Good day, everyone, and welcome to Leap Therapeutics' DKN-01 Clinical Investigator 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 Dr. Cynthia Sirard, Chief Medical Officer of Leap. Please begin.
Thank you, operator. Welcome, and thank you to those of you joining us today for an update on Leap Therapeutics' DKN-01 development program. I'm Cynthia Sirard, and with me today are Dr. Rebecca Arend, Assistant Professor and Associate Scientist of Gynecologic Oncology Clinic, University of Alabama Comprehensive Cancer Center Experimental Therapeutics Program, and Douglas Onsi, President and Chief Executive Officer at Leap. This call is being accompanied by a slide deck, so I will ask you please to turn to our forward-looking statements on slide two. 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 of the company's most recent annual report on Form 10-K, as well as other reports filed with the SEC. Any forward-looking statements represent our views as of today, April 23rd, 2020, 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 three. Good day. Today, we are hosting a call to share updated results from our clinical study of DKN-01 as a monotherapy and in combination with paclitaxel in patients with advanced gynecologic cancers. Our presentation will be given by Dr. Rebecca Arend, Assistant Professor and Associate Scientist, Gynecologic Oncology Clinic, University of Alabama Comprehensive Cancer Center Experimental Therapeutics Program.
Dr. Arend will provide background on endometrial cancer and carcinosarcoma and review her clinical experience with DKN-01 as a monotherapy and in combination with paclitaxel. We will end the call by opening the floor to questions for Dr. Arend or any of us from Leap. Turning to slide four. DKK1 is a secreted protein that modulates cell-signaling pathways known as the Wnt signaling pathways, as well as the PI3K and Akt pathways. In cancer, DKK1 has been implicated in facilitating tumor growth and metastasis, as well as promoting immunosuppression in the tumor microenvironment through the activation of myeloid-derived suppressor cells and the suppression of NK cell antitumor activity. Some patients' tumors have mutations in their Wnt signaling pathways that lead to higher levels of DKK1 being produced by the tumor cells.
We are developing an antibody that binds and inhibits the activity of DKK1, known as DKN-01. We have evaluated DKN-01 in a variety of preclinical and clinical studies. We believe that DKN-01 therapy causes tumor reductions through both changes in the tumor cells and activation of the innate immune system in the tumor microenvironment. Let me now turn to slide five. This slide shows the DKN-01 global development program with the ongoing studies and the timelines associated with each. The blue studies are those that are Leap company-sponsored and include two ongoing studies, one in gynecologic cancer, which Dr. Arend will describe during this presentation today. The second study is a study in collaboration with BeiGene, which is a follow-on from the study that was presented at ASCO GI earlier this year.
This study will enroll subjects to be treated with DKN-01 in combination with atezolizumab, either as a second-line agent or a frontline combination. We will be targeting the patients with DKK1 high disease in second-line GE junction and gastric cancer, as well as an exploratory study in combination with XELOX in the frontline setting. In addition, we have several studies ongoing that are investigator-sponsored and referenced in green on this slide. One such study is in collaboration with New York University in prostate cancer, in which we are studying DKN-01 as a monotherapy or in combination with docetaxel in patients with DKK1 high or Wnt-activated prostate cancer. The second study is a study in esophageal gastric cancer in collaboration with Royal Marsden and Roche, in which we are studying DKN-01 in combination with atezolizumab in second-line esophageal gastric cancer.
The third study is a study in collaboration with Massachusetts General Hospital and Bristol Myers Squibb, studying DKN-01 in combination with nivolumab in second-line biliary tract cancer. Lastly, we have a study in collaboration with University of Mainz in Germany, looking at patients with DKN-01 in combination with sorafenib in Wnt-activated first-line hepatocellular carcinoma. Now, I would like to introduce Dr. Rebecca Arend from the University of Alabama at Birmingham Comprehensive Cancer Center. Dr. Arend completed her undergraduate degree at Columbia University and received her medical degree from Albany Medical College. She completed her residency at Columbia-Presbyterian and her fellowship at the University of Alabama at Birmingham. During her fellowship in gynecologic cancer, she was awarded an AAOGF/ABOG Young Investigator Fellowship Grant that currently supports her own lab.
