Bexobrutideg, which we call Bexdeg for short, being a degrader. We've got an important new suffix on there to indicate it's a degrader. So I'll be calling it Bexdeg NX-5948. Okay. Bexdeg. Okay. Yeah, Bexdeg. Yeah. Awesome. So, maybe just to clarify, this EHA day will be focused on the phase 1A, more mature data, but not from the phase 1B expansion cohort for CLL. Right. It'll be on the 1A cohort, not the 1B. Okay. When should we see, start to see the 1B data, later this year? Yeah. The goal is, you know, by the end of the year to have that data set, which will essentially complete the disclosure on the phase one program. Got it. and as you know, we've had our end of phase 1 meeting already, and this is now to complete that disclosure. Got it. Okay. Since we mentioned the end of phase 2 meeting, because that's one other focus from the investors is the, what's the registration of paths forward, right? Because you potentially can have the accelerated approval for a third plus line, but also people wanna know what's the earlier line strategy based on your interaction with the FDA, what, what you can disclose right now, and then when we're gonna have a formal update for that front. We'll have a formal update on our next steps for pivotal studies in mid-year, and that's consistent with the guidance we have for our timing that allows us to include feedback from the FDA in terms of the design and dose level for that study, those studies, plural. That'll be mid-year, and we believe we'll have everything ready to first talk about a single arm phase 2 study in CLL in the double exposed population, so post BTK inhibitor treatment and then post BCL2 inhibitor treatment. That's where we have fast track status. We'll talk about that strategy and that study. After that, there will be a discussion on the confirmatory randomized phase 3 study in CLL. We'll outline those two programs, first the single arm, and then followed by our refinement of our plan for the randomized control arm. Our goal is to have all that in place this year. Mm-hmm. Okay. Good. And then, it seems the regulatory update not gonna be happening at the EHA, but also still kind of, potentially ahead of your formal phase 1B data updates. How should we think about the sequence of the event, before we see the expansion data? You will tell us the registration or path for third plus line and then versus the earlier line. Is that the right way to think? Yes. I think it'll be important, from a timing perspective for us to, first reveal the phase 2 and phase 3 plans, the regulatory update, and then, you know, it'll be followed by the data, you know, that drove those decisions later in the year. Obviously we wanna go as fast as we can to get these studies up and running. Key is to get the regulatory feedback, have a regulatory update, get those studies running, and then we'll present in major medical conferences the data associated with those. Okay. So the data will really continue upon the medical meeting and then updates will from your corporate event. Yeah. More of a corporate update and regulatory update. Got it. And then, given the, one of the key aspects of the regulatory update is the dosing, right? We know you are doing this 200 and 600 milligram. How should we think about when you give us the design of the phase two or phase three, you will tell us which dose you will go. And then the implication is, you know, basically you'll see the data in real time. So you already made the decision which dose you will pick before we have the data, full data. Yeah. I think, I mean, we will, as a company, obviously be examining the data soon, as soon as we can, and that'll inform our dose selection decision as well as interaction with the agency around Project Optimus and the dose. You know, both doses continue to look very similar. Certainly we get complete BTK degradation with both doses, in fact, almost all the doses that we've tried. And we see a similar safety profile between the two dose levels. I think, you know, the distinguishing features, you know, probably will be very subtle, if there are, if there are any, and it'll probably boil down to a medical sort of overall judgment, you know, about doses. There's a lot of ways we could go. Got it. Okay. That's why you can make the decision even before you see the full data, right? Yes. So you probably will see the early data. Okay. Good. And then, another key topics, we, you know, probably you also have with the FDA, with the investor is the, what are the active comparator for your confirmatory study in earlier line. What's the current thinking? We know you've guided it before at some high level, but what's the current thinking based on maybe some additional discussion with the FDA, maybe with your investigator? What is the appropriate active comparator for the earlier line confirmatory study? Yeah. Our current thinking really is consistent with our past thinking, which is number one, we would prefer to engineer and design a global study, one phase 3 randomized control study that could serve as being appropriate for many different populations, different countries, where there may be different standards of care, different approved agents as potential control agents. We have to take that into consideration. I think number two is that you want it to be certainly very relevant for U.S. populations too, whatever control arm, however that's designed, so that obviously that's the primary market. We're targeting the U.S. We have a very large number of U.S. investigators who are very interested in the study. We are in the midst of, you know, meeting with investigators, getting a lot of feedback on this phase 3 to design something that'll be