CytomX Therapeutics, Inc.
Q4 2019 Earnings Call Transcript

Published:

  • Operator:
    Good day ladies and gentlemen and welcome to the CytomX Therapeutics' Fourth Quarter 2019 and Full Year Financials Conference Call. At this time, all participants are in a listen-only mode. As a reminder, this call may be recorded. I would now like to introduce your host for today's conference, Christopher Keenan, Vice President of Investor Relations. Chris, you may begin.
  • Christopher Keenan:
    Thank you, Lee. Good afternoon and thank you for joining us. Earlier today, we issued a press release that includes a summary of our recent progress and fourth quarter 2019 and full year financial results. This press release and a recording of this call can be found under the Investors and News section of our website at cytomx.com.
  • Sean McCarthy:
    Great, thank you very much, Chris and good afternoon everyone. Thanks very much for joining us. It's a pleasure to be here to provide an update on our progress during the fourth quarter and throughout 2019. I'll begin with an overview and some recent highlights across the pipeline, and we'll then turn the call over to Amy to review our lead CX-072 and CX-2009 programs in more depth. Robin will then review our fourth quarter and full year financial update and I'll wrap-up with upcoming 2020 milestones, before opening up the call for questions. At CytomX, we see a major opportunity to more effectively target therapeutic antibodies into diseased tissue, generating new classes of anti-cancer therapies. We believe our unique Probody therapeutic platform represents a fundamental advance and we are highly focused on the discovery and development of a broad clinical pipeline of novel drug candidates to make a meaningful difference in the treatment of cancer. Our unique science offers the potential for new and highly effective anti-cancer therapies, including potentially best-in-class molecules against validated targets, first-in-class molecules against novel undruggable targets, and new combination therapies. Probodies are fully recombinant antibody pro-drugs comprised of a therapeutic antibody as a mask designed to block the binding of the antibody to its target until the mask is removed. Mask removal is achieved specifically and selectively within cancer tissue by certain disease-associated proteins called proteases. This allows us to localize antibody activity into cancer tissue, decreasing target engagement in normal tissues and broadening or in fact even creating a therapeutic window.
  • Amy Peterson:
    Thanks Sean. I'm pleased to be here today to report on the great progress we continue to make with our lead wholly-owned programs CX-072 and CX-2009, including studies that set us up to answer important questions over the next one to two years. Let's begin with our lead program CX-072. As previously reported, patient enrollment is complete for the Part D expansion cohort, starting in CX-072 at the dose of 10 milligrams per kilogram administered intravenously every two weeks to patients with multiple tumor types and we expect to present a summary of our finding from these expansion cohorts this year. Data presented to date most recently at ASCO 2019, showed that CX-072 functions as a checkpoint inhibitor, demonstrating encouraging activity where one would expect to see it with such agents, including triple negative breast cancer, anal squamous cell carcinoma, and cutaneous squamous cell carcinoma. CX-072 tolerability appears favorable as well. And while numbers are too small to be clinically significant, trends towards lower rates of immune-mediated adverse events have been observed. Clinical pharmacokinetic and biopsy data has shown that the CX-072 Probody behaves as designed. That is it remains masked in the circulation and becomes unmasked in tumor tissue, resulting in intra-tumoral saturation of the target and anti-tumor activity. These findings provide an important clinical proof-of-concept for our platform and a strong rationale for differentiation of CX-072 from other PD inhibitors, and support combination strategies with other anti-cancer agents.
  • Robin Knifsend:
    Thank you, Amy. I would like to review selected financial highlights for the year 2019. We ended the year with cash, cash equivalents and investments totaling $296.1 million, compared to $436.1 million as of December 31st, 2018. Our strong balance sheet allows us to comfortably fund operations into the second half of 2021, assuming no new collaborations and/or financings. Research and development expenses were $132 million for the year, compared to $104 million in the corresponding period in 2018. The increase was primarily attributable to additional costs related to our maturing pipeline, including personnel related expenses. In 2019, we incurred approximately $16 million of non-recurring charges related to the acquisition of technological knowhow, license fees to UCSB associated with entering into the amendment with UCSB and the license fee for the EpCAM program. General and administrative expenses were $37 million compared to $34 million in the corresponding period in 2018. Revenue for the year was $57.5 million, compared to $59.5 million in the corresponding year. The decrease was primarily due to a $13.1 million decrease in revenue from AbbVie under the CD71 co-development and licensing agreement relating to the $21 million milestone payment net of associated license fees earned in May 2018 of which $11.7 million was recognized in 2018. In addition, there is a slight decrease in revenue under our agreement with Amgen and decreases relating the Pfizer and ImmunoGen collaborations, which concluded in 2018. The decreases were partially offset by an increase in revenue from Bristol-Myers Squibb due to the accelerated revenue recognition related to the cessation of research on certain targets under our agreement with Bristol-Myers Squibb in the first quarter of 2019. With that, I will turn the call back over to Sean.
