All right, thank you. Good afternoon and hi, everybody. My name is Eric Joseph. I am Senior Biotech Analyst with J.P. Morgan. Our next presenting company is Nurix Therapeutics, presenting on behalf of the company. It's my pleasure to introduce CEO Arthur Sands to bring us through the story. There's a Q&A after the presentation. Just raise your hand. We'll bring a mic around to you for those who have questions. Then for those tuning in via webcast, you can submit questions via the portal. With that, Arthur Sands, thanks for joining us.
Thank you, Eric Joseph. I'd like to thank the entire J.P. Morgan banking team for inviting us to the conference. These are our disclaimers. Just to cap 2024, it was another terrific business year at Nurix Therapeutics as we continue to move our pipeline forward. I think some of the highlights are put here on this slide. The upper left, I think we really ended the year on a very strong note with our presentation at ASH most recently with regard to NX-5948, our pure BTK degrader being developed in CLL. We have completed the phase Ia dose escalation. Not only do we have the robust efficacy signals in CLL, but also Waldenström's, which we reported a little earlier in 2024 at an international Waldenström's conference.
We have also made really significant regulatory progress, both with the FDA and EMA, with now two Fast Track designations for NX-5948, one in CLL and one in Waldenström's in the United States. And we also gained PRIME designation from the EMA, which puts 5948 in a very strong regulatory position as we advance with the goal of starting pivotal trials in 2025. With regard to other compounds in our pipeline, we advanced NX-2127, a very interesting dual degrader of BTK and IKZF1/3 in very aggressive lymphomas. And also NX-1607, a first-in-class CBL-B inhibitor, CBL-B being an E3 ligase. And I'll just hit some of the highlights of these programs as we go forward. We really made great progress as well with our significant partnerships, three of them, Sanofi, Gilead, and Pfizer. A lot of interest here in the STAT6 degrader program with Sanofi.
This has made terrific progress towards a development candidate. And as well, our IRAK4 degrader with Gilead, which is in IND-enabling studies with Gilead. These are two programs that we've been working on for really now approximately four years or more in our drug discovery alliances with those two companies. And then we also have made great progress in our Degrader Antibody Conjugate Program, a really unique program initiated with Seagen to create degrader molecules as payloads for antibodies and a whole new class of ADCs. So we look forward to future updates in that category. And we ended the year in a really strong financial position with just over $600 million in cash. So we'll be discussing our pipeline a little bit more broadly, but I do want to give you how we think about building our pipeline in this slide here.
So in the first category, our BTK degraders represent our approach to hitting clinically validated targets like BTK, where resistance mechanisms are emerging, and also where scaffolding function of the protein has not been addressed by existing inhibitors. And we're seeing some of the great results we're seeing in CLL because of this strategy of attacking these targets with a degrader mechanism. Secondly, there are those targets like IRAK4 where the inhibitors do show some signs of working, but they're not hitting the target fully or strongly enough. And again, we believe this illustrates the scaffolding function as being critical to remove the protein being superior to inhibiting it. And then third, there are a category of what are the undruggable targets or historically undruggable. And these are targets like STAT6, which is a transcription factor with no real classic active site.
But with our degraders, we can remove those transcription factors and address the unmet medical need in this category in type 2 inflammatory diseases. So for those of you who may not be completely familiar with degraders, just let me walk through how these work. These are bifunctional small molecules with two binding moieties, one that binds to a target protein, imagine this purple protein being BTK, and then the other side of the molecule binding to an E3 ligase, thus creating induced proximity and event-driven pharmacology, which leads to ubiquitination onto the target protein, signaling it for destruction in the proteasome.
And so this is a very efficient catalytic process, which means that one drug molecule can degrade many target proteins and recycle within the cell, which from a pharmacology standpoint means less drug on board can hit the target and hit it harder by removing it rather than inhibiting just its kinase function. Now, how does Nurix develop all of these agents? And we have multiple as you'll see on my next slide. We develop what we call the DEL- AI platform, which is an integration of DNA-encoded libraries to find molecules that bind to these targets, to E3 ligases as well as novel targets to degrade, but also to use our machine learning capabilities to optimize those targets very efficiently. DEL gives us the kind of large data information to make machine learning usable in a drug discovery setting, DEL being, of course, DNA-encoded libraries.
