CytomX Therapeutics, Inc. (CTMX) Q2 2020 Earnings Report, Transcript and Summary

Good day, ladies and gentlemen. Welcome to the CytomX Therapeutics Second Quarter 2020 Financials Conference Call. [Operator Instructions] As a reminder, this call may be recorded. I will now introduce your host for today’s conference call, Christopher Keenan, Vice President of Investor Relations. Chris, please go ahead.

Thank you, Valerie. Good afternoon, and thank you for joining us. Earlier today, we issued a press release that includes a summary of our recent progress and second quarter 2020 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. With me today are CytomX President, Chief Executive Officer and Chairman, Dr. Sean McCarthy; and CytomX’s Chief Financial Officer, Carlos Campoy. During today’s call, we will be making forward-looking statements. Because forward-looking statements relate to the future, they are subject to inherent uncertainties and risks, including the uncertainty surrounding the COVID-19 pandemic that are difficult to predict and many of which are outside of our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov, including our Form 10-Q filed today. We undertake no obligation to update any forward-looking statements whether as a result of new information, future developments or otherwise. I would like to turn the call over to Sean.

Great. Thank you, Chris, and good afternoon, everyone. Thanks for joining us. It’s a pleasure to be here to provide an update on our progress during the second quarter of 2020. I’ll begin today’s call with a brief overview of our recent achievements, including our presentations at ASCO 2020 and the next steps for our lead clinical programs. I’ll also comment briefly on our preclinical discovery progress, and we’ll then turn the call over to Carlos to review our second quarter financial results. We’ll then open the call up for questions. At CytomX, we are pioneering a novel class of therapeutic antibodies designed to target cancer tissue, allowing for the development of an innovative pipeline of novel cancer therapies. Over the past decade, we have built a strong scientific foundation for our mobile technology, which has the potential to change the way we think about antibody therapeutics. Our technology called the Probody platform is designed to direct an antibody’s anticancer activity towards tumor tissue and away from normal healthy tissue, allowing us to attack new classes of targets that have previously been considered inaccessible to conventional antibody approaches. Our primary strategy is to use our technology to make first-in-class anticancer drugs for the potential treatment of a wide range of cancers by targeting these previously undruggable targets. We’re also utilizing our technology to discover and develop potentially best-in-class immunotherapies. We have four clinical-stage programs advancing towards or already in Phase II clinical studies. These are CX-2029, a Probody drug conjugate targeting CD71 that we are advancing into Phase II studies in multiple tumor types, including head and neck and non-small cell lung cancers. CX-2009, a Probody drug conjugate targeting CD166 that we are advancing into Phase II studies in breast cancer, CX-072, a Probody therapeutic targeting PD-L1 that we are advancing in combination with CX-2009 in triple negative breast cancer; and BMS-986249, an anti-CTLA-4 Probody therapeutic currently in a randomized Phase II study in melanoma, which is being run by our partner, Bristol-Myers Squibb. In parallel with building and advancing our broad clinical pipeline, we have formed many strong partnerships with leading biopharmaceutical companies, including BMS, Amgen, AbbVie and Astellas, all of whom are advancing novel product candidates utilizing our technology. We have integrated research and development capabilities, and our ambition is to ultimately commercialize our products ourselves and with our partners as we build a long-term sustainable values-based organization. I’d like to spend some time laying out the high-level strategy for each of our four clinical assets. And how the data we presented at ASCO 2020 has pointed the way to our Phase II programs as we evaluate the full potential of each product candidate in further detail. Let’s begin with CX-2029, a Probody drug conjugate targeting CD71. CD71 is also known as the transferrin receptor, a protein that is highly expressed on many cancer types, but due to its involvement in iron metabolism has been traditionally thought of as undruggable. We know, in fact, that antibody-drug conjugates targeting CD71 are not developable due to lethal toxicity at low doses in animal models. However, given the high potential of CD71 as a novel anticancer target, we have investigated whether our Probody technology could allow us to achieve therapeutic levels of an anti-CD71 drug conjugate in cancer patients, potentially unlocking this first-in-class approach across a range of different cancer types. Our Phase I results presented at ASCO 2020 show, for the first time that