Good afternoon. We will begin the MacroGenics 2019 Third Quarter Corporate Progress and Financial Results Conference Call in just a moment. [Operator Instructions] At this point, I will turn the call over to Anna Krassowska, Vice President, Investor Relations and Corporate Communications of MacroGenics.

Thank you. Good afternoon and welcome to MacroGenics’ conference call to discuss our third quarter 2019 financial and operational results. For anyone who has not had a chance to review our results, we issued a press release this afternoon outlining today’s announcements, which is available under the Investors tab on our website at macrogenics.com. You may also listen to this conference call via webcast on our website where it will be archived for 30 days beginning approximately 2 hours after the call is completed. I would like to alert listeners that today’s discussion will include statements about the company’s future expectations, plans and prospects that constitute forward-looking statements for purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our annual, quarterly and current reports filed with the SEC. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so, even if our views change, except to the extent required by applicable law. And now I’d like to turn the call over to Dr. Scott Koenig, MacroGenics’ President and Chief Executive Officer.

Thank you, Anna. I would like to welcome everyone participating via conference call and webcast today. Thank you for joining us. This afternoon, I will focus my prepared remarks on our more advanced programs and the near-term milestones expected during the remainder of the year. But before I do so, let me first turn the call over to Jim Karrels, Senior Vice President and Chief Financial Officer who will review our financial results for the quarter.

Thank you, Scott. This afternoon MacroGenics reported financial results for the quarter ended September 30, 2019, which highlight our financial position as well as the progress we have made over the quarter. As described in our release, MacroGenics had research and development expenses of $44.9 million for the quarter ended September 30, 2019, compared to $46.2 million for the quarter ended September 30, 2018. This decrease was due to decreased development and manufacturing costs for MGA012 and flotetuzumab, partially offset by increased clinical trial costs related to our MGD013 study. We had general and administrative expenses of $11.8 million for the quarter ended September 30, 2019, compared to $9.6 million for the quarter ended September 30, 2018. This increase was primarily due to consulting expenses and other professional service fees. We recorded total revenue, consisting primarily of revenue from collaborative agreements, of $18.7 million for the quarter ended September 30, 2019, compared to $20.8 million for the quarter ended September 30, 2018. The decrease was primarily due to decreased revenue recognized under our collaboration and license agreement with Incyte. This decrease was partially offset by an increase in revenue recognized from the deferred upfront payments under both our collaboration and license agreements with Zai Lab and Servier as well as revenue related to manufacturing services performed under our clinical supply agreements with Zai Lab. We had a net loss of $44.6 million for the quarter ended September 30, 2019, compared to a net loss of $34 million for the quarter ended September 30, 2018. Note that for the quarter ended September 30, 2019, this net loss reflected other expenses of $6.7 million, which included $7.6 million in unrealized losses recognized on corporate equity securities held. And finally, our cash, cash equivalents and marketable securities as of September 30, 2019, were $254.4 million compared to $232.9 million as of December 31, 2018. And now I’ll turn the call back to Scott.

Thank you, Jim. Let’s begin with margetuximab, our investigational Fc optimized anti-HER2 antibody being evaluated in SOFIA, our Phase 3 trial in HER2-positive metastatic breast cancer designed to compare margetuximab plus chemotherapy against trastuzumab plus chemotherapy. We have previously reported that progression-free survival in the margetuximab arm was prolonged compared to the trastuzumab arm, meeting the study’s first sequential primary endpoint. In October, we reported data from the second prespecified interim analysis of overall survival conducted after 270 events had been reached. The data showed a trend in OS in favor of margetuximab. In the intent-to-treat population, the median OS of patients treated with margetuximab and chemotherapy was 21.6 months compared to 19.8 months for patients who received trastuzumab and chemotherapy, a prolonged median survival of 1.8 months. The hazard ratio was 0.89 and the P value was 0.33. Margetuximab’s optimized Fc region binds with increased affinity to CD16A, including the 158F low-affin V allele carried by approximately 85% of the human population. In the prespecificed exploratory analysis of this major subpopulation of genetically defined patients in SOFIA carrying the 158F allele, median OS was 23.7 months in the margetuximab arm compared to 19.4 months in the trastuzumab arm, a prolongation of 4.3 months. The haz ratio was 0.79 and the P value was 0.09. We look forward to presenting further details of the second interim analysis at the San Antonio Breast Cancer Symposium on December 11. The final OS analysis is planned after 385 events have accrued, and it is projected to be completed in 2020. We believe that patients with HER2-positive metastatic breast cancer need access to new therapies. Margetuximab, if approved by regulators, will address an important unmet need and could become a valuable treatment option for patients living with this devastating disease. Therefore, we expect to…

