All right, good afternoon. I'm Eric Joseph, Senior Biotech Analyst with JP Morgan. Our next presenting company is Nurix Therapeutics, and presenting on behalf of the company is CEO, Arthur Sands. There is a Q&A session after the presentation. If you got a question, we'll bring a mic to you. For those tuning in via the webcast, you can also submit questions via the portal. So with that, Arthur, thanks for joining us.
Thank you. Thank you, Eric, and I'd like to thank the entire JP Morgan team for inviting us and for another great JP Morgan conference this year. I will be making certain forward-looking statements, and I, we refer you to our filings with the SEC regarding the risk factors that face our business. So at Nurix, we are focused on targeted protein modulation, a new approach to making small molecule agents that can do one of two things: either harness an E3 ligase, as pictured here in the center of the screen, harness it in order to degrade specific protein levels, this is targeted protein degradation, or inhibit a ligase, a particular ligase, which will result in elevation of cellular protein levels in a very specific way.
Now, the reason this can be achieved with this target class of E3 ligases is that there are over 600 E3 ligases in the human genome, and they have very specific functions, all of which center on modulation of protein levels. This is a natural cellular system, and with our small molecule drug engineering approach, we can, again, either harness this system or enhance it to achieve therapeutic outcomes. So we first directed this powerful technology, and we've been working on this for over a decade here. We're based here in San Francisco at Mission Bay. But we first targeted this technology in the area of oncology, specifically BTK, Bruton's tyrosine kinase, where we have led the field in applying targeted protein degradation to B-cell malignancies.
What we've identified and we've published on and continue to expand on is that these degraders have the potential to displace the BTK inhibitor class of agents, which have been very successful, but have certain liabilities, which include resistance mutations that are accumulating to these, these drugs. With degraders, we can tackle those resistance mutations, and we can also tap another part of the BTK signaling pathway, which is known as the scaffolding function of BTK, which is a structural component of the cell through which growth signaling can occur in B-cell malignancies. Secondly, in 2023, we were very excited to expand our therapeutic focus into inflammation and immunology. We have multiple programs in this field now, and we'll be speaking more about those in the future.
But the first one that has been licensed to Gilead was part of a drug discovery alliance with Gilead, actually, and it's a degrader of IRAK4, which was licensed in 2023. And it is being developed by them now in rheumatoid arthritis. We have our own plans for our lead BTK degrader, NX-5948, in autoimmune disease, and we plan to enable this molecule for potential IND filing in autoimmune disease this year. And thirdly, another major accomplishment this year, this past year for Nurix was the signing of a really milestone, a first-of-its-kind agreement to use targeted protein degradation as payloads on ADCs.
Certainly, the ADC field is very advanced and been very successful, but this is the next generation, known as degrader antibody conjugates, where a degrader molecule is the payload, as opposed to a classic toxin of some type. This lends itself to forming a new targeted, highly targeted cancer therapeutic class of drugs. Pictured here is our pipeline, which has now grown to be quite substantial. Of course, today I will not be able and have time to talk about all of these programs. I'm gonna focus today, my today's remarks on our BTK degraders, NX-2127 and NX-5948. But we are advancing NX-1607, which is an inhibitor of CBL-B, one of those over 600 E3 ligases, specifically focused on immuno-oncology here. By inhibiting it, we can raise the immune system.
We have multiple undisclosed products in development with Gilead, Sanofi, and Pfizer. The first one that, again, that we have disclosed with Gilead is the IRAK4 degrader, which is now we're picturing in this category of this growing group of I&I programs at Nurix. I also will only mention briefly the new, it's listed here now as Pfizer collaboration, but which was formed at Seagen. So these are targeted protein degraders. I'm picturing here how this functions and why it's so powerful. These are bifunctional small molecules, so they're small molecules that have a small linker region, and one portion of the molecule binds to a target, in this case, BTK in blue, and another portion binds to the ligase, in this case, the cereblon E3 ligase.
These bifunctional molecules bring the target in, in proximity to the ligase, which triggers the ligase's natural function of ligating, attaching these ubiquitin peptide sequences to the BTK protein. This serves as a signal for destruction by the proteasome. So this is a very efficient process and a very powerful process, one of the reasons being that the molecules, once accomplishing this degradation, can recycle and go to degrade another target protein. So one drug molecule can degrade many target proteins. This is fundamentally different PK/PD than you see with an inhibitor. It's one of the reasons why we think degraders have such a potential advantage over inhibitors. So specifically, what are those advantages, to enumerate them? Well, in the case of BTK, the big picture, as we titled it here, is that degraders have the potential to displace this inhibitor class.
