Thank you for standing by. This is the conference operator. Welcome to the Corvus Pharmaceuticals Second Quarter 2020 Business Update and Financial Results Webcast Conference Call. [Operator Instructions] And the conference is being recorded. [Operator Instructions] I would now like to turn the conference over to Zack Kubow of Pure Communications. Zack Kubow;Pure Communications: Thank you, operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals Second Quarter 2020 Business Update and Financial Results Conference Call. On the call to discuss the results and business highlights for the second quarter 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' quarterly report on Form 10-Q, which was filed today and 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 second quarter 2020 financials and then turn the call over to Richard for a business update. At June 30, 2020, Corvus had cash, cash equivalents and marketable securities totaling $59.3 million as compared to $78 million at December 31, 2019. Research and development expenses in the second quarter of 2020 totaled $7.9 million compared to $10.6 million the same period in 2019. The decrease of $2.7 million was primarily due to a $0.5 million decrease in ciforadenant clinical trial expenses, a $1.7 million decrease in CPI-006 drug manufacturing costs, a $0.5 million decrease in CPI-818 drug manufacturing costs and a $0.8 million decrease in outside service costs. This was partially offset by a $1.1 million increase in CPI-006 clinical trial expenses. The net loss for the second quarter of 2020 was $10.6 million compared to a net loss of $13.0 million for the same period in 2019. Total stock compensation expense for the second quarter of 2020 was $1.4 million compared to $1.9 million for the same period in 2019. Looking forward, we expect net cash used in operating activities for the second half of 2020 to be between $12 million and $14 million, a reduction from $18.8 million of net cash used in operating activities in the first half of 2020. This reduction is mainly due to careful management of expenses, combined with strong prior enrollment in our clinical studies and the focus on patient monitoring and follow-up in these studies. Our current forecast also includes the incremental activity related to our Phase I study of CPI-006 in COVID-19, which is relatively less costly than our core oncology programs. I will now turn the call over to Richard.

Thank you, Leiv, and good afternoon, everyone. Thank you for joining us today for our second quarter 2020 business update. We made good progress in the second quarter, advancing our pipeline of precisely targeted oncology therapies and working to initiate a promising new clinical program for a novel immunotherapy approach for patients with COVID-19. Corvus now has 4 active programs in the clinic, all of which are uniquely positioned and are expected to have meaningful updates in the second half of the year. It is an exciting time for Corvus, and I want to thank our entire team for the excellent work and dedication that brought us to this point in spite of the challenges created by COVID-19. Overall, we are fortunate that COVID-19 pandemic has had minimal impact on the company's progress. With our core oncology programs, our activity in Q2 and into the second half of the year has been focused primarily on patient monitoring and planning for subsequent trials. High enrollment in our trials enabled us to treat patients and acquire the necessary data prior to disruption caused by COVID. This enabled us to remain on track with updated ciforadenant data in renal cell cancer presented at ASCO and no significant interruptions for patients enrolled in our clinical studies. Moreover, as we recently announced, we have filed an IND and initiated a clinical trial investigating our CPI-006 B-cell-activating antibody in COVID-19. This study is proceeding as planned. Looking forward, we will work closely with our investigators to advance our studies with additional data updates expected later this year. We will do this while continuing to prioritize the health and safety of our employees, clinical partners and the patients they serve. Also, in support of our studies, we have been in regular communication with our manufacturing partners, and…

[Operator Instructions] Our first question comes from Mara Goldstein with Mizuho.

Can you hear me?

Hello?

Hello? Hi, Richard. Can you hear me?

Yes, Mara, I can.

Great. Awesome. Can you give us just a little bit more detail around patients who have the PR and 818 trial and what the trial would look like in CTCL? Will it be consistent with what you saw for the PTCL cohort?

Color around the peripheral T-cell lymphoma patient? Pretty straightforward patient with widespread lymphadenopathy that had failed CHOP chemotherapy, which is a routine therapy for PTCL. Then she went on to get high-dose chemotherapy and a bone marrow transplant. She failed shortly thereafter. She had growing disease when she came on our trial. She was on our trial receiving 818 one pill twice a day and was on it for several months and, slowly, over time, had complete resolution of lymphadenopathy, documented on CT scan and on PET scan and confirmed on follow-up scans, CR by RECIST criteria or any lymphoma criteria you want to use. And in terms of subsequent studies, we're going to enroll more PTCL and CTCL patients to just get more numbers on those 2 subsets. Those are the 2 of the most common subsets of T-cell lymphoma. They're very different. PTCL is a more rapidly aggressive tumor. CTCL is more chronic. Want to get a little bit more data on those 2. We have seen, in CTCL, responses not quite yet meeting -- in our dose escalation, not quite meeting RECIST criteria yet or Cheson criteria or Lugano criteria but very close, and we're continuing to follow those patients, and we're going to explore those efficacy signals further in the subsequent patients. And let's see -- what was the rest of your question?

I think that was it. But if I could just ask just on the RCC trial and Adenosine Gene Signature, what the realm, I suppose, of possible outcomes would be in terms of how you would use adenosine signature post the discussion with FDA. So if we think about -- is it in all-comer and you would just have different stratification categories based on that? Or would -- are you seeking to be able to enroll patients based on adenosine signature?

I'll let Dr. Mobasher, who has been doing a lot of work on that, answer that question. Mehrdad?

Sure. Yes. So the current thinking is that for the Phase III, we'll enroll all-comer patients, but we will have the adenosine signature status at study enrollment, and patients will be stratified based on the signature. However, the study will be powered based on the adenosine signature-positive population, and we'll have utility for the negative population. That will give us a lot of information about the negative population and also help us in further understanding of the signature and the biomarkers.