Thank you. [Operator Instructions] And our first question is from Jonathan Chang with SVB Leerink. Your line is open.

Hi, guys. Thanks for taking my questions. First question, any color on the business development front for margetuximab?

Jonathan thanks very much for the question. We continue our discussions with potential partners and are extending the discussions with others at this time. But at this point, I have no further updates to report.

Got it. Thanks. And how should we be thinking about the different allele populations in the SOFIA study? Is the plan still to file for approval in the overall population, or would you file for approval in just the F allele subgroup at this point?

Jonathan thanks very much for the question. As you know, we showed a statistically significant improvement in PFS in the margetuximab arm of the intent-to-treat population with a positive trend in OS in both interim analysis for margetuximab, and we think that the results are particularly profound in the CD16A 158 allele population. So as a result, given the magnitude of effect that we are seeing is primarily in that population, that will certainly be included in the filing of the BLA and we assume we will be reviewed in the context of the total package that we submit.

Got it. And just one last one for me, for flotetuzumab, how are you thinking about benchmarks for the overall study as well as just in the primary refractory population?

So as you saw from today’s abstract, we are very excited about the results, and we will be sharing, obviously, the definitive data at the upcoming ASH meeting. As you noted in the abstract, the additional patients that were included in this Phase 1 study we were seeing at the targeted dose that we are intending to move forward in the refractory population, we were seeing over 30% CR response rate, which again was consistent with the 29% response rate that we reported out at ASH last year. As also noted in the abstract, if you look at patients with refractory disease, after they have failed the first chemotherapy and then they’re treated with a subsequent chemotherapy, the literature suggests the best response in the low teens, and then subsequent salvage responses are almost close to zero. So given that we’re seeing responses, particularly in this population where the mean number of treatments were over 3 we think that we are in great shape to advancing this towards a registration study. With regard to the specifics on what the ultimate response we want to attain, obviously, greater is better. But clearly, if we are achieving responses greater than 20% or more, I think we will be in a nice range, but this is obviously a discussion that we will have with the FDA to discuss how to move forward in a registration study.

Got it. Thanks for taking my questions.

Thank you. And our next question is from David Lebowitz with Morgan Stanley. Please go ahead.

Thank you very much for taking my question. The other question on the SOFIA trial data, given that the subset was an exploratory endpoint, albeit it’s pre-specified, is it something that can actually be included in the labeling as a separate group or specifically approved for that group or is it something that would have to be studied separately with a primary endpoint for it to be included – to be labeled for that population specifically?

Thank you very much for that question. And you have pointed out quite correctly that we had predefined essentially a population which represents 85% of all patients and where we are seeing the predominant response. And as you again point out correctly, it was exploratory, which means we didn’t allot any alpha to this endpoint. We will include, obviously, the totality of data here, make a case to the FDA why such information should be evaluated, but ultimately it will come down to the FDA view on whether this is approvable. I am sure that they will seek additional guidance from outside clinicians. And it probably will be done at an ODAC if this is a point that they want to get further defined. But again, we will make a strong case. While we will be filing on an intent-to-treat population, we think that they should consider the data, given even in the recent overall survival, the interim data which is not complete, we are seeing in that population an overall survival benefit of 4.3 months in the marg versus trastuzumab population.

