Good afternoon, ladies and gentlemen. Thank you for standing by, and welcome to the Corbus Pharmaceuticals First Quarter 2020 Business Update and Financial Results Webcast. Please note today's conference is being recorded. It is now my pleasure to turn the conference over to Zack Kubo of Pure Communications. Please go ahead, sir.
Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals Q1 2020 business update and financial results conference call. On the call to discuss the results and business highlights for the Q1 of 2020 are Richard Miller, Chief Executive Officer Syed Lay, Chief Financial Officer and Lord Admiral Vacher, Chief Medical Officer. The executive team will open the call with some prepared remarks, followed by a question and answer period. I would like to remind everyone that comments made by management today and answers to questions will include forward looking statements.
Forward looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by those statements, including the risks and uncertainties described in Corvus' quarterly report on Form 10 Q, which was filed today with the SEC and other filings the company makes with the SEC from time to time. The company undertakes no obligation to publicly update or revise any forward looking statements, except as required by law. With that, I'd like to turn the call over to Laith Wang. Laith?
Thank you, Zach. I will begin with a quick overview of our Q1 2020 financials and then I'll turn the call over to Richard for a business update. At March 31, 2020, Core was our cash, cash equivalents and marketable securities totaling $68,700,000 as compared to $78,000,000 at December 31, 2019. Research and development expenses in the Q1 of 2020 totaled $10,200,000 compared to 9,400,000 dollars for the same period in 2019. The increase of $800,000 was primarily due to a $1,300,000 increase in CPI-six clinical trial expenses, partially offset by a $900,000 reduction in 818 drug manufacturing costs.
The net loss for the Q1 2020 was $12,900,000 compared to a net loss of 11 $600,000 for the same period in 2019. Total stock compensation expense for the Q1 of 2020 was $1,800,000 compared to $2,000,000 for the same period in 2019.
I'd like to note that
we continue to carefully manage our expenses, especially in light of the COVID-nineteen pandemic. Enrollment in our trials with our 3 programs has been strong, in some cases ahead of schedule. This allows us to focus on monitoring and follow-up and makes us less dependent on new patient enrollment, which has been affected by COVID-nineteen. As Richard will discuss, we believe the overall impact of this slowdown will have a minimal impact on our ability to continue advancing our lead program, cyforadenant. Given the COVID-nineteen situation and our advancement of the cicoradenant program with over 300 patients enrolled to date, we intend to deepen our focus on our lead asset as we develop our registration strategy and head towards a planned pivotal trial.
As a result, we now expect full year 2020 net cash used in operating activities to be between $29,000,000 $31,000,000 This is an approximate $10,000,000 reduction compared to our previous expectations of net cash used in operating activities of between $39,000,000 $42,000,000 I'll now turn the call over to Richard.
Thank you, Leif, and good afternoon, everyone. Thank you for joining us today for our Q1 2020 business update. In the Q1, we continued to advance our pipeline of precisely targeted oncology therapies, enrolling patients in our ongoing studies and presenting updated data on cifiratinib, the Adenosine Gene Signature and CPI-eight eighteen at medical meetings. At the same time, COVID-nineteen grew to a global pandemic that changed the daily lives for most people, health care providers, patients and businesses in the United States. At Corbus, the health and safety of our employees, clinical partners and the patients they serve is our highest priority.
Accordingly, we have worked quickly to communicate and collaborate with our clinical trial sites to adapt our protocols to accommodate potential disruptions for patients enrolled in our studies. The updates we made were in line with FDA's guidance for conducting clinical trials during the COVID-nineteen pandemic and focused on ensuring patient safety and maintaining the integrity of the studies. In addition, we have been in regular communication with our manufacturing partners and there is currently no significant impact on our drug supply. I would like to thank our clinical trial sites for their partnership during this difficult period, and I am pleased that there has been a minimal impact to our studies so far. To date, we have not received any reports of major treatment or follow-up interruptions for patients already enrolled in our studies.
Specifically, we have no instances of missed disease assessments and no significant variances in safety monitoring. There has been an impact on special studies, such as detailed pharmacokinetic assessments and on treatment tumor biopsies as clinical sites shifted toward preparing and caring for the potential surge of COVID-nineteen patients. There has been an impact on enrollment of new patients in some of our However, we believe the overall impact of COVID-nineteen on Corbus has not been significant to date. Prior to the emergence of COVID-nineteen, we had very robust rates of enrollment in all of our trials, positioning us now to focus primarily on monitoring and planning for subsequent trials. CPI-six is an excellent example.
