Johnson & Johnson’s (JNJ) Management Presents at UBS Global Healthcare Brokers Conference [Transcript]

Johnson & Johnson (NYSE:JNJ) UBS Global Healthcare Conference May 24, 2022 10:00 AM ET

Company Representatives

Dr. Mathai Mammen – Head of Pharmaceuticals R&D

Conference Call Participants

Laura Sutcliffe – UBS

Operator

Good morning everyone! And welcome back to day two of the UBS Global Healthcare Conference. I’m delighted to be joined on stage by Dr. Mathai Mammen, who is Head of Pharmaceuticals R&D at Johnson & Johnson. My name is Laura Sutcliffe. I’m a Pharmaceuticals Analyst here at UBS, and I’m very happy to be spending the next 36 minutes and 24 seconds talking to you about R&D activity at J&J.

If you’d like to ask a question, we’re going to throw you a curve ball, which is that the QR codes currently don’t do anything when it comes to talking to the iPad. So we’re going to stop halfway through and have you raise your hand if you have questions. Then again towards the end, we have a microphone and we’ll bring it over to you traditional style.

Question-and-Answer Session

Q – Laura Sutcliffe

So, if you could just give us a couple of words about yourself and the things your sort of most excited about at this moment, Pharmaceuticals R&D at J&J and then we’ll go into some detail.

Dr. Mathai Mammen

Sure thing. First of all, thank you for having me Laura. It’s a pleasure to be here and tell you a little bit about what’s happening at Johnson & Johnson. I’m extraordinarily excited about where we are with our portfolio. We’ve been on a build phase for some number of years right now, and both in terms of the composition of the portfolio being in places where I think there are multiple big products that are truly transformational and the bar is high and we keep it high, as well as build and continue to evolve in Ngen and we can talk more about this, but in Ngen that I believe is differentiated and complementary to the efforts in the broader ecosystem, making us an ideal partner in many situations.

Laura Sutcliffe

Perfect! So we’ll definitely be coming back to the Ngen. I’d like to just start with this sort of top of mind issue, so we cover off at the beginning of the presentation which is COVID vaccines. Just given your sort of recent limitations on usage, could you just outline how you see the role for that going forward, whether it’s in the U.S. or beyond, and just sort of tell us what happens now to that spend and manufacturing capacity that maybe you have. Is it like its redirected elsewhere or sort of how are you thinking about that vaccines piece on COVID?

A – Dr. Mathai Mammen

No really, thank you for that question. So the vaccine holds a very special place in the company and in our hearts really. We were part of a group that really gave it a go right, in the beginning at 2020 when we saw this. The vaccine has certain features that we anticipated and have actually come to be, just as a reminder of what those are. It is still a vaccine that works really effectively after a single dose; it’s a vaccine that covers a variety of types of viruses.

So as we’ve gone through various variants and as Omicron goes though BA.1 now through BA.5, being a heavy T Cell vaccine it still actually works pretty much the same against the latest version of the virus as it did the originator strain. And that depending on how COVID evolves and how everything – the pandemic evolves, may have varying utility with time.

That said, what we – how we position the vaccine today is as a global vaccine. We’re very excited that we continue to ship vaccine to parts of the world that remain largely unvaccinated. So here within the United States or Europe and other regions, we’re talking about boosters and boosters on top of boosters, but that’s not the conversation in many parts of the world. People continue to die of COVID, people continue to have great debilitation because of COVID and our vaccine we’re proud is helping with all of that.

You asked about redirecting resources and manufacturing. We have a very robust vaccine pipeline that I just want to talk about for a moment. The Ad26 as a vector is a way to deliver an antigen. It continues to be really effective. It is a way that causes this really robust two kinds of immunity, both antibody immunity and T Cell immunity, which is very helpful when you have a variable virus, a virus that can keep mutating.