Dr. Arend currently serves as the chair of UAB's Tissue Committee and as the co-chair of the Gynecologic Oncology Disease Oriented Working Group and the Precision Oncology Working Group. She is a member of multiple professional societies and committees, both regionally and nationally. She has authored numerous publications and been highly recognized for outstanding presentations. Dr. Arend has a background in hormonal and molecular pathways associated with uterine carcinosarcoma, and she is currently working on personalized medicine targeting the Wnt pathway in immunotherapy in gynecologic cancer patients. We are very pleased to have her here with us today to present our DKN-01 data in gynecologic cancer patients.
Thank you, Dr. Sirard, for that great introduction. First, I would like to discuss why DKN-01 is such an exciting potential new drug for patients with GYN cancers. This is in part due to the fact that the Wnt beta-catenin mutations that activate the Wnt signaling pathway have a high prevalence in GYN cancer. In that pathway, when there's actually no activating mutation or when the Wnt pathway is turned off, there's no Wnt ligand to activate the pathway. Beta-catenin is degraded in the cytoplasm of the cell and never travels to the nucleus. When the pathway is turned on or is constitutively activated due to a specific mutation, beta-catenin travels to the nucleus and triggers the expression of several target genes that lead to metastasis and cancer stem cell growth and renewal. One of these target genes is DKK1.
Part of our goal is to understand how DKK1 gets produced in higher levels by beta-catenin by certain cancers. We want to understand the specific mutations in cancer tumors that drive higher levels of DKK1, and in this case, mutations and alterations that result in activated Wnt signaling. DKK1 is produced by that pathway. Here are four genetic alterations found in cancers that lead to the upregulation of the Wnt beta-catenin pathway that I'll discuss later. DKK1, which is a target gene of the Wnt beta-catenin pathway, has many functions, which can make it very confusing. This also makes it a very exciting target for treating cancer. The primary function of DKK1 seems to actually be to inhibit the pathway by working through a negative feedback loop. The cell self-regulates the pathway from continuing to be turned on.
In cases where there's mutations, such as a beta-catenin mutation, DKK1 just continues to get produced, and it's not able to inhibit the pathway. The indirect effects of DKK1 are to activate the non-canonical Wnt pathway that is not driven by beta-catenin, that when that get turns on, it actually leads to tumor progression. It also affects other signaling pathways, such as the PI3 kinase pathway through CKAP4, which promotes cancer cellular proliferation. This actually may be the reason why we have seen some remarkable responses, which I'll show you later in patients with PI3 kinase mutations. In addition to the signaling pathways in which it activates, it is also that DKK1 promotes an immune suppressive tumor microenvironment. One way in which it does this is by decreasing activated NK cells and increasing MDSCs.
Therefore, when DKK1 is inhibited, this actually allows the recruitment of CD8+ T cells. These multiple mechanisms really make DKK1 a very exciting potential target for cancer therapy. DKN-01, which is the monoclonal antibody that blocks DKK1, has both direct anti-tumor effects, and it also has indirect effects, such as activating an innate immune response or acting as an anti-angiogenic agent. Tumors with Wnt activating mutations, this leads to high DKK1 levels, are going to be more likely to respond to the drug. We additionally have preliminary data from the combination of DKN-01 and pembrolizumab in esophageal cancer, which showed a longer progression-free survival and overall survival was actually associated with higher tumoral DKK1 levels. Our data to be presented today suggest the same trend in GYN cancers.
This was a phase II basket study evaluating DKN-01 as monotherapy or in combination with weekly paclitaxel in advanced gynecological malignancies. While the primary objective was objective response rate, the goal from the design of this study was actually to be able to address really some of the secondary objectives, which were to explore the genetic mutations in the Wnt signaling pathway and the tumoral DKK1 expression as predictive biomarkers, which is the focus of my presentation today. The trial included both recurrent endometrial cancer patients and platinum-resistant ovarian cancer patients and had a specific cohort for carcinosarcoma, whether it was ovarian or endometrial in origin. It was a non-randomized trial such that the physician could actually choose between giving the patient either monotherapy or the combination.
We did require that at least 50% of the patients in each group have a Wnt signaling alteration in order to have enough patients to evaluate our secondary endpoint. All patients underwent a mandatory biopsy if it was feasible before starting treatment and before cycle number 2. Genes that were defined either based on the literature, genomic analysis, or Foundation Medicine classification as causing a Wnt signaling alteration made up 50% of each group. There's a smaller subset of these genes that are specific alterations that are known to be an activating mutation, and these seven genes are listed on the table at the bottom, the specific gene alterations that coincide with it. The most frequent Wnt-altering mutations in GYN cancers are ARID1A and CTNNB1, which is beta-catenin. Both of these and all of the mutations are much more prevalent in endometrial cancer compared to ovarian cancer.