very attractive and really serve all the constituents for the program. At this time, we're not ready to disclose that. I'd put that in more of a Q3 timeframe. Mm-hmm. Along with our regulatory update. Yeah. Okay. Very good. And then maybe, you know, you have a few other things and let's just move on to the next. So for this, Bexobrutideg, Bexobrutideg. Bexdeg. Bexdeg. Yes. Bexdeg. We know you also have some cohort in the NHL, maybe more indolent parts. What, what, when should we see some updates from there and what's the plan for there? Yeah. So we've, we provided some updates on the Waldenstrom's group, which looks quite good and actually shows consistently, you know, approximately 80% response rate like CLL. Waldenstrom's being the closest NHL indication really to CLL and as an indolent lymphoma. Mm-hmm. We have accumulated quite a bit of other aggressive lymphoma information and data, and we've seen activity of 5948 basically across all of the indications. There, it's a matter of prioritization and really more of a combination approach to therapy in those aggressive lymphomas. I think 5948, we clearly have activity across all the subgroups, and it really becomes more of a question of prioritizing which indication and also thinking about the combinations. In the context of CLL, CLL is the number one priority. Mm-hmm. You know, it'd be wonderful to be able to do all these things at once, but that's not realistic. We try to focus our capital where we think, you know, we're gonna have the greatest impact. Mm-hmm. Yeah. Makes sense. You know, prioritization is appreciated by investors as well, right? In the company, you have the limited resource you can deploy, and then, obviously if you're unlimited, you can do everything together, right? Yeah. Okay. Good. And then, you know, BTK in lymphoma and then CLL makes a lot of sense. And also we know BTK inhibitor also works in the INI space, and then seems you may be the only, so far, the BTK degrader, and also try to expand to this INI. Maybe take a step back. What are the key rationale you think a BTK degrader can address for INI indication? And then we talk about the, the development plan. Yeah. We, we, there's so many indications that the BTK mechanism could be good in. Mm-hmm. We have looked across many, and one of the first criteria that we applied is, okay, what is the risk benefit for entering a particular indication? That is, we want to be in severe, you know, life-threatening indications that are really extremely important in terms of high unmet medical need. That is where there is the most demand, and it is obviously where our drug could perform the best because we have seen such great performance in very challenging oncology disease settings. We know that could translate into great performance in very challenging autoimmune disease settings. That is number one. Number two was speed to data readout, so that we could actually assess the, you know, potential in particular indications. Then the third would be addressable large, large markets. Those are the lens, that is the lens we applied. When we applied that, we looked at a warm autoimmune hemolytic anemia, life-threatening disease in the heme space. I think other cytopenias, you know, such as ITP could also be lumped together with that. Mm-hmm. We have opened a cohort, a cohort in CLL patients with WHA or warm autoimmune hemolytic anemia. Mm-hmm. That will give us our first look at the applications there. The other advantage about those heme indications is that the readouts are rapid. You can look for response in hemoglobin levels rising. They are also quantitative, which is very important in autoimmune disease where there can be confounding placebo effects in some indications, and some of the scales are very subjective. Here, hemoglobin is hemoglobin. In ITP, of course, you have objective platelet counts. Those would be very interesting in terms of early proof of concept. Mm-hmm. When you look at market size, they're meaningful markets. They're not huge markets. We are also looking and reevaluating indications like MS, where there is clear opportunity for BTK mechanisms. The recent publications continue to look very promising. Mm-hmm. for inhibitors there. Mm-hmm. We think a degrader that has established CNS activity, which we have with Bexobrutideg, we've seen really dramatic responses in patients with CNS lymphoma and leukemias. That tells us, and we have great drug levels. Mm-hmm. Established in the CSF of those patients. We clearly would be applicable, I think, to MS. Again, as the inhibitors have shown promise there, but it also seems that they're leaving some opportunity on the table for enhanced efficacy, and potentially safety as well. Mm-hmm. Mm-hmm. Seems you can potentially increase the potency or efficacy, compared to inhibitor, for using the degradation. Any risk using the degradation or degrader for INI, compared to inhibitor, as you start to expand to this? Because Bexobrutideg is the only degrader, is a BTK degrader for this INI. What's the reason that other people not trying to do that? There's not been any class specific, you know, degrader class specific, safety issue identified. Mm-hmm. which is excellent. I think that the safety potential of the degrader mechanism in general and Bexobrutideg in particular is that we can achieve complete degradation of the target, at very low blood levels of the drug. As compared to inhibitors, where I'm talking about 500-1,000-2,000 fold lower degrader drug levels than are required by inhibitors. Mm-hmm. To cover the target. That could bring with it a bigger therapeutic window, a better safety window. You have less chemical on board. Right. Some of the things