MacroGenics Inc (MGNX) 2018 Q2 法說會逐字稿

Good afternoon.

We will begin the MacroGenics 2018 Second Quarter Corporate Progress and Financial Results Conference Call in just a moment.

(Operator Instructions)

At this point, I will turn the call over to Jim Karrels, Senior Vice President and Chief Financial Officer of MacroGenics.

Thank you, operator.

Good afternoon, and welcome to MacroGenics' conference call to discuss our second quarter 2018 financial operational results.

For anyone who has not had the 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 www.macrogenics.com.

You can 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 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 Operating Officer.

Thank you, Jim.

I'd like to welcome everyone participating via conference call or webcast today.

Thank you for joining us.

During the second quarter of 2018, we made significant progress on several fronts, and I'm happy to provide an update that is focused on our most advanced product candidates and our financial position.

But before I do so, let me first turn the call back to Jim, who will review our financial results for the quarter and year.

Thank you, Scott.

This afternoon, we reported results for the second quarter, which highlight our strong financial position.

As described in our release, MacroGenics had research and development expense of $52 million for the quarter ended June 30, 2018 compared to $34.5 million for the quarter ended June 30, 2017.

This increase was primarily due to the continuous enrollment in our 2 margetuximab clinical studies, namely, the SOPHIA Phase III trial for metastatic breast cancer and a combination study with an anti-PD-1 in gastric cancer as well as the flotetuzumab monotherapy clinical trial in AML.

We also increased headcount to support our expanded manufacturing and development activities.

We had general and administrative expenses of $11.1 million for the quarter ended June 30, 2018 compared to $8.4 million for the quarter ended June 30, 2017.

This increase was primarily due to costs incurred related to the implementation of our new enterprise resource planning, or ERP, system as well as increased patent expenses.

We recorded total revenue consisting primarily of revenue from collaborative agreements of $18.8 million for the 3 months ended June 30, 2018.

This included $9.9 million related to the manufacturing services and clinical supply of MGA012, also known as INCMGA0012, to Incyte Corporation as well as $6.1 million related to 2 transactions entered into with Provention Bio, in which we received warrants to purchase a total of 2.4 million shares of their common stock.

Revenue of $18.8 million for the 3 months ended June 30, 2018 compared to $1.7 million for the 3 months ended June 30, 2017.

Revenue from collaborative agreements include the recognition of deferred revenue from payments received in previous periods as well as payments received during the year.

For the quarter ended June 30, 2018, we had a net loss of $43.2 million compared to a net loss of $40.7 million for the 3 months ended June 30, 2017.

Our cash, cash equivalents and marketable securities balance as of June 30, 2018 was $300.9 million, which compared to $305.1 million as of December 31, 2017.

And I'll point out that a significant portion of our accounts receivable balance of $17.8 million at June 30, 2018 relates to an amount owed to us from Incyte for the previously mentioned MGA012 activities.

Based on our current operating plan, we believe our cash, cash equivalents and marketable securities combined with collaboration payments we anticipate receiving should enable us to fund our operations into mid-2020, assuming our programs and collaborations advance as currently contemplated.

And now I'll turn the call back to Scott.

Thank you, Jim.

As I mentioned in the opening, MacroGenics continued to make progress across multiple fronts.

I will focus my comments this afternoon on our leading programs, which represent the most significant near-term value creation opportunity.

Let me begin with margetuximab, our novel immune-optimizing anti-HER2 antibody, which has an Fc domain engineered to enhance engagement and activation of the innate immune system.

Our pivotal SOPHIA study is evaluating the efficacy of margetuximab plus chemotherapy compared to trastuzumab plus chemotherapy in approximately 530 relapsed/refractory HER-2-positive metastatic breast cancer patients.

We expect to complete enrollment of the Phase III trial in the next few months, and based on the rate of PFS events which have accrued to date for the study, we expect to be in a position to announce top line results in the first quarter of 2019.

