Regeneron Pharmaceuticals, Inc. (REGN) Regeneron Oncology Investor Event, ASCO 2020 Conference (Transcript)


Regeneron Pharmaceuticals, Inc. (NASDAQ:REGN) Regeneron Oncology Investor Event, ASCO 2020 Conference Call June 1, 2020 4:30 PM ET

Company Participants

Justin Holko – VP, IR

Dr. George Yancopoulos – Co-Founder, President and Chief Scientific Officer

Marion McCourt – SVP and Head, Commercial

Dr. David Weinreich – SVP, and Head, Global Clinical Development

Dr. Israel Lowy – SVP, Translational Sciences and Oncology

Dr. Andres Sirulnik – SVP, Translational and Clinical Sciences Hematology

Conference Call Participants

Terence Flynn – Goldman Sachs

Max Skor – Morgan Stanley

Evan Seigerman – Credit Suisse

Alethia Young – Cantor

Geoffrey Porges – SVB Leerink

Geoff Meacham – Bank of America

Carter Gould – Barclays

Yatin Suneja – Guggenheim Partners

John Newman – Canaccord

Ronny Gal – Bernstein

Mohit Bansal – Citigroup

Kennen MacKay – RBC Capital Markets


Ladies and gentlemen, thank you for standing by and welcome to the Regeneron Oncology Investor Event ASCO 2020.

At this time, all participants are in a listen-only mode. After the speakers’ presentation, there will be a question-and-answer session. [Operator Instructions] And please be advised that today’s conference is being recorded.

Now, it’s my pleasure to turn the call to the Vice President of Investor Relations Mr. Justin Holko.

Justin Holko

Thank you, Carmen. And welcome everyone to Regeneron’s first ever ASCO investor webcast. Joining me today are Dr. George Yancopoulos, Co-Founder, President and Chief Scientific Officer; Marion McCourt, Senior Vice President and Head of Commercial; Dr. David Weinreich, Senior Vice President and Head of Global Clinical Development; Dr. Israel Lowy, Senior Vice President of Translational Sciences and Oncology; and Dr. Andres Sirulnik, Senior Vice President, Translation and Clinical Science Hematology. After our prepared remarks, we will open the call for Q&A.

Before handing the call over to George, I would like to remind you that remarks made on today’s call include forward-looking statements about Regeneron including those related to Regeneron’s business and research and development programs, anticipated milestone and regulatory matters. Each forward-looking statement is subject to risks and uncertainties that could cause actual results and events to differ materially from those projected in that statement. A more complete description of these and other material risks can be found in Regeneron’s filings with the United States Securities and Exchange Commission. Regeneron does not undertake any obligation to update publicly any forward-looking statements, whether as a result of new information, future events or otherwise.

With that, let me turn the call over to Dr. George Yancopoulos.

Dr. George Yancopoulos

Okay. Hey, there. I’m George. I hope you can all hear me.

Let me start by thanking you all for your interest in our efforts, and I will lead off the agenda by giving an overview highlighting our technologies and the rationale behind our prospectively designed combination approaches. And then, I will turn it over to Izzy Lowy, who will give an update on Libtayo as well as our bispecific efforts in other solid tumors. Andres, who you just heard, recently joined our efforts and he will discuss our approaches in the hem onc space; and then, to Marion to update you on our commercial advances.

So, I believe that any story about Regeneron has to start with the science and technologies that we have built over the years that empower and allow us to create our homegrown pipeline. From the Regeneron Genetics Center, which is highlighted in the yellow box on the left of the circle on the slide, that leads the world in human sequencing, including the entire UK Biobank, and which has created the largest genetics combined with electronic health record based big data set in the world.

From that to our turnkey approaches that are highlighted on the right side of the circle, such as VelociGene, VelocImmune, TRAPs and so forth that to make the best antibodies and bispecifics in the world. Now, including our highly synergistic technology collaborations with partners like Alnylam and Intellia that we believe will help make us leaders in the next generations of genetics therapies.

It’s really the power of our technologies that have delivered repeated breakthroughs over the years, the most urgent medical needs, such as blockbusters like Eylea, Dupixent. And the world looks to us to exploit these capabilities to deliver when there is an emerging crisis like Ebola, or now with the coronavirus epidemic. And I will shortly say a little bit more about that. And it’s also these technologies, which we believe are beginning to deliver in the immuno-oncology pipeline that we are hoping will really bring the promise of immune therapies to all the cancer patients still in need of better treatment.

Two of the most important foundational technologies for the foreseeable future remain VelociGene and VelocImmune. VelociGene remains arguably the world’s most powerful way to generate genetically humanized models for target discovery and validation, and which together with the Regeneron Genetics Center really gives us a unique combined capability in doing the best of integrated mouse and human genetics. VelocImmune remains arguably the most powerful turnkey solution to make fully human antibody therapeutics to any disease target.

We have created a next generation VelocImmune mouse that is designed to be a source of our bispecific platform. And now I remind you, this platform delivers multiple classes of bispecifics, from so called CD3 bispecifics to CoStims bispecific, all in a highly reproducible and turnkey fashion that allows us to repeatedly produce best-in-class therapeutics. And you’ll hear a lot more about these.

Using these repeatable and reproducible approaches to deliver these classes of therapeutics, we not only deliver best-in-class agents, but we can parallel process by — while also cutting timelines from years to months.

Next slide?

Okay. Now, I realize that today’s supposed to be focused on our cancer pipeline. But, I know many of you are also interested in our COVID-19 efforts, and the potential impact they may have on the pandemic. And I thought a short digression on this story might be a good way to highlight the very same technological capabilities that I’ve just been touting that we’re using in regards to our cancer pipeline. You all know that the SARS-2 virus has a critical protein on its surface known as the spike protein, and that the key portions of spike proteins are so called receptive binding domain or the RBD that binds to the ACE-2 receptor on human cells, initiating and allowing for lung infection.

Of course, we thought that our technologies were perfect for coming up with antibodies as drugs that could block this RBD from binding to the ACE-2 receptor, and preventing or even treating COVID-19 infection. One reason we thought this was the impressive track record we had in undertaking a very similar challenge with Ebola, which has its own counterpart to the spike protein, known as the GP protein.

If you can go to the next slide?

