Good morning, everyone, and welcome to the Lee Therapeutics DNK01 Clinical Perspectives Conference Call. Following the presentation, there will be an opportunity for questions. Please be advised that this call is being recorded at the company's request. At this time, I will now turn the call over to Mary Jenkins of Argo Partners. Please go ahead.
Thank you, Chanel. Welcome and thank you for joining us today for Leap Therapeutics' 1 Clinical Perspectives Conference Call and Webcast. I am Mary Jenkins with Argo Partners. And with me today are Douglas Anze, LEAP's Chief Financial Officer and Doctor. Samuel Koeffner, Director of Precision Medicine and GI Oncology Program at the Angeles Clinic.
This call is being accompanied by a slide deck, so I will ask that you please turn to our forward looking statements on Slide 2. Before we begin, I would like to remind you that any statements made during this call that are not historical are considered to be forward looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the Risk Factors section in the company's most recent quarterly report on Form 10 Q as well as other reports filed with the SEC. Any forward looking statements represent our views as of today, October 22, 2018 only. A replay of this call will be available on the company's website, www.leaptx.com, following this call.
With that, please turn to Slide 3, and I am pleased to turn the call over to Doug Anci, Chief Financial Officer of LEAP.
Good day, everyone, and greetings from Munich. I'm very happy to be here with Doctor. Samuel Klempner and to have the opportunity to discuss the combination study of LEAP's DK101 and Merck's KEYTRUDA at that midway point in the study. Doctor. Klempner will start off by describing the challenges of treating esophagogastric cancer patients and the unmet medical need.
Then he will review the clinical data presented in our poster yesterday, which was very well received by the attendees and we'll go into further detail with respect to a number of the patients. For those of us who work on the program day to day, the outcomes of individual patients have enormous impact. And then last, we'll take questions from the analyst community. We're enthusiastic about the data that's emerging and we hope that we can communicate that enthusiasm on the call. And now I hand it off
to Doctor. Putnam. Thank you, Doug. Thank you all for coming. I'm going to try to put this data in perspective of the larger esophagogastric problem in the U.
S. And also globally. So on this slide, we're just highlighting the scope of the problem. So this is a disease that, although somewhat less common in the United States, as you can see, globally represents the 3rd leading cause of cancer related death with between esophageal and gastric nearly 2,000,000 cases in a year. Unfortunately, we haven't made significant progress even though we've known this is a significant problem for a long time.
So within the United States, which somewhat differs from the Asian countries, most of our patients are actually not diagnosed clearly highlighted by the 5 year survival in advanced patients of less than 5%. Standard of care agents in the first line are active, but as you can see, the durable benefit is infrequent and later lines of therapy have limited activity. These are patients that I think when you're looking at any clinical trial in the esophagogastric space, you need to have an appreciation of the types of people that you're trying to help with these agents. The reason that this is a very difficult population is highlighted here. So these patients are highly symptomatic, owing to the fact that the tumors are located in areas that affect their ability to swallow, and therefore, the nutritional status of the patients would impact both their ability to tolerate standard of care therapies such as chemotherapy, but also significantly impact their ability to go on to clinical trials often owing to performance status alone and symptoms from the disease.
In fact, this is even more clear when you look at the fact that although the majority of patients who are diagnosed with metastatic disease do receive first line therapy, the drop off from first line to second line is dramatic and arguably the highest among the most common tumors treated globally. So there's been a lot of SEER analyses and Medicare claims data suggesting that only about 40% to 42% of patients who receive first line therapy ever go on to receive second line therapy. And this is highlighting the problem of the symptom burden of these patients. Although there have been some molecular classifications, which have added important understanding into the biology of the disease, we've yet to be able to translate some of these targets, largely receptor tyrosine kinases, such as EGFR and MET and HER2, owing to the problem that this is a very heterogeneous disease. So targeting with a small molecule inhibitor, there's a lot of escape mechanisms within the tumor.
So this has been a limited strategy. So there's clearly a need for novel agents and novel approaches in the second and later lines of therapy. So hence enter the trial, the LEAP study, which we'll be talking about. This is just highlighting the paradigm of esophagal gastric in the U. S.
