MacroGenics, Inc. (MGNX) Earnings Call Transcript & Summary

Okay. Great. Well, welcome back, everyone, to Citi's 2022 Immuno-Oncology Summit. I'm Yigal Nochomovitz. I'm one of the biotech analysts here at Citi. Most of you know who I am. As a reminder, if you'd like to ask questions during the session with MacroGenics, then just e-mail me, [email protected]. Most of you should have my e-mail address in your inbox. And I can relay the questions to Scott. So with that, I'd like to welcome Scott Koenig, CEO of MacroGenics. And we also have Jim Karrels, CFO, in the background to answer any financial-related questions.

So Scott, maybe just to start out the session. It would be great if you could just give us a high-level summary of MacroGenics' corporate strategy? What is the near-term mission of the company? What is the longer-term mission? Just to help those investors that are less familiar.

First of all, Yigal, thanks so much for the invitation today. It's always a pleasure to speak with you. So MacroGenics, many of you know, is a company that's developing immune-based therapeutics based on several antibody-like structures. The company has been in operation now for over 20 years. And we have built this company from the ground up, doing everything from early target and platform discovery all the way through commercialization, including a commercial-directed manufacturing facility and all preclinical development. We have 3 platform technologies, 1 focused on alteration of the Fc domain of antibodies to enhance immune functions, including ADCC and specific immune responses, addressing the treatment of cancers. We have a second technology around building bispecifics and trispecific molecules, which we call DART molecules, which are being developed in different indications and modalities, both incorporating redirected killing mechanisms as well as combination checkpoint therapeutics. And then finally, we have, through various in-licensing opportunities of linker toxin technologies developing suites of ADC molecules. The company is focused, as I said, primarily in developing new therapies, cutting-edge therapies for cancer, although we have some historical work and continued work through collaborations in the autoimmune and infectious disease areas. Our company has a very large clinical pipeline and preclinical pipeline. We've been focused in the last couple of years on advancing a number of molecules targeted to a ligand in the checkpoint family called B7-H3. We have 2 molecules being pursued there, 1 in ADC and another Fc engineered molecule. We have several combination, DART bispecifics targeting combination checkpoints. We have 2 molecules in development for treatment of AML and have additional other molecules, a collaboration with ImmunoGen, for instance, on an ADC directed to a very novel target called ADAM9. We -- this year, we will be discussing very shortly, advancing -- our plans for advancing the ADC molecule towards a registration-directed study in prostate cancer, building off the results we have recently presented at ESMO and ASCO. And we'll be providing additional updates on several of the other molecules during the course of the year. And with that, let me give it back to you, Yigal.

All right. That was a really good intro. And you mentioned B7-H3, which has obviously been in focus very much on the investor front. You have 2 molecules, the MGC018, which is the ADC as well as the -- just the antibody, enoblituzumab. So 2 questions. First of all, just tell us a little bit about why B7-H3 is such an interesting immuno-oncology target? And then also, interestingly, since you have both versions, the ADC and the non-ADC, what's the strategy there? Naively, I guess, one would think that the ADC would accomplish everything that just the naked antibody would accomplish. So why have both?