Here are the patient characteristics that were enrolled in our trial. I want to point out that this is an extremely heavily pretreated population with very limited, if any, treatment options left. Therefore, we do not expect drug activity to be what we see in the frontline or the second-line studies that we're used to. Almost every single patient had a prior taxane therapy, and patients who have failed prior taxanes previously are really not expected to respond to future taxane therapy by itself. For endometrial cancer, a third of the patients are stage 4, and greater than 75% of them had more than three prior systemic therapies with a significant Avastin and hormonal use previously. This is really a population that's very difficult to treat and is really in desperate need of additional therapeutic options.
Here is the specific tumor histology in each of the arms. In the endometrial cohort of patients, there was a higher proportion of the serous subtype in the grade 3 that got the combination therapy compared to the monotherapy. Here are the most common treatment emergent adverse events in both arms. The AEs were similar for monotherapy and combination, with GI disorders being the most frequent, and combination therapy had a higher frequency of anemia. Severe adverse events were only 4.5% in the monotherapy arm and 6.4% in the combination arm. DKN-01 was very well tolerated as monotherapy and also in combination with paclitaxel. Me witnessing how patients look when they receive DKN-01 really has been remarkable. It really does have an extremely good safety profile.
Patients who are monotherapy, again, they don't even feel like they're on therapy at all, which is really drastically different than the more toxic therapies that we're used to. This is extremely strong selling point when discussing with patients after they've received multiple lines of treatment and are really sick of being on chemotherapy at this time. Additionally, this makes DKN-01 an extremely good partner for chemotherapies or other potential combinations. Even seeing patients on the combination arm, it almost sometimes seems like DKN-01 actually would help with some of the side effects. This makes it much easier discussion with patients during the informed consent process or when discussing their treatment plans, especially for those patients who are receiving monotherapy, which was great in the trial that the physicians got to decide whether they were going to get monotherapy or combination.
I really do think that it was a beautifully designed trial that made it very easy to accrue to. Due to the mechanism of action of DKN-01, it would make sense that patients with higher DKK1 levels would have better outcomes. Part of our objective is to choose tumors that have higher DKK1 expression. In this slide, you can see a much higher number of endometrial cancer patients with high DKK1 compared to ovarian cancer. While the numbers are small in malignant mixed Müllerian tumors or MMMT, they also seem to have a higher DKK1 level. These tumors, which are, as I said, rarer, they are much more aggressive than actually either endometrial or ovarian cancer and have much fewer options than either one of those. It makes it an extremely difficult population to treat.
It's very exciting to see that they potentially have a biomarker that's targetable. Because of the higher DKK1 levels in endometrial and Triple MT or carcinosarcoma and the much higher number of Wnt-activating mutations, which we saw in the previous slide, we'll be focused on this group of patients in this presentation, where it really seems that DKN-01 has a real opportunity for making a significant impact on the highest number of patients. Endometrial cancer is by far the most common cancer we see in clinic, and really the majority of them have symptoms of premenopausal bleeding so that they have symptoms and they are diagnosed in an early stage and are cured with surgery alone. There still is a subset that recur or those that initially present with an aggressive histologic subtype or metastatic disease that have an extremely poor 5-year survival rate.
Initially, most patients are treated with surgery, but some receive surgery, chemotherapy, and radiation, and then still recur, and when they do, they really have very limited options. This slide really shows some of the single agent activity that we see in some patients. It's remarkable that when you look at this slide, I want to remind you that a core element of the study was to find out whether patients with Wnt signaling alterations should have a better response to DKN-01. Here you can see they clearly do with a 10% overall response rate, including a complete response and 50% with stable disease. This is in contrast to the blue, who are the patients without a Wnt alteration who experience really minimal activity with single agent.
It's important to note that in heavily pretreated patients, while tumor reductions are always the best outcomes. These are rare, and a durable disease stability is considered really a success in these patients who have no approved therapies left at this point. If you look at this spider plot, you can see how long patients with stable disease remain on therapy. This is a single agent with no toxic chemotherapy. We're really seeing clinically meaningful activity with monotherapy, with a reduction in tumor over time in many patients. Even if it doesn't meet that 30% decrease, we still see a durable response. You can see looking at the difference in the green lines compared to the blue lines, showing that using Wnt alterations as a biomarker really does work in predicting which patients are more likely to have a significant response to the single agent.