So we screen our targets with billions of compounds encoded by DNA. And using those DNA barcodes, we can decipher using AI what the patterns of binders are and actually predict ultimately new binders to new targets and ligases without potentially even running a physical screen just through the DEL- AI capability. So this is a new rollout for us here at J.P. Morgan. But we do intend to describe more about DEL- AI when we do our research day later in the year. And it's been very productive. Here's our total pipeline. And as you can see, we have many programs in the oncology space, which is at the top half of this, and then a growing pipeline in our I&I space as well. So moving really rapidly forward using our technology.
So let me now turn to the lead program NX-5948, which addresses this very large market opportunity in B-cell malignancies, primarily CLL. And what's pictured here are the current incumbent inhibitors and their sales over year over year. So this is now approaching a $10 billion a year market. And our goal is to use degraders, which we think can be superior to these inhibitors, to displace the inhibitors from this market, actually, and build new markets, not only in B-cell malignancies, but also in inflammation and autoimmune disease. And I'm speaking specifically about where we think NX-5948 can go. So why do degraders have this advantage or this potential? We can overcome resistance mutations, and we're showing that in the clinic. We can address the scaffolding function of structural proteins, including BTK and transcription factors. And we're seeing great clinical efficacy so far.
Let me just show you some of the highlights from ASH from this trial. Primarily, we have data from our dose escalation portion, although we now are in the upper right-hand corner here in the dose expansion to phase Ib/2 with NX-5948 at two dose levels, 200 milligrams once a day and 600 milligrams, and we're also expanding in other B-cell malignancies, marginal zone lymphoma, Waldenström's, and follicular. Just a quick look at the patient demographics in the CLL trial. I think what I'd like to point out here is, first off, very heavily pretreated patient population, about four prior lines of therapy. Essentially, all of them have had a BTK inhibitor, and that therapy has failed them, mostly covalent, but also, interestingly, a good number of non-covalent as well, about 20+% of non-covalents.
These patients also have failed BCL-2 inhibitors, mostly this being, of course, venetoclax, but also wave of smattering of CAR-T and other therapies, so heavily pretreated. And then you can see the mutational spectrum. These are very important resistance mutations in the case of BTK, about 40% of our patients, and other poor prognosis mutations, 40% of p53 and other mutations as well. So heavily mutational burden population. And the beauty of NX-5948 and its degradation mechanism is pictured here. So the different colors represent these different mutations that we've identified within our patients in the trial. This is BTK levels measured in our patients from a blood draw, which starts at day one of the trial. And you can see their starting points for BTK levels.
And then you can see, regardless of the mutational status of BTK, basically all the patients respond in terms of degradation to this drug, giving us a really substantial and encouraging response rate here as early as eight weeks, here being 75% plus of patients showing response to NX-5948. And then if you evaluate patients that have stayed on 16 weeks or the longer on therapy, that number goes up to 84%. And this is in a very advanced patient population, again. So we're really encouraged by these results. And we think that this can be extrapolated as we grow this trial and move into pivotal studies. If you look at lymph node reduction, it becomes even more obvious. This is one of my favorite slides. So on the Y-axis here, you're looking at lymph node size.
You can see virtually all the patients are showing some type of response to this drug. Then this orange outline, these patients, these also have CNS involvement from the disease, a very difficult to treat situation. We get a great response there. Then you can see the smattering of BTK mutations and other mutations. We have not seen any mutational profile that would tell us about resistance yet to NX-5948. This is really quite a great result for us. I won't delve into details here on the safety profile. This was all presented at ASH, but really we have, we think, a superior safety profile, which does bode well for the expansion of this trial and ultimately moving into earlier lines of patients in CLL.
But also in Waldenström's, this was data we presented at the international workshop in Waldenström's in, I think, around October. And again, we see this 78% response rate. So this further corroborates the effects of NX-5948 in CLL, but in Waldenström's macroglobulinemia. This is looking at the waterfall plot from that small group of patients, but the green triangles here are all the responses mounting. And we expect to follow this trial forward and to expand in our Waldenström's phase IB cohort, which is actually ongoing. So I mentioned some of these regulatory milestones already. I won't repeat them, but we're really excited about expanding this trial. We're working in opening up France, Poland, Italy, and Spain. And these are going forward, have gone forward in 2024, as well as moving and taking advantage of our Fast Track designation in Waldenström's.