we've seen with the inhibitors are, really some of this liver tox signal, which typically is an off-target, you know, effect of some binding that was not detectable during development or discovery of those molecules. I think there could be a safety advantage there. From an efficacy standpoint, the advantage is, of course, we're taking out the totality of the protein function by degrading the protein, which includes not only the kinase function or the enzymatic function, but also the scaffolding function. Yeah. Which we've established, I think, very strongly. We've actually led the charge on this, that that scaffolding function contributes to BTK B cell signaling quite significantly, more than people realize. Mm-hmm. BTK, Bruton's tyrosine kinase, is not just a kinase. It's not just an enzyme. It's a node, a structural node in the cytoplasm of the cell through which other signaling goes through as well. We would take, we take all of that out. Mm-hmm. That could, that's the rationale from a, you know, theoretical and scientific standpoint, which has been substantiated with data in oncology. That's the rationale that where degrading could be a better approach in autoimmune also. Got it. Okay. Great. You just mentioned you opened a cohort for CLL with WHA. How's the enrollment there? When are we gonna start to see the initial data? How about the non-hem INI cohort? Are the studies gonna be up and running? Yeah. In terms of the cohort that we have open now, we'll be able to, as we see what enrollment looks like, we'll be able to give an update. We'd like to include meaningful patient numbers. It is a subset of patients, and we just have to see at what rate that enrolls before we can commit to a timing on disclosure. Mm-hmm. and then I think in terms of a non-oncology IND and INI, you know, that would be an end of year or beginning of year timeframe. Start the trial or IND, the open cohort, by the end of the year? No, I didn't say that. I said that the IND would either be end of year or beginning of next year. Okay. IND. Yeah. Got it. Okay. You mentioned two indications, WHA and the ITP. Is that also the apply to the non-oncology INI as the priority indication, or you may have some other indication you will be able to do that? I'm sorry. Did you say IT, ITP? Yeah. You say WHA and ITP. Yeah. I, we haven't really outlined plans for ITP. I just mentioned that because it, it's very similar, essentially biology in terms of autoimmune reaction against platelets. Mm-hmm. And the other being, you know, red blood cells. It has been lumped together in studies in terms of basket trials. Mm-hmm. I think that'd be something to consider, but we have not outlined that yet. Yeah. Not off, not formal guidance for ITP. Right. Not formal guidance, just talking. Yeah. Okay. Good. Another example, right? So how these, indication correlate with each other. Okay. Good. So that's your BTK program. We spend most of the time, which is, you know, rightfully do, do so. But you also have this, other pipeline. Maybe excitingly, you recently have some announcement with your partnership, with Sanofi to find the first candidate for the IRAK4, STAT6. Yeah. So, tell us, what's the highlights from that announcement, and then, what's the next step for the program? Yeah. This is a very exciting program. This is our first development candidate, novel degrader of STAT6, within our Sanofi Alliance. NX-3911 is the number, designated for that compound. Mm-hmm. They have extended their license option, which means they now take over the IND enabling studies and ultimately then phase one and human proof of concept studies. Importantly, they fund all of that 100%. That allows us to see that program move forward aggressively with really the right partner who knows this, obviously the space extremely well. At the end of that, the way the deal works is we have an option to opt back in. Mm-hmm. At the end of human proof of concept after we see human proof of concept data into the program for a 50/50 cost profit share in the United States. That gives us an ability to have, you know, very valuable options on a very hot, you know, program, and yet, and yet not fund all of this in addition to our CLL work. Mm-hmm. So that came out Monday. It was, Mm-hmm. Simultaneous essentially with, you know, Chimera's data. Yeah. their first in human data on STAT6, which looked very, very good. Yep. I think got a lot of attention appropriately. Mm-hmm. That was very encouraging for our program as well. I mean, and it was a great day for the STAT6 as a target, you know, as it really advanced the field. Yeah. We definitely applaud the work that they've done there. Yeah. Obviously, it's a good day for STAT6. The timing, I believe it's a coincidence because you guys are probably not talking to each other on the release on that. On the other side, that's the first time we see from Chimera for the human data, even if it is a healthy volunteer. Sanofi already made the decision for that candidate, right? What's the criteria when they select that candidate to move into the IND enabling study? You know, they are probably looking at all the other pre, all the parameters across different programs. This program, I think, was really, you know, a very high bar to qualify as a development candidate, and was subject to multiple parameters being measured and a lot of analysis done by Sanofi, who again knows the space very well, knows what's required. All the benchmarking done on this preclinical study was incredibly thorough. The initial safety studies or toxicology studies, very thorough. This looks like a beautiful, you know, drug candidate. And as we disclose in the press release, we basically achieve gene