Yes, it's a pleasure to answer that. So as you know, we've been working on this target and potential clinical opportunities now for a number of years. We actually started exploring the development of molecules over 14 years ago when we developed over 50 antibodies to B7-H3. This is a very attractive target from a number of vantage points. First of all, it's overexpressed on most solid tumors with very modest expression on normal tissues, particularly associated with normal tissue membranes. We identified many different epitopes to this molecule. And from this large group of antibodies, we selected several variable domains where we would have very high binding to tumors versus normal tissues. Now with regard to the expression pattern beyond the tumor itself, it's found on both dividing tumor cells, the tumor vasculature, the endothelial cells as well as cancer stem cells or tumor-initiating cells, and we also find an upregulation on so-called Tregs. What's been demonstrated in the literature is a close association with overexpression levels of B7-H3 and poor clinical outcome in many, many solid tumor types. And so there is also evidence that has been reported, for instance, in lung cancer that there's an inverse relationship between B7-H3 expression and responsiveness to anti-PD-1 therapies. And the importance of this molecule for the treatment of cancer really stands out because of the selective expression pattern and may also contribute, for instance, to tumor growth in certain instances. So based on the studies we have been doing, we felt that it would be most valuable to develop different modalities to treat cancer. So when we first started out, we developed actually 3 molecules. The Fc-engineered molecule called enoblituzumab, where, as you know, that this mediates ADCC killing of targets using our enhanced Fc engineering technology. And we have also demonstrated that this Fc modifications can lead to upregulation of various checkpoints. And we have shown in various model systems as well as in clinical samples that there is an upregulation of various checkpoints when using the Fc modifications we've made in enoblituzumab. We've taken that molecule through various Phase I studies and expansion studies, and demonstrated a couple of years ago that enoblituzumab in combination with pembrolizumab in late-stage head and neck cancer and lung cancer gave responses in the mid-30% response rate, which was quite improved compared to historical data treating with anti-PD-1s alone. And so based on this, we decided to move forward in a front-line head and neck study, where we are combining enoblituzumab with our in-house developed anti-PD-1 retifanlimab. And currently, right now, we're enrolling up to 50 patients, which should be completed this first half of this year that are PD-L1 positive. For patients that are PD-L1 negative, which represents about 1/3 of all head and neck patients, we're treating those with our bispecific DART molecule, tebotelimab, the PD-1 LAG-3 bispecific. So the beauty of this is that we can enhance immune activity. It's -- the combination, we believe, will be quite safe based on historical data as well as the very large data set we've had with enoblituzumab as monotherapy. Now with regard to the ADC molecule, this molecule called MGC018 uses a distinct linker toxin technology called duocarmycin. It's a cleavable linker, which when taken up into B7-H3-positive cells will get cleaved in the lysosome. Will move into the nucleus and alkylate DNA, which then promotes apoptosis of cells. The free linker -- free toxin will be released and cells in the local tumor environment, which [ are in ] B7-H3-expressed will also be killed in that local environment. So back to your question of why develop 2 modalities? Well, the beauty is -- here is that certain individuals with certain tumor types may be responsive to 1 modality versus another. The combined ability with different molecules might differ. And it also allows patients who may respond to 1 and may not continue response, maybe also have a second opportunity to be treated with another B7-H3 modality. Having said that, we also are continuing to develop a lot of preclinical molecules. We had a historical bispecific molecule that we had in the clinic that we didn't pursue. But we have a now next-generation DART bispecific molecule that is in preclinical development. And you'll hear more about these things later this year.

Okay. Let's just talk a bit about the registrational path for MGC018. Are you thinking that this is going to be a monotherapy approach, for example, in late-line prostate where you had a north of 50% PSA 50 response and I believe a 25% tumor response? Or are you going to focus more on combinations for a registrational study?

Excellent question. So obviously, we were very encouraged by the data that we've seen to date as monotherapy in this 40-patient expansion cohort that we initially discussed at ESMO. With the basis of this data, we have designed a study with registrational intent. And what we are planning to do this quarter is to speak to the FDA on the design of that trial and all the aspects of that in terms of inclusion, exclusion criteria control groups, et cetera, statistics around that. Once we have that feedback from the FDA, we would then move forward and would hope that such a trial could be initiated by the end of 2022. So again, at this point, I still want to have the regulatory feedback, it is our intent to move forward with a single-arm registration study. Having said that, we have had very encouraging data preclinically in model systems combining MGC018 with various molecules. In particular, I have highlighted that we can see enhanced antitumor responses when combining these with various checkpoint molecules. We'll have more to speak about this in the course of the next couple of weeks because we expect to actually start a combination study with 1 of our checkpoint molecules and MGC018 in the coming weeks, and looking forward to discussing the prospects there. So in the end, while we are planning to move forward with a single-arm study, we do not rule out the possibility in the future that additional studies could be developed in combination with a checkpoint and other molecules as well.