Let me just talk about some of our early plans for our first pivotal studies. We do think there's an accelerated approval opportunity in this post-BTKI BCL-2 inhibitor population. We are also actively planning a randomized control trial as a confirmatory trial, which would be a head-to-head against a suitable comparator to then gain full approval based on the accelerated approval. But we have great ambitions to move into first line plus scenarios, both monotherapy, which would require a head-to-head study with NX-5948 against existing BTK inhibitors, and as well as then combinations with a BCL-2 inhibitor, likely venetoclax. So we envision a suite of trials starting with trials one and two pictured here, but as fast as we can, really opening up all four trials. Right now, we're focused on one and two in the first half of 2025. So that's a quick summary of NX-5948 in oncology.
We're also very excited about moving NX-5948 into immunology and inflammation. And so let me just give you a few words about that and show you a little data of why we think it has such an advantage. So BTK is, of course, a very central node in signaling in B-cells, but not only B-cells, but monocytes and other cell types. And really, by inhibiting the kinase, we're really not taking out the full function of this in autoimmune disease. And we do believe that we have an ability to take the same advantage of scaffolding function and move that into autoimmune disease. What are some of the evidence that supports this? So on the left here, you're looking at our comparison of NX-5948 in dark blue to some of the inhibitors that are currently in autoimmune disease trials, rilzabrutinib, evobrutinib, and acalabrutinib as well.
You can see by these potency curves; we get 10- to 100-fold greater potency in blocking B- cell signaling as measured by CD69 as compared to these inhibitors. Not only that, but we get to deeper levels of blockage of this signaling. We think this reflects the fact that we're removing the protein. This is the scaffolding function showing itself to us at the cellular level. It's not only in B-cells, but in myeloid cells as well. This is, again, a 10- to 100-fold greater activity with a degrader compared to inhibitor. That's the kind of advantage we think we can bring into patients into this autoimmune setting. It's fueled by what we've learned in oncology. This is the BTK degradation by dose level from our oncology trial. You can see that really we get basically complete degradation.
So this gives us, for autoimmune, a really wide dose range to choose from. This is why this is important, because different autoimmune diseases are likely to require different doses. And then, of course, I think established the scaffolding function as being very important. I did mention that we do have activity in the brain, and we've seen great results in those patients with CNS lymphoma. And so having activity in the brain really does open up things in autoimmune disease like MS. And our safety profile, we think, does actually bode well for autoimmune disease. And we've learned, of course, this from our oncology trials. So what are our next steps to move NX-5948 into multiple B-cell indications? So we've outlined opening of an autoimmune hemolytic anemia arm within our CLL trial.
There are CLL patients that get autoimmune hemolytic anemia, also known as WAHA or warm autoimmune hemolytic anemia, and so we're in the process of opening that cohort to accomplish proof of concept, and then we are contemplating an autoimmune IND in non-malignant hematology indications for autoimmune cytopenias, so a very logical place to start. In the heme system, we get rapid readouts. There are great biomarkers to see effects within these indications, so speed to getting data is critical to us. We're in the process of conducting a healthy volunteer study assessing a new formulation. This is underway. This will give us, again, this broad range of doses and formulation to use in a very wide spectrum of autoimmune disease, and we see future indication potential expansion in dermatology and also neurology.
As I mentioned, with our BTK activity, MS, I think, is within the realm of possibility for NX-5948, so NX-5948 has this potential to be this sort of pipeline in a product, if you will, both in oncology and in autoimmune disease, but we have more than that, than NX-5948, of course. I mentioned IRAK4 at the beginning. This is progressing well with Gilead. This is some of our preclinical data that was presented recently at the American College of Clinical Pharmacology. It was a Gilead poster, actually. We also had a separate poster on our BTK NX-5948 in autoimmune disease, but this is a very potent degrader. This is, again, a category of drug where inhibiting IRAK4 has really not proven itself to be sufficient, and by degrading it, we can really hit this master regulator of the toll-like receptor and interleukin-1 receptor pathways.
We're looking forward to great progress with Gilead on this program. The concept of the expectation is to have an IND filed. Gilead is planning to file that in the first half of 2025. The other area of great interest, again, is the STAT6 degrader. This is really gaining a lot of attention, this target, because it is a key transcription factor in the JAK-STAT pathway. It acts downstream of inflammatory cytokines, IL-4 and IL-13, and is a clear driver of the TH2-mediated inflammatory responses for allergy, asthma, and eczema, and many others. It has been considered an undruggable target historically. Of course, all of this is really made more compelling by the success of Dupixent as an extracellular way to hit this pathway. This design category is to be an oral version of Dupixent, if you will, and have broader reach potentially as well.
