Good afternoon, ladies and gentlemen. Thank you for standing by, welcome to the Corvus Pharmaceuticals First Quarter 2020 Business Update and Financial Results webcast. Please note today's conference is being recorded. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session, instructions will be given at that time. It is now my pleasure to turn the conference over to Zack Kubow of Pure Communications. Please go ahead, sir.
Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals First Quarter 2020 Business Update and Financial Results conference call. On the call to discuss the results and business highlights for the first quarter of 2020 are Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, and Mehrdad Mobasher, 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's 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 Leiv Lea. Leiv?
Thank you, Zack. I will begin with a quick overview of our first quarter 2020 financials, and then I'll turn the call over to Richard for a business update. At March 31st, 2020, Corvus had cash equivalents, and marketable securities totaling $68.7 million as compared to $78 million at December 31st, 2019. Research and development expenses in the first quarter of 2020 totaled $10.2 million compared to $9.4 million for the same period in 2019. Excuse me. The increase of $0.8 million was primarily due to a $1.3 million increase in CPI-006 clinical trial expenses, partially offset by a $0.9 million reduction in CPI-818 drug manufacturing costs. The net loss for the first quarter 2020 was $12.9 million compared to a net loss of $11.6 million for the same period in 2019.
Total stock compensation expense for the first quarter 2020 was $1.8 million compared to $2 million for the same period in 2019. I would like to note that we continue to carefully manage our expenses, especially in light of the COVID-19 pandemic. Enrollment in our trials with our three 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-19. 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, ciforadenant.
Given the COVID-19 situation and our advancement of the ciforadenant 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 million and $31 million. This is an approximate $10 million reduction compared to our previous expectations of net cash used in operating activities of between $39 million and $42 million. I'll now turn the call over to Richard.
Thank you, Leiv, good afternoon, everyone. Thank you for joining us today for our first quarter 2020 business update. In the first quarter, we continued to advance our pipeline of precisely targeted oncology therapies, enrolling patients in our ongoing studies and presenting updated data on ciforadenant, the adenosine gene signature, and CPI-818 at medical meetings. At the same time, COVID-19 grew into a global pandemic that changed the daily lives for most people, healthcare providers, patients, and businesses in the U.S. At Corvus, 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-19 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 on-treatment tumor biopsies as clinical sites shifted toward preparing and caring for the potential surge of COVID-19 patients. There has been an impact on enrollment of new patients in some of our studies. We believe the overall impact of COVID-19 on Corvus has not been significant to date. Prior to the emergence of COVID-19, 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-006 is an excellent example. Following on the presentation of positive initial results from the study at ASCO last year, we saw an increase in interest in enrollments.
We are tracking ahead of our internal enrollment plans for this program, having moved into the third and fourth arms of the study with CPI-006 in combination with pembrolizumab, which is now fully enrolled, and the triplet arm in combination with ciforadenant and pembrolizumab, both ahead of schedule. With ciforadenant, we have already completed enrollment of a 25-patient study designed to confirm activity in our biomarker-positive population. 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 ciforadenant, 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 ciforadenant 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 adenosine signature in renal cell cancer is confirmed.
We plan to meet with FDA in the third quarter to discuss the study design and plans for a ciforadenant 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-006, 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-006 has profound effects on B cells, leading to activation, transformation to plasmablasts, and secretion of IgM and IgG antibodies. In total, we have enrolled over 75 patients to date in our CPI-006 study, which is evaluating the antibody alone in combination with ciforadenant, in combination with pembrolizumab, and a triplet, combined with ciforadenant and pembrolizumab. We intend to present an update on this work at the SITC meeting in November later this year. One tantalizing new area is the potential to use CPI-006 as a therapy to enhance antibody responses. We have seen anti-tumor antibodies produced in some of our cancer patients treated with CPI-006.
Last, on CPI-818, our ITK inhibitor, we have established its safety, pharmacokinetics, receptor occupancy, and optimal dose, along with early signs of anti-tumor activity. Based on patient responses from the first portion of the phase I-B study, we plan to move forward with the next portion of this 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 three 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?
Thank you. Ladies and gentlemen, if you would like to ask a question, please signal by pressing star one on your telephone keypad. Our first question today will come from Mara Goldstein with Mizuho Securities.
Okay. Mara?
Can you hear me now?
Mara, your line is open. Yes.
