All right, everybody. I think we'll get started here with our next fireside discussion. My name's Derek Archila, I'm one of the Wells Fargo biotech analysts. With us now, we have Arvinas. From the company, we have Randy Teel, President and CEO, as well as Angela Cacace? Cacace. Cacace. Okay. Sorry about that. Chief Scientific Officer. Welcome and thank you so much for coming. Thank you very much for having us. Maybe, Randy, I'll turn it over to you. Give us the evolution of Arvinas here. A lot of changes, a lot of things going on. I'll let you take over from there, but just give us the high level view of the state of the business. Absolutely and t hank you again for having us. It is definitely a time of good change for us. I would say maybe four things to start off. First of all, it is great that we have a product that is in the market now. [VEPPANU], which we have sold and another company is now commercializing, is getting to patients and b eing a company that has invented a technology and then brought the first one all the way through regulatory approval is really rewarding, and we are excited to see that. I think two is, we are at a point where we have turned a corner from having the attention be on the pipeline writ large to the programs in that pipeline now getting very close to having data. The conversations that we are having today and this week are very different than we were having three months ago, now that we have multiple programs which we will go through that all have data really coming in the next 15 months or so. Across the pipeline, we have got four essentially in the clinic now. ARV-393 is a BCL6 degrader in hematology. That program will have its first phase I clinical data by the end of the year. The second one I will highlight is an SBMA program. Kennedy's disease is a rare disease, and we have a program that degrades polyglutamine repeat AR, or androgen receptor. That program will have its first phase I clinical data in the first half of next year in both healthy volunteers and in patients with SBMA. ARV-102 is our LRRK2 degrader for neurodegeneration, relevant for both progressive supranuclear palsy and Parkinson's disease. That is a program that has completed a phase I in Europe, and we have now got a number of regulatory body conversations going on at once across the U.S., Europe, and Japan. In the middle of that, we will share some additional biomarker data from the phase I study next month at MDS, so data coming there. The fourth program is an HPK1 degrader called ARV-6723. That program is just beginning in the clinic in this current quarter. It is our first IO program, so wouldn't guide to data there yet, but maybe expect by the end of next year or so. That means that now, as we have turned a bit of a corner from [vepdegestrant] to the pipeline, the pipeline is really coming into relief, which allows us to talk about expectations, lets investors really ask questions in detail about what is coming. I would say on the backdrop of that, I would say that since I took over as CEO about six months ago, I have been really clear to say that we will invest and be very careful to invest only where we think Arvinas is the right company to do that, and also look for opportunities to partner where it makes sense. I think we have already taken some decisions, most specifically around our G12D degrader, that illustrate that program. That will actually have data coming, but we have already said we will only progress if a partner is found to take that forward. The last thing I would say is from a capital perspective, our current guidance says cash into the second half of 2028, which allows us to get comfortably past all the milestones that we will talk about today. It's a great place to be. As I've taken over leadership this year, we've continued to focus on making sure that we are running as efficiently as we can be to make sure that we can get to the most important milestones, which are, of course, the clinical data that's now coming up. It's a great time to be looking at Arvinas and talking about it as we've transitioned to the pipeline and now very specifically to the programs that are about to share data. Excellent. Why don't we start off with ARV-393, and I guess maybe talk about some of the initial data that we'll see by the end of the year, and how we should be benchmarking some of that data relative to the competitors. Yeah. From a high level, the BCL6 program was one of our first programs that was squarely aimed at an undruggable target. Our first historical targets were AR and ER. BCL6 was one that no one had degraded before. It's been gratifying to see that as multiple companies have come to the clinic with that as a target, it certainly looks like a good target to be degrading. The program that we're running right now is a phase I dose escalation study. We have a broad range of patients across both B-cell lymphomas and T-cell lymphomas. The data that we will share by the end of this year or so will be biased towards the patients with T-cell lymphomas. We're also already thinking about a 2027 disclosure where we will share data and focus on B-cell lymphoma patients, both as monotherapy