So that covers some of our small molecule degrader applications. I'd like to just wind up here with a shout-out to our degrader antibody conjugate team, or DACs. I'm going to preserve plenty of time for Q&A with Eric Joseph. But this is such a great, really remarkable use of our technology. So basically, we're using degrader molecules as payloads on antibodies. And this has been a concept in the field that really hasn't moved forward, I think, until we really had the potency level that we need for these degraders. Because the key for a payload to work on an ADC or DAC is it has to be hyperpotent. And indeed, most of the payloads have been simply toxins, which are hyperpotent, but they're also extremely toxic even when attached to an antibody. But with this approach, you have double targeting.
You have the targeting of the extracellular antibody, which enables entry extracellular to target with the antibody, entry of the antibody into the cytoplasm of the cell and into the lysosomal compartments, and then liberation of the degrader antibody, the degrader payload, to then trigger that catalytic degradation of the target. So really, we have, I think, the best partner in the world for this program. When we signed the deal, it was with Seagen, of course, that evolved into a great deal with Pfizer. We're working really effectively with the Pfizer Seagen team to build these molecules. It had significant cash upfront. It had multi-billion dollar potential. There's many products that can come from this. You can imagine one degrader payload could be put on many antibodies.
Also, as with all of our deals, we preserve cost-profit sharing like we do with the STAT6 and with the IRAK4 program with Gilead. We always preserve that. We can opt in once we see human proof of concept with any of our partnership deals. This is just one bit of data on this, and then we'll close and go to Q&A. We really think that this can provide really exquisite selectivity. ADCs occupy a certain space here. The antigen does provide cell and tissue selectivity, but the toxin does not provide any specificity. Degraders, they provide a lot of specificity, but they're going to hit every cell in the body like any small molecule, oral molecule.
If you combine those and look for that space in between, this is where the DACs can really take the best of both worlds, the targeting of an antibody and combine it with the targeting of a degrader. Does this work? That's what the data is here on the right. Let me walk you through this. In light blue is a BTK degrader, a plain unconjugated degrader. You can see very potent degradation of BTK in B-cells. In purple is a BTK degrader linked to an anti-CD19 antibody, so directed delivery to the B-cell in purple here. Now, if you take that degrader, and instead of putting it onto an anti-CD19 antibody, you put it onto an anti-HER antibody, obviously, you're not going to hit the B-cell.
We've proven that if you expose this to B-cells, you do not see BTK degradation in any substantial way. So this proves B-cell-directed specific degradation of BTK via a DAC. Of course, we're working on other targets than BTK with Pfizer. But I can just tell you that we're seeing very similar results with those targets. This is a very exciting way to have the most exquisite, potentially, oncology-targeted agents really in the industry. Let me just close on a couple of notes of, again, strong cash position. We're funded to really hit on our key initiatives in 2025. I think top on the list is the pivotal trials for NX-5948 to get those to lift off. I covered those already. Secondly, expanding NX-5948's potential in additional cancer indications, but also most importantly, I think, in autoimmune disease.
And then move IRAK4 and STAT6 forward as rapidly as possible with our partners. And at the same time, advance our other wholly-owned pipeline, NX-2127 and NX-1607. And then tell you more in the future about DEL AI and this great platform and how we can broaden our discovery position. And of course, we always run a tight ship, and we maintain our strong cash position as we go forward through all these great events in 2025. Now, just to close, I do want to acknowledge some of you may have noticed that we've been using a new logo on all of our slides, and we have a new website. This is actually the old logo for Nurix, which was great for the decade plus that it served us.
When Nurix was founded, by the way, it was out of really breakthrough science from UCSF and Berkeley, where a Bay Area company. And the flame was to denote lighting the way into a new area of drug discovery. Because you have to believe me, when we started on this ligase-mediated drug discovery, no one believed us. In fact, the first company to believe us was Celgene. And we did a big deal with them. And that's because they have Revlimid, and they've been working in this space. But we were lighting the way, and I think we've done that. But we're rolling out a new logo as of really today. And so here it is as it transforms, hopefully in front of you. So this is the new logo. And let me explain this and why we've made this transformation. So first off, it has mechanistic meaning.
So each block here represents a ligase, if you will, binding to a target. So two proteins coming together. The N represents a bifunctional molecule that actually makes that happen. The other advantage for this is that it really is more of a patient-friendly, healthcare-oriented logo that you could see on a bottle of pills. We just couldn't see the flame on a bottle of pills, and it was kind of problematic in advertising as well. So this has really been a great transition, and it has a lot of meaning, and it's going to serve the company well as we go forward. So thank you all very much, and we can do Q&A.