Following on the presentation of positive initial results from NISTEDI at ASCO last year, we saw an increase in interest in enrollments. As a result, we are tracking ahead of our internal enrollment plans for program, having moved into the 3rd and 4th arms of the study with CPI-six in combination with pembrolizumab, which is now fully enrolled and yatripedon in combination with ciforadenant and pembrolizumab, both ahead of schedule. With ciforadenib, we have already completed enrollment of a 25 patient study designed to confirm activity in our biomarker positive population. So overall, our current efforts are now focused on patient follow-up and on monitoring with the aim of collecting data, analyzing results and designing follow-up studies. Of note, we will be analyzing our ciforadenant data in renal cell cancer in preparation for a meeting with FDA later this year to discuss our registration strategy and a pivotal trial.
Turning to an update on our programs, starting with cifiratinib, which is our small molecule inhibitor of the A2A receptor, we are now approaching a very exciting period for this program. We have a key abstract accepted for presentation at ASCO in late May. This data will provide an update on cifiratinib in combination with atezolizumab for the treatment of renal cell cancer and the role of the Adenosine gene signature as a potential predictive biomarker for patients most likely to respond to this therapy. Our confidence in the biomarker signature is enhanced by independent work from other groups that confirm its potential, including an abstract that will be presented at ASCO from a leading academic institution. In that study, the prognostic value of the Edenisene signature in renal cell cancer is confirmed.
We're told to meet with FDA in the Q3 to discuss the study design and plans for a cifiratinib randomized pivotal study in second, third or later line renal cell cancer using the Adenosine Gene Signature biomarker. We will also be exploring the potential for a single arm study based on the Adenosine Signature. As you recall, the Signature identifies a very unfavorable group of patients, a new subset of renal cell cancer. And we believe positive biomarker identified patients will do better with ciforadenant and do poorly with standard therapies. This provides a potential option in an area of unmet need.
Moving to CPI-six, our B cell activating anti CD73 antibody. We continue to be enthusiastic about this novel immunomodulatory antibody, which has demonstrated dramatic effects on circulating immune cells with B cell and T cell mobilization and redistribution. We are not aware of any other agent antibody small molecule targeting CD73 or any other target that has exhibited these properties. As we have previously reported, CPI-six has profound effects on B cells, leading to activation, transformation to plasmoblast and secretion of IgM and IgG antibodies. In total, we have enrolled over 75 patients to date in our CPI-six study, which is evaluating the antibody alone in combination with ciforatinib, in combination with pembrolizumab and Atripet combined with aciforabimabimplantpembrolizumab.
We intend to present an update on this work at the SICC meeting in November later this year. One tantalizing new area is the potential to use CPI-six as a therapy to enhance antibody responses. We have seen antitumor antibodies produced in some of our cancer patients treated with CPI-six. Last on CPI-eight eighteen, our ITK inhibitor, we have established its safety, pharmacokinetics, receptor occupancy and optimal dose along with early signs of antitumor activity. Based on patient responses from the first portion of the Phase 1, 1b study, we plan to move forward with the next portion of the study with an initial focus on cutaneous T cell lymphoma.
So far, this trial has succeeded in providing important information about the dose, selectivity, PK and target occupancy. This now positions us well for future studies, not only in lymphoma, but also in autoimmune diseases. In summary, we continue to make good progress with our pipeline. We have accomplished this with a very efficient use of capital across 3 programs in the clinic. Importantly, we have the potential to initiate a pivotal study of ciforadenant used with the Adenosine gene signature in renal cell cancer in early 2021.
We'll make an important step towards this with the presentation of latest data on the program at ASCO. We look forward to providing an update at that time. I will now turn the call over to the operator for questions and answers. Operator?
Our first question today will come from Mara Goldstein with Mizuho.
Okay. Mara?
Can you hear me now? Your line is open. Yes. Great. Thanks.
Sorry about that. Just a couple of questions. And the first is just on the ITK inhibitor. When you think about sort of advancing into next and the clinical path for that drug, what would be the most likely scenario in terms of clinical trial and understanding that you might not have a comparator, but how it fits into the treatment paradigm? And then I'm just curious about in the triplet combination
for CD73, sildofarent
and pembrolizumab, is that on fluenol yet?
Is that I didn't catch the end of that. Is it what?
