basically the communication hub of the kinase. Ideally, you wanna shut down both of these. What we saw with the prior attempts to come up with these SRC inhibitors is that they're only able to shut down the catalytic domain and not the scaffolding domain, whereas NXP900 is able to shut down both of them for a much more potent, we believe, and much more effective shutting down of the SRC kinase. As I mentioned before, the phase I-A and the drug-drug interaction studies have been completed. We'll talk about those briefly.
The phase I-B, which is kind of where the tire meets the road, started six or seven months ago, something like that, and is very much ongoing, with preliminary data expected in the summer, probably the late July, early August timeframe. This is the selectivity that I talked about. This is a kind of heat map comparing NXP900 to dasatinib, which is one of the three prior SRC inhibitors that were developed. You can see that dasatinib is very dirty, lights up like a Christmas tree.
So it shouldn't come as a big surprise as to why when you start treating patients with dasatinib, you can start running into issues because there's just too much crosstalk when you start, you know, hitting a whole bunch of targets. Whereas NXP900, as you can see, is very, very clean, and that was by design from day one to try to come up with a very selective SRC inhibitor. The second thing, and don't worry about the busyness of the slide, is this mechanism of action aspect that I talked about.
So you wanna be able to shut down both the catalytic domain, which is down there, and the scaffolding domain. The easiest way to see the difference is when you look at the three-dimensional crystallography pictures of the binding of NXP900 to the SRC kinase versus dasatinib, bosutinib, saracatinib to the SRC kinase. When you look at those three-dimensional crystallography pictures, what you basically see is that the kinase remains in what's called an open conformation. It remains basically upright. It's still partially active.
Those drugs are unable to shut down the SRC kinase completely. Whereas, in contrast, when you look at the binding or the three-dimensional crystallography picture of the binding of NXP900 to the SRC kinase, you see that the SRC kinase is in what's called a closed conformation. It's basically shut down, completely incapacitated, and that's really what you wanna achieve. We feel that's a better outcome. In terms of the phase I-A, that was the dose escalation, basically the safety study. It was in all comers, and we tested obviously a wide variety of doses. Started off very low, at 20.
We did 20, 40, 80, 150, 200, 250, and 300 mg per day. This is a once-a-day oral. In terms of safety, you'll see on the next slide, generally unremarkable. That's good. We certainly didn't see any of the major safety signals that were seen in the past with the other SRC inhibitors, the immunosuppression and the cardiovascular issues and things like that. We certainly didn't see any of that, and we haven't seen any of that in the ongoing phase I-B, so far so good. What was particularly interesting about this phase I-A is that we actually looked at a pharmacodynamic parameter, which was the level of SRC inhibition.
You can take blood from the patients and measure the before and after levels of SRC. What we saw was that at doses of 150 and higher, 150, 200, 250, and so on, you get to about 90%-95% SRC inhibition. That's very profound. We believe that's very potent. When you compare that to the pharmacodynamic data that was generated back in the day for these other three SRC inhibitors, they kinda max out at around 45%- 50%, whereas we're at 90% to 95% steady state. That's a pretty dramatic difference we feel, and hopefully, that'll play out in our favor in the clinical trials.
This is the safety chart from the phase I-A. Generally unremarkable. There's obviously a little bit of GI. There's always some, you know, some diarrhea and a little bit of nausea and things like that when you give an oral to oncology patients. That's kinda par for the course. We did have some cases of pneumonia. You can see it down below. I can assure you these things were scrutinized and adjudicated, you know, with a fine-tooth comb by, you know, a wide and respected panel of medical monitors, and none of these were adjudicated to be drug-related or possibly drug-related.
These had really nothing to do with the drug. This is this pharmacodynamic data that I talked a bit. I wanna draw your attention to the right side, the right table over there. This is basically steady state. What do we mean by steady state? Basically, patients have taken the drug for 28 days, every day for 28 days. They come in. That's a cycle. That's basically the first cycle. Then they come in on day 29, which is basically day one of cycle two. Before they take that 29th dose, the measurements are taken. What you can see down there in turquoise is the level versus baseline, and you can see that it basically comes down by a good 90%.
That's what we mean by 90% SRC inhibition at steady state, that is a very encouraging result from our perspective. In terms of the drug-drug interaction study, the combinations that we wanna run in the phase I-B, one has already started with the drugs of two drugs in non-small cell lung cancer. The first one's called TAGRISSO, the second one is called lorlatinib. Those drugs have basically in their package insert, contraindications with drugs that basically stimulate things like CYP3A, cytochrome P450, and things like that. We needed to rule that out in order to be able to combine with those drugs.