And this has been outlined in the NCCN guidelines as well as several kind of white papers from various institutions. But we break this down largely into gastric and gastroesophageal junction, particularly CBORD 2 and 3 and stomach that would be on the right hand side of the slide where it says gastric GEJ. And true esophageal tumors, including squamous and midesophageal adenocarcinomas are less common and somewhat of actually a worse prognosis population. So the standard of care is first line systemic therapy. Generally, this is 5 SU and platinum, although there is a lot of variability within the U.
S. In patients that are tested standard of care for HER2 and are positive, then Herceptin is added in both situations. And then you see the drop off between the first and second line therapy. Response rates in the first line approach 50% to 55%. And when you see in the second line, save for the Cyramza and taxol, which has a 28% response rate, this is the highest that we currently have available in the second line.
However, there is a significant portion of patients who are not candidates for Cyramza owing to comorbidities. And then you see the 16% response rate single agent taxanes in this setting. In September of 2017, pembrolizumab was approved for the treatment of beyond second line gastric and gastroesophageal junction adenocarcinomas. It does not carry an approval for squamous cancers of the esophagus. And highlighting the KEYNOTE-fifty nine data over here on the right, which shows the response rate that led to the approval.
So only 11.6%. And actually, if you subtract the MSI high patients from that, it drops into the single digits in around 9%. So clearly, there's not a lot of durable responses and benefit in the second and third line setting, so a clear need for novel therapies. And here we see the schema for the LEAP trial. You can see there was a brief lead in with the dose escalation of the DKN-one drug from 150 milligrams starting to 300 milligrams, which was the intended dose.
As you may well know, there was data from the taxol plus DKN-one trial in esophagal gastric cancers, clearly suggesting 300 milligrams was a safe and tolerable dose. Pembrolizumab was given a standard approved dose of 6 to 200 milligram dosing. And then after no safety signals were seen, this expanded to the larger study you see on the right hand side, with the primary endpoint being safety and multiple secondary endpoints of response biomarker analyses and traditional clinical outcomes of PFS and OS. This was assignment stage design. So if there were 3 partial responses, the study would expand to continue enrollment up to the full 60 patient study, which you see there.
I think it's important to note that there was both PD L1 naive patients. So these are not exposed to KEYTRUDA, but also an important and very unmet need is trying to tackle the PD L1 exposed and or refractory population. So this is the patient demographics of the currently enrolled patients. What you can see here is that this is quite representative of the modern care of esophageal gastric cancer in the U. S.
So the majority of patients have received 5FUN platinum therapy. And then you see the typical representation of second line and later therapies in the types of prior therapy with taxane, ramucirumab and immunotherapy, PD-one directed therapy well represented. You can see, I would call your attention to the PD L1 expression, which is reported here. Again, this is centrally tested PD L1 expression, and you see that the positive rates and negative rates are largely reflective of what we see in other study population. Importantly, looking at the micro satellite status of these patients, you see that the majority, if not all, are micro satellites stable.
There is a population that are unknown. And this is an important point because in the keynote studies, the MSI high patients are clearly driving some of the response. Tumor mutational burden, which is an emerging immunotherapy biomarker is collected and among the known is reported here. And again, MSI high tends to have very high tumor mutational burden. So there's no other suggestion that those patients are captured here.
This is the safety data, the treatment related adverse events. And really, this is an encouraging safety profile when you look at combining immunotherapy agents. For example, for context, if you look at CheckMate 32, which is ipinivo in esophagal gastric cancers, There is significant rate of treatment related adverse events, which is well described with the addition of ipilimumab to PD-one. Contrast that against here where you see that the majority of treatment related adverse events are very low grade and actually somewhat infrequent. So in summary, I think there was no clear additive toxicity when you're adding PKN-one to standard dose pembrolizumab.
As an investigator, that's obviously an encouraging thing because these are patients where we're trying to balance both the quality of life and the quantity of life. So a non toxic therapy is very important. Now we're getting into the meat of the study. This is the overall population with the objective response rate and then we will talk about the evaluable population lower down on this slide. So you see among the evaluable patients of which there are 23, so 62% of the accrued patients are evaluable.