Is that on fully enrolled yet? In that triplet, can you just kind of give us a sense of
the way
that it is? The triplet is okay. The triplet is almost fully enrolled. I think we still have 1 or 2 patients to go in it, but they've all been identified. That will be fully enrolled, and Murda, jump in here if I'm not missing something within the next week or 2.
So the No, you're accurate. Yes. So that's done. I hope that addresses that. The doublet has been fully enrolled.
Now the question about ITK and how to think about it. So first of all, the patient so the patients who have been enrolled in our study to date have been patients who failed everything, every approved agent for those diseases. So any activity we see in the T cell lymphoma patients and in the cutaneous T cell lymphoma patients in our studies is noteworthy because there are no other therapies for these patients. These patients are quite sick. Just to put that a little bit and just elaborate further, as you know, there's a lot of therapies for lymphomas.
Some have that one curative for these kinds of lymphomas, but they have some minimal activity. And it is we've seen patients coming on our trial with most of them, in fact, with greater than 5 lines of cryotherapy. So these patients are pretty beat up. So we think that activity any activity in the patients that we've been treating is noteworthy. Of course, the aim of our Phase I study of the portion of the trial we've done, which is important to emphasize, has been to determine various safety and target occupancy and effects on the immune system and things like that.
And we've the trial has succeeded along these lines in, I'd say, every aspect. We've learned a tremendous about this target and our drug. And in particular, there has never been, to our knowledge, a specific ITK inhibitor. And we are learning what the impact of very specifically blocking that target is. So that's where
we are
on that.
Okay. And just to confirm, are you the dose portion was a 4.50
dose? So we're going to go
with 600 milligrams of PID.
Okay. And just do you have a sense of the size of that kind of trial given TTSL, that patient population to begin with and the fact that you had these patients are going to have failed so many therapies around what size study you'll be looking for?
We're going to try to well, first of all, we're still in the 1b part of this. So we're going to treat some more patients. We're going to get a feel for the activity and then we'll design the new trial and go from there. The nice thing about 818 is that it's been very safe so far. And some patients have been on this treatment for every day for months now, several months.
And so it's very attractive now to think about this not only as a single agent, but as you know, Mara, most of our lymphoma therapies are combinations. And so we're also beginning to think now about what kind of therapies to put it together with, how we move it up earlier in the treatment paradigm, etcetera.
Okay. All right. Thanks. I appreciate it. I'll hop off with somebody else.
Our next question will come from Tony Butler with BOTH Capital.
Rich, a couple of questions as well. I'm going to go back to the CPI-six studies. And correct me if I'm wrong, in clinical trials, there were actually 6 cohorts. Is that correct? And within the presumption of 3 78 patients to be enrolled, is that divided equally among those 6?
It's cohort 1A 3C and of course cohort 2a3C. So that's the first question. And then the second question is again from the registration or the presumed registration trial for ciporab and then which you hope to start next year in 2nd, 3rd or 4th
in line
RCC. So I'm curious how do you what form do you think that takes? Is it just previous failures, as you know, atezo and or PD-one have been increasingly being used frontline.
Will you simply use scan of
the cure plus SIFO or would you throw atezo in conjunction? I'm just curious how you think about that from both a control standpoint and also from a registration standpoint. And this is regardless of what you do with the single lung trial. And obviously, those patients will be all having adenosine temperatures. Thanks very much, Richard.
Okay. So, Mehrdad, do you want to handle actually both of those questions? Sure.
The second question in terms of the landscape, you're right. Almost all patients now do get immunotherapy in frontline PD-1s in frontline. But remember, what we have shown with the signature is that this signature identifies the patients who are not going to do well to the immunotherapy. So what we are doing is that we are giving them ciparatnaments and the idea is that it will be in combination with a PD-onePD L1 given what we know also from the mode of action and resistance mechanism for those and that's how these patients will be rescued. The study will be powered for signature positive patients.
Did I answer the second question?
So maybe Go ahead, Richard, please. Go ahead and answer. No, no, no. Go ahead. I think you did answer.
That's fine. So the first question, if I gather, I guess I can't remember anything up on clinicaltrials.gov. But basically, Tony, and we added some cohorts to this after it was started. So basically, there were 4 cohorts. There are 4 cohorts in the study.