  • Sean McCarthy:
    Great. Thanks Robin. So, in closing, let me briefly review our anticipated 2020 milestones. For CX-072, our PD-L1 Probody, we anticipate presentation of final monotherapy data for the expansion arms in multiple selected tumor types, building on our ASCO 2019 presentations of last year. We also for the CX-072 ipi combination in relapsed or refractory melanoma, we anticipate initial data from Stage 1 of the ongoing Phase 2 study. For CX-2009, our CD166 targeting Probody drug conjugate, we anticipate presentation of updated Phase 1 dose escalation and dose ranging data to support the dose and indication selection for the ongoing Phase 2 study you heard about today. And then for CX-2029, our CD71 Probody drug conjugate, we anticipate initial data from the Phase 1 dose escalation portion of the Phase 1/2 study with additional proof-of-concept data from expansion cohorts targeted for 2021, assuming that the program transitions to that stage. Also and as I mentioned earlier on in my remarks, we do anticipate that BMS will present the Phase 1 data for the ipi Probody BMS-986249 sometime this year, and that of course will be the data that has supported the announcement that we made this week regarding their entry into the randomized Phase 2 study of the ipi Probody that we're all very, very excited about. So, thanks, everyone, for taking some time to join us today. It's obviously been a turbulent day out there in the markets. But we're very pleased with the broad progress we've made at CytomX last year and continuing into this year, both with our very unique technology platform and also with our advancing and deepening clinical pipeline. And all of us on the CytomX team are excited for an eventful 2020 ahead. So, I think with that, we'll turn the call back to Chris for Q&A.
  • Christopher Keenan:
    Lee, I think we're ready to open the call for questions.
  • Operator:
    Certainly. Your first question is from Christopher Marai from Nomura Instinet. Your line is now open.
  • Christopher Marai:
    Hi, thanks for taking the question and congrats on the progress. I was wondering if you could touch upon -- on the CD166 2009 Probody program. You updated us on the path forward there, including HER2 negative HR positive breast cancer. And that will constitute your expansion cohort in the Phase 2. Could you maybe elaborate a little bit on the potential path to approval that could emerge from that and how that might look? Is there a go-no-go decision that you're looking for? And then how might this fit into the evolving treating paradigm here? Obviously, other therapies are looking for approval in this setting as well. Thank you.
  • Amy Peterson:
    Sure. Thanks Christopher, this is Amy. Thanks for your question. Yes, so this study just to recap, the first part of the study we'll evaluate 40 patients with hormone receptor positive HER2 negative breast cancer. While we can't disclose the details around the eligibility criteria, what I can say is we have taken a sharp eye to that to ensure that the patient population is one that would be something that we could take forward to global health authorities, should be see activity commensurate with taking the molecule forward. And it is in patients who have received hormonal-based therapy. We recognize that other treatments are emerging and we always have an eye to that. But at this point in time, I can't really divulge further details around specifics of eligibility criteria.
  • Christopher Marai:
    Okay. Then just to follow-up perhaps a bit, the expansion component of the trial I assume would not be registration-directed. At what point does CytomX make a go-no-go decision on this and run out a Phase 3 and even the population that you may be selecting in this expansion cohort? Thank you.
  • Amy Peterson:
    Sure. Thanks for the follow-on. So, you're right. With 40 patients, that's not registrational. However, depending on what we see and depending on our discussions with health authorities, it could potentially lead to something that is registrational if we have the right sample size, if that answers the question.
  • Christopher Marai:
    Yes. And then just the go-no-go on data here, what do you want to see in those 40 patients? Then I'll jump back in the queue. Thank you.
  • Sean McCarthy:
    I think, Chris, as I mentioned, our goal there is to have initial data on this first 40 patients in 2021 and obviously, we'll take a look at that data and decide the path forward.
  • Christopher Keenan:
    Next question Lee.
  • Operator:
    Your next question is from Mohit Bansal from Citi. You line is now open. Your line is now open.