Thanks for taking my question.

Thank you. And our next question is from Yigal Nochomovitz with Citi. Your line is open.

Hi, this is Samantha on for Yigal. Thanks very much for taking our question. On enoblituzumab, in the Phase 2 portion of the study, I am curious that the go or no-go futility analysis, what are the thresholds that you need to meet in order to move forward for both the enoblituzumab plus MGA012 and also in the chemo combo group?

Thank you very much for that question. As you know, we are very excited about the prospects of enoblituzumab given the data that we presented at last year SITC meeting, where we were seeing in combination with an anti-PD-1 molecule, enoblituzumab response rates in the mid-30s in that population. Now as you note in this Phase 2 design, we’re comparing enoblituzumab and our anti-PD-1 MGA012 as one arm, a combination of enoblituzumab and MGA012 plus chemo as the second arm, and ultimately comparing this to the control arm, which currently the standard of front-line therapy is enoblituzumab and chemo, which as you probably know, had a response rate in the mid-30s. So without giving precision about an exact number, we would obviously like for one of those experimental arms, or both those experimental arms, to approach that range of responsiveness before we proceed to the Phase 3 head-to-head arm, where we’ll be looking at primary endpoint of OS.

Thanks for that. And if the arm that does not include chemo happens to be in that range, is there a potential for moving that forward as well for a similar accelerated approval pathway that you have for margetuximab in gastric cancer?

Well, that will be very exciting if we do achieve that range. Again, given that we did see that range of responsiveness in the later-line therapies, albeit it was small numbers of patients that clearly would give us reason to approach the FDA to discuss alternative ways of getting such a drug approved.

Thanks for that. And one more for me on flotetuzumab, is there – do you see a potential registrational path forward for also the relapsed AML? And is there any data to suggest that the combination with MGA012 could improve response rates in the relapsed population?

Terrific questions. So with regard to defining the population that we plan to move forward towards a registration study, as I stated, we will primarily look at the refractory population, given where we’ve seen the greatest response rate. However, focused on some of the biomarker data that we have shown to date and will be updated at the ASH meeting subsequently, there is a segment of relapsed patients who relapsed very quickly, even though they had an initial response to chemotherapy. And this may be a population that we will be able to evaluate as well and hope to see a salutary effect of flotetuzumab. Getting back to your second question on terms of combination of 012, our anti-PD-1 with flotetuzumab, I think again, this is purely speculative, but given a very strong preclinical signal that combining this with anti-PD-1 and flotetuzumab in various AML models and in vitro analysis leads to much more effective killing of AML targets, and actually, given some data that you may be aware of with trastuzumab studies more recently, which obviously is a completely different population combining with anti-PD-1’s, also enhancing responses in populations they’re exploring, the idea that there is up-regulation of checkpoints, both on the AML blasts as well as PD-1 on the T-cells that are being activated here, I think we’re very excited to, hopefully, see an improved responsiveness in the populations treated with AML. Now the way we are looking at this going forward is that this could be used upfront, but quite often what we have seen in our studies is that the longer the patients have been able to remain on flotetuzumab therapy, the better these patients tend to respond. And so again, if the opportunity by combining these two together leads to prolongation of flotetuzumab treatment and better outcomes, that would be obviously in the interest of the patients. So we look forward to having some data, hopefully next year as we have already begun the dosing of patients with this combination very recently.

Thanks very much for taking the question.

Thank you. And our next question is from Jonathan Miller with Evercore. Please go ahead.