We went in record time of nine months from the start of our effort to make an antibody cocktail against this Ebola GP protein to initiating human trials. And as demonstrated by the World Health Organization in its now well-known PALM trial, our Ebola antibody cocktail was highly effective in saving life. The fact that our approaches were so effective for Ebola, which as you all know, is much more universally fatal than COVID-19, motivated us to undertake a similar effort here. And in terms of timing, we broke our Ebola record in going from initiation of our program to human trials that we will begin in about five months from initiation and not just with the single antibody, but a cocktail again. And this is really important.

We use our technologies to create the largest collection of highly potent antibodies from both VelocImmune mice, and also from convalescent humans, thousands of antibodies, and selected picomolar antibodies their resistance to all naturally-occurring viral variants described to date. But we also showed that individual antibodies were not enough. We demonstrated rapid viral escape mutants to all of our single antibodies tested, despite their high potency and binding affinity. And we predicted this beforehand. So, a prospectively designed approach was based on the fundamental realization that, as previously demonstrated for HIV and other viruses, combination drug therapies could prevent viral drug-resistance by requiring simultaneous mutation at multiple genetic positions. We reasoned that the same approach might be required to prevent escape to anti-viral antibodies.

And thus while others focused on the potential of single antibody treatments, we prospectively pioneered and demonstrated the value of antibody cocktails, and how they are necessary to avoid rapid viral escape.

Shown on this slide in blue is the RBD portion of the spike protein, and colored in green on the top and yellow and orange to the right are two different antibodies that both bind to different portions of the RBD, which both block the interaction with ACE-2, and together, not only highly potently block the ability of the virus to infect human cells, but create enormous resistance against viral escape. So, that’s what we set out to do, create an antibody combination that could be highly effective and also resistant to escape. That’s what our technologies created. And that is what we are now about to begin testing in human trials in COVID-19 patients.

Next slide?

So, I am sure that the relevance and analogy in terms of our approach is to cancer does not escape any of you that our prospective approach in the field of immuno-oncology was to build a set of combination or cocktail approaches that could change the course of cancer treatment. And we are really excited about the progress we are making in becoming a leader in oncology.

It all begins with our efforts to have a leading therapeutic in the PD-1 class. And we believe that Libtayo is meeting that challenge. We have rapidly become leaders in the non-melanoma dermato-oncology space, based on our first-in-class data in two different skin cancers. That is squamous cell carcinoma of the skin, or CSCC, and basal cell carcinoma of the skin, or BCC.

It’s remarkable to me that these major opportunities had sort of been missed by the field, especially since the antitumor effects that we have demonstrated are as impressive as those seen in any other solid tumor settings for checkpoint inhibitors. And we are very excited that our monotherapy trial in first line non-small cell lung cancer was stopped early by the IDMC for overwhelming efficacy, allowing us to enter into another important cancer setting with Libtayo with data that looks as competitive as any. But most importantly, this is really just the beginning for us.

Just as I described before, all of our approaches and efforts, start with individual therapies that culminate in combination that we believe can take therapeutic benefit to entirely different levels. We now have over 10 different therapies in development in multiple cancer types. And we have two sets of foundational approaches, both of which have now been validated already in the clinics as being foundational.

Libtayo provides one of the powerful foundations for one set of combination opportunities, while our CD3 bispecifics act as a foundation for another set of combination opportunities. But moreover, each of these foundational opportunities can be combined with each other, as well as with another set of bispecifics, which we term our CoStim bispecifics. And importantly, just as now Libtayo is emerging as a leader in immuno-oncology space, in both dermato-oncology and in other settings, we have achieved proof-of-concept with our first two CD3 bispecifics programs. And I think many believe that our BiSpec programs there are emerging to establish us as leaders in this setting as well.

Next slide?

So, our entire strategy is built around the notion of creating agents that can compete in particular setting, particularly for example with Libtayo. We’ve shown Libtayo has impressive efficacy in settings now that either we’ve defined or the world has defined are responsive to PD-1 monotherapy, such as in dermato-oncology and lung cancer. And believe this is a very important opportunity. And we now have an important drug that really can make us players in this space.

Moreover, we believe that we can go beyond these settings where we are seeing and others are seeing PD-1 efficacy. So, we’re — of course, we’re looking for more efficacy, because we know that even in these responsive settings, more than half the patients do not respond to current bio treatment. And we’re now studying the addition of novel therapeutics to the Libtayo backbone to enhance responsiveness in these already somewhat addressable tumors, adding other checkpoints, or CD3 bispecifics or CoStims and a variety of vaccines adjuvant approaches that we’re interacting with.

Beyond enhancing efficacy in already responsive tumors, we’re also looking to extend the benefit of immune-therapy to tumor settings with currently very-limited response to checkpoint inhibitors. That’s where we think not only combinations with Libtayo but the opportunities that are being presented with our CD3 bispecifics and our CoStim bispecific really allow us to explore potential responses outside the space of where checkpoints have currently shown any activity.

So, our entire approach is built on this concept of integrating different opportunities to create combinatorial flexibility. Libtayo is a foundation for one set of combination, CD3 bispecific is a foundation for another set of combo opportunities. And moreover, the opportunities to mix and match all of these in all sorts of settings where the science points us to the potential benefits.

So, with that overall introduction, I’ll now turn it over to the person who’s been leading all of our cancer efforts to this point, Israel Lowy.

Dr. Israel Lowy

Thank you, George. Hi, everyone. This is Israel Lowy. I’m Senior Vice President of Translational Sciences and Oncology.

I had the privilege for about a decade before coming here, leading many of the foundational first studies of anti-CTLA-4 and anti-PD-1 at a company called Medarex. And after its acquisition by BMS, I came and joined Regeneron to join George and his team to really take combination immunotherapy to the next level.

So, we’re going to start with Libtayo and go to the next slide, 15.

And, as George mentioned, the successful treatment of cancer is going to require creative approaches to thoughtful and novel combination. And we view Libtayo as but the first foundational element in assembling a diverse array of foundational technologies that can be brought to bear in cancer, as in a very flexible fashion, as George said, in almost a plug and play manner.

So I’m going to take you through these three different things here. If we can go to the next slide?

This year at ASCO, we presented longer follow-up on our initial Phase 2 study that led us to registration in cutaneous squamous cell carcinoma with additional follow-up that remarkably enough, actually, we found an increase in the rate of complete responses. Initially, it was about 6% and then after about two years of additional follow-up, responses matured into becoming complete responses in nearly 20% of patients. At 24 months, we still have not reached the median survival in this group of patients for whom prior to this therapy, the mean survival was only a year with difficult treatment.