  • Unidentified Analyst:
    Hi, this is James on for Mohit. It looks like Bristol now has 986288 and 986249 in trials. Can you remind us how these two CTLA-4s differ and any insight on BMS' strategy to explore both?
  • Sean McCarthy:
    Yes, hi James. Absolutely. So, 249 is the Probody version of ipi itself. And I think as we've laid out that's the program that's being advanced into the randomized Phase 2 study. And that was the first Probody targeting CTLA-4 that we made with BMS in this alliance. 288 is, as we've said, a modified version of ipi that is designed to be more active than the parental antibody. I'm expecting them to probably say a bit more about this program this year, as the new leadership within BMS get their arms around these programs. So we're not at liberty to say too much about it. But we've made a Probody version of that modified ipi, and that has now also gone into Phase 1 dose escalation. So, as I said in my prepared remarks, the fact that they're putting one program now in Phase 2 and the other is moving into Phase 1, I think it really underscores a couple things. It underscores their continued commitment to CTLA-4 as a target and it very much underscores their interest and commitment to our technology.
  • Unidentified Analyst:
    Thank you. I've just got a follow-on. The press release mentioned the EGFR T-cell bispecific with Amgen is going to be advancing in 2020. Can you highlight what sort of developments have been made and then if we'll be seeing any preclinical data this year?
  • Sean McCarthy:
    We presented some preclinical data previously, as you may have seen in poster form. So, the basic concept and the basic proof-of-concept behind EGFR CD3 has been presented. What we've been doing with Amgen for the last couple years is really working through the detailed protein engineering and molecular biology of how to optimize that format. And as I'm sure you know, there's a lot to that and there's a lot of different formats to sort through, a lot of geometry to get right in terms of the activity of the two arms of this type of bispecific. And all I can say is that we've made good progress and we do expect to move towards lead clinical candidate stage over the course of this year with Amgen. One other note is, as I mentioned, we do at CytomX, much in the AbbVie alliance, we retain development control for this program through proof-of-concept. So, we'll be filing the IND once we get to the point at having a clinical candidate that we agree to move forward with our partner.
  • Unidentified Analyst:
    Fantastic. Thank you for taking the questions.
  • Sean McCarthy:
    Thank you.
  • Operator:
    Your next question is from Terence Flynn from Goldman Sachs.
  • Unidentified Analyst:
    Hi, this is Holly on for Terence. Thanks so much for taking the question. Two for us, one, so as we look towards the data from Stage 1 of the Phase 2 study of CX-072, which is especially later this year, what do you need to see in order to move that program into Stage 2 of the Phase 2 study? And then secondly on CX-2009, beyond the breast cancer indication that you outlined, what other tumor types might be appropriate for this treatment, considering the risk-benefit profile demonstrated thus far? Thanks.
  • Sean McCarthy:
    Thanks for the questions, Holly. I'll be happy to turn those over to Amy.
  • Amy Peterson:
    Okay, great. So, as far as the Stage 1 of the Phase 2 study for CX-072, what we would need to see to move forward, I don't think we're actually giving guidance on what sort of response rates we would need to see. However, I will say that from the data that is available in the public domain, response rates have been around the 20s and in some cases using immune resist as high as 45%. And we are well-aware of those and looking to see where we benchmark to that. For CD166 program, additional indications, as I sort of alluded to in the transcript, we saw monotherapy activity with patients in head and neck, triple negative breast cancer, hormone receptor positive HER2 negative breast cancer, and in the 2019 presentation there are other indications where tumor volume reductions were observed, for example, in ovarian cancer. And what we might think about then are moving forward into those indications where we at least observe activity with our agent. But at this point in time, we're focusing on the hormone receptor positive HER2 negative breast cancer population, which you probably know very well, is about 60% of all of patients with breast cancer. And at this point in time, there is no ADC approved in this particular indication. And then when it comes to CX-2009 in combination with 072, what I alluded to in the transcript is we would look to indications where either have had single-agent activity and think about bringing the combination forward in those indications. But we haven't disclosed what those indications are yet.
  • Christopher Keenan:
    Lee, I think we're ready for the next question.
  • Operator:
    Thank you. Your next question is from Terence Flynn -- it's from Mara Goldstein from Mizuho. Your line is now open.
  • Mara Goldstein:
    Great. Thanks so much for taking the question. Thanks for the additional color on the 2029 program. I just had a question with respect to the biomarker arm in that study and if you can provide a little bit more insight into that and when you might have information. And as well, given the novelty of this particular target, how should we think about it in terms of the sort of focus of tumor types, even though I certainly respect it's a solid tumor study? And then secondarily, I know you've spoken to Bristol having data on the 249 program sometime this year. Do you have any particular insight as to what venue that might be?