6 monotherapy, 6 together with cifirabine, the idea being that you're blocked 2 Adenosine nodes in the pathway. The 3rd arm was a doublet of 6 with pembro and the 4th arm is all 3 together, 6, Schiphol and pembro. We've enrolled all of those except for the final cohort now, the triplet, which is almost enrolled as we mentioned earlier. So after funding, there were dose escalation in each of those cohorts because you have to establish safety in each of the monotherapy and the combinations, although they were staggered a bit. But we went from 1 milligram per kilogram up to 24 milligrams per kilogram.
We found 18 milligrams per kilogram IV every 3 weeks to be the right dose for all across the board. So that's the dose we're using for each of the 4 cohorts. Now within each of those cohorts, there's the ability to expand, to look at renal cell and lung and prostate, and I think there's an other category. So there's sort of like 4 buckets for each of the 4 arms. And we have enrolled many of those.
But as we've been conducting the trial, we've tended to shift patients over because that's one of the beauties of this trial is that we can funnel patients over to maybe getting maybe looking more carefully at the combination versus the monotherapy. So we're not going to fill up every bucket of every 4 cohorts because we don't think that's necessary and we've seen evidence that maybe some of the combinations are more important.
Agreed. And if I may just continue on that theme. Correct me if I'm wrong, but I believe it was actually the triplet, which demonstrated some of the better data that we've seen all the different small population today. So I can understand why you'd shift patients, but I just want to confirm that, that was what you're seeing as well.
Well, the TRIP is we don't have enough data yet on it. The triplet is the last of the cohorts that we've been enrolling. So that has the least mature data and the least number of patients at this point in time. But that, of course, will mature as we go on. There are something like over 30 patients on this trial now still on active therapy.
So this is a work in progress. And one of the things that Leif emphasized in his introduction and I tried to emphasize is we've really because our enrollment and our execution has been so good over the past year or 2, we've really now loaded stacked the or loaded the fuel tank. And so now we can run and treat these patients and start to look at the safety and efficacy data and the biomarker data and start to make some decisions. And that's why I don't think this COVID pandemic has impacted us very much because we have really gotten most of what we needed from enrollment, fortunately before that happens. And so now it's a matter of letting this data mature.
We have a lot of patients on therapy now across our trials. Now it's a question of like the data mature, analyze it, and as I said, go to the next steps after we figure out the answers. Does that make sense?
Yes, sir. It did. Thank you very much, Richard. I appreciate my time.
So if you ask me which of the so if you ask me which of the 4 cohorts is better yet, I mean, there's a suspicion that the combination to better, but I wouldn't say there's proof of there's no proof of any of that. But one thing that is absolutely no question, no absolute no question now is the impact on the immune system, we believe, in a very positive way. The impact on B cells, on lymphocyte trafficking, on immuno immunity is profound. It's really, really amazing. And that occurs even at a dose of 1 milligram per kilogram.
There's new biology here that has never been described before. And it's not about Adenosine. I can't rule that out, but we see these effects in vitro even when we take adenosine out of the equation. This is not going to be seen. We have other antibodies to CD73 that also block adenosine production, react with different epitopes.
It's not about that. This antibody, 6, is reacting with a different part of the CD73 protein that has an immunostimulatory effect, which by the way was first described back in the 1990s. We knew that. So we don't think anybody that to our knowledge, we don't think any small molecule or any other antibody that we've heard about or seen has this property.
Our next question will come from swamampakula Ramakanth with H. C. Wainwright.
Thank you. Thank you, Richard. How are you doing this afternoon? I have a couple of questions. Since I've been jumping between calls, you might have answered this, but nevertheless, let me ask you this.
So on the supportive demand program, in the Phase IbII study, there is some data expected at ASCO. So what sort of data should we expect at that conference? And also, what's the path forward beyond the Phase IbII study that you're talking about? The second question is on the 818 Phase 1b study. What's the time line for data there?
And what is the expectations for the next development pathway from here? Okay. So let me start with the SIFO and then I might ask Murdo to comment as well. So recall that we published in January in cancer discovery, Larry Fong from UCSF is the first author. We published data on 68 patients with advanced refractory, mostly PD-one failure renal cell cancer.
And in that paper, we showed in patients who were Adenosine Signature positive, there was a 17% response rate by resist criteria. There were also many patients who didn't quite meet the criteria for PR that had substantial tumor regression. We also showed that there was a nice plateau, a long lived plateau on the progression free survival curve. And that was statistically significantly associated with the Adenosine Signature and was not nobody responded, 0 in the adenosine signature negative population. When we of course, we knew about this data before the publication in January and we said, okay, let's prospectively this is an observation now, let's prospectively corroborate that.