The response rate of 17.4%. Again, this is if you look back at the MSS, JE Junction and gastric patients in the KEYNOTE studies, this is just about a doubling of the response rate compared when you throw out those MSI high patients. Disease control rate, which I think is an important clinical outcome in esophilic gastric cancer of 56%. This is important because although it may not be direct tumor responses, you're seeing these patients these are patients who are having their symptoms controlled, which often translates to improved outcome. The median time to response of 3 months is consistent with what's seen.
In fact, it almost mirrors exactly what was seen in the CheckMate 142 study that was presented today at ESMO. So no major changes there, both early and late responses are seen with immunotherapy. This is a well described phenomenon. This is an important table. You see again the promising overall response and disease control rate, especially noting that some of these are heavily pretreated patients, which is an often difficult population to improve upon.
There is of note, this is 23 patients overall of therapy and the response rate is pretty similar between second line and second line and beyond patients of 18% 14.3%. So this is encouraging and also parallel somewhat what has been seen in other immunotherapy trials. Although, to be honest, this is somewhat of an improvement in the later lines of therapy where there has been a drop off in some other immunotherapy trial. Among the microsatellite stable known patients, so again, there's a portion that are not yet known. We see an excellent response rate and disease control rate.
And then PD L1, which is a biomarker for immunotherapy of honestly debatable importance, but it's something that you need to capture because it is linked to the label of pembrolizumab. What you see here, this is the centrally tested PD L1. So in positive population, where it's known, the response rate is 33%. But equally important here, although the numbers are small, one of the 4 patients with a known PD L1 negative population responded. And that's a very encouraging sign when you're an investigator because the response rate in PD L1 negative patients from KEYNOTE-fifty nine is about 6%.
So obviously, this will be exciting to follow as the number of evaluable patients increases as the data matures. But these are encouraging numbers to have activity in a PD L1 negative population that otherwise is generally not exposed to immunotherapy if KEYTRUDA is the only option. Here we see the waterfall plots and we'll see the spider plots as well from the evaluable population. So what you see here is similar to what was shown in the table, and I think it will be important on the next slide when you see that some of these responses are quite durable. So here, you see the partial responses in the stable disease, and this will be broken out by PD L1 and microsatellite status on some subsequent slides.
So here is the spider plot with durability and depth of response. I'm sure you all have seen plots like this in the past. So this is including all patients who are available, and this is on study and off study, and you can see that the lighter yellow is off study. So durable responses out to beyond 250 days. The reason that patient is a lighter yellow is that they are off study, but it was after the time of the data cut for the analysis.
Here we see again a subgroup analysis. So it's important when you look at this study, if you think back to the earlier table, it actually includes esophageal and esophageal squamous cell cancers, which are actually not part of the label of pembrolizumab and an even more difficult population to treat. They tend to have lower response rates to actually all therapies. So when you focus in on the GE junction and the gastric cancer patients, which is highlighted on this slide, that's a better comparator to the current approval for pembrolizumab. So that's what we're trying to show here.
And so here you can see that stratified by 1 or more prior lines and by microsatellite status when it's known. And so here in this perhaps more comparable population, you see the response rate of 23.5%. So that 17.4% previously was dragged down a little bit by the claims in esophageal, true esophageal that are less responsive. So this is probably a better comparator to put in context with the current approved landscape of GE junction and gastric cancer. So again, 23.5% is a little bit more than a doubling of the response rate when you look at single agent pembrolizumab given on label, and that's again shown down here on the KEYNOTE-sixty one and 59 data.
So, 61 is a true second line randomized Phase III trial against paclitaxel in the 2nd line and KEYNOTE-fifty nine is a single arm study of single agent pembrolizumab in after second line therapy. So this is the slide that would get me excited as an investigator along with this next slide, which is again just showing the spider plot for that population, again, the GE junction and gastric cancer patients. And you can see both durable responses in people with in the second line setting, so one prior line and microsatellite stable. And these are actually both my patients, so I can describe in a little bit more detail subsequently. And then you see the blue line as well, someone with more than 2 prior lines of therapy, microsatellite stable, also achieving a durable benefit.