by employing our technology, CD71 can indeed be targeted successfully in patients with advanced cancers. Our dose escalation study achieved therapeutic levels of CX-2029, and objective confirmed single-agent responses were observed in patients with squamous non-small cell lung cancer and with head and neck squamous cell cancer. The principal dose-limiting toxicity seen in this Phase I study was anemia, which was managed with red blood cell transfusions. These promising Phase I results for CX-2029 are particularly important because targeting CD71 is likely the most rigorous tests we have conducted to date to assess our Probody technology. And these results, we believe, underscore the broad potential of our platform. These Phase I data also resulted in CytomX earning a $40 million milestone payment from AbbVie, our partner for this program, which we received in the second quarter. CytomX continues to lead clinical development in this global co-development and commercialization alliance. We expect to initiate Phase II expansion cohorts of CX-2029 at the dose of 3 milligrams per kilogram every three weeks in head and neck squamous cell carcinoma, squamous non-small cell lung cancer, squamous esophageal carcinoma and DLBCL in the second half of 2020, with potential for the first data readouts in late 2021. Turning now to CX-2009, our wholly-owned drug candidate targeting the previously undruggable target CD166. CD166 is widely expressed across multiple tumor types, and we believe has broad potential as a novel anticancer target. However, like CD71, CD166 is present on many normal tissues, ruling it out as a target for conventional therapeutic antibody approaches. To unlock the potential in this novel pathway, we have designed CX-2009 as CD166 targeting Probody conjugated to the well-characterized cytotoxic payload, DM4. Similar to our experience with CX-2029 that we just discussed, our Phase I dose escalation study with CX-2009 in patients with selected advanced solid tumors, achieved therapeutic exposures of the drug candidate, and we observed evidence of single-agent anticancer activity in several tumor types, including breast cancer and ovarian cancer. CX-2009 was generally well tolerated. The principal dose-limiting toxicities were ocular, anticipated and well documented secular of DM4 conjugates and that we intend to manage with ocular prophylaxis in ongoing studies. With Phase 1 now complete for this asset, our program strategy is presently focused on breast cancer. Of note, CD166 expression is high in greater than 80% of hormone receptor positive HER2-negative breast cancer patients; and in approximately 50% of patients with triple-negative breast cancer. In our Phase I study, we observed durable clinical activity in both of these breast cancer populations, despite these patients being very heavily pretreated. Significant unmet medical need remains in breast cancer, and accordingly, we previously announced the initiation of a Phase II expansion study of CX-2009 in hormone receptor positive HER2-negative breast cancer. We didn’t like to pause this study in March 2020 due to the impact of the COVID pandemic. However, our team has used the intervening period resulting from the pandemic to further refine the study with a focus on patient enrollment criteria, including prior treatment regimens. This revised trial will continue to evaluate CX-2009 monotherapy at 7 milligrams per kilogram administered every three weeks, and we aim to enroll at least 40 patients. We expect to reinitiate the study during the second half of 2020. We’re also preparing to initiate Phase II expansion studies of CX-2009 in triple-negative breast cancer, both as monotherapy and in combination with our wholly-owned anti-PD-L1 Probody, CX-072. We have previously reported single-agent activity for CX-072 in triple-negative breast cancer and have also presented our preclinical data that provide experimental rationale for combination treatment of CX-2009 with PD inhibition, consistent with the well-established benefits of combining chemotherapy and checkpoint inhibition. We’re excited to also get this work underway in the second half of this year. These Phase II studies of CX-2009 in hormone receptor positive and triple-negative breast cancers are important next steps in our further evaluation of the potential of this novel first-in-class drug candidate, and we are working towards initial data by the end of 2021. Moving on now to our PD-L 1 inhibitor, CX-072 in further detail. Updated data from our Phase I/II trial of CX-072 from multiple expansion cohorts continued to show durable antitumor activity in patients with IO sensitive tumors, such as triple-negative breast cancer, anal squamous cell carcinoma, cutaneous squamous cell carcinoma and tumors with high mutational burden. This data was presented at ASCO 2020. I’d like to spend a few moments here highlighting the high tumor mutational burden cohort for CX-072, which is illustrative of the unique and potentially differentiated clinical profile of this asset. 