and in combination. That's a program that most folks are asking about, that data coming up in the very near term. In terms of the benchmarking that we're doing, as we think about T-cell patients, most studies in their phase I dose escalations have not been run in patients with T-cell lymphomas. They're generally large basket trials across B-cell and T-cell. As we look at what good could look like, we look at what's on the market now, and if you're a patient who's being treated for second-line AITL, what are you expecting to receive? At that point, you're expecting something like a 35%-40% response rate. Again, for therapies that are on the market. In a dose escalation trial where we already know that a large number of the patients will be dosed below the efficacious range, hitting that as a target would be great to do. But we will look even harder at efficacy as we get into expansion phases and start to expand at doses. What is really clear in the NHL space is that while there is a lot of competition for bispecifics and CAR-T and so on, there are not a lot of oral therapies that could look to displace non-oral therapies and either displace chemo in some settings combined with others and really provide new options to deepen and extend responses for patients across NHL. Gotcha. Can you talk to the level of degradation you think you need for BCL6 to confer efficacy? Do you need full degradation, or are there certain thresholds there? Yeah, and it is a great place to bring in Angela, our CSO. Look, at high level, we know we need high amounts of BCL6 degradation because it is a very rapidly resynthesized protein. But Angela can say a bit more and maybe talk a bit about our preclinical data that gets there. Sure. We have looked across high-grade and low-grade DLBCL models. We have also looked at AITL, which is nodal T-follicular helper of the angioimmunoblastic type. We found that around 90% degradation covers the amount of coverage of the target that we need to impact proliferation and then apoptosis induction within the tumor. Gotcha. Angela, you brought up some of the potential combos. Can you talk about how you are thinking about your strategy and development there, and what really makes sense, and what you would want to produce as a comprehensive early data set for proof of concept? Yeah. This is definitely one where the landscape is changing rapidly, and what is really clear is the most important thing for us to show is, first, some good solid monotherapy activity and some solid combination therapy activity. That feels like the bottleneck that we have to get to first. Over the longer timeframe, the way we think about it is monotherapy in later line opportunities and combinations in earlier line opportunities. If we look just at DLBCL, there is an opportunity to meet some unmet need in patients in third, fourth line as monotherapy. Ultimately, we would like to get to second line, potentially in combination with a bispecific, and there is an opportunity over the longer term even to go to first line. The general motif in NHL has been to add on therapies that can deepen and extend responses. Adding an oral therapy, we think, is a good opportunity to do that. We have started in combination with glofitamab, have a supply agreement with Roche to do that, and that is an important first step, and we can talk a bit about why we chose that. Beyond that, though, we certainly expect other combinations to come into play. We have a very broad range of preclinical evidence supporting combinations with BCL2, a bunch of different inhibitors. On the AITL side, or nTFHL, again, it is a monotherapy late line opportunity where patients, as I said, roughly get served with the 35%-40% response rate, but there is really no clear standard of care. On the AITL side as well, there is an opportunity in the first line perhaps there to combine with chemo, whereas on the DLBCL side, maybe it is an ultimate goal to try to displace chemo from the first line. I know there is a lot of potential opportunities there. It is not too specific on where we will go. Again, we have got to show good monotherapy activity, good combo activity, I think with multiple agents, and then we will get a little more clear about where we would like to take it as the landscape evolves. Understood. Just remind us in terms of the number of patients that we'll see in the update, and I guess because it's dose ranging, right? How many are we really going to see maybe at these effective doses? Where are you starting in terms of from the animal studies and the translation? Are we already at therapeutic level doses? Yeah, walk us through all that because these data sets can be not, say messy, but- Yeah -We just want to make sure we're looking at the right data set and looking at the benchmark we should be. Yeah, that is a great question and reminds me to say that as we started this phase I study, it was quickly clear that we were dosing quite a ways below the predicted efficacious range. That actually is one of the reasons that we've said that we'll focus the initial update on T-cell patients because we know, based on the modeling that we did preclinically, that the level