In June, at the ASCO Annual Meeting, we presented interim clinical data from our ongoing Phase II study of margetuximab plus the anti-PD-1 agent, pembrolizumab, in patients with gastric and gastroesophageal junction cancer.

The data we presented demonstrated that this chemotherapy-free combination may enhance anti-tumor activity in patients with advanced gastric cancer.

You may recall that earlier this year, we announced the expansion of the margetuximab gastric study by enrolling 25 additional gastric cancer patients.

We expect to complete enrollment in the next few months and we anticipate presenting results from the trial in the first quarter of 2019.

In summary, we are encouraged by our progress with margetuximab and we look forward to announcing additional results in the first quarter of 2019.

Our next program is flotetuzumab, our DART molecule that recognizes both CD123 and CD3, which is being developed as monotherapy for the treatment of acute myeloid leukemia, or AML.

We have completed enrollment in the dose expansion cohort, and we plan to present updated clinical data and announce next steps in the development of flotetuzumab later this year.

Our partner, Servier, has development and commercialization rights for flotetuzumab outside of North America, Japan, Korea and India.

You'll recall that MGA012 is a PD-1-directed immuno-oncology molecule that we licensed at Incyte in late 2017.

Under the terms of our agreement, Incyte has exclusive worldwide rights for the development and commercialization of MGA012, while MacroGenics retains the right to develop our pipeline assets in combination with this anti-PD-1 antibody.

In June, Incyte announced their intention to pursue monotherapy development of MGA012 in 3 indications.

The cohort of patients with microsatellite instability-high endometrial cancer will be further expanded.

And in addition, they are planning to open Phase II studies in Merkel cell carcinoma and anal cancer later this year.

Data from these studies is anticipated in the 2020, 2021 timeframe according to their disclosures.

In addition, Incyte will likely provide an update on the ongoing monotherapy MGA012 study that MacroGenics had initiated at a scientific meeting later this year.

We have additional DART programs in development and I will provide brief updates on them.

MGD013 is a first-in-class DART molecule that provides co-blockade of 2 immune checkpoint molecules expressed on T cells, PD-1 and LAG-3, for the potential treatment of a range of solid tumors and hematological malignancies.

MGD013 is currently being evaluated in a Phase I study, and we expect to establish the dose and schedule for MGD013 administration as well as initiate dose expansion cohorts by the end of the year.

Another DART molecule focused on co-blockade of 2 immune checkpoint molecules is MGD019, which is designed to target both PD-1 and CTLA-4 in T cells.

We anticipate submitting the IND application for MGD019 also by year-end 2018.

Let me shift to our B7-H3 franchise, another opportunity for value creation in 2018 and beyond.

Our most advanced candidate, enoblituzumab, is an Fc-optimized monoclonal antibody that targets B7-H3.

We have completed enrollment in our ongoing study of enoblituzumab in combination with an anti-PD-1 mAb and expect to present clinical data and provide guidance on future developments of enoblituzumab in the fourth quarter of 2018.

The second clinical candidate in our B7-H3 franchise is orlotamab, previously known as MGD009, a DART molecule targeting B7-H3 and CD3.

Orlotamab is being evaluated in a Phase I study across multiple solid tumor types.

We recently established the dosing schedule for orlotamab administration and initiated monotherapy dose expansion cohorts in 6 different tumor types.

In addition, we started a combination study of MGA012 in the first quarter that is currently accruing patients.

The third candidate in our B7-H3 franchise is MGC018, an anti-B7-H3 antibody drug conjugate that has shown potent anti-tumor activity in preclinical models.

We have submitted an IND for MGC018 and, in the coming months, anticipating initiating a Phase I study both as monotherapy and in combination with MGA012 in patients with solid tumors.

I'll quickly mention that we continue to progress 2 additional DART molecules in Phase I clinical development.

The first, MGD007, is a DART molecule that recognizes gpA33 and CD3.