We have evidence that we can overcome treatment-emergent resistance mutations from the inhibitors. This is a very important and very serious event when these occur in patients, and we've enrolled many of these patients in our trials. Again, we can eliminate the scaffolding function, this additional growth signaling pathway of BTK, and we think we can expand this market into autoimmune diseases and be the first to enter a BTK degrader into the field of autoimmune diseases. We have two of these degraders.
NX-5948 is a pure BTK degrader, a highly selective BTK-only degrader, while NX-2127 is a dual degrader of not only BTK but also the IKZF1 and IKZF3 growth signaling transcription factor pathways, which is the same pathway that lenalidomide has targeted so successfully in NHL and other B-cell malignancies. So in this cartoon, we picture why this destruction or this degradation of the BTK protein, as you see here on the right, is superior and how it actually provides the scaffolding function elimination. With inhibitors, the BTK protein still exists, and the scaffold, it exists with a number of other cytosolic proteins, and growth signals can continue to signal down these pathways. By degrading it, this is eliminated.
With regard to resistance mutations, what you're looking at here is what we call a heat map for cell killing. The most potent cell killing is at the top here. This is a nanomolar-level cell killing with NX-5948 across a variety of the actual resistance mutations that we've cloned out, and put into cell lines in order to test them compared to all the inhibitors. So these are some of the more common, resistance mutations to all of these classes of inhibitors. Of course, the first generation being ibrutinib, you can see it has failed most commonly because of a C481S mutation that forms at the binding site for ibrutinib, but also the L528W is a very important resistance mutation.
But all of these inhibitors, the next generation and now the non-covalent, they all have their blind spots here in this ability to kill these mutational cells. So this one, you know, non-clinical figure shows you the molecular basis for our belief that we can, in fact, ultimately displace the inhibitors in the marketplace. And it is indeed a very large marketplace. We're looking at now over $8 billion in sales combined. Ibrutinib here in the darker shades, starting to lose market share to some of the newer entries. These are covalent, next gen, acalabrutinib, and zanubrutinib. But again, we believe that the degraders are a truly differentiated approach that ultimately can eclipse most all of the inhibitor class, if not all of them. Now, we state here with degraders, resistance is futile.
I'd like to qualify that a little bit. There's always ways for a cell to gain resistance abilities to a drug. But what you want is a drug where it's, it fundamentally more difficult to become resistant to that drug because of the nature of the way the target is hit and how it is removed in the case of degradation from the cell, and we believe that's what we're witnessing with these degraders. So how do we see both of these molecules over this landscape of the B-cell malignancy marketplace? So chronic lymphocytic leukemia, or CLL, is one of the largest markets. That's also indicated by the size of the circle here. Waldenström's, marginal zone, and mantle cell lymphoma are also important BTK-driven tumor types.
We see NX-5948, and we list it across the top as covering potentially all of these as a monotherapy, and furthermore, being moved up to earlier lines of therapy, so second line and then ultimately first-line therapy, if we're able to displace the inhibitors. It also has potential in the more aggressive NHLs, such as DLBCL, in combination with other agents. NX-2127, we see more as a late-line drug. It is that dual-acting agent, and so it is already a combination agent in a single pill, if you will. And these dual mechanisms may have a particular advantage in DLBCL, and I'll share with you some of our data from here that encourages us that this is the case. So let me start with NX-5948.
In its current trial, we have two dose escalation protocols going on here, one in CLL. This is the most recent dose level. We've achieved 200 mg once a day, oral. And in NHL, we're already at the 450 mg QD once-a-day cohort. We intend to also include a primary CNS lymphoma, a very serious disease, as we have evidence that NX-5948 crosses the blood-brain barrier. I'm just noticing this timer is not actually working up here, so if I'm running over, I mean. Okay, thank you very much. Seems like I have lots of time. So, let's see. I skipped a slide. From a safety standpoint, we have an excellent safety profile. NX-5948 was very well tolerated in the trials.