  • Sean McCarthy:
    Hey Mara, thanks for the questions. I'll take the second question first, can't comment on that unfortunately. They're working that through, but appreciate the question. Regarding 2029, so our guidance at this point, so this is a big idea, this target. It's a very exciting target. And as I've said before, what we're doing is a pretty careful thoughtful dose escalation with a target. As we've demonstrated pre-clinically, if you don't mask it, it's actually extraordinarily toxic, in fact, lethal. So, we're taking it carefully to learn about this molecule in patients. And what we're working towards presenting this year is initial safety data from Phase 1 dose escalation. The biomarker biopsy data would come a little later in the study as we move to not quite to expansion stage, but the upper range of the dose escalation, so probably no biomarker data this year.
  • Mara Goldstein:
    Okay. Thank you.
  • Operator:
    Your next question is from Robert Burns from H.C. Wainwright. Your line is now open.
  • Robert Burns:
    Hi, thanks for taking my questions. So, I just wanted to circle back on the CX-072 plus Yervoy Phase 2 study. So considering that Idera Pharmaceuticals is currently running a Phase 3 for their asset, IMO-2125 plus Yervoy versus Yervoy in anti-PD-1 or L1 refractory melanoma patients after achieving a 24% objective response rate in their Phase 2. Could you comment about the sort of efficacy benchmark you believe you would have to hit in your Phase 2 trial for CX-072 plus Yervoy in order for your Phase 2 trial to potentially be registrational in nature? And then I have one follow-up after.
  • Sean McCarthy:
    Hi, Robert, great question. And yes, we've obviously noted that data and I'll hand over to Amy.
  • Amy Peterson:
    Okay, great. Right, so as far as what we would need to see in the Phase 2 single arm study, what we would need to see to make it registrational in and of itself, it's hard to pinpoint. Obviously, they went forward with a Phase 3 with a response rate of 24% and we're encouraged certainly by that. And so for registrational standalone, we're probably looking at something upwards of 24%, right? However, we do see that it certainly gives us justification to move forward into larger randomized studies, as they did. And we'll see what happens with their data, which I think we're expecting in 2022 from the Phase 3.
  • Robert Burns:
    Okay. Thank you for that. And then one more from me, so I just I'm curious as to how you see that sort of indication, the anti-PD-1 refractory melanoma patient setting evolving over time, when we consider some of the assets and combinations we see moving into that space. Thanks.
  • Amy Peterson:
    Let me make sure I understand your question. So, it's how does the anti-PD-1 refractory patient population evolve as other agents are moving into the space?
  • Robert Burns:
    Yes, I'm sort of curious as to how you see that sort of treatment pattern sort of evolve, considering all the data we're seeing from multiple different assets, just from a landscape perspective; your thoughts on it.
  • Amy Peterson:
    Yes, I guess first, nothing is yet approved. And so while there might be a lot of people dabbling in this space and testing in this space, I think until we have approvals, this space is open. And I guess I'm not quite sure what additional flavor you're looking to get from us on that.
  • Sean McCarthy:
    Yes, Robert, maybe just one additional -- sorry. Go ahead.
  • Robert Burns:
    No, I'm sorry, Sean for cutting you off. Go ahead.
  • Sean McCarthy:
    I was just going to add that we've moved into this patient population in large part of course because of the substantial unmet medical need. That could shift over time, right, if some of these other approaches are successful and if they move a lot faster than us, then we have to carefully monitor that. But we see this particular patient population as an opportunity to run a study reasonably quickly in an area of unmet medical need, where by the way, the combination that we're evaluating may afford advantages over others. Because we know for example, the depth and durability of response that can be afforded with this, still the only I-O/I-O combination that's been approved. It can be very impressive and very meaningful for patients. And so I think we'll just have to see how it unfolds. We haven't, as you well know, we haven't committed at this stage to large randomized study. We wanted to take it one step at a time. But we'll closely monitor the field and see how it unfolds.
  • Robert Burns:
    Awesome. Thanks guys.
  • Operator:
    Your next question is from Etzer Darout from Guggenheim. Your line is now open.