14 patients with various advanced tumor types with high TMB were treated with CX-072 at 10 mg per kg. Of 10 efficacy evaluable patients, three confirmed partial responses and one confirmed – one complete response were observed. The partial responses were in colorectal, cutaneous squamous cell carcinoma and neuroendocrine carcinoma and the complete response was in a patient with anal squamous cell carcinoma. CX-072 was well tolerated with only 2% grade 3 or higher immune-related adverse events. These data are particularly of note in view of Merck’s approval in mid-June this year of Keytruda in solid tumors with high TMB. As we now conclude our first clinical explorations with CX-072, which is the first Probody therapeutic to be evaluated in humans, we’re very encouraged that our platform is functioning as designed, and these findings provide rationale for differentiation of CX-072 from other PD inhibitors and support combination strategies with CX-2009 and other anticancer agents. Turning now to another exciting application of our technology in cancer immunotherapy and our work with our partner, Bristol-Myers Squibb, who presented data during the second quarter for 2 anti-CTLA-4 Probody programs, BMS 986249 and BMS 986288, which I will refer to you as BMS 249 and BMS 288, respectively. At ASCO, BMS presented the first clinical data for BMS 249, a Probody version of the anti-CTLA-4 antibody, ipilimumab. This is a novel therapeutic strategy to enhance CTLA-4 exposure in the tumor microenvironment, while potentially sparing systemic toxicity. The trial evaluated BMS 249 as monotherapy or in combination with the anti-PD-1 antibody, nivolumab in patients with advanced cancers with doses ranging from 240 milligrams to 2,400 milligrams of the Probody, which for reference is approximately 3 to 30 mg per kg. Ipilimumab is typically used clinically at doses of 1 to 3 mg per kg. Safety data from the Phase I trial showed that BMS 249 was generally well tolerated as monotherapy and in combination with nivo. The types of treatment-related adverse events were consistent with those seen with the parent molecule ipilimumab. And the incidence of Grade 3 and above adverse events were supportive of the Probody mechanism of action. Based on these Phase I findings, BMS has initiated a randomized cohort expansion, evaluating the tolerability and activity of BMS 249 in combination with nivo versus nivo with or without ipilimumab in metastatic melanoma. The advancement of BMS 249 into this study triggered a milestone payment of $10 million from BMS to CytomX that was received in the second quarter. This is an important study that has the potential to provide additional validation of this novel product candidate. Staying with CTLA-4 for a few moments, also in Q2 at AACR, BMS presented preclinical data for BMS 249 and also BMS 288, which is a Probody of a nonfucosylated version of ipilimumab. BMS 249 and BMS 288 demonstrated equivalent intratumoral pharmacodynamic activity and comparable antitumor activity relative to their parental antibodies. These data also showed that the Probody versions are significantly safer than each underlying antibody, demonstrating highest nonseverely toxic doses in animal models that were fivefold and threefold improved, respectively. These data support the strategy of using our Probody technology to expand therapeutic index for CTLA-4 therapy and are strongly consistent with the clinical experience to date that BMS has reported with BMS 249. The nonfucosylated Probody, BMS 288 is also in the clinic in a Phase I dose escalation study. Before I turn over to Carlos for a review of our financials, I’d like to provide brief updates on three early stage programs at CytomX that are emerging as a potential second wave of product candidates in our pipeline. Let me begin with CX-904, our T-cell bispecific Probody targeting eGFR and CD3, partnered with Amgen. We believe the application of our Probody technology has the potential to enable solid tumor targeting of this modality. Such targeting with unmasked T-cell bispecifics has been very challenging for the field due to narrow or non-existent therapeutic windows. We continue to advance this candidate towards IND-enabling studies and expect to file in late 2021. Turning to CX-2043, our wholly owned EpCAM targeting Probody drug conjugate, CX-2043 was developed utilizing CytomX’ Probody technology and ImmunoGen’s drug conjugate technology and arose from our previous strategic collaboration. We continued to advance this candidate towards IND-enabling studies. Lastly, as part of the strategic collaboration with Astellas that we announced in the first quarter, for which we received an $80 million upfront payment, we have now launched discovery activities surrounding the development and ultimate commercialization of novel T-cell engaging bispecific antibodies in masked form. This is our second alliance in this exciting area of research, and we have high hopes for this Probody format. With that, let me hand the call over to Carlos to review our financial update.