The next slide shows that in addition to being first-in-class in cutaneous squamous cell carcinoma, we have recently announced results from our basal cell carcinoma in the second line. Again, a setting where there is no approved therapy, and where we achieved impressive response rates, but more importantly durable responses, lasting well over six months. And pictures tell — speak a thousand — better than thousand words. And you can see below how these remarkable changes in lesions and changes in patients that are just life changing.

Next slide?

We recently shared our excitement about stopping our monotherapy lung cancer study in the population greater than 50% PD-L1 positive on the basis of an interim analysis conducted by the IDMC. At that time, we announced that the overall hazard ratio was 0.676 on the population of 710. What we’re sharing with you here is an additional analysis, a modified intent-to-treat analysis, which we conducted because for the first portion of the study, we were prevented from performing PD-L1 testing according to FDA standards for clinical trials. And the FDA therefore asked us to do an additional modified ITT analysis, as shown on this slide that included only the patients who tested above 50% according to this rigorous standard. And as you can see here, the data look even better. So, we are very excited about this. We’ll be presenting the data at a meeting coming up. And we can tell you that all the other analyses that go along with this, fall into place.

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Next slide?

So, we believe that combinations are critical. And we seek to join with novel and exciting combinations with partners who develop agents that are outside our wheelhouse. And so, what you see here is a list of just some of what are more coming of collaborations with companies that have novel vaccine approaches, oncolytic viral approaches, and more to come.

So, if I can go to the next slide, I’d like to turn it over now to Andres Sirulnik to tell you about the next foundational component in our armamentarium of bispecifics.

Dr. Andres Sirulnik

Thank you very much, Izzy.

I’m Andres Sirulnik. I’m Senior Vice President in Translational and Clinical Sciences Hematology. And as a way of brief introduction, I’m in hematology/oncology. Prior to joining industry, actually I spent several years at Dana-Farber and Brigham Women’s Hospital in Boston, focusing my work in hematologic malignancies. And I spent almost a decade at Novartis in oncology development, focusing my work in developing compounds in both, solid tumors and hematologic tumors, and more recently had a role in a biotechnology company, bringing several programs into the clinic in the immuno-oncology space.

Having recently joined Regeneron, I really truly look forward to the opportunity continue to further advancing existing dynamic, bring transformative new therapies to patients.

If we can move to the next slide, please? Next slide?

What makes Regeneron unique is a platform by which we can generate and combine antibodies against many cancer types. Libtayo is one pillar to our approach, but our portfolio consists of multiple classes of bispecifics, in addition to traditional checkpoint inhibitors. And our ability to meet and match tumor target with our CD3 bispecifics, CoStims or other technologies, highlights Regeneron’s progress of combinatorial potential.

Next slide, please?

I’d like to give you an update of where we are and our progress to-date on 1979, our bispecific on CD3, CD20 as a target. We have been making significant progress in this program. 1979 has shown encouraging responses in lymphoma with responses and rates of greater than 90% in late-stage follicular lymphoma with more than three quarters of a patient achieving complete response rate. And in aggressive diffuse large B cell lymphoma, we are seeing deep responses of 50% to 70% in patients with and without prior CAR-T therapy. Furthermore, we continue to be particularly encouraged by the durability of those responses.

Next slide, please?

We continue to advance our program and we now have initiated our potential pivotal Phase 2 program both Hodgkin’s lymphoma and in follicular lymphoma. And additionally, we are exploring also with potential for registration, other areas in lymphoma. These trials are occurring and advancing.

Next slide, please?

In terms of our upcoming milestones, what we would expect is that we will continue our work on our Phase 1 study, where we are combining 1979 with Libtayo. We also explore combinations with the standard of care and novel internal agents, including the CoStim bispecifics that was mentioned earlier. We will broaden the pivotal development program in diffuse large B cell lymphoma and follicular lymphoma, include earlier lines of therapy. And specifically also, we are and have started our subcutaneous formulation testing, which is a plan to start soon. We are starting to complete enrollment of our Phase 2 study in 2021 and we are — potentially will submit BLA in 2022.

Next slide, please?

We are also very excited with the progress that we’re making in our two BCMA CD3 bispecific programs. Our first BCMA bispecific is in the early stages of dose escalation. In the first two doses we tested, we already saw encouraging responses, including responses that resulted in MRD negativity. In addition to this, our second BCMA bispecific is already showing encouraging data. Not only these result make us believe that we will play an active role in the treatment of multiple myeloma, but these results also serve as a validation of our CD3 bispecifics platform, a platform where we have multiple additional bispecifics that will enter the clinic over time.

Next slide, please?

So, where do we look forward to in the upcoming half of the year? We will provide updates on the ongoing Phase 1 dose escalation by the end of the year; we plan potential registrational studies in relapsed/refractory multiple myeloma; we will be initiating combination studies with standard of care regimens and novel agents, and as we discussed earlier with our own CoStim bispecific another agent; and we will be initiating registrational trial in other lines of therapies in multiple myeloma.

Next slide, please?

I will conclude my remarks by showing you a broad set of monotherapy and combination efforts that are already underway or upcoming. And I am now pleased to turn the presentation back to Izzy. Izzy?

Dr. Israel Lowy

Thank you, Andres.

So, I’d like to speak now a bit to our efforts of looking at novel combinations of Libtayo and bispecific in solid tumors, as well as expand a bit more on the third category of the bispecifics, the CoStim bispecifics and why we’re so excited about them.

If we can go to the next slide?

So, MUC16 is an antigen widely expressed in ovarian cancer, it gives rise to circulating CA-125 often used for following the progress of ovarian cancer. As many of you know, PD-1, as a monotherapy is rather inactive in ovarian cancer. So, we’ve developed a MUC16 by CD3 bispecific that attaches to the MUC16 on the ovarian cancer cell. And from the outset, envisioned creating a study in which we would combine it with Libtayo. This study is ongoing. The dose escalation of monotherapy is proceeding. We’ve initiated combinations of MUC16 by CD3 with Libtayo, and that dose escalation is on its way. And we recently received an allowance from the FDA to initiate a study with a MUC16 by CD28, which will be actually our second CoStim bispecific to enter the clinic. And that can be combined with either MUC16 by CD3, or with Libtayo.

So, next slide, please?

So, why are we so excited about CoStim? So, these — we call these — these are all antigen by targeting CD28. And CD28 is the main second signal that T cells require after they recognize an antigen in order to have effective T-cell activation. Normally, they receive this via B7 molecules on antigen preventing cells. These molecules are quite plentiful on hematologic malignancies but pretty much absent on solid malignancies. And therefore, what we’ve done here is create an artificial bridge to use a tumor antigen and link it to CD-28, so that we can mimic this opportunity for co-stimulation.