Here again, it's just to try to put this in context and make it very clear for everyone on the call. So you have to look at the populations of patients that were studied. Obviously, the size of the trial is important, and this is a study currently that we're talking about that requires some maturing of the data to see the full set. But across the top row, you see the response rates from the registration trial. And what clearly stands out is an over and doubling the response rate in this LEAP trial.
Stable disease rate is intermittently reported in some of the studies. But again, here, we're seeing an improvement, again, a doubling compared to the KEYNOTE-fifty nine, which is perhaps the closest comparator study to this. PFS is something that is important, but remains to be fully matured from this data set. And again, trying to break it down by the standard stratification factors, including PD L1 and microsatellite status. So there is no microsatellite high patients that are known on the LEAP trial.
So that 23.5% overall response rate is presumed to be all in MSS patients, and it is. PD L1 positive patients, the response rate is 33%, which again is an improvement upon monotherapy. And response rate is actually quite important in these patients because the burden of disease is what causes the symptoms. So patients who respond, their symptoms improve and they feel better and that I think will be highlighted in some of these vignettes that I'm about to show. So I'm going to highlight a few patients.
These happen to both be my patients, so I can certainly speak in detail if there's questions. This is a patient of mine who was heavily pretreated and was presented on the prior call for those that were there. He had extensive metastatic disease, which is highlighted here, both in the liver and the perinephric mass. And this is actually somewhat important because the rates of response with immunotherapy tend to actually be a little bit lower in the liver. So when you see activity in visceral metastases like the liver, it's something that gets you a little bit more excited about a drug in general.
So clearly, a significant decrease here. This is an 82% decrease by RECIST. Patient remained on study over 9 months with significant symptomatic improvement as well. This is another patient that had previously shown some of the early data and this is a follow-up showing what is sometimes seen as a pseudo flare phenomenon where if you actually look between the December 'seventeen and the January 'eighteen scans, the mass is actually in the liver increased slightly, but then subsequently decreased and converted more to a cystic appearance. This is somewhat typical for some immunotherapy responses and it's also mirrored by the serologic response in CA99 decrease.
Again, this is a microsatellite stable patient with a low tumor mutational burden, so someone who may have been predicted to be less likely to benefit PD-one monotherapy. So if you're potentially expanding the group of responders, that's an important component by adding a second drug. This is another microsatellite stable GE junction adenocarcinoma. So again, you see a low tumor mutational burden, microsatellite stable status and what's called a CPS 1%. So one can be either accomplished by tumor cells or the responses are relatively low in this PD L1, CPS1 population.
So previously treated with FOLFOX, you can see the baseline disease sites there, highlighted on the 3 CT scans vertically and then going in time across in rows. And you can see that what's highlighted by the best response over there is actually not the overall response per RECIST, but the decrease in each lesion going across. So lesion 1 going across in a row decreased by 12%, whereas lesion 3 decreased by 62%. Again, another GE junction, adenocarcinoma, which is the most common subset in the United States. This is a patient of mine who is ongoing on trial, a younger man previously treated by first line as well as local regional disease with significant nodal burden of disease causing symptoms and pain, particularly that para aortic node.
And you can see on his first scan, a relatively rapid decrease in the size of that lymph node, which was associated with a normalization of his DEA and complete resolution of his pain. I do expect personally this patient to go on to become another responder, but that remains to be seen with follow-up scan. Again, another patient highlighted here that would be somewhat less likely to be predicted to respond. So a PD L1 positive patient with an intermediate mutation burden. This is an actual esophageal adenocarcinoma.
So these are patients who are tend to be harder to get access to immunotherapy as well as tends to be less responsive. So this was quite an encouraging single case. So here, another chemoradiation, first line therapy, increasing lesions in the lung, esophagus and nodes. And by central read, this is actually a clear PR, but by investigator assessed response, it was also a near PR with a 28% decrease. I can certainly answer questions about the discrepancy there if asked, but we presume this will go on to become a PR.
When you look at any drug, you have to wonder about the mechanism of action and whether or not there can be any predictive biomarkers either for responders or people who will not benefit. This is very early data looking at the potential biomarkers for DK101 in combination with pembrolizumab. So what you're seeing here is an RNA scope assay for DKK1, the hypothesis being that higher DKK1 expression may be associated with response. And here you see the difference between a partial responder and someone who was primary progressive, suggesting that lower DKK1 expression by RNA scope at baseline may be associated with lower response rate. This remains to be validated in all of the samples that are collected and in certain area of ongoing interest.