We have vaccines for RSV that are – that’s a Phase III asset right now and moving along, that means resource. We have a different technology that we depend on to create a quite unique vaccine for E. coli. So E. coli being a Gram-negative bacterium, it has not been easy to develop a vaccine for – in the last 30, 40 years. So we have a unusual, special differentiated technology, and we have this product in Phase III. That too needs resource and we’re able to redirect that way, and earlier than that we have multiple other vaccines including a terrific vaccine that’s coming into development for Staph Aureus that I’m very excited about.

Laura Sutcliffe

So can we pick up on the RSV since this is actually a pretty unique vaccine. Could you just talk people through sort of the steps that’s been through in develop and how you’ve tweaked this vaccine to get to your Phase II product? And then maybe after that we can sort of think about how the RSV market might look and how we treat or prevent.

Dr. Mathai Mammen

So first on the disease itself, Respiratory Syncytial Virus (RSV) is a very debilitating disease for both the very young and very old. We are developing this vaccine right now as a senior vaccines for older individuals, and when older individuals do contract RSV it can be really bad, and it can cause a step down in lung function, it can cause long term disabilities, it could cause death.

So we see an RSV from a history standpoint has been very difficult to create a vaccine for where it’s a robust enough immune response, especially in the elderly that don’t, that where it’s difficult to create a robust immune response. We’ve taken it through a number of different paces, where not only do we have the vaccine itself that is within Ad26, but we’ve added a protein component to it, to give it even more oomph. And it’s – oomph isn’t a technical words, but it’s really – it’s a powerful immune response that we’ve been able to induce against RSV and now we have Phase II data called the CYPRESS study.

That is very exciting data and FDA has granted us breakthrough designation based on that data and asked us to submit additional safety information from an ongoing Phase III as part of maybe a – as a registrational package. We will also of course have efficacy data from our Phase III, but right now we will be a company that we hope are one of the leaders. We have a couple other companies that are coming forward with great products as well, but we will be a leader that has multiyear data, so durability data and hopefully what turns out to be really robust data against types of RSV data out there.

Laura Sutcliffe

So I guess there are a few different questions. The first is your vaccine is constructed somewhat differently. For instance, we’ve got a – from the other two main contenders out there, we’ve got us a plain subunit vaccine and then we have an adjuvanted subunit vaccine. Is it a case of wait and see or are you sort of confidence there are some benefits to the way that you’re constructing the vaccine?

Dr. Mathai Mammen

I always, never want to get in front of data and so this year’s a big data year for all of us together, and you know I never – I always think of its patients first and so patients have not benefited from any RSV vaccine all this time, so let’s see how it goes. The features of our vaccine are that a pure protein vaccine is particularly good at drawing an antibody response, but those kinds of vaccines sometimes don’t have quite the durability over the years, so – but I would say let’s just wait and see and see what the data looked like, both on the immune side and of course the efficacy side.

Laura Sutcliffe

So, I suppose the potentially related question, when everyone has data, nobody will really have data over multiple seasons or…

Dr. Mathai Mammen

We will

Laura Sutcliffe

Not – will you have enough data then to say this is an annual vaccine or this is something longer.

Dr. Mathai Mammen

We’ll have several seasons’ worth of data.

Laura Sutcliffe

Okay, which is potentially an advantage, because some of us won’t have that.

Dr. Mathai Mammen

Potentially, yeah.

Laura Sutcliffe

I’ve just been handed the iPad back, so possibly the iPad questions are working again. So if you’d like to have a go submitting questions on the iPad, please do. I should also mention that Jessica Moore and Rachel Cooper from J&J’s IR team are here as well. So if you have questions which are not from the R&D questions, we can get those answered for you as well, but save them to the end if you don’t mind.

Okay, final question on the vaccines front then, so hindsight 2020, but what have you learned from the COVID efforts? These have been sort of accelerated, concentrated. There must have been something in there that you can learn and take from sort of vaccines R&D going forward.