Thank you, Sean. I would now like to review financial highlights for the second quarter ending June 2019. The revenue for the quarter was $16.6 million compared to $9 million in the corresponding period in 2019. The increase is primarily due to a higher percentage of project completion of CX-904, our Amgen EGFR product candidate. And also the recognition of revenue related to the $80 million upfront payment received under the Astellas agreement that we entered into in March 2020. Research and development expenses were $24 million for the quarter compared to $30.8 million in the corresponding period in 2019. The decrease was largely attributed to onetime licensing fee paid in 2019 and a decrease in clinical trial-related activities in 2020. We ended the quarter with cash, cash equivalents and investments totaling $346 million compared to $296 million as of December 31, 2019. We expect our strong balance sheet to allow us to meet projected operating requirements into the second half of 2022, assuming no new collaborations or financings. With that, I’ll turn the call back to Sean.

Great. Thanks, Carlos. So let me wrap things up here, and then we’ll go to questions. In summary, CytomX made broad progress across our clinical and preclinical programs during the second quarter as we further advanced our technology, partnerships and lead drug candidates to several important inflection points. We have continued to show leadership in defining new therapeutic antibody modalities with potential to address significant unmet medical needs in the treatment of cancer, a mission that remains as important as ever, despite the unprecedented challenges being posed by the COVID-19 pandemic. We have now brought two previously undruggable targets into play in the oncology field with our platform, CD166 and CD71, both of which we believe have broad potential in multiple cancer types. And we’ll be learning a lot more about these product candidates from our Phase II studies that we expect to start to read out in late 2021. We’re further extending our undruggable target strategy with the advancement of our bispecific program targeting CD3 in EGFR. And with the drug conjugate targeting EpCAM, these preclinical programs are taking great shape as our next INDs. We have also continued with our cancer immunotherapy strategy, leveraging clinically validated targets. The clinical data for our wholly-owned anti-PD-L1 Probody CX-072 has continued to mature, affording us unique opportunities to advance innovative combination therapies, starting with CX-072 plus CX-2009 in triple-negative breast cancer. Our collaborative work with BMS on CTLA-4 has also provided important proof points for our platform, both clinical and preclinical, and we’re delighted to see BMS 249 continuing to advance in the randomized Phase II melanoma study in combination with nivo. Our broad partnership strategy has also continued to deliver with $130 million of cash proceeds so far this year, including the initiation of a major new alliance with Astellas and the progression of many additional preclinical programs across our collaborations, adding to the strength and depth of our pipeline. We continue to enjoy a robust cash position and remain highly focused on making the biggest difference we can for cancer patients as we continue to build our company. Regarding COVID-19, CytomX has continued to execute very well, despite the uncertainties and challenges presented by the pandemic. All of us at the company hope that you and your families are well and keeping safe during this time. And I would like to close by thanking our employees, our patients, our investigators, clinical trial staff and everyone involved in helping us continue to drive forward with our mission of developing new medicines for the treatment of major unmet medical needs in oncology. With that, I’ll hand the call back to Chris, and we’ll open up for questions.

Thank you, Sean. Valerie, please open the Q&A session.

[Operator Instructions] Our first question comes from Peter Lawson of Barclays. Your line is open. Q –Waleed: This is Waleed on for Peter. Just maybe initially on the expansion study for CX-2009. Just wondered if you could give us a little bit more color and details on the revised patient enrollment criteria for the study. And also based on your discussions with the FDA, what does the bar need to hit and what would be considered positive results in both HER2 negative breast cancer as well as triple negative?