And so we set out to enroll approximately 25 patients. I think we've enrolled 26 or so. And those 26 additional patients are both Adenosine Signature positive and negative. Because again, you have to confirm the data not only for the positives, but for the negatives. And those additional patients with the follow-up that we have, again, some of the follow-up is short on those additional 25, 26 patients, that is going to be the subject of our ASCO abstract.
And I can I mean, it's not going to be a surprise? The data is holding up. I mean, we expected it to hold up. It's holding up very nicely. In addition, at ASCO, as I mentioned in my remarks, there's very nice paper by workers at Swan Kettering, I guess I can say the name, in hundreds of patients where they basically looked at the Adenosine Signature independent of us and said, what's the prognosis of these patients?
And they find exactly what we do. That if you're a Dennison Signature positive, you have a very bad outcome. And if you're and those of course, the Sloan Kettering patients are not treated with the advancing antagonist, that's where they're the extended therapy. So we feel pretty good about this signature now. Now in turn so that sets us up for a biomarker defined trial.
Now I should say that we've also found in our initial work, we found about 60% of patients with renal cell cancer are then a signature positive. I think our most recent data is like 68%. So it's in the same neighborhood. So it's probably 60% or 2 thirds or so of patients are signature positive. So it's a substantial fraction of the patients.
And they do very poorly. Our work, the Sloan Kettering work and work of other companies that we've talked to, I don't think there's any question that we've identified a frankly new disease because they do so poorly. And this is the population that our drug is active in. And this is sets us up for a very nice trial where we can where we have some options now. We can take everybody and do some sort of hierarchical analysis or we can just focus on the signature positives.
And those are the things that we'll be deciding in the coming months. But Doctor. Mobasher is working with the experts, top people in the field in renal cell cancer. They're well on
the way. There's a protocol
that would define a pivotal randomized trial. So I'll let him comment some more on that. Rudyard, do you want to then just talk about generally what our plans are on that?
Yes. And like you mentioned, the plan based on the initial data that we have identified this full risk patient population that they actually need new treatment. And based on our data, we think these are the patients who would benefit from our treatment. So we have 1 steering committee. We are working on our pivotal data that will be powered in signature patients.
And that's the path that we think is a meaningful path that will be discussed without the
Yes. Thank you, Richard. Thank you. All right. Now on the you also asked about 818 timeline.
So the 818 timeline is we're going to enroll some more we're following new patients that are on the study now. We're going to enroll some more patients with cutaneous T cell lymphoma only because we think that's a very appropriate business for this drug. Frankly, you could make an argument to enroll more patients with the other T cell lymphomas as well, but we're trying to focus a little bit here. We're also getting very, very interested as other people are in some of the autoimmune disease applications, and we're starting to look at that. We think this might be a very interesting disease in autoimmunity.
We don't work in that area so much ourselves, but we've begun collaborating with certain people at NIH, for example. So I think ASH meeting might be a good place for us to give an update on that, but we'll see how things go there. Great. Really appreciate that, Richard. Thanks.
All right.
Thank you. Next we'll hear from Gabriel Fung with Mizuho Securities.
Hi, guys. Yes, this is
Gabriel from Mizuho Securities. Actually in addition to NARA. Congrats on the team. It's good to hear pivotal program around the corner. And just a follow-up on what was you said on the pivotal study.
Do you think that will be required for a Ciproadenant sorry, for an all comers arm to be compared directly to an adenosine signature selected arm? And how do you think that will change the market opportunity? I mean, you mentioned already that it will be 68% approximately 68% of the patients are adenosine positive. How do you think this could actually maybe be used in earlier life as they are given that this works that is? Thank you.
So, Murdad, do you want to take that?
Sure. In terms of whether the better study would be enrolling everyone or would be enrolling just signature positive patients. All our data for until now suggests that signature positive patients are the ones who have objective responses. And as Richard mentioned earlier, they have actually pretty long duration of provision free survival that has given us a tail in that curve. From the operational perspective, both are viable options.