We recently commenced a combination study of MGD007 with MGA012 in patients with colorectal cancer.

In addition, we expect to commence the Phase I study of MGD014, a DART molecule being developed to kill HIV-infected cells, during the third quarter of 2018 under a contract with NIAID at the NIH.

Finally, I'll provide a brief corporate update.

MacroGenics has completed the build-out of a GMP suite in our headquarters building in Rockville, Maryland to support larger-scale clinical and commercial manufacturing, and we recently completed a successful engineering run.

We have initiated GMP production runs in this facility in the third quarter of 2018.

This is a major milestone in our development and supports our goal of becoming a fully integrated biopharma company.

So as you can see, this has been another busy and productive quarter for MacroGenics.

We continue to be excited by the progress we have made and look forward to continuing our efforts to advance our programs and to develop innovative new therapies for the treatment of cancer.

And now I would be glad to address any questions that callers may have.

Operator?

(Operator Instructions) The first question comes from Peter Lawson with SunTrust Robinson Humphrey.

On the margetuximab in breast cancer, what would you view as success in that 1Q '19 top line data?

Thank you very much, Peter.

Obviously, as you recall, the readout for the study is the sequential primary endpoints of PFS and OS.

The study was designed based on historical controls for testing in a population of HER2-experienced individuals.

And the expectation on baseline, we used was the [trastuzumab] control arm for which [Ketsala] was approved.

These patients had a PFS of approximately 3.3 months, while we have set as our base is approximately 4 months on the controls for PFS.

And we're looking at, optimistically, as much as 2 or more months of improvements on the experimental arm.

As you know, we've set out the PFS with a hazard ratio of 0.67, and this is powered to 90%.

If successful, we would then go on follow the patients for the overall survival and the overall survival was powered at 80%.

And then just on the H7 -- sorry, the B7-H3 franchise.

What's the strategy there?

How do you think that sort of differentiates and plays out the 3 different approaches you have?

Do you think you'll get to the position where you just move one forwards, or do you think there's enough differentiation there?

And at what point do you think you have a single molecule to move forwards?

Thanks for that question.

As you know, we've put a lot of effort into exploring the B7-H3 target, given that this target is highly overexpressed on most solid tumors with very low expression on normal tissues.

Preclinical studies have shown that, mechanistically, we could exploit an Fc-enhanced antibody, a biospecific which engages the CD3 on T cells to recruit T cells to kill tumor targets as well as an antibody conjugated with an ADC.

As you also know, the preclinical models don't necessarily predict the efficacy and -- oh, as well as safety in human studies.

We've had a very long experience now with enoblituzumab as we pointed on the call earlier.

We'll be updating our results on enoblituzumab in combination and the pembrolizumab, the anti-PD-1, later this year, where we look at 4 different tumor types.

And we plan at that time to also give you revised guidance in terms of next step for further clinical development of that molecule.

Second is, as you heard today, we have selected a dose for MGD009, or orlotamab, as monotherapy and we've just begun to expand into 6 different tumor types.

We expect by next year to have approximately 100 patients dosed with orlotamab as monotherapy.

And early this year, we began the combination study with our own MGA012 anti-PD-1.

Again, mechanistically, this makes a lot of sense and support -- it's supported by preclinical data that, combined with an anti-PD-1, will enhance the effect of the monotherapy effects of MGD009.

Today, as you heard, we announced the filing of the IND for MGC018 and we found that this molecule was extremely potent at eliminating tumors in preclinical model systems even with single dosing.

And so we think that there is an opportunity for all 3 molecules to succeed, potentially, either alone or in combination with checkpoint inhibitors.

But we will have more data by next year to be able to give better guidance on which of these molecules we will advance further to registration studies.

The next question comes from Umer Raffat with Evercore.

[Mike], I wanted to focus on the CD123 for a minute, if I may.

And I guess our question was really aimed at understanding the efficacy data we've seen as it relates to CR rates, and specifically, should we or should we not be including CRis when we think about the overall efficacy profile of this CD123?