Hi, guys. Thanks for taking the question. I think I heard you maybe imply that the FDA would have some more complicated things to say about that subpopulation for the margetuximab trials. Do you think there is a possibility for an ADCOM to get that on label or a potential bottleneck there? And then on the flipside, even if the IGT population is approved, what do you think the commercial bottleneck is, or the adoption in the ITT population? I know you plan on having a test available. In your conversations with docs, how much importance have they put on that subpopulation?

Okay. Thanks Jon for the questions. Let me go back over the stuff from the beginning. The FDA has not said anything to us about specifics about an ADCOM. I was speculating that given that the study was designed as an intent-to-treat population, but given that the major response appears to be in the F allele population, I was speculating that they would likely hold an ADCOM to address these questions. But at this point, it’s theirs to decide after we submit the data in the BLA and for them to review. But if I had to guess, I would assume that that would occur. With regard to the commercial size of the population, clearly we would like to have the – if approved by the FDA, the discussion of labeling to include information regarding the F allele population. If it is not there, we certainly will be publishing the data in scientifically reviewed journals and so it is obviously out there and available for physicians now but obviously the more details will be provided subsequently. With regard to the opportunity commercially, it’s just too early to assess at this point. Our commercial teams are looking at the landscape which, as you know, is continually changing. Right now we are working with two potential vendors to develop a laboratory-developed test because we think it would be important for both the oncologists and patients to have that test available if the drug is approved so that the populations that would most benefit from margetuximab could be selected and be included. So was there anything else? Did I miss anything?

No, thank you. That was perfect. Moving on from margetuximab, I had 1 or 2 about the other pipeline. It seems like the PD-1 and LAG-3 by specific timing is getting pushed out a little bit. Is there a reason for that? Do you have any color for why expect that now in 2020 as opposed to the second half of this year? And then secondly, do you have any more details on the flotetuzumab plus PD-1 combo trial, which I know it is not on Clin Trials.

I’m sorry, from the flotetuzumab and PD-1, did you say?

Yes, details on that trial, which is not on Clin Trials.

Yes, okay. So let me answer the first question, which is on PD-1 LAG-3 bispecific DART molecule. As we noted today in my earlier remarks, we are actually now up to over 150 patients being treated with the PD-1 LAG-3 DART molecule in over 9 tumor types. And what – we made a decision because a significant proportion of those patients had not either been received their first scan, or had only received 1 scan. We didn’t think the data was mature enough to give a fair evaluation of the results. What I have said previously, we are very excited about the prospects of this molecule given that we’re seeing responses across multiple different tumor types. But we felt it would be valuable to have a few more months of maturation of the data to be able to provide this in a very balanced manner. So as was noted, we expect to submit to one of the major scientific conferences in the first half of the year for presentation. With regard to the flotetuzumab and PD-1, the reason why you don’t see it on clintrials.gov, we’ve started the study, but the study is being conducted outside the U.S. currently in, I believe, 3 countries at this point.

Alright, thanks very much. I think we are all very excited to see that PD-1 LAG-3 data.

Great, terrific. Thanks, Jon.

Thank you. And our next question is from Debjit Chattopadhyay with H.C. Wainwright. Please go ahead.

Hey good afternoon guys. First, a clarification, in terms of the activity you’re seeing primarily in the refractory patients, how does this – or why is this different from, say, some of the other CD123 ADCs, for example?

Great question, Debjit and it really gets to the core observations we have recently made with regard to a biomarker. And again, that will be updated in an oral presentation at ASH. As was pointed out at the last ASH meeting, it seems to be a segregation of patients that respond to chemotherapies and patients that respond to immune-based therapies, based on immune-based markers. So clearly for the population that are responding to flotetuzumab, we’re seeing a very significant gamma-interferon associated signature with other immune parameters. It turns out that patients who respond to chemotherapy fall in the other group, which are essentially immune depleted. And so while it’s not 100%, there is a clear segmentation of the responsiveness in this population. And so given that current drugs, which include, as you described, ADCs, are essentially directed chemotherapy therapeutics, they fall in the other group that do not have likely to have the immune signature. And therefore, quite distinctly, I think flotetuzumab provides a mechanism of action that other therapies that are being explored right now cannot address.