  • Etzer Darout:
    Great. Thanks for taking the question. Just a couple of questions from me. First on CX-2009, just wondered if you could talk a little bit about the population that the study you're going into, the hormone receptor positive HER2 negative population as far as sort of response rate expectations and how we can think about what sort of the clinical hurdle is in that setting. And then secondly, just wondered, given that we've seen Opdivo CTLA-4 combinations being successful beyond melanoma, if there's any expectations that Bristol could take programs forward beyond just the melanoma expansion. Thanks.
  • Sean McCarthy:
    Let me answer the second question first. And thanks very much for the questions. And I'm sure Amy will be happy to take the second on the 2009 patient population. So, obviously, BMS has made a pretty substantial commitment to the melanoma, the randomized melanoma study. I can't comment on what their thoughts might be in terms of other indications. But as we've said, with our combination, of 072 plus ipi, we do see opportunities beyond melanoma that we could potentially move into. And the team, Amy and Alison and the team are very actively working those through, so no specific update at this point, but we certainly see additional opportunity on our side.
  • Amy Peterson:
    Great. And then I'll address your first question, which was I think trying to better understand what response rate we might be benchmarking to in this patient population, given the competitive landscape. So, I can't give guidance on what response rate we're benchmarking to. I mean it's known that hormone receptor positive HER2 negative breast cancer responses are not as easy to have with chemotherapy or with other agents, which doesn't mean that these patients aren't getting benefit. So, we will be looking at a couple of things in addition to response rates. Clinical benefit rate, for example at 24 weeks, is often used to assess whether or not the drug is doing anything. And when it comes to other drugs moving in the area, there are certainly drugs moving in and there are drugs moving out, and CDK4/6 inhibitors, for example, are possibly moving to adjuvant spaces. Sacituzumab, we're interested to see what ultimately happens with that. But we don't anticipate that data for quite some time. So, I can't give you a number.
  • Etzer Darout:
    No, that's fair. Thank you.
  • Operator:
    Your next question is from Biren Amin from Jefferies. Your line is now open.
  • Biren Amin:
    Yes, hi guys. Thanks for taking my questions. Maybe I guess one more, Sean, on the refractory melanoma trial. I think on this call you talked about a 20% to 24% ORR is a good benchmark. How do you position that if we look at the 14% ORR that was presented by FDA? I think they published this data in Lancet in 2017 in about 2,500 patients that fail PD-1, but continued to be treated with PD-1 post-progression. So, essentially you're getting a 14% ORR on PD-1 after they progress. So, do you think a 20% to 24% ORR in that population with the combo would be a differentiator? Thanks.
  • Sean McCarthy:
    Hi Biren, good question. I want to be clear though. I mean we're not guiding to -- I don't think we did specifically guide to a 20% to 24% response rate on this call. I think what we said when we look at the -- and by the way, that data that you cite is of course interesting in terms of continued PD therapy in failures. But what we're saying, let me try to be as clear about this as I can be, is that if we look at the published evidence or the publicly available evidence for how patients who have been pretreated, treated previously with a PD inhibitor, how they fare on a PD-CTLA-4 combination. Those response rates are in the 20% to 40% range. And the landscape is shifting, as Robert asked and other have asked, right, with other combinations in this patient setting. So, the bar is probably getting higher, not lower. So, we'll do the best we can do and we're obviously looking for the best response rate we can get. But we're not specifically guiding 20% to 24%, just to be clear. We have to do better.
  • Biren Amin:
    Okay, that's helpful. And then on the EpCAM, can you just talk about this is a target that is also expressed on normal cells. And can you just talk a little bit about what you're seeing in the animal data and whether that will correlate in terms of off-target toxicity?
  • Sean McCarthy:
    This is on EpCAM. Yes, so we're really interested in this target. And you know, ImmunoGen has been for some time, as you know. And just the program became available in the context of ImmunoGen's strategic reprioritization last year. So, we were able to negotiate to bring it back into CytomX. So, the target, it's been thought of for a very long time as a very good cancer target. It's actually a reasonably well-validated target in that there is data out there, there's Phase 2 data for a fusion protein, an EpCAM targeting fusion protein, which actually is a different kind of a toxin. It's a recombinant toxin fusion that is quite effective in Phase 2. So, we know this target can work. The preclinical data has shown that the -- and again, ImmunoGen just presented this. The ADC is quite toxic. It induces a range of toxicities, including in the skin. The Probody is protected in that regard and yet the Probody retains the anti-cancer activity of the underlying ADC, just like our Probody drug conjugates do. So, it's an interesting and exciting program. We've just brought it back into the company. So, we're in the process of evaluating the data to decide what our timeline is going to be for moving that program forward. But we think it's a really interesting market.