And I ask because we've read varying takes from FDA on whether or not CRis should be included or not and that was partially dependent on whether the durability response is different between CRs and CRis.

So just looking to get your sort of color on that broader question on how we should think about this drug, is a 20% CR rate, CR/CRi, or is it closer to low teens?

And then, I had a follow-up.

So thank you very much for that question.

As you know, we presented our initial data on the first 14 patients at ESMO last year and follow-up data on another 8 patients at ASH last year.

As I announced on the call, we completed enrollment of the remaining patients in the 25 expansion cohort, the relapsed/refractory patients, and continue to follow those patients and we'll update this at a scientific meeting later this year.

With regard to your specific question with -- regarding the importance of CRi, as you know, these relapsed/refractory patients, many of these patients have undergone very extensive chemotherapy treatments that in large part reduce the bone marrow reserves of stem cells.

And so even under the best circumstances, if the blast cells and the leukemic stem cells can be controlled, there may be insufficient precursor stem cells of the normal variety to explain -- to expand to completely reach normal levels.

So in patients, for instance, for example, with a CRi that achieved 50,000 platelet recovery, which is not a normal value but will reduce the opportunity for bleed would be considered a success here.

With regards to how the FDA looks at this, obviously, we cannot predict that on a case-by-case basis.

But as you know, some products have been approved based on CRhs as well as [full state] CR.

And of course, durability will enter into this.

So again, we will be looking at these parameters as we go forward.

And as we hope to update you, we will not only discuss the opportunity for flotetuzumab as monotherapy later this year with updated data but also give some guidance on how we move to the next step both as monotherapy and, as we have noticed previously, we expect to initiate very soon a combination study of flotetuzumab with MGA012, our anti-PD-1 molecule, based on a very compelling data that we showed last year at ASH, where we showed that after single course of -- single cycle of flotetuzumab, we see an upregulation of PD-L1 on AML blebs, which gives a lot of rationale where a combination of the 2 molecules may result in a better outcome.

So this is how we kind of view the scene at this point.

All right.

That's really helpful, Scott.

And perhaps can you give us some color on what type of durability of responses are you seeing overall and how that differentiates between our CR patient -- a true CR patient versus a CRi patient?

So as we pointed at the ASH last year, we were seeing responses that were durable as long as 6 months, and some of these patients continued further in their durability to their initial response.

A lot of this is also dictated by how long the patient maintained the drug as maintenance therapy, and that can also dictate how long the durability will be sustained.

But we will update with this kind of data at the scientific meeting later this year.

The next question comes from Christopher Marai with Nomura Instinet.

This is Jackson Harvey on for Christopher Marai.

I have another question on flotetuzumab.

I'm just curious if you're still doing the continuous infusion or if you're working on a next-gen technology.

And if you could elaborate a little bit on your registrational path if you believe it will be for the continuous infusion.

Thank you very much, Jackson, for your question.

With regard to flotetuzumab, as you'll recall, we had worked on identifying a dosing regimen that would maximize the therapeutic benefit and minimize the side effect profile.

And we arrived at a dosing strategy where we start with a leading dose of 30 nanograms per kg.

We increase it up to 100 nanograms per kg and then ends up at 500 nanograms per kg for the remaining 3 weeks of infusion.

At that point after 4 weeks, the patients are evaluated and then if they continue on additional dosing as a result of favorable laboratory evaluation, they will then be put on a dosing regimen of 4 days on, 3 days off and maintain that schedule for 1 or 2 or as much as 3 additional cycles depending on the patient.

That is the strategy we are anticipating moving forward with monotherapy.

We are exploring other dosing regimens in combination with MGA012 as we described, and we'll be updating that dosing regimen later this year.

With regard to a next-generation molecule, as we pointed out, we have had great success at creating long-acting Fc-bearing DART molecules, and a CD123 with an Fc domain that enhances the half-life of this molecule is no different here.