Got it. Thank you. And then moving on to more of a 40,000-foot question here, given where the stock is and the Street’s reaction to the SOFIA data, how do you prioritize the prospects of potentially running 3 or 4 registration directed studies over the next year and your balance sheet constraints?

Obviously, the company is spending considerable amounts of time currently both to prioritize the programs that we think will have the greatest chance of success and continue to have a prolonged runway with the current cash position. So with regard to the prioritization, what I can first state is that given the signal that we’ve seen, obviously, with margetuximab, not only in breast cancer patients but in the gastric cancer patients, we believe that advancing the front-line study in metastatic gastric cancer should be a priority. And given, particularly as we’ve described this trial as a 2-module study, we’re going to put a strong emphasis to get objective data next year on the subpopulation of the PD-L1 positive IHC3-plus positive population so that we can make a decision whether the signal is strong enough to proceed forward for expansion, given that the opportunity that is afforded us for that study is a potential accelerated approval if we meet the results, both from an efficacy and safety perspective. So that will be given, certainly, a priority. As you’ve heard today, we’re very excited about flotetuzumab, and we’ll have more to speak early next year on how do we move forward towards registration studies there. And again, given that we can hone in on a specific population, we think that that could be executed in a very cost-effective and a, I would say, fairly rapid manner, relatively speaking, compared to some of the more, other larger potential trials. Again, we still have further conversations with the FDA to get an understanding of how the best way to move forward on flotetuzumab. With respect to the other programs, obviously, we are about to initiate a study in the head and neck population with enoblituzumab. And here again, we have partnerships with that molecule…

Great. And just one last follow-up, so independent of what happens on the regulatory front for SOFIA, if you were to have another do-over with margetuximab in breast cancer, would you consider doing a combination with an estrogen receptor inhibition plus a CDK4/6 inhibition?

So that’s a nice speculation. I haven’t thought about specifically on the hormone receptors or CD4K combinations. Clearly, the opportunity, given the signal of margetuximab, irrespective of how the regulators opine on approval, we think this drug is quite effective. And given the enhanced signal we’ve seen in gastric cancer with anti-PD-1’s and the design, as you know, with the anti-PD-1 and anti-PD-1 LAG-3, we think the opportunity is quite ripe to look at combinations of margetuximab with these checkpoints in breast cancer, particularly late-line and potentially early-line as well. And so irrespective of how the outcome comes out on the regulatory front, we think that there is certainly merit to proceed forward in that manner. And certainly, given the recent successes reported on TKIs, particularly to [Technical difficulty] study that was reported out and will be updated at San Antonio in late-line patients, again, we think mechanistically these work orthogonally and could enhance the responsiveness of patients, both in late and early-line treatments, but I think your points are well taken. This could be a broader discussion to include families of estrogen blockade as well as on the CDK4/6 molecules.

Thank you.

Thank you. Our next question is from Stephen Willey with Stifel. Your line is open.

Yes, good afternoon and thanks for taking the questions. I guess just a couple on margetuximab first. So with respect to the upcoming San Antonio presentation, just curious if we are going to see either, a), the impact, if any of post study therapy and then also whether or not you’re going to be breaking out overall survival as a function of allele status, specifically in those patients that are homozygous for the V allele?

Steve thanks very much for the question. I have not seen a final package of slides. I know obviously we have a very large dataset that we would like to present there by the investigators, so I can’t comment what ultimately will get in front of the presentations. But there is a clear interest in giving an in-depth analysis of the various subpopulations that, although exploratory, can potentially benefit by this treatment and looking at differences among those populations for some insight here. So we’re very happy to share that with you, but I can’t give you the specifics on what’s going to be included in the final presentation at this point.