Our first one in the clinic is a PSMA by CD-28. Again, we envisioned this as from the beginning a combination with Libtayo. And in fact it is dosed with in combination with Libtayo from the outset. So, this is underway and has enrolled several cohorts and is ongoing in dose escalation.

People shied away from targeting CD-28 after the TeGenero debacle in 2006, which caused — where widespread CD-28 super agonism caused severe side effects and almost killed some healthy volunteers. But, we’ve created antibodies that are highly specific to activating CD-28 only in the context of the tumor in — with the tumor antigen.

Next slide, please?

So, this slide here gives you an example of the type of data in the preclinical setting that gave us such excitement about this. What you have on the left are growth curves of tumors, either targeting with a control, PD-1 alone, or PSMA by CD-28. And you can see, they do not impede tumor growth. So, when we combine PD-1 with the CoStim PSMA, we do. And by the way, we never — we always sort of take this for granted. But all of these are done in models where everything is humanized, so that we can use the actual clinical molecules in these models, another testament to the power of VelociGene that George and his colleagues have worked tirelessly over the years to develop.

We also show on the right initial data with a PSMA by CD-3 antibody bispecific, that also has promising activity and was just recently published in Cancer Immunology Research.

Next slide shows additional preclinical data that gives us the basis for our excitement about combining CD-3 bispecific with CD-28 bispecific. Again, you see here that each one on its own in this model is insufficient to control the tumor, but the combination effectively controls the tumor. And in the bottom right where you see the glows or where the tumor is, there is no glowing when you use the combination.

So, what you have here now is a summary of the types of various combinations that are coming into the clinic that we are very excited about. Not only do we have Libtayo as a foundational element within the checkpoint family, we have a LAG-3 antibody that is exploring a variety of combinations with Libtayo, and we’ve recently received an allowance from the FDA to explore a GITR targeting antibody which we think is differentiated from others, which we will be taking into the clinic soon as well.

We have a number of these combinations with CD3 bispecifics, CoStim bispecifics and ultimately you could imagine all three. But as they say in the old commercial, wait, there’s more. So, I’m going to turn it back now to George to talk through some new things that we’re thinking about that add even further combination.

Dr. George Yancopoulos

Well, thank you, Izzy and Andres for reviewing those programs.

I hope you guys on the outside share our enthusiasm for these stories. It doesn’t matter whether we’re talking about coronavirus or cancer. All of our efforts are involving the powerful and elegant and expansive combination opportunities that allow us to bring different classes of molecules together to enhance and extend therapeutic efficacy in these variety of different settings.

And we’re particularly excited that these foundational class members, such as Libtayo for the checkpoint inhibitors, such as the CD3 bispecifics for our entire bispecific platform, are demonstrating their capabilities in the early human trial experience and really suggest that the combination opportunities that we have to look forward to, could really take cancer therapy to another level. And in terms of that, I’m going to just very quickly give you two short stories, just to whet your appetite about the sort of things that our technologies allow us to do, to layer on even more unique steps of combination opportunities that allow us to, once again, enhance any of the previous therapeutic approaches in various settings.

This is one that might have application and combination opportunities in lung cancer for variety of other settings. I’m sure many of you know that the MET tyrosine kinase receptor, which is a receptor for HGF, can — as a mutated version or as an amplified version can promote tumor genesis and cancer activity. Well, thanks once again to our technological capabilities, we’re able to make a very novel type of bispecific antibody that does something very different to this pathway that could be explored before.

So, our bispecific not only binds to MET receptors, blocks their interaction with the native ligand, the HGF, and thus blocks that growth signal very effectively. But moreover, it rapidly induces a change in the complex structure information to rapidly result in degradation of the entire MET receptor complex. And this seems to induce a powerful apoptotic signal in the resulting treated tumor cells, which we think could amplify the potential benefit of targeting this pathway.

This agent — this novel bispecific is already in clinical trials as a single agent. And as I said, one could also imagine opportunities of combining this unique reagent or this class of reagent with other sets of opportunities, some of which we’ve already described to you. So, that’s one unique class of bispecifics that we’re able to make based on our technologies and capabilities.

Another very exciting one is summarized on the next slide. We refer to these as Peptide-in-Groove targets. I’m sure you’re all familiar with the fact that T-cell activation is driven by peptides that are processed from intracellular proteins, proteins that are normally not accessible to the outside of the surface. But, these peptides are processed and presented on the surface of cells on HLA molecules, so that they can be recognized by T-cells, which are constantly interrogating to look for stealth versus non-stealth. Of course, this is the basis of transplant rejection, but it’s also the basis of this emerging new power to use T-cells to attack neo-epitopes on tumor cells.

Well, heretofore, T-cell receptors had been the only approach to detect and address these sorts of Peptide-in-Groove targets. So we’ve been able to generate a new class of antibody and the antibody that we can generate in bispecific format that can do sort of exactly what T-cell receptors are designed to do, but now in a highly selective fashion, once again generated from a next generation version of VelocImmune mice. So, antibodies that can be made, much higher affinity and much more specific for these Peptide-in-Groove targets, than you can normally get from the natural TCRs themselves. But once again, these are very natural created by an in vivo system, Peptide-in-Groove, antibody reagents that can be reassembled into highly potent bispecific antibody.

We believe these create a whole new class of reagents that allow us to attack potentially the many tumor specific proteins that are intracellular and otherwise inaccessible to traditional antibody efforts, but will be presented as these peptides and will now be accessible to our PiGs put in various format. And not only as bispecific format as these bispecifics that you heard about from Izzy and from Andres that can either directly kill or cause post simulation, but they can also put into formats powerfully into genetically engineer T-cells to create new classes of empowered T-cells that are now directed by these new classes of reagents, as opposed to limited by either the traditional chimeric antigen receptors or the utilization of actual native T-cell receptors to drive the T-cells to recognize tumors.

And obviously, we’re taking great advantage of the opportunities and the possibilities that are presented to us with this whole new technological capability, not only internally, not only by using a bispecific formats, but in our powerful collaboration with partners that we have, such as Bluebird who are focused on using engineer T-cells to attack cancer.

Next slide?