I want to go through a couple of case vignettes to highlight some of the responses that we are seeing. For example, this is a 60-year-old patient who had received prior radiation and chemotherapy, which she really tolerated poorly, to the point where we were actually unsure whether she was even going to be able to get additional treatment. At this point, we usually send a tumor to get what we call next-generation sequencing to see if there's any targetable mutations on the tumor itself. When her results returned, and this trial was an option for her, we enrolled her in July of 2018. Initially, the tumor size reduced by 37.5% after eight cycles. After 10 cycles, the patient had a 56% reduction, and by cycle 14, she had a complete response, which was due to single-agent activity.
This is a woman with recurrent endometrial cancer with almost no other options, who came on to study suffering from neuropathy and thrombocytopenia, and now has no evidence of residual disease after 21 months of being on monotherapy, and she continues to do great. To me, as the treating physician and to this patient, this has truly been like an absolute miracle drug. Here's an example of another lady with recurrent endometrial cancer who experienced such horrible toxicity from Taxol that she had to discontinue it. After cycle 2 of monotherapy, she had a 41% reduction in her tumor, which was confirmed after 4 cycles, and she remained on therapy for over six months, when otherwise she should have definitely died at this point. It's important to note that this patient did not have a high DKK1 score, with 38 really being the threshold.
Hers was only 19. This does show that even some patients respond to it even without a high DKK1. I think it's important, as I showed previously in the mechanistic slide, that this patient did have a PI3K mutation. When looking at the response rates to combination therapy, we see stable disease in actually over half the patients, even though they had received prior taxane therapy with a median of six prior systemic therapies. This is really much better than what would be expected with Taxol alone. Here in the forest plot showing that some patients with stable disease have been on combination therapy for over a year.
If you look at both patients on monotherapy and combination therapy and compare the Kaplan-Meier curves for progression-free survival in patients with a WNT activation mutation, which is the blue line, to those without, the green line, this confirms our hypothesis that patients with WNT activating mutations have a longer progression-free survival. Interestingly, if you separate those that were on monotherapy and combination therapy, the best outcomes were for the patients receiving monotherapy that had a WNT activating mutation. It's remarkable that in these patients, DKN-01 monotherapy, while not statistically designed for this, outperforms the paclitaxel combination. This really indicates that paclitaxel does not appear to add any benefit to DKN-01 in patients who have received a prior taxane and have a WNT activating mutation. If you look at those without a mutation, the combination does better, suggesting that paclitaxel does add benefit to DKN-01.
Carcinosarcoma, which I mentioned previously, is made up of both carcinoma and sarcoma, but does much worse than either carcinoma of the endometrium or of the ovary, and worse than sarcoma does. It really does not respond well to chemotherapy at all, and it has a horrible prognosis with very limited treatment options. While the numbers are small, you can see that even in some of these patients with carcinosarcoma, they have a nice, durable, stable disease on monotherapy. The red dotted line here actually represents one of my patients who continues to shock me. She is on single-agent therapy, and initially, her tumor decreased in size, and despite the fact that she's had a slow increase since that time, clinically, she continues to have an excellent response, and she's doing fantastic with no side effects at all. She continues to be on monotherapy for almost 2 years now.
Even though we only have 6 evaluable patients in the combination arm, we have 2 partial responses, which is a very promising start in this patient population where paclitaxel has a low single-agent response rate. Here is one of those 2 patients with a partial response. She also, to me, is a miracle. She's a 46-year-old who was treated previously with neoadjuvant chemotherapy and then underwent debulking surgery. She received the combination DKN-01 and paclitaxel, and she has had a complete resolution of her lung lesion, which had a CTNNB1 mutation. The other patient with a partial response actually started on combination therapy, and the Taxol was discontinued after 9 cycles due to neuropathy. She continues on the single agent, and this is the third patient that we have seen who has had a deepened and durable response on DKN-01 monotherapy after discontinuing combination therapy with paclitaxel.