A – Dr. Mathai Mammen

COVID is devastating a situation that’s been for everybody, for all of us. It has had silver linings within our company and multiple companies and we paid very close attention to what’s been possible.

As an example, there are many things operationally with the use of data and analytics that we’ve wanted to do, want to do and we were on our way to get there, but with COVID given that we couldn’t, we didn’t have options. COVID serves as a catalyst for us to just go very quickly to those solutions we want. For example, our ability to do trials where the patient doesn’t have to come to a site or our ability to use heavy data science to locate where subjects are that might have a disease and make sure there is a site that’s there or ways of collecting patients where the patients actually are.

Amazingly you would think that’s kind of obvious and that should always happen, except that the way clinical trials generally operate among companies is through relatively well known PIs, investigators, and those aren’t – there’s sometimes a disconnect between where the data tell you one should be and where you end up. So this was a catalyst to go beyond networks of relationships and so forth, to be able to use Data Science to accelerate clinical trials generally, both through technology and through patient finding.

There are many other learning’s that the company has had on processes that we shot right through for our COVID vaccine that now we say there’s no going back on. So we’ll continue in this new nimble, even more agile way from here onwards.

Laura Sutcliffe

Can you give us an anecdote to about nimble and agile?

Dr. Mathai Mammen

Yeah, I mean it’s – in any company, any group of people there are stakeholders and there is decision making processes. Right now we have highly streamlined some of those and how they work for particular programs that where speed is everything and weeks might matter.

Laura Sutcliffe

I think we’re probably coming closer to the sort of Ngen piece that you mentioned at the start of our discussion. Could you just maybe help us sort of put some meat on the bones there and explain to us sort of how you’re running this Ngen, what it’s been delivering for you and how it’s shaped? What we can see when we look at the J&J pipeline on your sites or on your website?

Dr. Mathai Mammen

Yeah, so what’s visible on the outside is a fraction right off what’s happening. Overall with regard you see the portfolio and you see projects that are in mid-phase or late phase development, and so let’s just start there. Like we are – we’ve radically changed and evolved this portfolio. As we said late last year and it remains, it remains correct right now, we are committed starting last year through 2025, end of 2025, registering or filing for 14 products that we believe are really important, like with the average figure sales of $4 billion for those 14 products.

We’re on top of that seeking to continue to build on products that are very important, that are in line marketed products with 36 new filings for new indications and new uses for these products that will change the impact in a big way that the products would have. So those 50 products if you will or indications if you will were very much on track for. So that’s the portfolio and that’s what’s seen.

The Ngen behind that, both impacts the near term, our ability to execute, like decrease execution risk on those projects, but in addition continues to evolve what we can do. Loss of exclusivity, which is on everyone’s mind is part of what we do. I tell my team, our goal is to reinvent the entirety of our portfolio every 10 or 15 years. Every 10 or 15 years we need an entire new portfolio, so the Ngen becomes everything, and so right now I’m very pleased about for starting in development, how we think through and evolve the regulatory signs.

For example, I’ll talk about data science with respect to the regulatory science. You know, we had a lot of talk over the years of synthetic control arms, external control arms and using single arm studies or predominantly or to augment randomized control studies with external data drawn from our interactions with the healthcare system in general in the real world.

So that’s a lot harder to do than it might sound on the surface and the predominant reason for that is, two. One, when you randomize in a clinical study, you do – don’t have to think a lot about what factors you’re controlling for, because there’s randomization that takes care of it. And second, the endpoints in a clinical trial can be whatever you make it. They can be quite particular bespoke measurements that don’t happen in the real world, but you can take care of it in trial.

When – if to use, you have to solve both those problems for external control arms and what our company has been able to do and in close collaboration with the regulators is use very advanced methods for propensity matching and for convincing ourselves that have a high bar on what denotes rigorous data. And we’ve been able to have multiple successes in oncology and outside oncology for external control arms. That is – there is two main impacts of that, that I would say that’s part of our Ngen.