What you can see on the right of the slide is that among the patients with DKK1 baseline status known, you can see that there does seem to be an enrichment for the responders and the stable disease patients in a higher baseline DKK1 expression. So that's encouraging when the potential mechanism can be tied to the clinical outcome. And finally, another interesting aspect of immunotherapy in general is how to expand upon PD-one therapy. And so there's a lot of interest in combining agents that manipulate the adaptive immune system. So that's PD-one therapies that are primarily acting on T cells, CD8 positive T cell.
But of course, there's another important arm of the immune system, which is the innate immune system. These are the primary defenders you can think of them. And so here you see some preclinical mouse models suggesting that DKK1 functions clearly superiorly in a NK intact model. So if you deplete the NKs from a mouse and give DKK1, there's certain significantly less activity than with an NK competent model, suggesting that the mechanism may be mediated through NK cell activation, which is an area of intense interest in the immunotherapy field. So again, tying complementary mechanisms of action, which may improve the proportion of patients who would benefit and maybe bearing out in the study itself where you early signal of significantly improved response rates with the combination.
So I will conclude the overview of the publicly available study data and just suggest that this is clearly a safe combination with very little additional side effects that we saw from the adverse event slide. The combination has a very promising overall response rate. And I can tell you from participating in this trial, since the beginning, that our patients have clearly benefited from this, including some of the stable disease patients that the disease control rate is high on this trial and that translates directly to patient benefit in my opinion. This is a heavily pretreated population and you've seen activity both in the much later lines as well as the second line. And the mechanism and the response rates, I think, tie or may tie together nicely, which is always a good thing when you're thinking about how to carry a drug forward.
And biomarker exploration is an area of intense interest, but there seems to be a suggestion that DKK1 expression may be associated with the identification of responders where higher expression predicts for perhaps a better chance of response. The clinical study is ongoing. It's nearly fully enrolled. One thing that I'll remind you of that the evaluable population that we presented is roughly half of the overall study. So there's a significant portion of patients who remain on study who have yet to be scanned to see where their responses are to be included in the evaluable population.
And consistent with other immunotherapy trials, particularly the HCC data and actually some of the CheckMate 142 that was presented today, there are patients who have been on therapy in some of those other trials for over a year before achieving a response. And if you look back to the spider plot, which I showed, you see that the same thing has been shown here. So it just highlights the importance of for investigators unless there's clear progression to give that disease control rate a chance to convert over to a partial response and that can sometimes take quite a lot of time. I will give it back to the rest of the team and happy to take any questions.
Our first question comes from the line of Reni Benjamin of Raymond James. Your line is now open.
Hey, good afternoon guys. Thanks for taking the question. I guess just a couple for Doctor. Klempner. Can you give some more color on the STs that are seen in the trial?
And in your opinion, really kind of how meaningful are they? I think there were a couple that you mentioned have the potential to turn into a PR and I guess I want to know why. And then separately, separate from the company, could you give us your own thoughts on how you'd like to see this combination developed going forward? And then what indications, for example, you think we should stick with esophageal, gastric or should we start exploring tumor agnostic indications and target MSI stable patients? Thanks.
Sure. I'll try. I can tackle the first one relatively straightforward. The second is a big question, but I'll try to give you some thoughts about it. So the reason you asked about why might there be some patients who I believe will be converted to PR and I can certainly speak to my one patient who I presented the scans on where he had a serologic biomarker, a protein called CEA and that normalized from quite elevated to normal after about the first two doses, first two cycles.
And so by the time his first scan happened, his marker had already normalized. And in my experience, when the marker goes from elevated into the normal range, that person is clearly responding. And sometimes it just takes a little bit longer than the first interval of the scan, so sometimes done 6, 8, 9 weeks depending on the trial. So sometimes the scanning interval can play a part into when you see the response. But I'm literally 100% convinced that my own patient is going to convert to a responder, which of course will be encouraging when you were to add that into the evaluable patients, your response rate would obviously increase in that situation, which only adds my own excitement about getting more patients on to the combination.