Yes, great. Thanks for the questions. So regarding patient enrollment, the kinds of things that we’re looking at, obviously, are – given that the Phase I data for CX-2009 was generated in a very heavily pretreated patient population with a median number of prior treatments of 7 or 8, depending upon whether it’s TNBC or hormone receptor positive. Obviously, we’re looking to enroll a substantially less heavily pretreated patient population in the study. So we’ve been fine-tuning that in the recent months. Also, given the evolution of the landscape, giving a little bit more thought to prior treatment regimens that are allowed in the study in regards of the patient population. So those are the kinds of things that we’re doing in this intervening period. Regarding the bar for activity, still, I want to emphasize, this is still a relatively early expiration of CX-2009 in breast cancer. It is a rapidly evolving field, both in hormone receptor positive and triple negative. We haven’t yet had formal discussions with FDA on these types of matters. But the – in triple negative, of course, we’re very well aware of the approval now of the sacituzumab and the activity that we’ve seen with that molecule in hormone receptor positive, where sacituzumab is also active. So we’re mindful of the need to be competitive in this evolving landscape.

Great. And then maybe just a question on BMS 249. Do you have any idea of when we can see the next data readout from that study?

Unfortunately, we don’t at this stage. They are actively enrolling. Patients have been – we can’t speak to their time lines, unfortunately, or to impact that COVID may be having on their enrollment. So we’re just going to have to wait and see how that unfolds.

Our next question comes from Etzer Darout of Guggenheim Securities. Your line in open.

The first one for me is a little clarity on the CX-072 combination with CX-2009. Is that what you said was that you plan to sort of initiate a study there in the second half of this year? And then just a quick question on the Astellas bispecific collaboration. Obviously, hematologic malignancies are where we’ve seen sort of the most success, but it’s also kind of more crowded. I wondered if you could talk about – a little bit about maybe where you and Astellas plan to sort of concentrate or focus sort of your energy, if you will, in terms of sort of the bispecific landscape and where you may find indications, I guess, that are more appropriate for the technology?

Yes, great. Etzer, thanks for the questions. So yes, we are actively gearing up to start an expansion cohort or expansion cohorts of CX-2009 in triple negative, both as a monotherapy and in combination with CX-072. I want to reiterate that we have seen single-agent activity for both probodies, CX-072 and CX-2009 in triple negative. So we think this is an exciting experiment to do with the potential for competitive differentiation further down the road. So that study, we aim to get up and running second half. With regard to Astellas, we haven’t guided on the specific focus of the programs there in terms of tumor types. I would just say, broadly speaking, that our strategy in using our Probody masking technology on CD3 bispecifics is from the CytomX point of view, is largely directed at solid tumors where we see the need for substantial improvements because this has been a very tough area to break into for reasons, a very, very narrow and compressed therapeutic window with solid tumor targets. So broadly speaking, we’ve developed the technology to address solid tumors. It certainly could have application in hematologic, I can’t speak specifically for Astellas.

Our next question comes from Terence Flynn of Goldman Sachs. Your line is open.

Was just wondering on CX-2029 regarding the Phase II program. I know you ran through, it sounds like three different tumor types you’re focused on there. Can you maybe just give some insight in terms of how many patients you think would be eligible if you look at U.S., EU5 and Japan for treatment here with CX-2029? Just trying to kind of think about the potential market opportunity.

Yes. Terence, great question. So let me just run through the four expansions again for clarity. So squamous head and neck, squamous non-small cell lung, squamous esophageal and then DLBCL. The first two indications we demonstrated confirmed partial responses in Phase I dose escalation. Squamous esophageal, we’ve shown preclinical activity in xenograft models. Similarly, DLBCL, strong preclinical activity in that indication. That’s the first hematologic indication. That’s one that has arisen through our discussions with our collaborator AbbVie, they have a strong interest in hematologic malignancies as you know. In terms of penetration of the patient population and the market size and the line of therapy, it’s really too early to tell at this stage. We are optimistic based on the Phase I data, of course, that we have a very unique, active single agent against a previously undruggable target that has shown in some of the case studies that we presented previously at ASCO, some pretty profound tumor regressions in patients with very late stage, very heavy tumor burden. The therapeutic window is clearly there at 3 mg per kg. We need to do more work to establish how wide that therapeutic window is, which will dictate ultimately how far forward in lines of therapy we can bring this exciting drug candidate. So Terence, we just have a lot more work to do there. But we’re excited, and we think this program is going to have broad potential.