The other two patients were esophageal cancer patients. Additionally, this is another example of a patient with a relatively low DKK1 score, but she also does have a PIK3CA amplification. Now I want to focus on the 102 patients for whom we have available genetic data. This is patients from all tumor types treated with monotherapy. In this pooled analysis, you can see that patients with tumors with WNT activating mutations had three times longer progression-free survival than those without a WNT activating mutation. If we look at the overall survival in the same cohort of patients, the median overall survival was not yet reached for those with the WNT activation mutation, which shows that the progression-free survival advantage is really holding up into an overall survival advantage.
Now I want to turn your attention to the data on the patients that we have DKK1 RNAscope expression. There will be more to add to this group, but not every single patient, due to the lack of available biopsy specimen for testing. Here's an image on top of a patient with a CTNNB1 mutation and a high DKK1 H score compared to a low H score at the bottom. If you look at those patients with Wnt activating mutations and compare them to those without, confirming the association that we expected due to the fact that these mutations should turn on a production of DKK1. I'd like to point out that there are patients with high DKK1 scores that do not have an activating mutation.
If we look at all tumor types treated with monotherapy, patients with DKK1 high tumors also have three times longer progression-free survival, which is also what we saw in those with the Wnt activating mutation. This progression-free survival advantage is, again, holding up into overall survival. This correlation between DKN-01 response and DKK1 expression was also seen in the esophageal gastric cancer study in combination with PD-1 antibody. I want to conclude by emphasizing the fact that patients with advanced and recurrent endometrial cancer, and especially patients with carcinosarcoma, are in desperate need of new effective agents. The options of available therapies in these patients is actually much more limited than ovarian cancer patients, and the number of cases continues to increase. DKN-01 is extremely well tolerated, with significant activity as a single agent in a biomarker-targeted population.
Given the fact that endometrial cancer and carcinosarcoma patients have more WNT-activating mutations and thus more DKK high tumors compared to ovarian cancer, these are the patients that we expect to see a greater clinical benefit. It is absolutely essential that we continue investigating this agent. A trial in which WNT activating mutation or high tumoral DKK1 score are used as integral biomarkers is needed in order to confirm what we've seen in this basket study. Every time I have a patient with a CTNNB1 mutation and recurrent endometrial cancer, I wish I could offer her DKN-01. I would like to see combination treatments developed further, specifically with immunotherapy and potentially even triple combinations, because the toxicity profile of this drug is so good.
Thank you, Dr. Arend, for your participation in today's program, and thank you all for your time and attention today. We'd now like to open the call for questions. Operator?
Thank you. To ask a question, you will need to press star 1 on your touch-tone telephone. If you would like to withdraw your question, press the pound key. Again, if you would like to ask a question, press the star, then the 1 key on your touch-tone telephone. Our first question comes from Badu Kumar with Baird. Your line is open.
Yeah, thanks for taking our question. You mentioned that there seems to be a non-overlapping pattern for DKK1 high expression and WNT mutations. Kind of effectively, when you look at the landscape of these patient populations, do you expect that non-overlap to be larger? Do you expect that, based on the kind of feedback signaling that you mentioned at the beginning, that most of the patients who have high DKK1 expression will be patients who have activating WNT mutations?
Yeah, I can take that. Dr. Arend. I think what you said was that while we do see some patients with high DKK1 that do not have an activating mutation or vice versa, they have an activating mutation but have a low or medium level of DKK1. I think the majority, you will see a positive correlation. Because we are seeing some where it's not a kind of a double positive, I think for that reason it would be important to be able to include both populations in a future study. All patients with DKK1 high and/or WNT activating mutations, if that makes sense.
Okay. Just, I guess, to the company, what are kind of the next steps you would envision for pursuing DKN-01 in gynecologic cancers in terms of target indications and kind of scope of trial development?
Sure. I guess I'll jump in. Thank you for the question, and thank you, everybody, for participating on the call. We obviously need to discuss this data with the investigators, our partners at BeiGene and the regulatory authorities to determine the next steps for future development. We are very interested in continuing to explore DKN-01. In patients with activating mutations, patients with high DKK1, and also very interested in whether there's the opportunity to combine with PD-1 antibodies in endometrial cancer patients. We can't comment yet on exactly what the next steps and studies will be, but we're very excited by the data that we've seen and think there's an important opportunity here for us to bring DKN-01 to these patients.
Okay, great. Thank you.
Thank you. Our next question comes from David Novak with Raymond James. Your line is open.