  • Biren Amin:
    Okay. Thank you.
  • Amy Peterson:
    The indications where it is clinically validated, it's in bladder cancer. And they're actually moving it -- they moved into a pivotal study. Additionally, EpCAM as a naked antibody is used for the treatment of ascites and ovarian cancer in certain regions of the world. So, there are two clinically validated areas where EpCAM has demonstrated activity resulting in continued progress forward to registration studies or approval.
  • Biren Amin:
    Great. Okay. Thank you.
  • Operator:
    Your next question is from Joe Catanzaro from Piper Sandler. Your line is now open.
  • Joe Catanzaro:
    Hey guys. Thanks for taking the questions. Just a couple quick ones from me. Would you be able to say how many patients enrolled into the dose ranging portion of the 2009 Phase 1 study and whether we should expect that cohort of patients to be less heavily pretreated than six or seven prior lines of therapy for the initial dose escalation cohort?
  • Sean McCarthy:
    Hey Joe, it's Sean. Just let me make sure I understand the question. So, you're asking about the Phase 1 study enrollment, right?
  • Joe Catanzaro:
    So yes, so like the dose optimization that you had done in implementing the prophylaxis measures for ocular toxicity.
  • Sean McCarthy:
    Right, yes. So, again, I've got all this to present in a pretty comprehensive update on all of that work sometime this year. What I can say is that the patient population really throughout the work that we did that led to the selection of dose and indication was all done in pretty late-stage patients. And so now, as we're moving into the Phase 2 expansion, the team has revised our enrollment criteria and is working hard to tighten up that patient population relative to the Phase 1. So, I don't want to comment on specific numbers at this point, but it should become clearer as the year goes on.
  • Joe Catanzaro:
    Okay, got it. And then maybe following up along those lines, I know it was kind of asked earlier. But with Phase 1 dose escalation and optimization complete, what triggers via expansion of additional cohorts beyond the initial hormone receptor positive cohort that you just kicked-off?
  • Sean McCarthy:
    Yes, no one thing, really. I think it could be additional data. It could be thinking about priorities across the portfolio. Of course it would be data that we've already seen from the Phase 1. So, it's something that we're looking at in real-time, and particularly Amy and Alison now that they're here and firmly on board, are looking at very closely.
  • Joe Catanzaro:
    Okay, great. That's all I have. Thanks for taking my questions.
  • Sean McCarthy:
    You bet.
  • Operator:
    Your next question is from Varun Kumar from Cantor Fitzgerald. Your line is now open.
  • Varun Kumar:
    Hey good evening everyone and thanks for taking the questions. First on CX-2029, I understand the toxin used in this one is MMAE versus DM4 being used in 2009. Can you provide some context as to how we should think about the MMAE or when we see the first data and some of the off-target that we should expect from the initial data?
  • Sean McCarthy:
    Thanks for the question Varun. If I could paraphrase your question to some extent, it might be would we expect to see ocular toxicities with MMAE. The answer there is that we probably wouldn't expect it, based on the wealth of clinical experience with that payload. Ocular toxicity is a particular consideration with DM4 and the maytansines. So, the toxicities with MMAE that are best characterized are hematologic in nature, neutropenia, anemia and then also neuropathy. So, those would be the kinds of things that we'd be looking out for in the Phase 1 study.
  • Varun Kumar:
    Thanks Sean. And just maybe one question on the 072 combo. Any color on inclusion criteria being used based on Yervoy, prior Yervoy therapy in the patient?
  • Amy Peterson:
    When you say the 072 combo, you're referring to the ipilimumab combo. And right, we are not allowing prior CTLA-4 exposure.
  • Varun Kumar:
    Okay. So, all the enrolled patients will be CTLA-4 naive enrolled cohort?
  • Amy Peterson:
    Correct.
  • Varun Kumar:
    Okay, great. Thank you, Sean and thank you, Amy. Congrats on the progress.
  • Sean McCarthy:
    You're welcome.
  • Amy Peterson:
    Thank you.
  • Christopher Keenan:
    So, we're reaching the top of the hour and I don't see any more questions. I'm going to turn the call back over to Sean.
  • Sean McCarthy:
    Yes, great. Thanks Chris. Well, once again, 2019 was a very big year for the company, very important for advancements across the pipeline. And I think we're off to a great start in 2020. So, thanks for your time and we'll talk to you next time.
  • Operator:
    Ladies and gentlemen, this concludes today's conference. Thank you for your participation and have a wonderful day. You may all disconnect. Good bye.