Okay. And with respect to the checkpoint of choice, it sounds like you're not quite ready yet to disclose which one that is? Or can you tell us?

We're a few weeks away from discussing it. As you know, with the start of the study, that will be up on ClinicalTrials.gov, and we will be providing some of the rationale behind this very shortly.

Okay. And so you mentioned the FDA feedback on the registrational program. Obviously, that's an important catalyst. Are there other data updates for the MGC018 program this year that we should be aware of?

Yes, as you know, we are in other smaller expansion cohorts right now that -- we presented some preliminary data at ESMO on non-small cell lung cancer. We have several others that are continuing. And so what we would like to do is have that data continue to mature and would plan in the second half of this year, providing updates as that data matures.

Okay. And then on the safety side of the equation, I think in the past, you've talked about exploration of alternative dosing strategies to further improve the toxicity profile. How far are you from ironing out an optimal dosing strategy for 018?

We think we have a very good plan in place. What we did following ESMO and with the continued evaluation of the patients, both with regard to activity and safety side effects. We went back and took samples from a large number of those patients and looked at the pharmacokinetics, looking at area under the curve, Cmax associated with this, correlating them with both side effect profile and clinical responses. We then modeled that to come up with what we think is a go-forward dosing that will be part of the discussion that we'll be having with the FDA based on this analysis.

Okay. Great. And then just shifting over to the naked antibody enoblituzumab, you're doing a Phase II proof-of-concept study in squamous cell head and neck cancer and you're combining, I believe, with PD-1 as well as with your bispecific, the PD-1 LAG-3. So I'm just curious what's the thinking there? I guess I would think that if you're doing the PD-1 x LAG-3 combo, you achieve everything you would with just combining with PD-1. So I'm just trying to understand why do both of those cross combos?

If I had my preference, I would have done it that way. But as you know that these are 2 experimental agents. And so when we first designed the study, investigators were more comfortable -- certainly at the time when we first designed the study, we didn't have as much data on the tebotelimab. We now have a lot more data on tebotelimab and the PD-1 LAG-3. So they're very comfortable given the historical data we had with pembro and enoblituzumab to start out in the PD-L1 positive population using the retifanlimab, the anti-PD-1. As you probably know, if you look at the standard of care for frontline head and neck cancer, which is pembrolizumab plus chemotherapy, the response rate overall in that population that got approval in frontline head and neck study was about 36%. But if you look at and segregate these based on PD-L1 status, patients with PD-L1 negativity did not do very well. And so again, back to what I was saying before, is that we have some very good data that when you combine our Fc modifications with a checkpoint, you get the benefit there that the Fc modifications upregulate molecules such as PD-L1, LAG-3, other molecules, and therefore, would get an additional benefit by having this bispecific. But again, it was more to satisfy the investigators -- that putting these 2 novel agents together. Ultimately, once we have the data from both sets, one could, in fact, go to a tebo regimen as the next step forward, combining that with enoblituzumab if that turns out to be very robust data. It also gives us the opportunity if we achieve [ the reply ] that we hope to see to even also combining with chemotherapy to get even better responses. So we're looking forward at least in the second half of the year to provide an update on the first cut of the data from the PD-L1 positive, where, as I said earlier, we should have those 50 patients enrolled in the first half of this year.

We just have a question coming in from one of the investors. Just if you don't mind, just flipping back to the prostate for a second. I just want to -- if you could just clarify, when you talked about the registrational study for prostate, did you mean a single-arm registrational or a monotherapy but randomized?

I've been very clear about that if you listened to some of my previous talks. We will do a randomized study against the control. So it would be monotherapy of MGC018 as the experimental arm and then the control arm would be there. So it will be a controlled study.