In fact, what we ended up seeing is that NXP900 is in fact a weak inhibitor of CYP3A and those families of enzymes. That's actually a good thing, and obviously that facilitated the ability to conduct these combination arms. I'm not gonna go into too much detail here, but what's important to understand and I'd be happy to talk offline with any of you about this slide. This basically is the rationale for the different biomarkers and genetic signatures that we look for in the patients that are coming into the phase I-B.
We're enriching the patient population for different mutations and alterations of things like YES1 overexpression. That makes sense, right? YES1 being the main culprit within the SRC family. If that's overactivated, yeah, that's a patient we want because we feel that we can shut down YES1 pretty effectively. Obviously that we believe increases the probability of success. There are some other proteins and mutations that we're looking at that we're including in the phase I-B, things like FAT1, YAP1, and some others.
They all basically make a lot of sense when you do a deep dive into the mechanism of action and the cascade and where the SRC kinase sits. This is actually a very interesting case study we feel. One of the three drugs that were tested back in the day was a drug called saracatinib. This was AstraZeneca's attempt to come up with a SRC inhibitor, and one of the studies that they conducted was this study here. They enrolled about 25 non-small cell lung cancer patients. These were all refractory non-small cell lung cancer patients, and what they saw was the following.
They actually had two PRs and one stable disease that almost added up to a PR, 29% tumor shrinkage, where the cutoff is 30%. You know, roughly a 10, maybe 12% response rate, something like that. Obviously, that's not enough to move forward, certainly not for a big pharmaceutical company like AstraZeneca. A couple of key takeaway points that are important for us. First of all, number one, there was a signal of activity. You don't get PRs by chance. We know that this SRC inhibitor did something to these patients.
That's one. Two, AstraZeneca did not enrich the patient population that came into the study. They did not look at any of these biomarkers that we're looking for to enrich the patient population. This was an all-comers refractory non-small cell lung cancer patient population that came in. The third thing is, when you look at saracatinib objectively, we feel versus NXP900, it's not nearly as good as NXP900 in terms of its ability to inhibit SRC. Again, maximizes at around 45%-50% in terms of its ability to shut down SRC in the pharmacodynamic models that they did back then.
When you add all this up, we really like our chances. We're enriching for the patient population. We've got a much more potent SRC inhibitor, and we're on our way in the phase I-B. You know, fingers crossed, we'll see positive data. The phase I-B program has several cohorts in it, basically several shots on goal, if you will. There are actually five monotherapy cohorts where the drug is acting on its own. You've got two distinct subpopulations within non-small cell lung cancer, adenocarcinoma patients and squamous lung carcinoma patients.
You've got renal mesothelioma and a basket group that looks at patients that have these different mutations, which are mostly, it ends up being that these are mostly head and neck, esophageal type of patients. That's basically what we're seeing in this basket group number five over there. We've got two combination arms. The first combination that has already started is with osimertinib, which is TAGRISSO. TAGRISSO is an EGFR inhibitor, major blockbuster. It's an AstraZeneca drug. It's going to do about $7 billion this year or something like that, the mainstay of EGFR inhibition.
Unfortunately, patients can, you know, benefit for extended periods of time with osimertinib, sometimes even for two, three, four years. Inevitably, you know, patients will stop responding, and they'll become resistant to TAGRISSO treatment, and that's when you want to try to catch them and try to reverse that resistance. That's one of the combination cohorts. The second one, which is gonna start in a few weeks, is with an ALK inhibitor, also a non-small cell lung cancer called lorlatinib. That's a Pfizer drug. Second line, ALK gives a very prolonged benefit.
The median PFS is approaching five years with lorlatinib, obviously, it's a very effective drug. Again, same story. Eventually, patients will stop responding, and that's when you wanna try to catch them. That's basically the rationale for, you know, doing these combinations, and this is kind of what prompted this whole idea of doing these combinations. Just to draw your attention to the right side over there, this was the highlight of a publication. It came out about 3.5 years ago in Nature Communications, a very prestigious medical journal. This was actually done by the AstraZeneca R&D group.
This wasn't us. This was independently done. What they did here was, they took TAGRISSO-resistant cell lines, and they tried to re-sensitize these cell lines to TAGRISSO treatment by taking TAGRISSO in combination with a bunch of other drugs to see which combination could reverse the resistance. Lo and behold, the combination with NXP900 won this dog and pony show. By the way, they refer to the drug here as eCF506. That's a name that The University of Edinburgh, which is where we in-licensed the compound from, that's a name that the university had for the drug, but it's NXP900.