One is that you can go faster. You can – if you don’t or can reduce or not have an external control arm in the years to come, that can be a big advantage. The second is in many – in oncology say, there’s not one standard of care, right. But in the clinical trial you’d pick – you’re not picking 10 standards of care, you pick one typically. So the way you go from a regulator to a payer then is to develop evidence sets that your drug is preferred over other standards of care.

If you can develop through Phase II and Phase III the right real world endpoints that correlate to rigorous endpoints, and validate them on route to registering the product, then as you gather evidence for payer conversations with multiple countries and within the United States, you’re on much surer footing, because you have a legitimate way to compare your products without further evidence generating the trials. So that’s another way that the Ngen is very important to us as we generate these methods and ways of thinking and pathways with regulators.

If you look further back in early development and in research, we also see really good evidence of the Ngen. So one of the pieces of science that I emphasize at Janssen generally is immunology. Immunology has gone through a terrific revolution over the last five and 10 years and it’s become far more specific as a read of who you are and your status. You know your immune status gives rise to all sorts of things. Every one of our therapeutic areas has an immunology group, now. So not just autoimmune inflammatory group, but every one of our therapeutic areas, from infectious disease to neuroscience, to cardiovascular and metabolic disease has an immunology group, and that is a very distinctive way that the organization thinks, and has collective power that I think not a lot of companies have.

The second major things that I’d point to is that we have – we’ve used data science also in that realm. You know for identifying an appropriate patient – what is an appropriate patient for an IL-23 inhibitor. Like right now diagnosis mostly happens clinically, you say that someone has Crohn’s Disease or you have some other clinical diagnosis. But as data evolves on what denotes – your drawing a boundary around responder or a non-responder, we can define patients in a way where if we run them in a clinical trial, the probability is much greater of a positive effect, because you’ve pre-defined that group, and the effect sizes tend to be deeper, and so you’re doing more with your medicines in a more efficient way if you run it that way. And there’s – and people I think automatically think, well, that’s precision medicine and you’re splitting all these groups, but there’s as much lumping as splitting when you think rigorously through patient identification and try to match them with mechanisms.

Like one example of where we’re doing that is in our neuro psychiatry group. So depression for example, there are drugs and you know it’s technically a generasized market, but the drugs don’t work that well, and unfortunately many of us know. And so matching or defining patients that are respondwes allow first of all more efficient manageable trials and demonstration of superiority in clear ways. And so how to do that and how we’re thinking about that with different mechanisms we can talk about if we wish, but that’s an example of drawing boundaries around unwanted phenotypes or diseases that are more mechanistically related. Data science is critical, it’s at the center of that.

Another important way we use data science is to identify patients at all for rare diseases. A really good example of that is in pulmonary arterial hypertension. You know unfortunately like many of us have learned what PAH is, probably somewhere along our training, but you know probably half the physicians wouldn’t recognize it if they ran into a patient with PAH, and the unfortunate consequence of that is many people are diagnosed with a disease like that at autopsy. And so it’s not – its they never had a chance to get treated with effective medicines.

So what we’ve done is we’ve said, okay what’s the best way to address this problem. We have to be able to use something that’s collected in real life, like as they live and interact with the health care system, and we picked a variety of potential data sets and what we found is the use of ECGs was where the magic was. Where we can look at 12 lead ECGs and even outside of a physician’s ability to diagnose PAH, and because it’s hard to see in there, even an experienced cardiologists, but the machine learning algorithms with enough training data have been remarkably effective at picking up PAH and flagging that this is possible. So that’s a collaboration, a great internal group and a terrific company, and we’ve worked together to create that algorithm and it’s a software deployment on top of standard data that’s collected.

And then even further back, about how to discover molecules in the first place, the path of various barriers that might get in the way, we’ve – using images and other methods and analytics on top of images, we’ve created quite a bit of – quite a bit of promising, like a acceleration I would say to reduce the number of cycles it takes to discover a product, and to shorten the cycle time that it takes to discover a product. So all through R&D, I would say data science is a strong differentiator and that’s part of the evolution of the engine that we have, let me stop there.