So, we tried to summarized a vast number of potential opportunities that we are creating with individual agents, but also in combination to attack cancers of all class. As you might expect, we’ll be amplifying our approaches to attack all sorts of solid tumor cancers as well as hematologic cancers. And we’re excited about these unprecedented capabilities that we’ve created of combining all sorts of checkpoint inhibitors, CD3 classes of bispecific, CoStim classes of bispecific, as well as new emerging classes of molecules and bispecifics that we can make, such as the MET that I briefly mentioned, PiG reagents and PiG bispecific, not to mention the assortment of now collaborations that we’ve created from companies that we’ve discussed that allow us to take these reagents and further increase the opportunity to create clinical benefit.

So, with this overview of our ongoing programs, our pipeline, and future classes of reagents, I’d like to turn it over to Marian McCourt, our Senior Vice President of Commercial to describe the commercial advances that we’ve been making in this space over the last couple of years.

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Marion McCourt

Thank you, George. Hello to everyone. It’s a pleasure to talk to you today.

We have been able to accomplish a great deal commercially in oncology since launching our first indication for Libtayo. We collaborate, as you know, with Sanofi on Libtayo and Regeneron is the lead in the United States. Together, we’re very proud to have established Libtayo as the standard of care in CSCC.

In addition to growing the market since our approval in 2018, we’ve taken significant patient share from chemotherapy. Further, we’ve taken share from in-class competitors, demonstrating that even when physicians are familiar with specific treatments, they prefer choice, and they’re open to trying clinically compelling therapeutic alternatives according to patient needs. We believe this is important as we look ahead to potential future indication approvals for the Libtayo.

Our commercial team is eagerly preparing for two potential new launches for Libtayo, basal cell carcinoma and non-small cell lung cancer. Starting with lung. There are approximately 20,000 first line advanced NSCLC patients with greater or equal to 50% PD-L1 expressions diagnosed annually. Only one to PD-1 antibody has been commercialized as monotherapy in first line NSCLC.

As you heard from Izzy, our Libtayo survival data is strong and competitive. As I mentioned earlier, physicians prefer choice. And if approved LIBTAYO would provide additional product choice for oncologists, providers and their patients. We look forward to potential commercial preparation in this important category.

Moving to BCC, this is the most common skin cancer in the world with approximately 3,000 patient cases of advanced BCC in the U.S. alone. Like CSCC, this represents another potential first-in-class approval. There are currently no approved second line therapies and significant unmet provider and patient need exists. If approved, this would demonstrate Libtayo’s potential in patients with another difficult to treat non-melanoma skin cancer.

Before turning the call back to George, for closing and Q&A, let me briefly summarize some of our commercial accomplishments in just the last couple of years.

First, we successfully launched Libtayo and built a new immuno-oncology advanced CSCC market. Second, we’ve created an experienced, talented and competitive oncology team with our future portfolio in mind. Many of the individuals who have joined Regeneron have worked in oncology for their entire careers. Third, we’re very well positioned to apply and extend capabilities for not only new indications, but also our future product portfolio.

And with that, I’ll turn things back to George.

Dr. George Yancopoulos

Thank you, Marion. And with that, we’ll talk about upcoming milestones and catalysts. Well, we’ll show you that slide. And while we’re showing you that slide, we’ll open it up to Q&A.

Question-and-Answer Session


Thank you. And we will now begin the Q&A session. [Operator Instructions] And our first question is from Terence Flynn with Goldman Sachs.

Terence Flynn

Hi. Great. Maybe just two for me. I was wondering, if you can talk about your confidence level in the safety tolerability profile of 1979, such that you’ll be able to move into earlier lines of lymphoma. And I was wondering specifically if you comment yet if you’re going to conduct a head-to-head trial versus re-toxin. And then, maybe for Marion, just wondering, do you think you can get the modified intent-to-treat data on the Libtayo — future potential Libtayo lung label? Thank you.

Dr. George Yancopoulos

Well, in terms of Regeneron’s 1979 and its safety profile, when Izzy had initiated this program, he devised a whole new approach of how to divide the dose to minimize cytokine release syndrome and other untoward effects, leaving us with a very comforting safety profile to date. In terms of any details about it, I guess, I’ll leave it to Andres, who’s inherited this program and who’s been intensively looking into the safety aspects of it, to make some comments.

Dr. Andres Sirulnik

Hi. So, in terms of your question, we think that we have a very competitive safety profile and that we also believe that they what has been put in place in terms of mitigating CRS, which as you know, is one of the major concerns. We have addressed that issue really well with the schedule and dosing and premedication that was put in place early in the program. And since then I think that the safety profile of the drug now has changed dramatically. And I think that the updates that will be presented in due course will show how competitive the program is in that regard.

When it comes to what you asked, in terms of our plans moving forward in combination and early lines of therapy, we are planning to move forward and expand our program in other lines of therapy and combination therapy. And we will eventually disclose where we’re going.

Dr. George Yancopoulos

Okay. And in terms of the mITT analysis and the label, I’ll turn it over to Marion.

Marion McCourt

Sorry. My name was mentioned. I actually think Izzy ought to take that and give the latest view from a clinical perspective?

Dr. Israel Lowy

Sure. So, as I mentioned, when we were showing the data, the FDA actually asked us to do this analysis to be — to show that in a rigorously tested PD-L1 population greater than 50%, that our study — what the study showed. So in fact, you could argue that this is the key data. And we do believe that this will be included in the label, although that’s a forward-looking statement. Exactly how it will be included? We’ll have to turn out with discussion.


Thank you. And our next question comes from Matthew Harrison with Morgan Stanley. Please go ahead.

Max Skor

Hello, this is Max Skor on for Matthew Harrison. I just have a quick question. Regarding the REGN1979 trial, when can we expect an update from the DLBCL cohort? Should we be looking towards ASH 2020? Any insight would be greatly appreciated. Thank you.

Dr. George Yancopoulos

Alright. Well, we’ll ask Andres to speak on when we hope to have any upcoming presentations.

Dr. Andres Sirulnik

Yes, we are aiming to provide an update towards the end of the year.

Dr. George Yancopoulos

Next question?


Thank you. And our next question is from Evan Seigerman with Credit Suisse. Please go ahead.

Evan Seigerman

So just going back to the mITT, HR you presented, can you just elaborate, just a little as to what differences are in the way you measured PD1 in this particular population versus the overall population? I think we’re a little confused there. And is this specific hazard ratio part of your broader strategy to compete? Then I have a follow-up on with the LAG-3 bi-LIBTAYO data.