Okay. And they were also wondering if you could just be any more specific about when we -- when this year we might see updated data from the prostate cancer studies?

Again, probably the second half of this year we'll provide updates as patients are still on study, so we'd like to have that data continue to mature.

Okay. All right. And then shifting back to B7-H3 in the head and neck, when might we expect some of that Phase II proof of concept data for head and neck?

Well, as I said earlier, the 50 patients in the -- of the PD-L1 positive should be completely enrolled this first half of the year. And so what we will do is provide an update -- at least the first cut of data at a scientific conference second half of the year. The PD-L1 negative, which, as I said earlier, is about 1/3 of the patients, it's been slower enrolling. We're planning to enroll 30 patients in that cohort. We expect to have that completed enrollment in the second half of this year. So for the PD-L1 negatives, it's more likely in the first part of 2023, we would provide updates there.

And is there any thought being given to combining 018 with the PD-1 or the PD-1 LAG-3 in head and neck or not?

With regard to head and neck, as you know, we have a cohort right now as monotherapy. That has not completed enrollment in the monotherapy head and neck expansion study. The plan is to enroll up to 20 patients there. So that is continuing there. With regard to combinations with checkpoint molecules, as I said, we're just about to start a dose escalation study of MGC018 and 1 of our checkpoints. We'll just define which one very shortly. With regard to the specific tumor types we'll include, we'll also discuss it at that time. With regard to the possibility of head and neck being there, certainly given the expression of B7-H3 in head and neck as being very strong and upregulated, that would be one that -- whether it be in this study or in future studies, that would [ be one ] we would certainly entertain. Let me just also point out the difference. The MGC018 is being tested in late-line patients. The -- obviously, the enoblituzumab is being tested in front -- in newly diagnosed frontline patients.

Great. Got it. And then if we could shift over to flotetuzumab and the CD123 x CD3 programs, correct me if I'm wrong, but it seems like the Phase II single arm for flotetuzumab in relapsed/refractory AML has been going on for some time. So just wondering when we're going to see data from that one?

So we've been enrolling patients in this single-arm study of flotetuzumab. We have a preplanned looks at various times during the course of enrollment. And we'll be providing some updates on this program and more broadly, the whole approach to CD123 x CD3. As we've said, we have a study that we expect to start very soon with our next-generation version called MGD024, where we have a modification in the CD3 in this CD123 directed molecule that will allow us, we believe, to have dramatically reduced cytokine release and also be able to give this drug intermittently as opposed to flotetuzumab, which is given by continuous infusion. So we're very excited about the prospects of starting this MGD024 study.

And presumably, that would be in AML as well?

It's going to be in AML and broader than that. We're looking at other CD123 expressing tumors. So the opportunity, we think, is even greater than that with flotetuzumab. We had presented some very exciting preclinical data combining MGD024 with various other treatments for AML at the last ASH meeting, where we have shown that we can synergize and increase the antitumor responses using things such as cytarabine and venetoclax and others. So we think that the opportunity for MGD024 may be even greater than that of flotetuzumab.

And you did -- it sounds like you did not make any modifications to the CD123 part?

Correct. Correct.

Okay. All right. Let's talk about some of the other programs. You also have a PD-1 x CTLA-4 bispecific, that's MGD019. And I believe you're in dose expansion with that one. Help us just with the data readouts for that for this year?