I like the space. So yeah, for any questions that the audience has, just raise your hand, and we'll bring the mic over. But let's just kind of pick up on the NX-5948 and CLL, particularly as it relates to your pivotal trials getting underway, both as part of a single-arm trial and with an active comparator. Maybe just kind of orient us around sort of the getting steps to final dose selection, perhaps going into both of those studies. And as it relates to the randomized trial, what ultimately are you kind of considering as a potential comparator there?
Let me just start with the dose selection part. We have expanded at the 200 milligram and 600 milligram dose. We believe these doses are aligned with Project Optimus as per our end of phase one meeting with the FDA. That project being a requirement now to dose optimize early, and the two doses you select need to be sufficiently distanced in terms of PK. We went with 200, where we're seeing great responses, and 600, which is about a two to threefold PK increase over the 200. It satisfies that requirement. But also, it has a safe profile. We can't see any different safety profile so far at 600 versus 200. We need to see the results of the phase Ib/ 2 of the pure 200 versus 600, which is what we're doing now, and that'll enable future dose selection.
We think it may actually enable a range of doses to be used ultimately with this compound because of the safety profile, so that's the answer to your dose selection. In terms of the comparator arm, that's a big question, and our goal is to determine that in the near future, again, in discussion with the FDA. The randomized confirmatory trial, whatever the comparator arm is, it needs to be approved agents in a second-line plus situation, so the accelerated approval would be third-line plus. For the comparator, we want to move up a line, so we're looking at those agents that could serve a global trial, and different countries have different drugs approved and different histories in terms of their prescription tendencies, so we're considering all that, and we'll update you when we can.
I'm going to try and follow up on that with.
Okay. I didn't really answer the question.
I wonder whether, just to try and narrow down some of the considerations here as a comparator regimen, would the idea be to just kind of weigh whether to kind of have a physician's choice as a comparator regimen, or do you want like a standard single comparator in a pivotal?
We're looking at both options. The advantage of investigator's choice is that it is seen as a more real-world situation. In this second-line plus, what that boils down to is chemoimmunotherapy, so something like bendamustine, rituximab, which is still widely prescribed in that setting, or potentially pirtobrutinib, which does have accelerated approval and may gain full approval. We're weighing that. Of course, pirtobrutinib is not approved everywhere. I mean, it's going to primarily be U.S. and parts of Europe to start with. We really have to weigh what is the real-world situation in terms of comparator arms. Investigator's choice between some of these may serve that purpose. Now, you lose some control when you do investigator's choice because they can choose, but it is really the way medicine is practiced in those settings. There are some advantages.
Yeah. And venetoclax's, I guess, single agent, does that factor in at all as a consideration, or is it more kind of?
So it does factor in. It's actually trial number four on our list of four trials to do a combination trial with venetoclax. And so that would require another perhaps safety dose escalation run-in with venetoclax, selecting doses in combination and seeing how this behaves. I think people will be very excited about a degrader in combination with venetoclax because these inhibitors have driven some pretty deep responses in that setting, and the degrader could do better.
Question from the audience.
Hi. Thank you. So I have a question for the DAC, the next generation. So in comparison with ADC, the first step, because you conjugate the antibody to degrader, so the CMC of DAC will be more complicated than ADC. That's the first one. The second one is how to differentiate for different indication applications later between ADC and the DAC? Yeah. Thank you.
Did you get most of that, Eric Joseph, that question?
I didn't quite hear you.
Could you repeat the first part of that?
It says CMC.
Oh.
CMC.
CMC
Oh, okay. For a degrader?
Yeah.
Yeah. So degraders are mid-size small molecules. So they tend to be 700 +. So CMC can be a bit of a factor in terms of manufacturing. We've overcome those. We don't have any issues with NX-5948. And it ultimately will be cost of goods similar to a small molecule once you get the scaling right, which we're working on. So that's not an issue. And the second part of your question?
As application, indication, application later comparison CMC.
So that is why different indications and different applications, that is why we're looking at different formulations, because we do think, especially in autoimmune disease, that different doses may be required in the spectrum of autoimmune diseases.
A bit of a competitive dynamic between yourself and another BTK degrader. I guess as you look to launch your pivotal studies, how do physicians view the relative clinical profiles between yours and BeiGene's BTK degrader? And what levels, excuse me, levers do you see to kind of keep recruitment pace as your pivotal programs get underway?