Obviously, that was kind of the first time where we actually saw third-party independent data supporting the thesis for, you know, possibly combining with TAGRISSO to try to reverse the course for TAGRISSO resistance. We ourselves replicated this experiment here, and we did some in vivo studies as well. Everything came back very consistent, very strong. Now, this is a cohort that's very much off and running. We started enrolling patients into this group, into this specific cohort a few months ago. On the left side, same type of rationale with lorlatinib.
Also, this was an inbound that came to us from Vanderbilt University. They had conducted some work with SRC inhibition as it relates to lorlatinib resistance. They saw very good results, and obviously, we amplified that from there. That's basically the basis and the foundation for the combination cohort with lorlatinib, which is gonna start in a few weeks. Another combination that we're looking at potentially is with RAS. There's been some data that's been generated. This is actually data that was published last month at the AACR conference.
I can tell you that there are two independent, very well-known universities that have approached us, wanting to conduct some experiments of their own, because preliminarily, they've shown some very interesting activity in their own labs, looking at SRC inhibition as it relates to basically amplifying the RAS signal. You know, hopefully, we'll be able to do something along those lines as well. In terms of the market opportunity, this is where we feel this, you know, this pipeline and the pill opportunity really, I think comes to light.
When you look at the potential addressable patient populations here, they're very substantial. They're in the tens of thousands. Just to give you an example, back in our prior lives at UroGen and at Stemline, the two companies that I mentioned before, the first approval for UroGen for JELMYTO was in a disease called upper tract urothelial carcinoma. That's about 2,500 patients. For ELZONRIS, it was an indication called BPDCN, a hematological tumor, about 800, 900 patients on a good day in the U.S.
This is really orders and orders of magnitude bigger than anything that we've dealt with in the past. This is just for the monotherapy potential, looking at these different alterations. YES1 amplification, FAT1 mutation, and so on. When you look at the combination approach, at any given point in time, in any given year, there are about 20,000 patients, roughly, maybe even 25,000 patients that basically fail TAGRISSO. Don't worry about, you know, AstraZeneca. Unfortunately for humanity, you know, they can replenish this patient population very easily with newly diagnosed patients.
The fact of the matter is that roughly 25,000 patients drop off that merry-go-round every year. Those are the patients that we want to try to treat to try to reverse the TAGRISSO resistance. ALK, about half of that, and then there's some other possibilities for combinations. I think, you know, the take-home message here is that the addressable patient populations we're talking about here are very substantial. A little bit of housekeeping. We finished the first quarter with about $25 million of cash.
Our burn rate is very controlled. It's about four and a half million dollars per quarter, which is, I think, pretty rare in our industry to come across a company that I think is very financially disciplined. We have about 16, maybe 17 months of cash of runway from where we sit. Keep in mind that we expect to have a preliminary data readout in this summer, so in late July or early August, and of course, some subsequent data data readouts after that every three months or so.
Hopefully, you know, that'll give us more than ample opportunity to refill the tank at hopefully much higher prices, and everyone will be happy. I don't think anyone will complain. In terms of the analyst coverage, obviously, Joe is one of the covering analysts. He's very, very well-versed on the story. You know, if you do have questions, you know, obviously, I think Joe is a very, very good address to be able to answer those questions.
Again, in summary, we're talking about a drug that has tremendous potential, a very unique SRC inhibitor, trying to learn from the shortcomings of the prior attempts, and really trying to, you know, rationally design a drug that can really, after, you know, having seen the experience with the other SRC inhibitors, to be able to come up with something that is much more potent, much more selective.
So far, at least on in terms of safety, we certainly haven't seen any of these, you know, really horrible and prohibitive things that those other SRC inhibitors encountered that really prevented them from getting these all-important solid tumor approvals that everyone wants to get. So that ends the formal part of the presentation. Thank you all so much. Really appreciate your time. Joe.
Thanks a lot, Ron. actually just have one question here for time's sake. When you consider the commercial profile for NXP900, you touched upon this earlier a little bit, but what role do you think a diagnostic will play, and is this a commonly available diagnostic, and will you use it to identify patients?
Thank you, Joe. I'm glad I'm on the platform. For 5 minutes in my life, I can be taller than you. It's a very important question. All these biomarkers and all these mutations, fortunately for us, we don't need to come up with a companion diagnostic. That would be pretty horrific. These are all things that are available with the standard next-generation sequencing panels that are out there in probably 95% of the oncology centers in the country. Foundation, Illumina, these are all standard panels, so that's very fortunate for us.
Great.
Thank you very much.
Thank you very much.
Thank you.