We have chosen based on the CD123 expression pattern on both blast cells as well as normal tissue to be cautious and start with a short-acting molecule.

But we do have a long-acting molecule in the wings.

We're continuing the preclinical development of that molecule.

I should note on that we had, earlier this year, presented some data with some alternative CD3 molecules that may be incorporated with such a long-acting CD123 molecule.

The advantage of such a molecule is that we've observed in both small and large animal studies a dramatic reduction in cytokines without any effect on the reduction of or the elimination of CD123 cells.

So we're very encouraged that our next-generation molecule may be able to be used, for example, in a maintenance-type therapy along with MGD006 or for other indication where patients may be getting drugged for longer periods of time.

The next question comes from Yigal Nochomovitz with Citigroup.

Maybe I missed this but I didn't hear any updates on the enoblituzumab neoadjuvant prostate cancer study.

Is that still underway?

Is there a comment there?

And then I thought there was also a combo study with ipilimumab?

So with regard to the prostate study, this, we didn't have -- bring -- have an update today about that.

This is an IST study that is being conducted at Johns Hopkins.

As you recall, earlier in the year, the study was expanded from the initial 8 patients to enroll another 8 patients.

As I understand it, they are getting close to completing enrollment of that study but have not finished it out.

And my expectation is that sometime within the next 6 months to 1 year, they should be providing an update at a scientific meeting with regards to those results.

With regard to the enoblituzumab and ipilimumab, if you recall on an earlier earnings call, we had noted that we had stopped enrollments very early in that combination study.

Not so much for issues about effects of enoblituzumab and ipilimumab, but we thought from competitive standpoint, given that we did not have a CTLA-4 molecule that we were developing ourselves, that from a commercial standpoint, this was not right best for the company at this time.

So we had -- that study that we enrolled a small number of patients continued as closed for additional enrollment.

But I do believe there is at least 1 patient on that continues to get the drug in combination.

Just a quick correction -- just a quick clarification on the neoadjuvant prostate study, that's actually expanded from 16 patients to 32.

Oh, I'm sorry.

Okay.

And then regarding the ADC molecule, MGC018, I just wanted to get a sense as to the level of understanding you have of the -- at least preclinically, obviously, the safety of the linker and the warhead.

As you know, there have been some reports of unfortunate patient deaths with the Daiichi ADC as well as the Mersana ADC.

I know those were HER2-directed ADCs, but nonetheless, I'd just like to understand the work you've done to be comfortable with the safety of that molecule in, I assume, maybe nonhuman primates heading into the human studies.

Yes, thank you for much, Yigal, for that question.

We're very excited about the prospects of MGC018.

As you know, the linker-toxin technology, we in-licensed from Synthon with their linker/payload.

As you recall, or may recall, Synthon has actually started a Phase III study with the exact same linker-toxin technology for a HER2-directed molecule.

They had an update at the June meeting at ASCO.

From my understanding, from the data they have presented publicly or from what we know, there's no toxicity with regards to Grade 5 or deaths, as seen with some of the other molecules that you've reported.

There obviously was some toxicities associated with the drug which is specific but managed quite nicely.

Our preclinical studies were conducted both in mice and in primates, in cynomolgus monkeys.

We are -- I believe we have a very good dose and did not have -- achieve the dopamine toxicity in the ranges that we intend to introduce for human studies.

So we'll obviously have to see as we start the study if the primate studies and the mouse studies are predictive of what is seen in humans.

Okay.

And then just on 009, are you providing any more details on the dosing schedule at this point that you've established, or is that...

I'm actually happy to do that.

I wasn't limiting that.

We are on [our Q2] weekly dosing regimen right now.

There is a [lead-in] dose as we have done for other drugs where we start with a low dose and then move them to a higher dose, and that's being conducted right now, so.

The next question comes from Boris Peaker with Cowen.

So my first question is in the SOPHIA trial.