Alright, that’s fair. And you’re planning on filing here before the end of the year. Is there a scenario by which you guys supplement the BLA filing with final OS data if that final event is triggered before some kind of regulatory decision is reached, if the hazard ratios continue to trend in the right direction here, and is it your expectation that that would potentially constitute a major amendment that could delay a regulatory decision?

That’s an excellent question Steve. Given where we see the rate of OS accumulation to get to the 385 events, and knowing what the timing will be for, and yet until we – for regulatory review, whether there will be an ODAC meeting and the timing, I certainly put it on the table that if there is results for a final OS, which obviously continues to not only trend favorably, but particularly, if you look at the P values and the hazard ratios for the F allele population, although it would be an anomalous statistic if that obviously crosses over into significance there, it would be, obviously, important to share that information. So ultimately, I can’t – I don’t have the vision right now to know exactly when all those events will occur, but that certainly is something for us to consider.

Okay. And then maybe just a clarification question on flotetuzumab, so it sounds like you’re still enrolling primary refractory patients. Are you using biomarker selection criteria to enrich the patient population from here on forward? And what are the logistics of trying to secure biomarker data in this patient population, specifically just given that a lot of these primary refractory patients are in the midst of an acute medical emergency?

Yes now that’s a great question. So let me be quite clear on this, which is yes, we are continuing to enroll patients mostly for refractory patients but are also treating some relapsed patients as well. As we pointed out before, not only treating as monotherapy, but we also obviously just started the combination study with the anti-PD-1. However, it is not our intent to specifically use a biomarker to select these patients. We are pursuing the data. It’s better to find populations that may mechanistically respond, but in the current plans for design of future studies, it will be based on clinical criteria, specifically on failures of previous treatments or lack of responsiveness to treatments. But again, as I pointed out earlier, we will have some follow-up discussions with the FDA shortly to get a little more – to get clear definition on how to move forward.

And I think you may have mentioned in your prepared comments as to when you may be in a position to communicate that to investors, but could you just repeat that, if you don’t mind?

Yes, it will be in the first part of next year. We’re in a very good position to be able to do that.

Okay thanks for taking my questions.

Thank you. Our next question is from Michael Schmidt with Guggenheim Securities.

Hey, guys. This is Charles Zhu on for Michael Schmidt. Thanks for taking the questions. The first one is a bit of a follow-up from previous ones on flotetuzumab. But could you provide any color around why it, for whatever reason, seems to work better in primary refractory or early-relapsed as opposed to late-relapsed patients and whether or not the ASH presentations will provide any insight on this front?

Charles, you might have missed it. One of the responses to one of the questions earlier is that in a very thorough analysis that was presented initially last year and which will be updated in an oral presentation this year, there’s been evaluation of looking at patients who respond to chemotherapy based on a NanoString 770 marker profile, which is focused primarily on immune responsiveness. And it tends – it seems to be a segregation that in what are so-called immune-depleted signatures, the patients who will respond to chemotherapy tend to fall in that bucket, whereas those, in theory, who will respond to immune-based therapies fall in sort of the immune-enriched population markers, which particularly include up-regulation of gamma-interferon associated genes. We then did an analysis of the patients with refractory disease and who were treated with flotetuzumab. And in fact, the majority of those patients fell in that immune-enriched gamma-interferon signature bucket. And so clearly mechanistically, there is some reason that in an environment that has a lot of inflammation, for some reason chemotherapy isn’t working very well. And I can’t give you the specifics why, but that’s certainly an avenue of further exploration.

Got it. Okay, thanks. And could you also just remind me again, given the mechanism of action of the PD-1 LAG-3 bispecific, would you expect activity in the post-PD-1 setting for those 150 patients, and how do you evaluate the PD-1 pretreated versus naive patients for this particular agent? Thank you.