Our next question comes from Biren Amin of Jefferies.

So on CX-2029 for the dose expansion cohort, have you made any adjustments in this cohort that could lead to lower grade 3 or higher anemias and neutropenias that you observed in the dose escalation part?

Yes, Biren, well, I would just say that we’re – a couple of things on the hematologic side with CX-2029. The – as we’ve discussed previously, these are anticipated adverse events with this payload and to some extent with this target. We are doing more work to understand the etiology of the anemia over time. But in terms of steps that we’re taking, they will include treating patients with red blood cell generating growth factors like EPO derivatives. And that’s really all we can say right now. But I want to just remind everybody that the Phase I experience demonstrated that we were able to manage the anemia with red blood cell transfusions. This is something that oncologists are very used to doing, given many decades of experience with chemotherapies. And we’re continuing to get a handle on the overall therapeutic window, and will continue to get a handle on the therapeutic window of this target, and this agent as time goes on.

And on the dose expansion, are you enrolling for patients with high CD71 expression?

We’re not – let me answer the question this way. We don’t believe we have enough data yet, either preclinical or clinical, to draw any conclusions regarding the target level versus response. One of the things to consider is that CD71 is such an interesting target because it cycles so rapidly off the cell surface and then back, is an unusual target where expression level may or may not ultimately correlate with response, and so we’re not drawing – we’re not making too many assumptions about this at this stage, and so selection strategies will be developed over time.

Our next question comes from Mara Goldstein of Mizuho. Your line is open.

I had a question on CX-072 and the environment for triple-negative cancers, triple negative breast cancer therapies. And if you should decide that, that is not the best indication, given the competitive landscape, is there a sort of plan B of what you might look at – what other trials you might look at? That’s first of all. And second of all, I do have a question on CX-2029 and the decision to focus on squamous tumors rather than nonsquamous? And is there’s something in the biology that we should be aware of?

Yes, Mara, great questions. So with regards to CX-072, a lot of this is about follow the data. And as our data has continued to emerge and mature over time for CX-072 monotherapy and CX-2009, the concept of combining the two of these agents, which, as I mentioned earlier, both have single-agent activity in TNBC, combining them in that indication, we think, makes a lot of sense in the context of the current competitive landscape on the assumption that the activity of the 2 together has the potential to do something interesting, really interesting. So we’ll see. We’ll run this expansion, and we’ll see what we get. You’re right. The landscape is evolving. It’s not a huge patient population, but we’re really interested to see what this combination can do in TNBC. The question of squamous tumors. And actually, I’m sorry, let me answer the second part of your question on CX-072, which really relates to the program strategy overall, which is, as I said, we continue to follow the data where we’ve evolved towards a combination strategy, as you know, rather than driving the monotherapy to registration. That’s where the competitive landscape we see is just too – way too crowded for us to – at this point, without a partner to invest in driving the monotherapy to registration at least at this stage. We do remain interested in potentially finding a partner for this asset over time. And that could help inform future strategy as well. Regarding squamous tumors in CX-2029, again, follow the data. The clinical observations are really interesting. And the kind of thing you keep your eyes open for when you run Phase I studies. We are intrigued by the activity that we’ve seen in squamous head and neck and squamous lung. Why might that be? And is it a real signal in terms of that relative to other tumor types? That’s why we need to run the expansions. Why might it be the case? It could relate to target. But as we just discussed, we have a very early understanding of target versus response for CD71, we need to learn more there. Could it relate to the microenvironment, possible. So we just need to do more work. But we think it’s an intriguing clinical hypothesis and sometimes Phase I studies give you these great opportunities to all of the data into Phase II, and that’s exactly what we’re doing. So we’ll be learning more.