Laura Sutcliffe

Those are brilliant insights, thank you. The iPad is working again. We have some audience questions. We have a few audience questions. One of them we can tackle now, it’s about asset selection. Would you consider vaccines in other areas like preventing exacerbations associated with human rhinovirus, pan-species immunity has been a real challenge here.

Dr. Mathai Mammen

Yes, so the way I think about infectious disease vaccines right now is there’s – for the acute respiratory infections, we have two strategies actually. So maybe I can expand the question a little bit with our small molecule therapeutics as well.

Laura Sutcliffe

Great.

Dr. Mathai Mammen

And so with infectious disease vaccines we try to pick off the most serious, serious diseases that humanity faces first. So RSV is a big one, and within viruses we also look at metapneumovirus and other viruses that are very important. We’re not at the moment tackling influenza virus with a vaccine, but we have a – we’re thinking about pan flu, it’s a hard problem. And then behind that we would think about the broader range of viruses that afflict us. We don’t have a rhino virus vaccine right now, I think that would be much later, and we’ll tackle the very serious viral infections first.

But small molecules, I just want to talk about that for a moment. You know you can treat an small molecule – you can treat an acute infection in principle with a drug like a [inaudible] for influenza, but the challenge is you have to get diagnosed. You probably need a prescription and you need that, and you have a very short window to intervene and make a difference when you have an acute respiratory viral infection.

And the strategy we’ve therefore taken is very different from what others are doing, as the concept of pre exposure prophylaxis that everyone will – where everyone will know from HIV, but we’re applying it to acute viral infections. Meaning, if there is a category of patient that is particularly fragile, if they get an infection or an influenza they may have a problem. What we have is, we have a portfolio now of products for RSV for influenza, maybe for COVID in time where a long acting prophylaxis will yield very high levels of protection for that person, and that’s very different from using a vaccine to stimulate your immune system to protect that person. So that’s our overall prophylaxis effort. We use both a small molecule approach in prep and vaccines.

Laura Sutcliffe

Got it. If we could turn to oncology, we’ve got a couple of audience questions and then maybe in the last five minutes touch on the immunology piece. So on oncology, could you just sort of talk about your experiences with oncology over the last say five to 10 years? Do you think step changes in oncology are going to be harder to come by going forward? I think top of mind is the recent TIGIT failure over at Roche. Yeah, just your thoughts on what we can expect from efficacy improvements in the oncology field.

Dr. Mathai Mammen

So, I think the short answer is we can continue to expect step changes for the next five and 10 years. There is no area of biological science, medical science that has more effort in it right now than treatment of cancer, understanding cancer, treatment of cancer in both, understanding particular drivers of cancer that come through mutations, and through use of the immune system to treat cancer. There will be many failures as many hypothesis are being pursued simultaneously, but there are many successes as well and we’ll see them.

They won’t – they are not predictable like when they come, but my suspicion, my every expectation is we’ll see a lot over the next five and 10 years and it’s the reason why half our effort is in oncology. And we have distinct approaches, we think are distinct of how to approach oncology. For example, localized treatment for bladder cancer, for early stage bladder cancer, creating regimens that are complementary to one another as opposed to single products, sequencing them or a use of regimens as combination therapies and in many diseases and we try to take a distinct approach whenever possible.

Laura Sutcliffe

And then a specific question in an area where you have been successful – it’s actually an audience question, but very similar to one I have in mind. What’s your view on Carvykti potential and earlier lines of treatment, including the transplant in eligible population, as well as potentially replacing stems cell. What’s necessary to move into the front line setting and is the reimbursement environment conducive?