Dr. George Yancopoulos

Yes. So basically for various reasons we’re not going to get into now. We did not have access to the ability to do our PD-L1 testings according to the FDA standards for clinical trial. When we acquired that ability that resulted in accrual of the majority of the patients in the second half of the trial and the FDA asked us to do this additional modified ITT analysis, which we showed on the slide, to include only those patients who were validated as having PD-L1 greater than 50% according to their standard. We believe that, that represents in some ways the most appropriate data set to use when reviewing the study. And it represents the patients who were validated by that study done according to the FDA standards to represent the patient population that is greater than 50%.

We certainly are quite buoyed by the efficacy that’s seen in that population. What we can say is that us — when patients who were tested the previous way according to the other standards, were retested, a substantial number of them actually had lower PD-L1 level substantially lower than the 50%, which raised the concerns in the first place. But as one might expect, if you limited your analysis to those who were truly PD-L1 greater than 50%, you would get there your most convincing and best data.

Justin Holko

And haven’t yet to follow up on LAG-3?

Evan Seigerman

Yes, for sure. Thanks, Justin. So I noticed that your expansion cohort is enrolling. Any characterization as to what you saw in the dose escalation part of the trial?

Dr. George Yancopoulos

Izzy, I’ll ask you if you want to make any comment on that.

Dr. Israel Lowy

I think it’s still a bit premature for us to talk about the efficacy data. I mean sufficed to say we think the place that is going to really be active is the combination. And we’re exploring a couple of leads there to convince ourselves that we have appropriate activities to proceed further.

Dr. George Yancopoulos

And I think what everybody should realize, as I think we have demonstrated with LIBTAYO, it’s not always so easy to make the best checkpoint inhibitors. Not all of them are created the same, even against the same target. And not everybody always picks or predicts the right settings and the right indications where particular checkpoint inhibitors might have the best efficacy. And I think that, as led and demonstrated by Izzy and his team, they can pick some of the best setting and situations and combinations. And our technologies can deliver, in some cases, the best-in-class reagents.

Justin Holko

Thanks Evan. Next question please.


Thank you. Our next question is from Alethia Young with Cantor. Please go ahead.

Alethia Young

Just one from me. I just wanted to talk a little bit more about how you plan on positioning with your BCMA programs, with like so many on the market? Is it again the combination approach or is there an inherent differentiation you believe you can achieve from the agent?

Dr. George Yancopoulos

Was that question about basal cell carcinoma?

Justin Holko

No, no, BCMA.

Alethia Young

Alright, BCMA.

Dr. George Yancopoulos

BCMA, oh, Sorry, we didn’t hear that. BCMA. Yes, I think the critical thing is once again, as I’ve just said, not all agents and reagents even against the same targets are created equally. And I think that the track record of our technologies is that they tend to give reagents that deliver best-in-class or match the best-in-class in efficacy. So that’s one thing. There may be a lot of agents out there, they’re not all going to be delivering the same amounts of efficacy. Secondly, is of course, this opportunity that we have which I think is unmatched in terms of combining the right type of targeted agents to maximize the efficacy. So we are excited that not only have we now generated as you heard from Andres, two different BCMA biospecifics, using two different CD-3 arms that are both clinically active but that we can use these essentially as starting points as hopefully very active starting points where then we can layer in our additional therapies.

So for example, for these combinations we are very excited about fusing in our CD-28 co-stim agents that will at least based on what we’ve seen pre-clinically, combined very powerfully and hopefully in a safe enough way to enhance efficacy. So, we are very excited about having potentially best-in-class initial agents based on the BCMA approach, but also the ability to mix and match them with additional plasma cell co-stim agents that will enhance that initial activity.

Next question. Operator next question, please.


Yes. And our next question is from Geoffrey Porges with SVB Leerink. Please go ahead.

Geoffrey Porges

George, since you opened up the flamboyance of your CoV-2 antibodies, I just want to clarify a couple of things there. I’ve one question on the oncology side. So previously, you said that you had two cocktails in development, the CoV-2. And I’m just wondering if that’s still the case? And then could you just talk a little bit more about this mutant escape, how fit was that escape variance, what species did you see that should we be concerned about that? And then just last question. We’ve seen some pretty encouraging data about TIGIT at this year’s ASCO. You don’t have a TIGIT. You have a history of being able to catch up very quickly when promising a new target to identify. Do you have any intentions or interest in developing a TIGIT antibody?

Dr. George Yancopoulos

Okay, 15 questions for Geoff. Okay, try to remember them in order. But yes, we have multiple antibody cocktails that we are considering. One of which will be entering into clinical trials within the next week or two, which is our prime cocktail. We do think that there is enormous reason to be concerned about viral escape. We have shown in our preclinical experimentation that it is trivial to select escape variants, with even the most potent single antibodies that have ever been described against any virus. We do not think that this is a surprise. This is the entire history of viral drug therapy. And there is no reason to think that antibodies should represent some new immune class, immune from mutation viral escape. What we have shown that you could actually, if you have single antibodies, multiple single antibodies that all bind to a similar region of the spike protein, a single amino acid change in the spike protein can eliminate the binding of that entire shared class of single antibody.

We think there is enormous danger that if people contaminate the population with single antibody treatments, they may select for these escape mutants and be wiping out whole classes of therapies. When you use a cocktail, it becomes much harder and the virus is much harder to derive resistant viruses. This is just exactly what’s been seen with combination drug therapies in the past for HIV and other therapies.

So we are very excited about the opportunity with our initial cocktails and we have our backup cocktails, as well as we need them. We think the world should be very concerned about people prematurely going out with single antibody treatment, and contaminating the world with escape mutants. We actually already know escape mutants do not result — the mutation is not caused by the antibody. It’s just selected by the antibody. And we already know that escaping into individual single antibody exist today in the human population. And if we go after these populations with single antibodies, we will teleologically bring out and amplify the representation of these single escape mutants. And eventually if we do too much of that, we will even make viruses that will then be resistant to cocktails, which I believe right now, they are not.

Okay, so that’s the first set of questions that you asked.

The second set of questions about TIGIT. As you might expect, we have a plethora of our own TIGIT antibodies. Right now I have to say that we are not overly convinced or excited about the TIGIT opportunity. The space seems to be overlapping with the PDL high population and it’s not clear to us that will actually add to any efficacy over a potent PD-1 blocker on its own. We do think and we are excited about our GITR antibody, which in some ways leads to interactions or relationships with the TIGIT space.