Yes. Again, we're very excited about this molecule. Just to give you for those who have not heard, the data that we presented to date was extremely encouraging. We designed this molecule as a tetravalent bispecific molecule. So we have greater avidity for the both PD-1 and CTLA-4 that is how expressed usually in a tumor environment. We designed this as an IgG4 molecule. So it will not mediate ADCC activity. The major side effect that we believe is observed through combinations of ipilimumab and nivolumab is derived from the fact that CTLA-4 is upregulated on a lot of Treg cells. And as a result, by eliminating those cells, you get some severe toxic effects, in particular, GI toxicities associated with higher doses of ipi or nivo in those combinations. And in fact, what we demonstrated clinically and preclinically is that we could dose to very high levels without the associated toxicities observed beyond that, which one sees in an anti-PD-1. So we went through dose escalation. We got it up to 10 mg per kg. We decided on advancing dose at 6 mg per kg on a [ queue ] 3 weekly basis, and we have been conducting enrollment in 4 expansion cohorts right now, MS stable, colorectal, melanoma, prostate and lung cancer. We expect most of those patients to be enrolled in this first half of the year. So by the second half of the year, we should start -- be able to begin talking about some of those data sets from these expansion cohorts. So stay tuned for that.

So just thinking about the design of MGD019. You chose PD-1 and not PD-L1. Is there any -- is there a reason for why you decided to do it that way?

Yes. As I said to you, remember on the immune cells that we are targeting, we're seeing -- we're looking -- if you look at in the tumor microenvironment, the cells that are around the tumor, the highest percentage are those that are co-expressing CTLA-4 and PD-1. Obviously, the PD-L1 will be on the tumor side of things. So rather than the reassortment of those cells, we're actually hitting those immune cells to block those checkpoints. In fact, what we showed in our published studies is that compared to ipilimumab, the MGD019 was about a hundredfold better at blockading the interaction between CTLA-4 and the B71, B72 of family. So it's very effective. You get this tremendous avidity advantage for the expression and the binding of 2 molecules of each on those cells. And again, as I pointed out, we're not seeing the elimination of single expressed CTLA-4 positive Treg cells, which contributes to the toxicity profile of ipilimumab.

I'm not sure if you've talked about this yet, but if you were going to do a combination of 019 with another one of your molecules, what would you be looking to combine with?

I think that the opportunity here is extremely broad. This can be essentially -- if the profile continues as we are seeing this, this could be combined with additional checkpoints with ADC molecules, with Fc-engineered molecules. It is -- we think that this has the potential both to be used as a monotherapy bispecific as well as combination with both small molecules and large molecules. So we're very excited about that prospect here.

Okay. Let's talk a bit about HER2-positive gastric cancer. Now there you're doing a triplet at the checkpoint, PD-1 or the PD-1 LAG-3 with margetuximab and with chemo. So the obvious question, which I'm sure you've got before, but it's worth going through it again, is how will that stack up against what we saw in KEYNOTE-811, which obviously was Merck's triplet of pembro plus HERCEPTIN plus chemo?

Yes. So just -- you may have missed an update we had from a previous call. We had decided not to proceed with that study and enroll patients in that study. When we decided that we would not proceed with module A of the MAHOGANY study, we also decided not to proceed with enrolling with MAHOGANY B. So that decision was not based on activity. You make a very good point that as you -- as was shown combining pembrolizumab with HERCEPTIN and chemotherapy gave a response rate of about 74% in that population in frontline gastric cancer. This led to an accelerated approval by the FDA. We felt that given the many things in our portfolio for us to expend additional resources on this did not make most sense. That takes nothing away from what we think the prospects there of using margetuximab in combination with checkpoints and chemotherapy wouldn't be very good. In fact, the initial data looked very good, but it just did not make from a priority standpoint sense for us.

Would you -- are you considering that triplet in HER2 breast potentially or no?

I think right now, that certainly is something to think about in late-stage patients as opposed to early-stage patients. But right now, as a resource issue, not something we would prioritize at this point.

Okay. What about the earlier pipeline? How much of that can you discuss in terms of discovery efforts and new targets that you're working on or new bispecific combos?