Dr. Mathai Mammen

Yeah, so Carvykti Cilta-cel we think is a very unusual BCMA CAR-T cell and the reason we’ve tried to understand and we’re still understanding frankly, why it’s this effective. And what we think it’s got to do with, and there may be other reasons as well is the binder. Is the way – this is a bivalent binder. It engages BCMA in a particularly high avidity manner, and can we believe see low levels of BCMA on tumor cells and for that reason you can have deep effects. And plus the whole signaling machinery, and there are many other parts of how it’s constructed and then made that could easily be contributing as well to why it’s this good.

So what we continue to see is that it’s a – it’s got a very durable response even for a quite patient experience – I mean treatment experience patients, and so therefore we’ve gone down the lines all the way to, as you alluded to, treatment, transplant ineligible and transplant eligible patients. We are running those trials right now.

So CARTITUDE-1 through now seven and eight they are running and they’ll read out over the coming years at different times. And my hope and expectation is they will be – it will be an effective treatment for even very early stage tumors.

Now what would be the challenges that we have to overcome there, we’d like to make this a regimen that’s very, very well tolerated. It’s a powerful therapy, the CAR-T cells in general, and so how to manage cytokine release syndrome and any other effects that the therapy might have, we’re good at that now and we’ll continue to get better. Perhaps we’ll identify ahead of time which patients using data science can – which patients may be most at risk for that kind of side effect or who are the best responders, we’ll learn that over time.

One thing that’s necessary, I think absolutely necessary as we learn to manufacture the product much more efficiently. And so a major effort on my team is a combination of automation of what we do right now through partnerships and internal work, but also just understanding the science of what we’re transfecting. Like there are many T Cells that we remove from a patient and we transfect all of them.

So are there smaller and smaller subsets that are necessary, that give most of the efficacy and are safe as possible, that would take a lot last Lentivirus. It would be a lot less expensive to manufacture and we look forward to the advances, the leaps forward we can have to make the cost of goods much lower. And the turnaround time from when a patient, physician and patient together decide they want a treatment to getting the treatment, which is too long.

Laura Sutcliffe

Could you just talk a little bit about the durability piece, because we have got the response and we have durability of response and the likelihood is I think that you can treat with BCMA only once; at some point it will shed. What’s your sort of – what’s your view on being able to create something that’s efficiently durable that it really can be used in the first line.

Dr. Mathai Mammen

Yes, so the shedding of BCMA is a theoretical problem. We haven’t seen that as a source of treatment failure really, but it’s been for years right now, the conversation and how to stop the shedding and so forth, but we haven’t seen that play out. You will presumably, like you know cancers cancer and there will be a portion of people that relapse, and our goal is to understand why they are relapsing. Is it because the tumor is avoiding the CAR-T’s that are still present or is it that the CAR-T cells are going away, and then what you do with that depends on what you see, and we’re preparing for anything as we watch for who might relapse.

Q – Laura Sutcliffe

Okay, fascinating. We could go into this topic for ages, but let’s move on to immunology in the last five minutes. A question I have from the audience on your FcRn. I know you – the line is you tend to have a best-in-class asset with nipo. The [inaudible] product has had a very good launch in myasthenia gravis, you have a study on that, but your otherwise sort of not too much overlapping with the [inaudible] clinical trial program, so if you could just give us your thoughts on that field and what you aspire for your FcRn?

A – Dr. Mathai Mammen

For nipocalimab, nipocalimab you know here again, just like with RSV vaccine, I do wish all people with health that are developing drugs in this space, because it’s a terribly difficult aspect of the immune system that no one has hackled yet. Like we think of the innate responses and the adoptive responses as mostly what the autoimmune disease therapies have tackled, but the actual antibodies that are pathological, this is the first go.

So we’re together I would say as companies that are in the space, figuring out how to treat the – sometimes the entirety of the population like myasthenia gravis or the appropriate subset of a population, like I suspect might be rheumatoid arthritis, where not every one of the rheumatoid arthritis patients which trial we’re underway on will have a strong pathological autoantibody piece, but how to figure that out and to go forward.