Since you have a sequential analysis of PFS and OS, I'm just curious what happens if one endpoint hits statistical significance and the other one does not.

How does that work out?

Well, technically, we need to pass PFS, have a statistically significant difference for us to proceed for an OS readout.

Clearly, if we don't hit PFS, we will still follow up patients for OS.

And if the OS is quite remarkable in terms of its status of the patient, it still provides opportunities to present that data to the FDA.

But we'll have to see what data readout looks like.

Got you.

And I'm just curious, for flotetuzumab, how many patients of data will we get at -- I'm assuming this is going to be ASH at the end of the year.

And what you consider to be good data?

So I'll let you make the decision on what's good data.

When my -- our plan was to present the full dataset that we conducted at the targeted dose, which was at least 25 or more patients.

The next question comes from Debjit Chattopadhyay with H.C. Wainwright.

So enoblituzumab, it has been in development for a long time, and obviously, the checkpoint inhibition landscape has evolved considerably over that the same period.

So given that we get some data from you guys over the next few months, how should we interpret that data given the evolution in front-line and even second-line treatment, and what do you plan to take forward?

And then just a follow-up.

With MGD009, you're starting that program up.

Is that a read into something in the combo study with enoblituzumab plus KEYTRUDA?

So the answer to the second is quick.

As I pointed out earlier, they would be totally independent programs and one doesn't rely on the other.

We're looking to develop these independently as molecules and looking at the opportunity of combining these with different molecules.

That could be including other molecules targeting B7-H3.

So that's the answer with regards to 009.

With regards to the enoblituzumab and the combination with anti-PD-1, as you recall, we are looking in combination with enoblituzumab because, at that time, we didn't have MGA012 ready to go into the clinic in combination.

And so we wanted to get a dataset in 4 different tumor types, which include head and neck, lung, bladder and melanoma.

Within the both the head and neck and one cohort, we're looking at both PD-1 -- PD-L1 experience as well as unexperienced individuals.

So as you hear, we have a fairly large dataset with regard to different populations.

And what we plan to, obviously, present are the data that we think that potentially could have the best therapeutic benefit going forward.

Clearly, we will also outline the next steps in the development of this molecule for a particular indication based on internal set response rate, and this has been garnered both from our own experience with enoblituzumab as monotherapy and then, of course, what the experience has been with other checkpoint molecules and other current therapies for each one of these indications, both our frontline as well as late-line therapy.

So stay tuned.

We'll be able to provide an update later this year on that.

And just a follow-up on MGD01 -- the anti-body drug conjugate at enoblituzumab.

Could you remind us what the drug-to-antibody ratio is for that, for the construct?

It's 2.7 toxins -- the toxins on each antibody molecule.

(Operator Instructions) The next question comes from Jonathan Chang with Leerink Partners.

This is [David Roush] dialing in for Jonathan.

I know we've touched on MGD009 a bit on this discussion, but I was wondering if you can provide any context on which indications do you plan on exploring and what you might be looking at for benchmarks there.

Thanks very much, [David].

We've actually outlined that.

So with regard to the monotherapy studies, we're looking at testing this in much more for lung cancer, bladder cancer, head and neck, mesothelioma, melanoma and prostate, approximately 16 patients each for the monotherapy cohort.

For the combination study with our anti-PD-1 MGA012, we're looking at approximately 20 patients when we get to the expansion.

We're still in dose escalation right now for essentially an all-comers study.

But once we get to expansion, we're looking there at other small cell lung, renal cell cancers, sarcoma, mesothelioma, prostate and MSI-High tumors.

Obviously, we have the opportunity to change that as we get closer, depending on what we see in the earlier part of the study.

Great.

Just a quick one more question.

With Incyte presenting the monotherapy data on MGA012 later this year, do you have any insight on which indications they present -- they plan to present in?

And have they given you any insight on what to expect regarding endpoints and data?