Very few Grade three or greater adverse events, but most notably, we have witnessed no atrial fibrillation or hypertension, which has been identified as a risk for BTK inhibitors. So it's early, but this is a very favorable profile to start with. Showing you here the PK on the left, the blood levels of the drug achieved in patients, and then what you're looking at here is this very rapid and robust BTK degradation on the right, and you can see even at the lowest doses of this is from a blood draw in patients, we basically eliminate the BTK protein, and this works in 100% of patients. This is now looking at the waterfall plot. You're looking at reductions in lymph node size, and so we see. Okay, great. My timer now says 11 minutes. Is that actually what's left? Okay.
Is that about right? No. Okay. All right. I'm gaining time now. I've got them up to 26 minutes then. Anyway, I'll focus on the slides. The lymph node reductions are substantial, and again, all patients are experiencing this. Furthermore, anecdotally, we hear how patients feel better within the first week of dosing on the drug, and if you remember on that degradation slide, BTK comes down. Within two days, it's already basically eliminated from circulation. We had approximately 40%, 42% PR rate, stable disease, 42.9. We expect several of these to progress to PRs. And so early on, six out of seven patients have experienced some clinical benefit from this initial trial.
This is looking at the duration of therapy in the swimline plot, and we're already approaching almost a year of therapy with some of our CLL patients, and most of them actually have stayed on treatment and continue in treatment. In DLBCL, or, I'm sorry, NHL, so this includes many forms of non-Hodgkin lymphoma, we see substantial lymph node reductions. These are very advanced patients, also very heavily pretreated, but still, a PR rate of approximately 21%, stable disease of 21%, and some very interesting long duration of therapies in NHL. So looking good at the early stages. We're eager with NX-5948 to expand in CLL, and we are doing so.
First going to complete, of course, our dose dose escalation trial, but we're already recruiting new sites and planning for the dose expansion, and that's one of our goals for 2024, identify the doses to expand. But this slide captures our longer-term vision for development of this agent, and CLL in the, in the highlighted box here, really offers probably the most, the largest and the most direct path to first approval. Pictured here, we think there's a potential for second-line, therapy, demonstrating superiority to a current, a standard of care in this, in this category, which would be a major marketplace. And then ultimately going head-to-head to, move degraders to the frontline.
And again, the goal there being faster responses, deeper responses, and a lower resistance rate occurring and suppressing those resistance mutations. One thing that was interesting at ASH last year in December was all those mutations that we see actually exist in patients from very early on in their therapy. They're there in the background, and then they are selected for as the therapy is administered. So really, many, many patients are vulnerable to this resistance mutation story. So we see opportunities in MCL as well, and DLBCL. So the grand vision would be to launch several phase III when we're ready to move this to again, second or frontline in some of these major indications. Also not lost on us is the opportunity in autoimmune disease, which is perhaps even larger than the oncology opportunity.
What you're looking at here, in the red and blue lines, are NX-5948 as compared to many benchmark compounds, and you can see that we, in this arthritis model, completely block the inflammation process. On the right, very interestingly, in multiple sclerosis model, we're in blue compared to purple, which is Gilenya, a very potent drug, a very successful drug, but one with toxicities, and we can see that NX-5948 performs very well. This is further evidence of NX-5948 crossing the blood-brain barrier. We know also we degrade BTK in the microglial cells of the brain, which are the inflammatory and immune-responsible cells. This year, we're really excited to enable this IND indication.
This will require additional preclinical toxicology studies, which are already underway, and a healthy volunteer study. Then we'll be in a position to consider an IND and an autoimmune indication. I'm gonna turn to NX-2127. This is in both CLL and NHL. We have expanded NX-2127 at the 100 mg dose cohort level in CLL, and we're at the 300 mg dose level in MCL and DLBCL. So this drug started first in its development and really gave us proof of concept over the degradation mechanism. And as it's evolved, looking at lymph node reduction here in CLL, you can see the vast majority of patients showing lymph node reduction, and we expect NX-5948 will even better this in CLL. But this is really quite a nice result.
This also gave us the first resistance mutation data, which is in the asterisks here. These are patients that harbor these growing resistance clonal lines, and we're able to address those. When we first presented NX-2127 in ASH 2022, we had a 33% response rate. That's now up to about a 41% response rate, so it's growing over time. And again, we think that that reflects that we see more responses with time, and that NX-5948 can easily do this, if not better, for CLL. This is getting a little bit crowded as a swim lane plot because we now have a good number of patients here.