Our strength as an organization is going to be – we have a great product and we’re going to figure out disease by disease, the right regulatory path and the right sub-setting mechanisms, so that we’re maximizing effect size for those that we choose to treat.

Our GenX has a great product and they’ve chosen a different set of diseases largely and based on their hypothesis of where pathological antibodies are important. The good news is, I think that if you sum up all of our efforts, there’s probably like double that of the number of places one could use an FcRn antagonist. So it’s early days in this mechanism and let’s – hopefully everyone will make progress.

Q – Laura Sutcliffe

Super. And then another audience question here on immunology. Some data outflow by some other [inaudible] earlier today, just maybe your thoughts on the future of IL-23 field and sort of use in preservation of prescribing in that field.

A – Dr. Mathai Mammen

Yeah, so I go back to the general statement of what I tell my team, like every 10 or 15 years we need an entirely new portfolio. So loss of exclusivity per se is known – we knew about loss of exclusivity obviously like a decade ago, and so – and that happens at a regular clip and big portfolios, there’s always those dates coming up.

So every one of our products is selected based on our understanding of what will be you know inexpensively available and we need an unequivocal promoter bill advantage with any product that we have, and that’s the name of the game. It needs to make a meaningful difference to a person.

So we believe our product Tremfya right now is a strong inhibitor of the IL-23 pathway. We believe it as a product – and we’re starting to release date along these lines. It as a product distributes in a very good way to sites of inflammation and it’s durability of response is very good. So we believe Tremfya will be a fantastic play in the IL-23 place as an antibody.

On top of that, I would like to highlight, we talked about this late last year. We’ve made progress on an oral small molecule that is an inhibitor of the IL-23 receptor. That is looking good and this is a very serious effort within the team. We have a lead that’s in Phase II right now. We have a follow-on product of a different nature that’s a little bit further behind, we have a robust space in this class and we think we are leaders in the oral IL-23 receptor space. So between Tremfya and that program, we believe there is lots of good to do for patients in the IL-23 pathway.

Q – Laura Sutcliffe

Okay, and then I think just one more here in the last minute. Your myeloma franchise, could you just talk a little about your appetite for a next generation CD 38 and what you’d need to kind of go down that pathway and also the role for the bispecifics that you have say to teclistamab and so on and so forth.

Dr. Mathai Mammen

Yeah, so multiple myeloma, we have DARZALEX our CD38 inhibitor now in a subcutaneous format call DARZALEX FASPRO. We believe it’s a great product and the uptick is terrific and it’s used in the way that we were hoping. We don’t plan on currently ourselves with the next-generation CD38. We believe there is more mileage for our resources invested in other mechanisms. So obviously if we have a partner in Genmab that’s looking at a next-generation CD38 and we are doing that study together, so let’s see how that goes, but where I’m interested in is using other mechanisms and other approaches.

So we have Carvykti right now; we have Teclistamab, which is CD 3 BCMA bispecific that’s coming, and we have Talquetamab, which is a GPRC5D CD 3 redirector. GPRC5D is a very interesting way of targeting T-cells to multiple myeloma and that is not a particularly crowded space. We don’t see lots of others pursuing that epitope.

We do also believe that for CD 3’s to be their best, they need to be combined potentially or used alongside activating mechanisms for the CD – for the T-cells that do come in, so we’re looking at more combination regiments to treat people that are on CD 3 directors going forward, and that’ll be part of our own portfolio of approaches that might be used together. That’s important I think, because this is an area where you know the barrier to entry of making a CD 3 redirector isn’t particularly high, so the differentiation comes from how we do clinical development, how we gather evidence, the wall of data that we can put up and the potential for creating regiments that are partially or wholly owned.

Laura Sutcliffe

Perfect! I think we are just about out of time. So Dr. Mammen, thank you so much for being with us today.

Dr. Mathai Mammen

Pleasure.

Laura Sutcliffe

And everyone else, enjoy the rest of the day too!

Dr. Mathai Mammen

Thank you very much.