So as you know we had initiated expansion studies of over 100 patients before we transferred the molecule -- the IND over to Incyte.

And we have -- we know the data as of now, but we're not at liberty to describe the data.

But stay tuned.

I can say that given that we are expanding our effort in combination, they are expanding their efforts both as monotherapy in the 3 -- 2 additional new indications [they will] describe.

As I pointed out earlier, the MSI and endometrial patients were a part of the original expansion cohort.

And they intend to look for a registration pathway for that indication as well.

So -- and they are intending to expand into combination studies going forward in for many of their molecules.

So I would say stay tuned for results.

And the next question comes from Stephen Willey with Stifel.

I joined a little bit late, so my apologies if this has been asked.

But just kind of curious with respect to the gastric cancer study, the Phase II data that we're going to be getting at ASCO GI, presumably, in the first quarter of next year.

Should we assume that if that data continues to look consistent with the response and the progression that we've to date that, that is essentially the trigger for a go-forward decision?

And then, I guess, maybe just along the same lines, if you can talk a little bit about where you are in terms of the decision of perhaps swapping out what has been a pembro arm with MGA012 and perhaps what that timing consequences of that might be in terms of just a program reset?

Very good question, Steve.

Thanks very much.

As you know, the plan was to enroll 25 additional patients with the -- in the gastric study with an IHC 3+ HER2 expression.

We're getting close to a full enrollment in that study, as I pointed out earlier from the call, in the next couple of months.

We actually want to see that data mature.

And as you point out, early next year is a good place to present that data.

My sense is that if that data looks good, it would be in our sight to plan out registration pathway for this molecule in HER2-positive gastric cancer.

Obviously, things to consider is whether this should be preceded along second-line therapy as is being connected right now.

Should we consider frontline therapy and also, as you point out, using pembrolizumab or swapping out MGA012 or something else?

We haven't come to a final decision about that.

I can tell you this is part of an internal discussion, but we will be very clear by the time we present the data what the pathway will be.

We have a follow-up question from Debjit Chattopadhyay with H.C. Wainwright.

I apologize if I kind of missed this.

But for the gastric cancer study, is the enrollment primarily in Asia currently because the preliminary efficacy data had -- the data was obviously much better in the Asian patients versus Caucasians?

So thanks for the question, Debjit.

So as you know that in gastric cancer and gastroesophageal cancer, there's a higher proportion of gastroesophageal cancer patients in the U.S. and a higher proportion of gastric cancer patients in Asia, both in terms of numbers and the overall percentages that gastric cancer represents.

We are enrolling both in the U.S. and in Europe.

I would say that there is a higher proportion right now still of being enrolled in Asia for the 3+ gastric cancer patients.

But there clearly are patients coming from the U.S. side.

And just one quick follow-up on the MGD007, the gpA33, that program was put in back burner as of the last conference call.

But did I hear you correctly that you're bringing that forward again in combination with your in-house PD-L1?

So what we -- just a clarification is that our goal for monotherapy was to establish an acceptable safety profile and dose of the drug as monotherapy.

But we did not believe that, as monotherapy, the signal was sufficient to go on to further development in this as monotherapy.

And so I've said all along that then combine it with the [allele in] anti-PD-1 MGA012, and so that's what we initiated and the patients are enrolling in that study.

So we are continuing to follow a few of the patients that are still on the original monotherapy study.

But ultimately, if we continue to develop the combination going forward, if the results are successful later on, it will be in combination with the anti-PD-1.

And this is a pan-CRQ study just based on the gpA33 expression and not MSI our MSS patients, right?

Correct.

This concludes the question-and-answer session.

I'll now turn the call back to Dr. Koenig for closing remarks.

I'd like to thank everyone again for joining us and let you know that we look forward to continuing to advance our programs in the coming months and provide updates on our progress.

Have a good day.

Ladies and gentlemen, thank you for participating in today's conference.

This does conclude the program, and you may all disconnect.

Everyone, have a great day.