Yeah. We shared the podium with BeiGene at ASH. It was a very exciting session. It was a packed room and an overflow room. I think it reflects that there's a lot of interest in seeing what's happening with these two degrader programs. It has been, I think, excellent to have BeiGene with us and actually providing confirmatory data, if you will. We were the first to move into this space. But for many years, we were the only one talking about BTK degradation. I have to say it was fairly difficult to convince people. But with BeiGene's entry, it's actually helped, I think, the entire field and the awareness levels and the enrollment rates, to your point.
I think it's really excellent to have, when you have a novel mechanism of action, to have confirmation, independent confirmation, a second company, expert in the field company to show that this does actually work and works really well. Really, it's been a positive.
Just outside of CLL, as you kind of look to expand into immune and inflammation indications, and in some ways, one of your programs looking at warm AIHA secondary to CLL is a bit of a bridge towards doing that. I guess just stepping back, how much of the safety data generated today in CLL is kind of leverageable to I&I indications? And even specifically within warm AIHA, is some amount of the existing data gathered so far potentially de-risking for the activity profile in warm AIHA?
So definitely it is de-risking because even in our CLL program, we're seeing elevation of hemoglobin levels. We're seeing elevation of platelet counts as people's bone marrow recovers. And that is seen as a signal of bone marrow recovery, but it's also maybe seen as a component of CLL really is an autoimmune killing of some of these other cell types, including neutrophils. So we think we've got strong rationale from the oncology trial. The safety profile fits. Obviously, it's a stepwise approach, which we think is wise as we move into autoimmune disease. And then we could foresee going non-oncology heme as a next step. And that is, as I mentioned, a lot of advantages because of the accessibility of the blood compartment and the biomarkers that come with the territory, hemoglobin levels being really what you measure for approval. And the unmet medical need in warm AIHA.
It's really quite significant. There's a pool estimated of around 50,000 patients. It's really primarily steroid use and treatment. And if you had a targeted therapy that could really restore people's hemoglobin levels, I think it would be terrific. So that's how we got into WAHA and our stepwise approach.
And so you're evaluating a new formulation or additional formulation of NX-5948. Maybe just kind of talk a little bit about sort of the pharmacological parameters you're optimizing with that formulation. I mean, there's probably perhaps both clinical and commercial considerations driving that new formulation. Or maybe that's not the case, but perhaps you can kind of speak to the sort of rationale to evaluate a new formulation.
Yeah. So let me address that. So these degraders, as I mentioned, are relatively large small molecules or mid-size molecules. So they, in general, are not absorbed well orally. That's one of the problems. But there's a lot of compounds that are in that category. And so then this motivates additional formulations. Now, our results are so excellent, honestly, with our response rates in CLL. I don't expect an additional formulation to impact or improve that. We're already at the very top end of this. I mean, it's quite impressive in this patient population. So the motivation would be we would improve cost of goods, potentially absorption, and maybe make it a more versatile agent in some regards, depending on food or no food. So we're getting into this next category of optimizing the drug. And we're starting it early. And many companies might start life cycle management later.
Because of the autoimmune indication, I think this is emphasized as potential. But let me give you some numbers just real fast. I think we have enough time. For example, our blood levels of NX-5948 in CLL are 5,000-fold lower than pirtobrutinib's blood levels. And they're about 100-fold lower than ibrutinib. So we don't get much drug in, but it doesn't take much degrader drug to actually get these effects we're seeing. So we can optimize PK, but we're already really hitting these targets very hard. I think it would mainly be an improvement in cost of goods, potentially. I don't think it really is going to affect efficacy that much, to tell you the truth. But just to think about how much more effective the degrader is at much lower blood levels.
I think that speaks to the potential improvement in safety window over inhibitors because inhibitors have to sort of flood the system and stay bound to that target the whole time. That's what we're looking at, PK.
Okay. Well, we talked about one question here in the corner.
One question?
Yeah.
You can shout. I'll repeat it.
I'm just curious about conversations with BD interest. How do you think about autoimmune CNS kind of expansion? Any push from the BD community on where to go next?
So we have a lot of interest for autoimmune use from the BD side of things. There are a lot of BD meetings here at J.P. Morgan. But I think that the groups at these large companies are very different from the oncology group. So it's like a different product discussion, frankly, in the business development realm. Thank you.
Okay. All right. We'll wrap it there for time. Thanks everyone much for joining the session.
Thank you.
Thank you, Arthur.
Thanks.
Yeah.