Okay. And if I could just also squeeze one more in. And just – I know, obviously, Bristol is in charge of the program for BMS 986249. But can you just remind us what is maybe the next financial milestone for that program?

So for BMS 986249 for the ipi Probody, it would likely be the initiation of a registrational study, but I’d have to go back and check that.

Our next question comes from Mohit Bansal of Citi Your line is open.

So I just wanted to probe a little bit further on the cost-related Probody approach. If I’m – so can you please help us understand what fucosylation actually, what difference does that make to the Probody or antibody? And if I’m not mistaken, it seems like if these nonfucosylated version was also tested in clinic, so is there anything we have learned from that compound, which could be used in here.

Yes. Mohit, thanks for the question. So the concept, and this is articulated in the AACR poster that CMS presented a few months back. The concept is that nonfucosylation of ipi increases its ability to deplete intratumoral T-regs based on the way that it interacts with the target and Treg cells in the tumor. So the basic idea is that increased intratumoral Treg depletion by the nonfucosylated antibody results in more potent anticancer activity because many believe that Treg depletion is the principal mechanism through which CTLA-4 blockade works. Challenge is that the more potent you make ipi by making the NF version, the more toxic it gets because it activates immune cells peripherally, more effectively as well, in part by – again, by more powerfully down regulating immunosuppressive Tregs. So if you look at the AACR poster, what it shows – it’s actually really beautiful work. It shows that the underlying – the potency of the underlying antibodies for each – for ipi and for the NF is maintained with the Probody despite the mask. So that’s consistent with unmasking in the tumor. From a toxicity standpoint, they demonstrated that the HNSTD, the highest nonseverely toxic dose for ipi and for the NF Probody were five and threefold higher based on the masking that we achieved with the Probody. And in the case of the nonfucosylated, you can see from the data how much nontoxic the NF Probody – the antibody is and how the Probody protects. So the basic idea is with the NF Probody is we’ve got a more – we’ve got a more active antibody, but it’s more toxic, if we can improve the therapeutic window of NF, we can further improve on the BMS-986249 ipi Probody. So it’s kind of a next-generation ipi Probody, if you like. I hope that makes sense.

No, this is very helpful. And if I ask one more, it seems like your R&D expense quarter-over-quarter has declined significantly. So maybe a question for you, Carlos. I mean, how should we think about the expense, especially in R&D going forward, especially when you are starting some more trials and probably the enrollment will speed up now.

Yes. That makes sense. You noticed that we had a significant number of expenses that happened in Q1 that are onetime, particularly around licensing fees that were associated with the milestones that we’ve received in Q1. So Q1 was the aberration, not Q2. And you should see it continue at a lower level than what you saw in Q1, but we haven’t really guided for the full year R&D expense line.

Our next question comes from Joe Catanzaro of Piper Sandler.

Maybe just one quick one. Just wondering if you have any thoughts or whether the recent AdCom for the BCMA ADC and the ocular tox discussion provides any insight or future plans around CX-2009 around whether it’s collecting the data or just how the FDA thinks about that toxicity in the context of an advanced cancer population?

Yes, Joe, great question. Certainly something that we’re looking at. And at the time being, we have and continue to remain confident that we can manage ocular toxicities with the regimens that have been used previously with DM4 conjugates, but we’re certainly going to learn everything we can from those discussions and make any additional modifications or improvements that we may be able to make, but work in progress.

I’m showing no questions at this time. I’d like to turn the call back over to Dr. McCarthy for any closing remarks.

Great. Thank you very much. Once again, I’d like to thank everyone for listening in today. We had another very strong quarter. And as I said, despite the many challenges presented to all of us by the COVID-19 situation, very proud of the team and proud of our progress as we move the pipeline and platform forward. So I hope everybody stays well, stay safe, and we’ll look forward to talking to you all again soon.

Thank you. Ladies and gentlemen, this does conclude today’s conference. Thank you all for participating. You may have a great day. You may all disconnect.