Great. Thank you. Sorry about that. Just a couple questions, the first is just on the ITK inhibitor. When you think about advancing into the 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 comparative of how it fits into the treatment paradigm? Then I'm just curious about in the triplet combination for CD73, cifo and pembrolizumab, is that on fully enrolled yet?
I didn't catch the end of that. Is it what?
Is that on fully enrolled yet, in that triplet?
Okay.
Can you just give us a sense where the?
Okay. The triplet is almost fully enrolled. I think, we still have one or two patients to go in it, but they've all been identified. That'll be fully enrolled, and Mehrdad jump in here if I'm missing something, within the next week or two.
No, you're accurate.
Yeah. That's done.
Okay.
I hope that addresses that. The doublet has been fully enrolled. The question about ITK, and how to think about it. First of all, the patients who have been enrolled in our study to date have been patients who failed everything, every approved agent for those diseases. Any activity we see in the T-cell lymphoma patients and even 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 elaborate further. As you know, there's a lot of therapies for lymphomas.
Right.
Some have non- curative for these kinds of lymphomas, but they have some minimal activity. We see patients come on our trial with, most of them, in fact, with greater than five lines of prior therapy. These patients are pretty beat up. We think that 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 dosage safety and target occupancy and effects on the immune system and things like that. The trial has succeeded along these lines in, I say, every aspect. We've learned tremendous about this target and our drug. In particular, there has never been, to our knowledge, a specific ITK inhibitor.
Right.
We are learning what the impact of very specifically blocking that target is.
Okay.
That's where we are on that.
Okay. Just to confirm, the dose question was a 450 dose? Is that correct?
We're going forward with 600.
Oh, you are. Okay.
600 milligrams of BID.
Okay. Just do you have a sense of the size of that control given CTCL, that patient population to begin with, and the fact that these patients are going to have failed so many therapies, around what size study you'll be looking for?
First of all, we're still in the phase I-B 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 trials and go from there.
Okay.
The nice thing about CPI-818 is that it's been very safe so far. Some patients have been on this treatment every day for months now, several months. 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. We're also beginning to think now about what kind of therapies to put it together with, how we move it up the ladder in the treatment paradigm, et cetera.
Okay. All right. Thanks. I appreciate it. I'll hop off, let somebody else ask.
Our next question will come from Tony Butler with ROTH Capital.
Richard, a couple of questions, as well. I'm going to go back to the CPI-006 study. Correct me if I'm wrong, in ClinicalTrials, there were actually six cohorts. Is that correct? Within the presumption of 378 patients to be enrolled, is that divided equally among those six as cohort 1A through C, and of course, cohort 2A through C? That's the first question. Then the second question is again, from the registration of the presumed registration trial for which you hope to start next year in second, third, or fourth-line RCC. I'm curious, what form do you think that takes? Is it just previous failures, as you know, atezolizumab or a PD-1 have been or increasingly been used frontline. Will you simply use standard of care plus cifo, or would you throw atezolizumab in conjunction?
I'm just curious how you think about that from both a control standpoint and also from a registration standpoint. This is regardless of what you do with the single arm trial. Obviously those patients will be all having adenosine signatures. Thanks very much, Richard.
Okay. 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-1 in frontline. 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. What we are doing is that we are giving them ciforadenant, and the idea is that it will be in combination with a PD-1, PD-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-
You did.
Okay, sure.
Go ahead, Richard, please.
Go ahead. I have this.
No, go ahead. I think you did answer it. That's fine.
Mehrdad on the first question around CPI-006.
The first question, if I gather it, because I can't remember everything up on clinicaltrials.gov, but Tony, and we added some cohorts to this after it was started. There were four cohorts. There are four cohorts in this study. CPI-006 monotherapy, CPI-006 together with ciforadenant, the idea being that you're blocked two adenosine nodes in the pathway. The third arm was a doublet of CPI-006 with Pembro, and the fourth arm is all three together, CPI-006, cifo, and Pembro. We've enrolled all of those, except for the final cohort now, the triplet, which is almost enrolled, as we mentioned earlier. After finding 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.
We went from one milligram per kilogram up to 24 milligrams per kilogram. We found 18 milligrams per kilogram IV every three weeks to be the right dose for all across the board. That's the dose we're using for each of the four cohorts. Within each of those cohorts, there's the ability to extend, to look at renal cell and lung and prostate, and I think there's an other category. There's sort of four buckets for each of the four arms. We have enrolled many of those, but as we've been conducting the trial, we've tended to shift patients over because, and that's one of the beauties of this trial, is that we can funnel patients over to maybe looking more carefully at the combination versus the monotherapy.