knockout levels. Mm-hmm. In all the animal models. We include STAT6 gene knockouts literally. Mm-hmm. In our animal models, the 3911 degradation of the STAT6 protein basically takes it down to knockout levels. Mm-hmm. You know, zero. Plus shows the efficacy in animal models. It really checks all the boxes. Again, it was all developed with oversight from Sanofi. Yep. This is a program, you know, that we've been working on in the discovery capacity for five years. So this is not a new program. This is a mature program. Had a great joint scientific team on it, Sanofi and Nurix. Mm-hmm. For several years. It's great to see it advance. Yeah. Great. Now Sanofi taking over the IND and enabling, they probably will, you know, kind of accelerate the development plan. So what's the rough timeline we should look at this program? You know, I can answer that generically, but I mean, you know, typically it's 12-18 months, depending on all of the toxicology package that's put together. We'll have to wait for future disclosures from Sanofi. I did sit in on their presentation today. I was happy to hear them mention the Nurix program and talk about it in excellent terms as part of their future pipeline. That was really encouraging. Yeah. That's absolutely encouraging. Okay. You do have the rights to up and back, but that's after the human proof of concept data later on. Nurix still keeps the rights for significant economics down the road. Yeah. The 50/50 in the United States is a very, very valuable option for us, again, and it allows us to build our pipeline, product right pipeline with a significant product right opportunity, 50/50, and yet not have to fund that stage of the program while we're building our own phase 3 program in CLL. Mm-hmm. In addition to STAT6, we do have a similar structured deal with Gilead for the IRAK4 degrader. Yep. And then we're, as talked about, Bexobrutideg's ability in INI or potential ability. We're building a, really a, I think a very potentially powerful portfolio in INI. Mm-hmm. but doing it in a really capital, you know, conservative way. Yeah. Okay. Very good. You mentioned Chimera, obviously you're a little bit early in the clinic, but when you look at the data, do you think that's a fair kind of a benchmark moving on for the, the new, you know, STAT6 degrader, for INI? Yeah. They definitely set a good benchmark. I think that that's impressive. They shared a lot of data, on not only the degradation, but also biomarker effects in healthy volunteers. I think they did an excellent job of describing it and putting it in context of Dupixent data, when Dupixent was at that stage of development. I think they really provided the public with all the key parameters I think needed with about as much information from healthy volunteer data as you could get, you know, frankly. It was really an excellent job. Yeah. I think Sanofi probably think they may have a chance to be even better, at least from the early stage, kind of, looking at all the parameters. Yes. Our design goal is to be best in class, with, basically all of our programs. And there are many different parameters by which that could be achieved. Mm-hmm. I think that 3911 will achieve those and has achieved those parameters such that we can measure them all preclinically. Mm-hmm. I think it's going to be a very, very competitive compound. But then, you know, this space is so large, the market opportunity. Yeah. There's room for multiple drugs. There's multiple indications. There will probably be multiple STAT6 programs that go forward and parse up this large autoimmune landscape, different pricing, you know, potential and different things. Mm-hmm. There's room for, you know, many winners here. Mm-hmm. We're definitely in that first mover class with Chimera. We're happy to be in that class. I think Sanofi has, again, been analyzing the space for quite some time. I believe that, again, we have a great partner here and we'll be able to be quite competitive. Got it. And then the partnering, you just mentioned Gilead, IRAK4, understanding that's your partner. So any updates from that program, you can tell us now? Recently, we did announce that the IND was accepted. Yep. they are moving into their healthy volunteer stage. That I think will be a very important set of studies done likely in the next 12 months. Mm-hmm. And then, so we'll be looking at, you know, data, healthy volunteer data, I would hope in 2026. Yeah. Again, I'm not, I can't speak for their timing and such and they will control publication, but in general, generically that's about what you would expect. Yep. I think there'll be, you know, quite a bit of data in this emerging field, in terms of degraders in INI that'll be very exciting. Yeah. Absolutely. And then just lastly regarding the 2127 and then 1607, that's another two pipeline. And then, what, any updates from there? Should we expect to, say, see some data this year, next year? So, 1607. Yeah. 1607. That's okay. It's the Cbl-b inhibitor, and we do anticipate having an update probably this year. We did give a brief update at ASH that just that we have over 60 patients in the dose exploration portion of the trial, phase 1A, that is coming to a close. We'll have a data set to evaluate there. I think that's a first-in-class agent, inhibiting Cbl-b in immuno-oncology. We're across 11 different solid tumors that have been enrolled. It's a basket study, and we'll, you know, I think it has great potential. 2127's a little earlier. It is in dose escalation. Not clear if we'll have enough data for the end of the year, but if we do, you know, we'd certainly like to give an update on that. Excellent. Okay. I think the time is good. And then. And then.