Our GITR antibody we believe is very different from any other GITR anybodies out there. We have shown that ours have the ability to very effectively deplete Tregs, that suppressor cells that are holding back tumor responses, while actually sparing the effector cell that you want to go after the tumors. We’re very excited about this. We’ve been able to — because we have the velocity and technology that allows us to create these multiple humanized models that are we think more faithful replicas of what’s going on in the actual human, because so many components we can humanize, we’ve done a variety of head-to-head comparisons, which make us very excited about the unique ability of our GITR antibody to target intramural Tregs and shift the Treg to T effector ratio which is something that we’ve not been able to see with competitors and head-to-head studies in our humanized models. So we are very excited about that program and as you heard from Izzy that is already in the clinical.

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Justin Holko

We saw several callers in the queue. If you could limit your question to one, we’d like to get through as many as possible. Thank you. Next question please.


Thank you. And our next question is from Geoff Meacham with Bank of America.

Geoff Meacham

Just a question on your LIBTAYO combos with bispecifics, you guys were evaluating a number of the less immunogenic tumors or cold tumors. And obviously, this has been an area historically which hasn’t been so fruitful, I mean I have a feel. So, the question is, what gives you confidence in these settings with the prostate and ovarian in particular? And do you have a sense for how your combinations may compare in some of the preclinical models to other PD1 combinations in cold tumors?

Dr. George Yancopoulos

Yes, I think that the reason tumors are so called cold is because they are not generating the assortment of signals that are necessary in order to allow for T-cells to be attracted, to be activated, to proliferate, to create a type of so called hot environment. This is exactly what our cop-stims are designed to do, which is why we want to add these combination of signals. Most reagents to-date as you know are focused on this so called Signal 1. So our co-stim bispec that you mentioned in prostate cancer or co-stim bispec that you mentioned in the ovarian cancer can hopefully provide this missing Signal 2 and allow for turning hot tumors into cold. We should also mention that our CD-3 bispecific also offer the opportunity of engaging independently of whether the T-cells are there already or not, of engaging in bringing T-cells by targeting them to recognize and bind to the tumors of interest.

Izzy, would you like to add some more to that?

Dr. Israel Lowy

Sure. Thank you, George. First of all, cold is relative. I mean the idea is to really get the sparks going and get the inflammation going. And that’s what we seek to do with these approaches that can rely not on specific T-cell recognition per se, an influx of T-cells that have been there before, but to get stuff going, where they haven’t — where it hasn’t really started. So, the CD-3 bispecifics basically roundup T-cells in the neighborhood and say come on in and let’s attack this common antigen. And the co-stim bispecific say, listen, if you’re here, we can boost your signal, whether it’s via a CD-3 bispecific or if you’re augmenting an authentic recognition by a T-cell of tumor antigens, but it just doesn’t have enough oomph even with PD-1. And so you give it that extra kick.

So these have all been supported by our preclinical models, which is we keep saying, we use our clinical candidate in these models. So we’re not using surrogates. So the proof will be in the clinical trial but we think we are excited to bring these forward.

Dr. George Yancopoulos

Now, thank you, Izzy. Much better than my preliminary answer. Luckily, that’s why he is in charge of the program. Operator, next question please?


Thank you. Our next question is from Carter Gould with Barclays.

Carter Gould

I guess George and team, to what extent should we expect Regeneron to continue to invest and explore in trials in the compete section of your strategy, particularly once you get past the chemo combo in lung? And if that’s too vague, I’m trying to understand how you weigh strategic choices of pursuing things like LIBTAYO, mono and adjuvant lung? And maybe rewinding the playbook of your competitors versus focusing more on combinations or can you do both? Thank you.

Dr. George Yancopoulos

Well, I do think that we are very interested in some of the settings where there are enormous numbers of patients who can benefit. Lung represents such an opportunity. We now think that we have compelling data that really creates a competitive profile in lung. We are excited about the cancer settings where we were first-in-class where we think we have the opportunity to build the opportunity but we also — are also — as you said, the next generation of technologies are going to allow us to bring the next generation of potential treatments to patients who really need them.

So our focus, as you said, after a lot of these settings in which we’re either creating the market, or we’re very willing to compete, will be in settings where we are now hoping to enhance and extend tumor responsiveness where there isn’t enough of a benefit. And that will be a large part of our bonus — we think a large part of our future. So we think that there’s enormous opportunity now to be competing with a therapeutic that has such an attractive profile in terms of the LIBTAYO, but we think there’s enormous opportunity to enhance and extend the benefits of LIBTAYO to other settings, either by combining it with all these other agents that you’ve heard about, or they’re going to these other settings with these other combinations with or without the LIBTAYO. It’s really, I think, an enormously exciting time for us and I think for the field, and a time that offers a lot of hope to cancer patients, which is why we’re in this business in the first place.

Dr. Israel Lowy

Chapter one.

Dr. George Yancopoulos

Charter one Izzy just said.

Justin Holko

Next question, please.


Thank you. Our next question is from Yatin Suneja with Guggenheim Partners.

Yatin Suneja

So just a broader question. Can you really just talk about the fundamental differences between your approach for CD3 versus CD28 bispecific, specifically in terms of the tumor or the cancer target they might be applicable to? And then what you might be doing just to sort of mitigate the potential CRs or cytokine syndrome issue that might seem to follow after you stimulate either CD3 or CD20?

Dr. George Yancopoulos

Okay. Well, there’s a lot sort of in there. Okay. We think that we have a unique platform that allows us to create the best-in-class reagents, as we’re already been demonstrating over the last years. We can make them that are either targeting or using reagents that create the Signal 1, or that create the Signal 2 and we have a variety of different versions of these and different versions of Signal 3. We believe that we are the leaders in establishing not only these classes, but also in the ability have a turnkey system that creates them, that allows us to do this plug and play approach that Izzy described like few others could possibly even imagine. And along with that, we’ve been pioneering and developing ways of trying to figure out how to give these; either create them so that they’re safe or give them that they’re safe. Izzy, would you like to amplify again?

Dr. Israel Lowy

Yes. So there’s no tumor that can’t be thought of as a target for both the CD3 and/or a CD28 co-stim. So that’s number one. Number two, the extent of cytokine release is probably going to be different for individual agents and our preclinical data suggests, for example, co-stim bispecifics are very mild. And what we’ve already established, we talked earlier that we know how to manage PRs with our CD20xCD3. And obviously, everything we do when we go into the clinic, we do it cautiously. But we think that the benefit to be gained by combining these is tremendous and it’s really this combination approach that’s going to be the key towards really getting effective therapies out there.