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. If I may just continue on that theme, correct me if I'm wrong, but I believe it is actually the triplet which had demonstrated some of the better data that we've seen, albeit in small population, to date. I can understand why you would shift patients, but I just want to confirm that that was what you were seeing as well.
Well, the triplet 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. That, of course, will mature as we go on. There are something like over 30 patients on this trial now, still on active therapy. This is a work in progress. One of the things that Leiv emphasized in his introduction, and I tried to emphasize, is because our enrollment and our execution has been so good over the past year or two, we've really now loaded the fuel tank. 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.
That's why I don't think this COVID pandemic has impacted us very much, because we had really gotten most of what we needed from enrollment, fortunately, before that happened. 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 let 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 it. Mehrdad.
If you ask me which of the four cohorts is better yet, 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. One thing that is absolutely no question, 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 humoral immunity is profound. It's really amazing. That occurs even at a dose of 1 milligram per kilogram. There's new biology here that has never been described before. It's not about adenosine. I can't rule that out, but we see these effects in vitro even when you 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, 006, 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. We don't think anybody, to our knowledge, we don't think any small molecule or any other antibody that we've heard about or seen has this property.
Richard, thank you very much. Appreciate the call.
Again, ladies and gentlemen, it is star one to ask a question at this time. Please note if you're using a speakerphone to make sure your mute function is turned off to allow your signal to reach our equipment. Our next question will come from Swayampakula Ramakanth with H.C. Wainwright.
Thank you, Richard. How are you doing this afternoon?
Good.
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. On the support of the CPI-006 program, in the phase I-B/II study, there is some data expected at ASCO. Also, what is the path forward beyond the phase I-B/II study that you're talking about? The second question is on the 818 of phase I/I-B study, what's the timeline for data there, and what is the expectations for the development pathway from here?
Okay. Let me start with the cifo, and then I might ask Mehrdad to comment as well. Recall that we published in January in Cancer Discovery, Lawrence Fong from UCSF was the first author. We published data on 68 patients with advanced refractory, mostly PD-1 failure renal cell cancer. In that paper, we showed in patients who were adenosine signature positive, there was a 17% response rate by RECIST criteria. There were also many patients who didn't quite meet the criteria for PR but had substantial tumor regression. We also showed that there was a nice plateau, a long-lived plateau on the progression-free survival curve. That was statistically significantly associated with the adenosine signature and was not, nobody responded, zero, in the adenosine signature negative population. Of course, we knew about this data before the publication in January, and we said, "Okay.
This is an observation now. Let's prospectively corroborate that. We set out to enroll approximately 25 patients. I think we've enrolled 26 or so. 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. 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. It's not going to be a surprise. The data is holding up. We expected it to hold up. It's holding up very nicely.
In addition, at ASCO, as I mentioned in my remarks, there's a very nice paper by workers at Sloan 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?" They find exactly what we did. If you're adenosine signature positive, you have a very bad outcome. Of course, those Sloan Kettering patients are not treated with adenosine antagonists. They're getting the standard therapy. We feel pretty good about this signature now. That sets us up for a biomarker-defined trial. I should say that we've also found in our initial work, we found about 60% of patients with renal cell cancer are adenosine signature positive.
I think our most recent data is like 68%, so it's in the same neighborhood. So it's probably 60% or two-thirds or so of patients are signature positive, so it's a substantial fraction of the patients, and they do very poorly. Our work, Sankyo work, and work of other companies that we've talked to, I don't think there's any question that we've identified, frankly, a new disease, because they do so poorly. This is the population that our drug is active in. This sets us up for a very nice trial 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. Those are the things that we'll be deciding in the coming months. Dr. Mobasher is working with the experts, top people in the field in renal cell cancer.
They're well on their way. There's a protocol that would define a pivotal randomized trial. I'll let him comment some more on that. Mehrdad, do you want to just talk about generally what our plans are on that?
Yes. Like you mentioned, the plan based on the initial data is that we have identified this poor 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. We have formed a steering committee. We're working on our pivotal data that will be powered in signature patients, and that's a path that we think is a meaningful path that will be discussed with the health authority.
Thank you, Richard. Thank you, Mehrdad.