Hey, this is Arshad on for David. Thank you for taking my question, and congrats on the data. Just a quick question on the impact of COVID-19 on any potential on enrollment numbers in your DKN-01 trial in gastric cancer with BeiGene, and what kind of impact are you seeing, and how you expect enrollment to continue through the year? Thanks.
Sure. I'll take that one. This is Cyndi. Like most biotech companies, we have seen many major academic institutions pause or delay opening new clinical trials so that they can focus their resources on treating, of course, the COVID-19 patients and opening the COVID-19 related clinical trials. We continue to monitor the COVID-19 impact carefully and will provide updates in our SEC filings and other communications.
Thanks. That answers my question. I'll hop back in the queue. Thank you.
Thank you. We have a question from Wang-Chien Lee with Ladenburg. Your line is open.
Hi. Thanks for taking my question. My question is also about the path forward for combination. Of course, you mentioned for PD-1, what do you think about combined PD-1 and also the nivolumab, given they are approved the combo for second line, and Dr. Arend mentioned the safety profile is pretty good. I don't know what's your thought on that and also, because that could make it easier for the regulatory pathway, but I don't know if you have any theoretic or pre-clinical data support for the triple combination.
I'll take that, and then I'll let Cyndi chime in. I would say having treated a fair number of patients with the nivolumab pembro combination, it's actually extremely toxic. While the response rates are around 40%, 38%, I think that part of what's really exciting here is the fact that there's sort of an inverse correlation with the Wnt pathway and hot tumors. The idea that these cold tumors, the fact that DKN-01 may be synergistic with a PD-L1 or a PD-1 targeted therapy, my suspicion is that in the DKK1 high patients or those with the Wnt activating mutation, DKN-01 plus PD-1 or anti PD-L1 actually would have a better response rate than the pembro nivolumab combo, which would be way less toxic.
While the triple combination, I think could potentially bump that response rate in some patients who can tolerate it, and that might be interesting to look at the triple combination, I'll defer to the company on whether that's something that they're interested in. I would be more enthusiastic about potentially combining it, without the nivolumab, just due to the toxicity profile.
Got it. Makes sense. Maybe I missed it for the carcinosarcoma patient. For the two responders, do they had prior paclitaxel?
Yes. In the carcinosarcoma patients, they all had prior paclitaxel. That's even more exciting given the fact that we don't see the response rates in carcinosarc with prior taxanes is around 10%. They have had prior taxanes as part of their treatment.
Got it. Okay, that's very helpful. Thanks a lot.
Thank you. Our next question comes from Matt Phipps with William Blair. Your line is open.
Good morning. Thanks for taking my question. Congrats on the update. Dr. Arend, it seemed like, and sorry if I missed this, but both of the endometrial responders and one of the carcinosarcoma responders had PIK3CA mutations. Still kind of curious how common that is in endometrial, if you know, and maybe if you looked at some of the longer stable disease patients, see if they also had that mutation.
Yeah. I thought that that was remarkable and very interesting as well because I see PIK3CA very commonly. It's actually not on our chart that we provided because initially it wasn't considered an alteration mutation or an activating mutation. Due to the fact that those patients who had a partial response or complete response had a PIK3CA amplification, makes me very enthusiastic to include that in any future trials. I'm very interested in the mechanism of action. On that one slide, I did show how DKK1 potentially affects the pathway through CKAP4, and it could be a direct activation that's independent of the immune pathway. I'm excited to see where this is headed. I don't know that we fully understand why, but I do think even though the numbers are small, it's hypothesis generating that there is a correlation between PIK3CA amplification and response to DKN-01.
Thanks. I guess maybe it's more for the company, but maybe for Dr. Arend as well, have you had a chance yet to look at some of the on-treatment biopsies, look for some of those changes in kind of immune cell infiltration and such?
Sure [crosstalk].
How successful have you been in collecting the on-treatment biopsies as well, I guess?
Yeah. I'll take that one. We have not yet fully analyzed the biopsies as it relates to immunohistochemical changes and immune infiltrate changes between the screening biopsy and the on-treatment biopsy. In fact, we have a number of analyses left to complete on the biopsies, including some additional patients with the DKK1 RNAscope. We anticipate that we'll have much of this data toward the end of the calendar year.
Great. Thank you.
Thank you. We are showing no further questions. Thank you again for dialing in to today's conference. Have a good day.