But I think the main take-home here is we've had patients now over two years on therapy, and we've seen significant responses. In NHL, the very aggressive lymphomas, we've seen complete responses, partial responses, and also long duration of therapy. So we're very encouraged by this profile as well. We do, however, just to be clear, think that 2127 dual activity will probably be more of an advantage in NHL than in CLL, and that's why 5948 is going to be prioritized in CLL. You know, these all these patients are not just, you know, lines on a graph. This was our most recent complete response patient that we reported on.
In the red circles here, you see very significant lymph node growth at baseline, and then after eight weeks of therapy, all the lymph nodes are gone. She continued on therapy for over 16 weeks, and then since she really had no signs of disease, stopped therapy. As of our last contact with this patient and her investigative site, she remained in complete response even after having stopped therapy. This is quite an encouraging result. Again, as I mentioned, we're really focusing on DLBCL and MCL for 2127. We think it has certainly, we've seen already, potential for responses, complete responses in relapsed refractory setting.
Again, remember, this is a once-a-day oral pill, so these are patients that have either had CAR T and failed, or are not eligible for CAR T, or have had transplant and failed, or have had bispecific antibodies. So this is a very advanced patient population group, similar for MCL. We do have strategies where 2127 could move up in lines of therapy in DLBCL, and the real, the real goal, I think, for the field would be to identify a non-chemotherapy-based first line, 'cause right now that's Rituxan or CHOP, a successful therapy, but very old therapy with a lot of toxicities, and then other lines of chemo as well. And so we think in, and with the right strategy, we could, with 2127, actually move to either displace or augment our CHOP.
So it does have some frontline potential as well. And then I'd just like to close out with talking about our latest deal with Seagen, now Pfizer, in the DAC space or degrader antibody conjugate space. So just first off, on the mechanism of this, so what is a DAC? I described it verbally earlier, but of course, here's the antibody on the right, and it is an antibody that is conjugated to a degrader, a targeted protein degrader, against a specific target. Now, this is obviously not drawn to scale. Our small molecules are much smaller than the antibody. And so we're working now with the Seagen team, but now Pfizer as well, to engineer these molecules. So we are responsible for creating the targeted protein degrader. These are against certain targets.
It's exclusive around the cellular target that we're degrading, and then working with their linkerologist to create these combined molecules. So the deal terms, $60 million upfront, so very significant upfront. $3.4 billion in potential research and development milestones. This is a big number for most deals, and the reason it's large is that the way this works, one of our degraders could be attached or conjugated to many antibodies. And so under the deal terms, each one of those would be a separate product opportunity. And so there are multiple product opportunities, which could yield multiple streams of milestones and revenues. So we really think this could create this whole new class of drugs, for the ADC world or what will become the DAC world.
We do maintain options on all of our deal programs, and so these take the form of an option for Nurix to opt in after human proof of concept into cost-profit sharing relationship in the United States. And this is for two products out of this particular collaboration. So a new era for ADCs that we think with degraders. You know, it also does something for us in our pipeline, which gives us access to large molecule pipeline as well, and so not just small molecules in the future. And this has, I think, a lot of implications for the longevity of some of the value generation of large molecules versus small molecules.
Certainly, that would be very challenging for Nurix to do alone, but with a partner like Pfizer, we can actually bring these things forward and then exercise, hopefully one day, our options. Just to close out here on summarizing our major milestones for 2024. Number one, for 5948, I think most eyes are focused on 5948. We'll present our phase I-A updated data this year. It'll support our phase I-B expansion. We anticipate expanding this year at least two doses. We'll accelerate our phase I enrollment overall. We're opening sites in Europe, the U.K., and the United States currently, and we'll complete our IND-enabling studies for the autoimmune disease. For 2127, we will resolve this partial clinical hold.
I didn't mention that earlier, but this is something we disclosed in November. This is because we've embarked on a new manufacturing process, which gives us a chirally pure form and a commercially viable form of the drug, and to introduce that into the clinic will be a goal for 2027. NX-1607 will present our phase I-A data, not only as monotherapy, but also in combination with paclitaxel, and select a phase I-B dose for expansion. And on the research front, we expect to identify a new clinical candidate, a new degrader, targeted protein degrader candidate, either from our internal pipeline or with our partners, and we do anticipate achieving substantial additional research collaboration milestones throughout 2024.