Thanks for that question and as you might recall, Charles, what we have observed in our preclinical studies when we assessed separate in vitro analysis of T-cell activity restoration, in a bispecific dog molecule configuration, that configuration was much more effective in activating T-cells as compared to anti-PD-1 or anti-LAG-3 antibodies alone. To assess your question clinically, we are including patients that are both PD-1 experienced and that have progressed on therapy. And I should note that for one example, for instance, when we spoke at the time of ASCO with regard to the design of our MAHOGANY study, we presented a patient with gastric cancer who had been on multiple lines of therapy, which included a refractoriness to nivolumab. And yet this patient was able to respond with complete resolution of his target lesions for, I think, over a year. And what we believe, and based on very strong data that has come preclinically, combinations of PD-1 and LAG-3 blockade seem to induce an immune response that is superior to individual treatment alone, and there is synergy there in terms of either expanding populations that are in the activation phase or restoring cells that have an exhaustion profile. So again, we will be examining the populations of patients that are both anti-PD-1 naive, looking at historical responsiveness to those patients with those particular tumors to PD-1 therapies, and obviously, looking for improved responses in the anti-PD-1 naive as well as looking to the PD-1 experienced patients to look for responsiveness.

Understood. Okay, last question from me, and I don’t know if you kept up with this one. But there was something that happened a couple of days ago. There was another company had a Phase 3 trial, hit PFS, had OS as the secondary endpoint yet, and they ended up pushing out an NDA or a BLA. And has this event changed your view on the FDA’s level or willingness these days to accept a BLA or NDA filing based only on a PFS endpoint with OS pending? Yes, that is the question.

So I’m not aware of the specific case you’re citing, but as you probably are quite well aware, there are a very large list of oncology drugs that have been approved based on PFS data that ultimately do not meet OS criteria and OS data statistically as long as there are trends in terms of favorable responses for the experimental drug. Given the magnitude of effect we are seeing here, particularly in this F allele population, we think that it is prudent to file the BLA at this point. Ultimately it will be the decision by the FDA whether to accept the filing and review it, but we are optimistic that they will accept it and review it, and we’ll see very shortly.

Got it. Thanks for taking the questions.

Thank you. And we have a question from the line of Boris Peaker with Cowen. Your line is open. Boris, your line is open. Mr. Peaker, please check your mute button. Okay, Doctor, can I move to the next question?

Yes.

Okay. And we have a question from Christopher Marai with Nomura Instinet. Please go ahead.

This is Jackson Harvey on for Christopher. Thanks for taking the questions. I was just curious if you could provide some more color around the durability of response that you’ve seen with the flotetuzumab in the monotherapy trial. And with regards to the PD-1 combo study with flotetuzumab, what do you think, based on the preclinical data, should be the primary expectation for enhancement? Do you think we should be looking for longer duration of response, higher overall response rates or maybe an expansion of the AML populations that respond thank you.

Thank you very much for the question Jackson. With regard to the durability of response, I’m going to leave that to our ASH presentation that’s coming up in a few weeks. What we had noted before, as I recall from last year’s presentation, the responding population was a little over 3 months. My expectation is that it is now longer in the responsive population, but I’ll let the data speak for itself when it comes out in a few weeks. With regard to the combination with anti-PD-1, I think you’ve hit all the high points. I think we have the opportunity here for greater duration of response, increased responsiveness, and expansion of the population. In one way, what I’m hoping is that this, and as we study this, is that particularly in the subsequent cycles of therapy or during periods of consolidation, that we will be able to dramatically improve the length in which these patients respond. But obviously, we’ll have to wait for the data.

Great, thank you so much.

And this concludes the question-and-answer session. I would like to turn the call back to Dr. Koenig for his closing remarks.

Thank you, operator. I’d just like to thank everyone again for joining us this afternoon and to let you all know that we look forward to continuing to advance our programs in the coming months and providing updates on our progress. Have a good day.

And thank you, ladies and gentlemen. This concludes today’s conference call. Thank you for participating. You may now disconnect.