We haven't been disclosive as of yet. We have a number of -- as I said, the 1 thing we have is sort of a next-generation B7-H3 DART molecule that we are developing. But in addition to that, we have a large number of molecules. Obviously, some are -- we talked about is through partnership with Zai, where we have some preclinical molecules that are being developed that we disclosed earlier last year. But some of the newer molecules, which include ADC molecules, which include other checkpoint molecules, other bispecific molecules. We will provide some updates likely later this year and next year.

Okay. And then there's another one, I believe this is a 50-50 with ImmunoGen, the IMGC936, which targets ADAM9. What's the status of that one? I believe you're in a Phase I in a variety of tumor types -- solid tumor types?

That's true. So this is a study that's being developed with ImmunoGen using their next-generation maytansinoid DM21. This is an antibody we developed to ADAM9 that has very nice properties of incorporation into cells. In dose escalation, the ImmunoGen clinical group is actually conducting that Phase I study. They're still doing some dose finding and expansion at particular doses, have not selected the dose yet. But once they have selected the dose, the plan would be to move forward in an expansion in particular tumor types. And the plan, as described by ImmunoGen, is providing some updates later this year on that program.

Is that of a different payload from MGC018 or is it the same?

No, no, no. It's a maytansinoid, where, as I said, MGC018 is a duocarmycin. It's a streptomyces derived synthetic. We licensed that one in from a company called Byondis.

Okay. So you mentioned Zai, I mentioned ImmunoGen. But you have quite a few other partners -- well you have EVERSANA for the launch of MARGENZA, Incyte, also Provention Bio and Janssen. Just help us understand how those partnerships fit into your broader corporate strategy? How important are they to your advancing the mission of the company?

Well, I think that they all have a lot of value, both from a potential generation of revenues as well as advancement of the technology. So for example, on the Provention side, as you know, we developed a molecule called teplizumab a number of years ago for the prevention of -- or the treatment of newly diagnosed type 1 diabetes. As you may know, last year, Provention Bio received a CRL on their study called At-Risk -- data from that study, which would prevent the development type 1 diabetes in individuals with autoantibodies to certain components and who have a family history of type 1 diabetes. Recently, Provention indicated on a call several weeks ago that they had an agreement with the FDA on a move-forward basis on the outstanding issues regarding some of the manufacturing and the PK of teplizumab. And so they have said that -- this quarter that they will be providing a resubmission of the BLA which is on an accelerated approval. If that is successful, we would be -- do a $60 million milestone and certain royalties on that molecule. So that obviously is a value to us. With regard to the Janssen collaboration, we are working with Janssen on a DART like molecule with 2 undisclosed targets in -- outside of oncology. That collaboration is going exceedingly well. And again, it's up to Janssen to provide specific updates on that program. But it's, again, a nice validation of our bispecific DART technology and its utility beyond oncology in other areas. And -- so those are the 2 ones to highlight.

Anything you wanted to add regarding Incyte?

With -- regarding Incyte, yes, we've got a very good collaboration with Incyte. As you know, they are responsible for the clinical studies on retifanlimab, the anti-PD-1. As you recall, last year, they did receive a complete response letter with regard to the anal cancer indication and had indicated that they would be conducting -- and they are conducting enrolling patients in a frontline anal cancer study to provide supplemental data for that indication. They are also enrolling studies in patients with lung cancer in combination with chemotherapy with a study with endometrial cancer and Merkel cell cancer and then other combinations with novel molecules. Again, it's up to Incyte to provide the updates with regard to plans for regulatory filings and other studies going forward. But it's been a very significant collaboration for us and obviously look forward to getting that over the finish line in the near future.

Okay. And of course, I don't want to forget the fact that you have an FDA-approved product in margetuximab or MARGENZA partnered with EVERSANA for commercialization. So can you just give us an update on how that partnership is going? How they enhanced the launch? And how is the launch going?