These milestones are shown here in green, and the upfront payments from all of our collaborations in blue here. And you can see that, this does amount to a very significant source of non-dilutive capital for us and one that has grown consistently over the years. We do have $329 million in cash, but that is. If you add in the $60 million upfront, that, that includes that $329 million, okay? So that, that puts us in a very strong cash position. And this is a summary of all the deals we've signed.
So part of our business development strategy is to be able to build a pipeline, with partners and have these 50/50 options or, or cost profit share options available to us while we're getting non-dilutive funding to achieve that, growth of our pipeline. Our internal wholly owned pipeline is also advancing its three programs, and we do anticipate, as I've already alluded to, significant, milestones over the coming year in 2024. So with that, I, if my timer is trustworthy, I left us 13 minutes to talk and, take questions. So thank you very much.
Great. Thanks, Arthur. And just a reminder, if folks have questions, just wait for the microphone. But, Arthur, maybe just to pick up on the collaboration agreement with the DAC collaboration agreement with Seagen, now Pfizer. Perhaps I could get you to sort of expand on how this approach sort of complements the activity or the, yeah, the activity profile of TPDs alone. I guess, is it a play that would sort of, I guess, the tropism versus with an antibody conjugate allow for perhaps a better therapeutic window you might achieve with the targeted degrader alone? Or is it more to kind of perhaps go deeper or give Seagen, Pfizer, additional optionality where there are already players with their ADC platform?
Well, definitely, Pfizer sees this as a real path of innovation in ADCs, which have centered so far on toxins, traditional toxins that attach to antibodies and have been successful. So in this case, this would be a highly precision medicine approach to ADCs. So the delivery of the ADC, or of the degrader on board an ADC, could target in a very specific way a cancer driver protein that would otherwise be too toxic to create a traditional small molecule, too. Now, by way of example, for example, RAS or MYC, these are very interesting growth driver targets, and we all know they're involved directly in cancer, but they have been very challenging to treat with an adequate safety profile.
Now, headway has been made, but I'm not saying those are targets in the Seagen collaboration, but that's an example of the kind of oncogene driver target that would be otherwise very difficult to degrade. So that's one category. Another category are those targets where really there's no active site, so a traditional small molecule can't work. So really strong growth drivers, but also no active site. Those have been basically off-limits to drug therapy, and so we could address that category as well. The targets that we would select are all highly genetically validated through oncology and genetics, but that would be the two categories.
Plus, I think it would increase the therapeutic window, as you mentioned, because the ADCs with the current toxins really, if they break off and are widely, you know, spread, they are truly do carry deficits. So that could be overcome as well. So it's a very interesting new way. It'd be easier drugs to handle also, I would say, in general, medically.
Sorry, just, and just to clarify, the scope of the collaboration is primarily just within oncology, or are there other fields outside of oncology that you might look to explore within the agreement?
Yeah, we're focused on oncology.
Yeah.
Yeah.
Great. So I guess just going back to the update with your pure BTK degrader NX-5948, you presented an update at ASH there. And it is a study where dose escalation is ongoing. I guess, given sort of the, you know, the high levels of degradation you're seeing so far at 50 mg, I guess, can you just talk a little about sort of the. What's behind the incremental efficacy that you at least seem to be trending towards so far at the higher dose of 100 mg? And whether you think that you expect, you know, further dose gains, I guess, in efficacy as you continue to dose escalate.
Yeah. So, you may have noticed that even at the lowest doses of 50 mg once a day, we get basically complete BTK degradation, but that's from a blood draw, so that's in the bloodstream, that's not in the tumor. And so we think we do get increased efficacy with better tumor and tissue penetration of the drug, which does take higher doses. And now, having said that, at 50 mg, we also have seen clinical responses. But I do think these tumors, they vary greatly in their mass, and therefore, the tumor burden can be better covered with a higher dose, and it varies between patients. So you have to account for that at your higher dose. You want a dose that can really handle the full spectrum of the types of patients we get.
And so tumor burden is a factor. The other factor are those resistance mutations that do argue for making sure those are adequately covered, thoroughly covered by our drug. We know our drug does cover them, all that we've tested, but you need to have a, an additional efficacy window above a certain, degradation target level. So those are two of the rationale: tissue penetrance, tumor penetrance, covering thoroughly covering all the resistance mutations, so you suppress resistance all along the way in CLL. So I think we're close now. You know, and for NHL, we were at the 450 mg dose level. On our slide, we list one more dose level, which is 600 mg.