And that is what we are trying to actually fine tune in collaboration with our steering committee and also with the health authority. I think that was the first part of your question, the way I answered it. And for the second part, we think this would be a perfect treatment in terms of treatment landscape for 2nd line and third line patients because these are the patients that are giving immuno oncology treatment. And based on, again, mode of action, we believe these are the patients who will not respond and they will respond well to our treatment because in oncology, typically, you want to rescue patients in early on. There is a potential to move this treatment in combination with zeflatinib, whatever the backbone will be in frontline as well, but that is not our focus now.
But that's something we're looking into in the future.
That's a good point there. I'd like to just to add to that. So one of the nice things about ciforadenin, and we now have data like over 3 50 patients, We have patients who've been taking this drug now for over a year. I think we have some over 2 years every day.
3 years.
And so it's 3 years, sorry. You're older than I thought. So this driver, we've already been asked about this, would be very, very easy to combine from a safety standpoint with frontline stuff. So there's no question that, like many drugs, we try to get approval in the late line and then we move it up earlier. Now renal cell cancer is changing a lot.
Obviously, the landscape is changing very quickly. Patients are living longer. They make it the 2nd, 3rd, 4th, 5th lines of therapy. It's becoming somewhat like the chronic lymphomas in a sense. And that expands.
Now you're in the point where you start to think about not incidence of the disease, but the prevalence. The prevalence is probably going to increase. And this is something we actually had predicted 3 or 4 years ago. Now in terms of the market, so I think the market for us for renal cell would be very, very good. Certainly, as a small company, it's attractive.
But don't forget the Adenosine signatures in other tumors. And we've been looking at that. In fact, we have a paper that was just submitted for publication by Stephen Willingham and Drew Hodgson that is looking at that and shows the distribution of the dendency signature from TCGA data. And it is present in other tumors. So it leaves us to identify which tumors our drug will be applicable to based on the use of that signature.
So that's more work to be done in the future. But I wouldn't I think it would be wrong to just limit this or think of this just as a renal cell cancer play. The biology is very similar. Very similar for all of these. And one of the things you'll see on our assay, and it's in our abstract, I guess the abstracts haven't published yet, is the UDENYCE signature is just related to other things and other cell infiltrates, myeloid cell infiltrates.
Other people refer to this independently as myeloid signature. And we've identified those myeloid cells. That's going to be in our ASKET presentation. So those myeloid cells are not just the renal cell cancer, they're in many other cancers as well. So I would say the upside of this is the potential application in tumors outside of renal.
But just to back up a second, identifying a new subset of a disease based on a biomarker doesn't happen every day. And so I'm very proud of my team, scientific and clinical team, biometrics team, Identifying a new category of a disease is a big deal and that makes a career. In academic medicine, that's a career making move. And you think about that, you think about these other cancers and how we now talk about squamous versus nonsquamous. Well, there was a day when people differentiate those where Hodgkin's lymphoma and non Hodgkin's lymphoma.
Again, there was a day when you didn't know what the difference was, were diffuse large B cell lymphoma from follicular lymphoma. Again, it took real breakthroughs like this to determine, to differentiate these diseases that we didn't guided the therapy that gave greater opportunity to develop drugs because then you knew what the differences were in these diseases and what you can look for. Otherwise, you're treating a bunch of different things with different biological, morphologic and clinical characteristics. So that's a big, big deal. Now we've got to try to make sure it's accurate, and that's what we're trying to do.
Awesome. Actually, that leads me to a really quick follow-up because I know you have also programs in our blood run and prostate. What are your plans when do you expect to hear from those? So,
well, prostate, we just presented data on that a couple of months ago. We see activity in prostate. I think other people are reporting some activity in prostate. We've got our patients on that trial. We're following them.
We're looking we're interested in what the long term outcome is on those patients. We'll probably do more work in that area, but I'm not sure what that is right now. Again, we're looking for prostate is a competitive area. There's lots of good treatment. So it's not good enough to just be active.
You have to have some advantage. So and on the lung cancer, we're following patients on the Morpheus program with Genentech. I think there's some plans to maybe present that data at ESMO. I'm not sure about that. It's a small number of patients.
So I don't really know what to expect from that.
Got it. All right. Thank you.
And at this time, we have no further questions in our queue. I'll turn the conference back over to our speakers for any additional or closing remarks.
Okay. Thank you, operator. First of all, thank you very much for joining today. This is an unusual time. We're happy that all of you could participate in this call.
Enjoyed speaking with me, and we look forward to giving future updates someday soon at ASCO and beyond that. Thank you very much.
Thank you. And that does conclude our conference for today. We thank you for your participation.