So we have had a great relationship with EVERSANA. This was their first oncology product that they were undertaking as a true partnership, they are participating in the costs associated with the marketing and sales of this molecule. As you know, we have been selling this since March of last year. Given the competitive situation with regard to a number of available molecules for late-stage HER2-positive breast cancer, we have always indicated that this would be a modest revenue from the sale of this product. But obviously provides opportunities for treating late-stage patients that cannot have progressed on other approved products or have side effect profiles that would not be fitting and for which margetuximab MARGENZA would be appropriate. So we will, obviously, on our earnings call, provide updates on the sales this last quarter and the year. And -- well, in the future after we have at least a year of sales under our belt, we have an opportunity potentially to provide projections going forward on this. But it's been a good collaboration for this molecule. I should also say we are enrolling in an IST or -- an IST is organization that is being led by people at Dana-Farber are enrolling in an adjuvant study -- a neoadjuvant study in breast cancer comparing in the Fc -- F allele population comparing the use of marg and -- versus HERCEPTIN and -- in that population. So again, that will continue to enroll in the next year or 2. This is actually in combination with Perjeta, I should say that as well.

Okay. Obviously, the mechanism of MARGENZA's binding HER2 on the tumor cell and generating ADCC with engagement with the NK cells via the Fc gamma receptor. Have you given any thought to whether you'd want to partner with -- like an NK cell therapy company, perhaps to see if margetuximab in combination with an engineered NK cell might be interesting therapeutically?

Having said that, very interesting you bring that up. There has been interest from groups about pursuing that type of strategy, either in vivo or ex vivo, in that regard. So those are some conversations we are having regarding that potential mechanism. That also applies also for enoblituzumab because it has the exact same 5 amino acids substituted to enhance ADCC through our Fc engineering.

Okay. Interesting. Looking forward to hearing more about that. I don't want to leave Jim out of the conversation. Jim, could you just give us just a quick overview of the cash, the runway and those sorts of things?

Sure. Sure, I'll be happy to. Thanks so much for the question. So we announced on our earnings call -- our third quarter earnings call back in November that our September 30 cash number was $299 million. And at that time, we indicated that we believe that that cash plus our anticipated milestones, which, by the way, we risk adjust. We believe that, that combined cash takes us through 2023. Now an important footnote is that, that runway through the end of '23 does not include the effect of undertaking a late-stage Phase II/III development program for 018. So that additional funding will be required to pursue that.

Understood. Okay. And then, Scott, maybe just to finish up the session. It would be great for the benefit of everyone listening, everyone loves catalysts and data readouts. So if you could just kind of walk us through across the development pipeline, what are the key data milestones that we need to be watching for, for the balance of 2022?

Great. Thanks, Yigal. So again, to summarize, first on MGC018, number 1 is a follow-up from the meeting that we have with the FDA on plans for a registration-directed study. Second is the start of enrollment in a combination of MGC018 and one of our checkpoints and more detail about the design of that study going forward. Next is additional expansion cohorts in the latter part of this year, providing some updates on that, plus the prostate expansion cohort. With regard to enoblituzumab, first cut of data from patients that are PD-L1 positive in the second half of the year. With regard to MGD019, the PD-1 x CTLA-4 molecule is now called lorigerlimab. Again, providing some initial updates on 1 or more of the expansion cohorts the second half of this year. And then the start of a MGD024 study and then follow-up on the flotetuzumab program. And then finally, from ImmunoGen a follow-up on the study, the Phase I dose escalation study and selection of the go-forward dose for the 0936 ADAM9 program.

Perfect. Well, I think that concludes the session unless you have anything else you wanted to highlight or any other of the molecules that I may have missed?

No. I think we have -- this has been a good summary going forward. And obviously, lots of data. And we are also excited, as I said before, a lot of exciting preclinical new assets that we'll be talking about in the future.

All right. Great. Well, we covered a lot of territory in 46 minutes. So thank you both very, very much for the time. And of course, best of luck as you continue to advance the molecule portfolio.

Thank you so much, Yigal. Appreciate it.

Sure.