I think we're gonna look at the totality of the data, and I think we'll find that in terms of the higher upper dose level that we'd expand at, we're probably either there or, you know, almost there. And then the idea would be to pick a lower dose as well. So the FDA would like to see two doses under Project Optimus at in meaningful expansion cohorts, so you can then really select the Optimus or optimal dose. So we'd expand at two levels, but I think we're already looking at those levels, you know, that we've shown, so.
I guess in terms of the types of patients that you've been, you know, you, you basically have been enrolling NHL and CLL separately in parallel with one another, CLL being a little bit behind, nevertheless, seeing responses in both cohorts. I guess, ultimately, do you anticipate perhaps, you know, two different doses being pursued, one for CLL, differing from that being pursued in NHL? Or, ultimately, you'd want to harmonize that with a single dose for both the subpopulations.
If I were to speculate now, I'd say different doses for two different histologies, CLL plus all the others. And the FDA has indicated that they would like to see different doses for different histologies. These diseases are very different from one another, CLL being primarily a liquid tumor, although it can have also mass disease, but NHL definitely being solid base lymph node disease. So they are different and will likely take different doses. NHL likely would take a higher dose, may require a higher dose. We have included primary CNS lymphoma patients in the 5948 trial. That may require higher doses to make sure we get the kind of brain penetrance that we've seen in the animal models and see efficacy. So that's how we're thinking about the different histologies with regard to dose.
Okay.
It's really lovely work, Arthur, and thanks so much. It's Jake Kushner from.
Oh, my! How are you?
Yeah, nice to see you. Great work,
Thank you.
As I think about the Seagen deal, and I think about essentially the platform that you've developed to conceivably target a vast array of proteins, it seems like you could do some really creative things. For instance, deliver a molecule that could cause very precise tissue-specific death, say, by unfolded protein response, by knocking down BiP or GPR78, things like that. Really creative toolbox. I mean, it's spectacular. And obviously, it's very nice to have Seagen and Pfizer as partners, so I look forward to seeing how that folds out.
Well, thanks, Jake. Yeah, I think this field is going to be quite large of DACs. And after we announced that deal, we did see a couple other deals get done. I think one with BMS and another one with Merck, I believe, but with other companies. So, the awareness is there. We know Genentech has worked on this. There's been initial publications, but to really drive it into the therapeutic category, I think it does take teaming up with an expert like Pfizer now in this area, because you have to have the exquisite potency and directed antibody binding to particular tissues, as well as the exquisite potency and engineering of the degrader. And I think this team that we've formed really brings sort of the top class groups together to do that.
So I believe it does have great application in the future, and we see this as a high priority for us. From a portfolio standpoint, I just wanna mention again that this does give us a large molecule potential in addition to a small molecule potential in a partnership mode. But that has profound portfolio value creating implications over the long run.
Maybe just picking up on that final point here.
Mm-hmm.
with the last question. I guess really just how to think, the deal was, is very recently signed. I guess, how to think about perhaps just, you know, perhaps the first development candidates being brought forward from that collaboration?
So we haven't really forecast timing, but the idea would be that to move as quickly as possible. I think we signed the deal in September. It's probably unrealistic to have a development candidate in the first year of the collaboration, but I wouldn't put off the second year. So, we'll have to have future, more refined estimates of that, Eric, as we go further into it. What I can say is I really was excited to and attended the kickoff meeting of the scientific teams, and both sides are very enthusiastic, and it is very exciting. Already preliminary data, some of which Seagen has generated on their own. So we're off and running, and we will keep you posted.
I hope we could give more, also scientific updates as we go, not just wait for development candidates and development updates. So we'll work on that as well.
Is business development of this sort the type of thing we should expect more of in the next 12 months?
Of this in the DAC space? Well, all I can say is.
Not necessarily DACs, but just with, you know, collaborations with your platform, perhaps another.
Oh, yeah. No, you know, to be successful, really, it's a team sport, and so we're big believers in smart collaborations that also involve shared ownership of rights, so there's high value there. A compound like five nine four eight, I think, with the right partnership, would be a far more valuable product, far more valuable from a cash perspective, and for patients, get to more patients, if we were to team up rather than if we were to try to just do it 100% ourselves. So, we can create much more value with partnerships, I think, especially with the breadth of opportunities for 5948 .
Okay, excellent. I think we'll leave it there for time. So thanks again, Arthur, and thanks everybody for attending.
Thank you.