As to some of the other patients who remain on study in that stable disease kind of period, I think if they're tolerating the combination, which is clearly tolerable, then as my clinical judgment would be to keep them on for as long as delayed period of time. And scientifically, I think that this trial offers a couple opportunities to maybe get at some of those questions, which when the science and outcome tie together, then that's when I think anyone gets very excited about a drug. But one could hypothesize that perhaps the DKN-one and maybe the NK mediated mechanism may actually be up regulating the PD L1 expression and then the pembrolizumab that if that process takes a little bit of time, then the combination with pembrolizumab, 1, makes a lot of sense, but 2, it may explain why the responses can sometimes be seen a little bit later. I don't know if that answers the first part of your question, but your second question is about globally putting this in the context of esophagogastric cancer and then more importantly, where do you go from here. So globally, I tried to put this in the context of what is out there.
So the approved agent in the U. S. Is pembrolizumab as a single agent for gastric and GE junctions who have failed more than two lines of therapy. Independently, there is a tumor agnostic MSI high indication. For the sake of this trial, there is no known MSI high patients and I suspect there won't be at all.
So I don't think we need to talk about that part of the population. Although it is worth noting that that does kind of beef up the response rate and some of the durable responses seen in 59 are accounted for by those MSI high patients. You have to take that number probably a little bit inflated by the MSI patients in the KEYNOTE-fifty nine-sixty one, it's a little bit less. So if your comparator is pembrolizumab, then I think this is early data demonstrating a significant improvement in response rate, which again translates to benefit and allows people to stay on study, perhaps giving them the chance to convert 2 responders. How do you go forward from there?
I think the most important thing is really to see the data mature a little bit and increase the number of valuable patients and see those response rates and see if some of those other people convert. If it holds up with more mature data, then I think you definitely have to explore it because that would be a very exciting improvement upon the current standard. So one could envision a like a randomized Phase 2 trial in PD L1 positive patients of pembro versus pembro plus DK101, I think that would be extremely convincing data. I think this trial will be an exciting trial for me and I think the gastroesophageal community. But yes, I think 1 out of 4 people who are confirmed centrally PD L1 negative have the patient that won, they don't even have access to pembrolizumab on label because the label is for PD L1 positive patients.
So if your mechanism is expanding responses into the PD L1 negative patients, then I think something along the lines of expanding responses into the PD L1 negative patients, then I think something along the lines of pembro DK101 versus investigator choice would be a way to really confirm that activity in the PD L1 negative population. But certainly, this is going to be driven by the data. I think in my own opinion, the company has gone about it in a smart way rather than jumping, which other companies have done jumping from too early to Phase 3 trials that have only been met with kind of mixed response. So going about it in a logical way, trying to explore the activity, see something promising, successful strategy rather than jumping into a study before you will really understand your combination.
Thank you. Our next question comes from the line of Wangzhi Li of Ladenburg. Your line is now open.
Hey, thanks for taking my question. Maybe a few. The first one is the 1 suffragile patients, you mentioned it considered as a partial response by central review, but stable disease by the local side. Can you elaborate more why is such a big difference?
Yes. This is kind of a nuance aspect of RECIST. So in RECIST version 1.1, if you call a lesion minimally visible, then your default measurement is supposed to be 5 millimeters, whereas if you call the lesion completely gone, then it should be 0. And when that patient, if you add up the lesions on RECIST, the difference between the 0 and the 5 accounts for a difference of that PR versus stable disease. So, I think it's rare that a central review actually improves the outcome.
Usually central reviews when you look at trials tend to lower the response rates. But in this case, I think it's the central reviews are independent, which is obviously a strength. And I think that in this case, that patient clearly has benefited and has had decreased and bicentral review is a response. I don't know if that answers your question.
But it's So sorry, you shouldn't
Yes, in pulmonary lesion.
Okay. And the The Lucas side considers a 28% reduction, but the Century review is 74% reduction. But the same lesion, I mean the total the sum of the lesion size, is it the same scan, right?
Yes. They use the central review and the investigators use the same scans and the investigator, which is not me in this case, deemed that pulmonary lesion, although significantly decreased, still technically visible. So therefore, it's defaulted to 5 millimeters and the central reviewer reads it as completely gone. So it's recorded as 0. And resist uses the sum of the longest dimension.