You also asked about 818 timeline. The 818 timeline is we're following the 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 disease for this drug. Frankly, we 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 interested, as other people are, in some of the other immune 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 ourself, but we've begun collaborating with certain people at NIH, for example.
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. This is Gabriel from Mizuho Securities, actually, in addition to Mara. Congrats on the team. It's great to hear pivotal program around the corner. Just to follow up on what was just said on the pivotal study. Do you think that'll be required for a ciforadenant, sorry, for an all-comers arm to be compared directly to an adenosine signature-selected arm? How do you think that will change the market opportunity? I mean, you mentioned already that it'll be approximately 68% of the patients are denosig positive. How do you think this could actually maybe be used in earlier lines of therapy, given that this works, that is? Thank you.
Mehrdad, 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 until now suggests that signature positive patients are the ones who have objective responses. As Richard mentioned earlier, they have actually pretty long duration of progression-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 authorities. I think that was the first part of your question, the way I answered it. For the second part, we think this would be a perfect treatment in terms of treatment landscape for second-line and third-line patients, because these are the patients that are getting immuno-oncology treatment.
Based on, again, mode of action, we believe these are the patients who will not respond, and they will respond well to our treatment. In oncology, typically, you want to rescue patients in early on. There is a potential to move this treatment in combination with the ciforadenant, whatever the backbone will be, in front line as well. That is not our focus now. That's something we're looking into in the future.
That's a good point, Mehrdad. Just to add to that, one of the nice things about ciforadenant, and we now have data, like over 350 patients. We have patients who've been taking this drug now for over a year. I think we have some over two years, every day.
Three years.
Three years, sorry. You're older than I thought, Mehrdad. This drug, and we've already been asked about this, would be very easy to combine from a safety standpoint with front-line stuff. 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 to 2nd, 3rd, 4th, 5th lines of therapy. It's becoming somewhat like a chronic lymphoma in a sense. That expands, and 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. This is something we actually had predicted three or four years ago.
In terms of the market, I think the market for us for renal cell would be very, very good. Certainly as a small company, it's attractive. Don't forget the adenosine signatures in other tumors. We've been looking at that. In fact, we have a paper that was just submitted for publication by Daniel Willingham and Drew Hotson that has looked at that and shows the distribution of adenosine signature from TCGA data. It is present in other tumors. It behooves us to identify which tumors our drug will be applicable to based on the use of that signature. That's more work to be done in the future. I think it would be wrong to just limit this or think of this just as a renal cell cancer play.
Right.
The biology is very, very similar. Very similar for all these.
Right.
One of the things you'll see on our ASCO, and it's in our abstract, I guess the abstracts haven't published yet, is the adenosine signature is this related to other things, and other cell infiltrates, myeloid cell infiltrates. Other people have referred to this independently as myeloid signature. We've identified those myeloid cells. That's going to be in our ASCO presentation. Those myeloid cells are not just in renal cell cancer. They're in many other cancers as well. I would say the upside of this is the potential application in tumors outside of renal. Just to back up a second. Identifying a new subset of a disease based on a biomarker doesn't happen every day. I'm very proud of my team, scientific and clinical team, and 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. You think about that, you think about these other cancers and how we now talk about squamous versus non-squamous. There was a day when we didn't differentiate those. Hodgkin's lymphoma and non-Hodgkin lymphoma. Again, there was a day when we didn't know what the difference was. Diffuse large B-cell lymphoma from follicular lymphoma. Again, it took real breakthroughs like this to determine, to differentiate these diseases that really guided the therapy, that gave greater opportunity to develop drugs, because then you knew what the differences were in these diseases and what you could look for. Otherwise, you're treating a bunch of different things with different biological, morphologic, and clinical characteristics. That's a big, big deal.
Now we've got to try to make drugs that cure it. 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 non-small cell lung cancer and prostate. When can we expect to hear from those?
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 interested in what the long-term outcome is on those patients. We'll probably do more work in that area. I'm not sure what that is right now. We're looking for prostate's a competitive area. There's lots of good treatment. It's not good enough to just be active. You have to have some advantage. 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. 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 us today. This is an unusual time. We're happy that all of you could participate in this call. Enjoyed speaking with you, and we look forward to giving future updates someday soon at ASCO and beyond that. Thank you very much.
Thank you. That does conclude our conference for today. We thank you for your participation.