Our next question comes from Tony Butler with ROTH Capital Partners.

Richard, 3 questions, really. If you were to do a trial with an A2A receptor antagonist today that was not an RCC, would you still use adenosine signature as a biomarker? Or is it -- does it pertain more to an RCC trial with an A2A receptor antagonist? That's question one. The second question is with 006. And given that 3 cohorts have been -- have completed dosing and are being monitored, could you give us some thought as to what might be demonstrated later this year when you do present some data? Will it be from all 4 cohorts, that is, and will it just be -- will we be able to make a distinction between 1 of the 4 cohorts or maybe 2 versus the other 1 or 2? That's the second question. The third question is in funding 006 for COVID, is there a mechanism behind which either DARPA can help you with some of that funding? Or would you just take it on your -- all by yourself?

Okay. Well, this is a test of my memory, Tony, so I'll try to answer all 3 questions. So the first question is yes. The second question is combo. And the third question is yes. No, seriously, the answer to your first question is, yes, we would use the adenosine signature in other tumors. The adenosine signature is present in many other tumors, albeit to different degrees. We definitely would explore that in other solid tumors. I don't know if I would restrict enrollment based yet on that because we just don't have enough information on the predictive value of the adenosine signature in other tumors, but it's definitely something to look at. So we -- so basically, any patient, I would say, alert here, anybody using an adenosine mediator blocking agent for anything would be wise to look at the adenosine signature, including CD73. So yes, we would use it. But its role in other tumors is not as well understood as we have it for renal cell cancer. Renal cell cancers, clearly, I mean, you don't need any statistics for this. You have approximately 20% good responses versus 0. Now on your second question on the 006, we've looked at monotherapy, we've looked at combo with ciforadenant, we've looked at combo with pembro, and we've looked at triplet. Combinations look better, and the triplet is looking very interesting. But I think that's all I can say now. There's another component to this, which is also interesting. Remember now we've looked at all different kinds of cancers. And the -- each of these individual arms is not powered to show that one is better than the other. There's just not enough patients, and there's multiple different cancer histologies. But I think something that's going to be very interesting in the cancer story is the induction of antibodies to certain tumors and the role that induced antibodies might have in tumor response. Now the third question was COVID-19 and exploring government funding applications. We are looking at that. We are and have prepared certain applications. But at the moment, we need to get more data. This is a completely new area. Our plan is to get more clinical data, more safety data. The antibody data we're getting in vivo is quite interesting. Concomitant with that, we have an absolutely fabulous stuff happening in vitro. In other words, you can modulate B cells and antibody responses even in vitro. I'm hoping that we have a very nice presentation on all of that together at the SITC meeting in November. But the biology here is quite interesting. Remember, my team at Corvus has some knowledge of these cells, having worked on a couple of drugs you may have heard of, Rituxan, ibrutinib and now 006.

And Richard, if I may. I appreciate the explanation, but if we go back to the 006 combinations in oncology. The reason I ask is because there might be, for example, PD-1 -- if [ you're doing ] refractory patients, [ which you are ], PD-1 clearly may not work in a number of those cohorts and, therefore, there could be a number of patients who are refractory to PD-1, yet you may actually have better outcomes perhaps in one combination or in the triplet than you may have in the other combination. And that's really where I'm trying to drive this question, if you will.

Yes. So I mean I know what you're asking. Can you take a PD-1 refractory tumor like colon cancer or something and suddenly make it responsive? I mean I don't know if we're going to have that kind of information, but I get where you're going. So...

Maybe in non-small cell lung cancer.

Or you could take a PD-1 responsive tumor that failed or something like that and restore responsiveness. I mean that seems to be the case with renal cell. I mean the conclusion you can draw on renal is you take a PD-1 failure, and we see both kinds of patients. We see patients who've -- who are truly refractory to PD-1. That is, they grow right through a PD-1. And then we give them a combination, and they respond. We also see people who respond to a PD-1 then fail and then you recapture it later when you put it together. So those could be very different mechanisms, as you know.

[Operator Instructions] We have one more question from Arthur He with H.C. Wainwright.

Can you guys hear me?

Yes.

So I have 2. So first, regarding the RCC pivotal study design, I just want to clarify, are you guys going to use the original adenosine signature you proposed as a biomarker or you are also going to use the CD68 plus as a biomarker? Could you guys clarify for that? And the second one is regarding to the -- the second one is regarding the CPI-006 in the COVID study. I'm just curious, have you guys evaluated the neutralizing antibody titer?

Yes. Okay. So let me take those questions. The first one on the signature. So we're doing a lot of work on the signature, and it's going to be some combination of what you've discussed. In other words, you can incorporate all those into the same kind of gene signature. So we've continued to refine that a little bit, and we're still looking at that. But basically, it's focused on these genes that are expressed in myeloid cells, including those CD68 cells. Now the second question on neutralizing antibodies, yes, these patients are making neutralizing antibodies. I mentioned in my call -- in the call we just had that this day 14 patient had an anti-RBD of greater than 100,000. When you have a titer of greater than 100,000 to the receptor-binding domain, I guarantee you will have very high neutralization. There's -- all the studies are showing very close correlation with anti-RBD and neutralization. I mean eventually, people won't do neutralization because it's much more difficult assay, and the RBD is much simpler. But the correlation is very good. But when you get titers of 100,000 to RBD, that's for sure going to be neutralizing.

This concludes the question-and-answer session. I would like to turn the conference back over to the management for any closing remarks.

Well, thank you, everyone, for attending the conference call. Of course, we look forward to providing more updates on all the programs as the year progresses. Thanks very much.

This concludes today's conference call. You may disconnect your lines. Thank you for participating, and have a pleasant day.