And so that accounts for the difference. So if you have
a Okay. Got it. And just to clarify for the other responses, it's all just by the RECIST 1.1 criteria? Correct. Okay.
IR RECIST which is used in a lot of immunotherapy trials is essentially identical to RECIST other than the use of a confirmation scan. Obviously, in the responders on the spider plot, they've been on long enough that they've had
another question is about the I know that all the data is focused on the PD-one naive cohort. We do have 7 patients in the PD-one refractory cohort. So far, looks no response rate. Can you have any further color on any benefits or patient performance in that cohort?
Yes. I think as you pointed out, the numbers are quite small. But again, stable disease in 2 of the 6, so a third of the patients, I think is that's encouraging. Who knows, maybe they will ultimately there will be other PD L1 negative patients that may convert to responders. This is a population that is extremely difficult to treat.
These are patients who have seen essentially all the tools we have for stomach and esophagus cancers. And there to my knowledge, there hasn't really been any approach that has been able to reliably show activity in the PD L1 refractory population, really across tumors. I mean maybe some of these injectable approaches may add responses in those patients in melanoma, but we don't know if that holds true for tumors outside melanoma. But I think the stable disease rate is encouraging. To me, the lack of true responses is actually not that surprising because we haven't really solved that one.
So I would say that bigger numbers are needed. A stable disease rate of 33%, if it holds would be enough for me to be excited and want to explore that population. But I think you just need to see the data mature a little bit.
Got it. One more question about the Sacagio subtype. You also indicated so currently if this one patient is turned to a partial response out of 6, so you do see about 15%, 16% response rate, right? On the other hand, if I remember correctly, the PKAN V001 plus paclitaxel, should I think a 42% of response rate in taxin naive patients, Sacagial cancer patients. I think it's Sacagial plus GG junction, right?
So I think the company is going to provide data update on that in this quarter. I just want to ask you, will you given this I mean maybe too premature to judge the DKAN V1 plus KEYTRUDA in the suffrageous subtype versus DKAN V1 plus paclitaxel in subtype. But I mean, so far, I'm thinking, do you think it's plausible to maybe the DEACON Z1 plus I'm sorry, the DEACON Z1 plus KEYTRUDA, it's so far most data in the gastric and the GEG junction subtype and then the DGNV1 plus pravitaxel may be more active in the sub g or subtype?
Yes, I think that's a good observation and it's something that I can certainly speak to the tax alpha CKN-one because that data has been presented and it's relatively mature and the response rate that you quoted is accurate and that's a significant improvement upon either the rainbow or single agent taxol data. So I think independent of this study that data is interesting and exciting. And it's hard to really draw a lot of conclusions in this pembro plus DKN-one in the esophageal adeno or squamous from 2 and 4 and 2 respectively. I think the fact that there is a responder in that population is in and of itself interesting and exciting because those are groups that are excluded from all of the KEYNOTE studies. So if you look at the inclusion for KEYNOTE-fifty nine and 61, they actually restricted it to GE junction and gastric, partly because of that known phenomenon of lower response rate.
So to me, it's just a it's a signal and it's interesting, but it's really hard to say a lot more than that.
Okay, I understand. Thank you very much.
Sure.
Thank you. And I'm showing no further questions at this time. I would now like to turn the call over to Mr. Doug Anze for closing remarks.
Well, thank you all for your time on the call today and on the webcast. We appreciate your interest in LEAP and your interest in the DKAN-1 program. We're very excited about where we are today and in this ongoing study really look forward to being able to present the more mature data from the full data set to you next year likely in the Q2. And we very much appreciate Doctor. Klempner's time today, the insight of treating a patient, I think, makes the data more real and easier for people to appreciate and understand.
And we appreciate the work of all of our clinicians and their staff and the patients who are part of this study, it's something that is terrific for the clinical population and what is a very underserved esophagogic cancer patient population. So thank you all for your call time today. And if there are any questions, please feel free to follow-up with us at the company directly.
Ladies and gentlemen, thank you for participating in today's conference. This concludes today's program. You may all disconnect. Everyone have a great day.