Justin Holko

Thank you. Next question please.


And our next question is from John Newman with Canaccord. Please go ahead.

John Newman

Just a quick one. Do you have any plans to explore combining the gamma-secretase inhibitor with any of your bispecifics targeting BCMA?

Dr. George Yancopoulos

To Notch pathway, maybe you can tell us why we should consider that because we have not to-date.

John Newman

So it’s something that some of the other companies in the CAR-T arena are trying. Some people believe that if you inhibit gamma-secretase, it can present pre — high levels of pre-BCMA circulating but it hasn’t been proven yet. So I’m just curious.

Dr. George Yancopoulos

Well, we will keep our eye on that and consider adding it into our collection of potential combinations. Though I have to say I think we’re more excited about our internally derived combination opportunities.

Justin Holko

Thank you, John. Next question?


Our next question is from Ronny Gal with Bernstein. Please go ahead.

Ronny Gal

I’ll ask one and I have a second one, is a pretty quick one. First, if can try and compare the timing of your chemo combo in non-small cell lung cancer with the KEYNOTE-189. It seems you should be in a pretty good position to have your interim analysis pretty soon after you complete enrollment. If you care to give us an AIA either/neither, I would appreciate? And second, your — since you’ve taken the antibody approach to that, I got a follow up on Geoff’s question and ask you, as you think about the sustained approaches, which obviously is [clinical] Cov antibody, do you see the mutability of Cov to be a risk of escape there as well, or is it something that’s you think unique for the single antibody on deliver?

Dr. George Yancopoulos

Well, let me take the coronavirus question first and I’ll turn it to Izzy for the question of the timing for our combination chemo studies in lung cancer. So, we do not think that the virus is mutating at a very high rate. It’s just that as with any virus, a selective pressure that does not understand how to avoid selection of rare mutants by allowing for combinations can lead to potential catastrophe even undermining the possibility of future vaccines. Meaning that if you select for new spike proteins that are now resistant to immunodominant epitopes, which some of the first single antibody treatments are designed to attack, then you can actually weaken the benefit that you might see from vaccines, because you will now have selected in the population variants that have now taken over that are missing these immunodominant epitopes. So I think that there’s a lot of danger there.

We should point out that the history of viruses has shown how rapidly single amino acid mutants that create whole different classes of resistance can take over populations in just a few months, over entire globe. So anyway, with that, I’ll turn it over to Izzy in terms of the timing for the chemo combination.

Dr. Israel Lowy

So we have announced that we are expecting to complete enrollment in the very near future. And we’ve given guidance that some time in 2021 as when we expect to see our first analyses that we think may have a chance to be positive. Obviously, if we do one earlier and it’s positive, we’ll let you know.

Dr. George Yancopoulos

Next question, please.


Thank you. Our next question is from Mohit Bansal with Citigroup.

Mohit Bansal

Just wanted to understand your Peptide-in-Groove approach a little bit better in the sense of, how does it compare with the traditional TCR-based therapeutic approaches? And how do you envision your therapeutic in terms of, do you think it will be off the shelf or autologous at this point? And lastly, when could we see something from this program entering clinics? Thank you.

Dr. George Yancopoulos

So it’s a great question. But to get into the nitty-gritty, as many of you may know, T-cell receptors are designed to be low affinity agents that recognize in what’s called a high avidity state, their counterpart peptide. Antibodies are intended to be high affinity reagents that can essentially monomerically bind to and attack their target. So what we’ve been able to show is that our Peptide-in-Groove antibody can on average be higher affinity and more specific reagent than T-cell receptor. And thus they can be used in soluble both approaches, i.e. biospecific approaches for which T-cell receptors are not designed by nature to be able to work in. So it’s a whole different level, a whole different class, because antibodies that are recognizing what T-cell receptors recognize in the higher affinity and can work as soluble reagent.

That said, they may also have advantages in terms of binding affinity and specificity to T-cell receptors, even when engineered into T-cell. I think that the first examples that we may hope to see of these in the clinic maybe when they are incorporated into engineered T-cell approaches with our collaborators such as bluebird for example. And that could be within the next one to two years. Next question?

Justin Holko

I think we have time for one more question.


Thank you. And our last question is from Kennen MacKay with RBC Capital Markets.

Kennen MacKay

Hey, thanks so much for squeezing me in and congrats on the progress, especially with LIBTAYO. On LIBTAYO, wondering which of the combinations the team was most excited about? If you think with some of these newer targets, the field will be able to surpass the synergistic or [adjuvant] efficacy bar set by CTLA-4. Thanks and congrats again.

Dr. George Yancopoulos

Well, by the way, I should have probably mentioned in my earlier remarks, I hope you all realize that LIBTAYO was all part of a big and ongoing collaboration with our partners in Sanofi. And I hope you have heard from their own investor conference that they are equally as excited about LIBTAYO as we are.

In terms of which of the sets of combinations we’re most excited and interested in terms of extending LIBTAYO to a previously unresponsive tumor or increasing responsive, I think everybody you ask at Regeneron will probably give you a different answer. But since he’s running most of these programs, I will turn it over to Dr. Israel Lowy for his thoughts.

Dr. Israel Lowy

Well, we love our children. And yes, they each have their flaws and their pros but…

Dr. George Yancopoulos

Some of them like on Wednesday, the other ones are like better on Thursday.

Dr. Israel Lowy

But we wouldn’t be pursued — we’re not doing a throw stuff at the wall and see what sticks approach. We really take each of these, we vet them very carefully. We think them through. I mean, obviously, the combinatorial universe is impossibly large. So we try to make really good guesses. We look for where there’s a need, we look for where we can find an antigen that we can target specifically, where we can model it properly and be convinced that what we’re taking into the clinic has a shot. And that’s the approach we take. And we sort of mentioned this earlier. From the very first days, this is all about combination. That’s going to be the future. This is — people said, oh, there’s a PD-1, it’s over. It’s not over, it’s just beginning. And the future is going to be and coming up with various types of combinations. And the more flexibly and facile way you can test intelligent combinations, the more likely I think you’ll be towards hitting on some good treatments for previously difficult to treat cancers.

Dr. George Yancopoulos

Thank you, Izzy, and thank you to the team. We appreciate everybody dialing in today we know it’s a busy time during ASCO. Hopefully, you found today insightful. As always, the Investor Relations team is around to answer any questions you may have.


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