of exposure we were reaching in the early cohorts, we were not expecting to be efficacious for DLBCL. It's only just now in the past couple of months that we've started to reach doses that we expect to be efficacious in DLBCL. Really what happened over time was that as we saw responses in patients with T-cell lymphomas and B-cell lymphomas, but the T-cell was what got investigators' attention. We certainly saw as the study began and ran a predominance towards patients with T-cell lymphomas, and it's taken a bit longer to get to an efficacious range for B-cell lymphomas. Imagine in terms of the data coming at the end of the year, for patients that we have, again, across pre-efficacious and efficacious range, it should be in the dozens of patients. I would put it that way. But what I'd focus on, again, is we'll focus on the T-cell patients this year and BCL6 patient. Sorry, DLBCL patients in the update for next year as mono and combo. What sort of responses should we be focused on? Is there a benchmark 20%, 30%? What should be classified as good data? Well, as I said, in T-cell patients, there is really no phase I trials to look at that were run specifically in those patients. Yeah. We are looking at what a patient would typically get in second-line AITL. Again, these are going to be patients that are pretty heavily pretreated, but something if you were in the market, you would be looking for something like a 35% or 40% response rate. Okay. Again, I think that the long-term play here is clearly as a combination. Yeah. Showing an initial monotherapy response will get boosted a lot in our eyes by combination responses that we can then use to expand into other combination agents over time. Can you comment on what we should be expecting from a safety perspective? Ultimately, is there really any reason to think that there's any issues with degrading meaningfully BCL6 for long periods of time? Maybe the best way to answer that is what our preclinical data would've predicted for safety? Yeah. We did look at cytopenias in general, and we do have a very nice margin relative to those. I would say that we're keeping an eye out, but it did tell us to look out for those types of events. What do you think is acceptable in this population? Well, when we say this population, we're ultimately looking as monotherapy and late line and to be combinable. I think that sets a bar, right? We want to have a drug that is active as monotherapy, but is very combinable. From the phase I, it's important to see that we can dose to an efficacious range without any untoward effects. As we've looked at other therapies that have come already and had some clinical data while hitting BCL6, we haven't seen massive data signals or safety concerns that we're worried about. As Angela said, I think coming out of our GLP tox, eosinophilia was the one that was predicted that we should look for. We'll certainly look for that. But overall, we want something that's going to be combinable with bispecifics and with other therapies. Excellent. Anything else that you would point to for this update that we should be looking for or paying attention to? The only other thing I would say is that I think this is an area where, as I said on NHL, there's a lot of bispecifics, there's a lot of other therapies. There's not a lot of oral therapies. I don't see this as a winner-take-all kind of category. This is one where I think companies and patients will be looking for combination agents to go with a wide range of other potential therapies from different companies. We are thinking about this much more as a proof of concept, getting the data out there, making sure that investigators are highly aware that we have clearly reached an efficacious exposure to help drive continued interest in making sure that as we head into the multiple combinations that we'll want to run, that we're able to do that in an efficient way. Basically T- cell data or T- cell indications this year, next year may more focus on B cell. Yeah. How do you think about the development path for both of these? Basically, if we figure out we have got good activity, would you do a monotherapy late line, or would you just want to run the early line combos? What is the development path do you see for both of these? We would anticipate late line monotherapies. Certainly those are not the biggest commercial opportunities as compared to the earlier line combinations, but they are areas of incredibly high unmet need, especially for patients with T- cell lymphomas. Getting the drug to market sooner, even in a population that is relatively smaller, and they are not tiny, but they are smaller than the earlier line therapies both allows patients to benefit sooner, but also it makes it a lot easier to run ultimate combination studies with a bunch of other agents too. We definitely see value in exploring the drug in late line monotherapy, even as we are simultaneously pushing towards earlier lines in combination. When would those decisions be made? Is that a 2027 event in terms of understanding that? Yeah. Okay. Yeah. Yes. Got you. Maybe shift gears to ARV-102. LRRK2 degrader, you guys are looking at PSP. We did see the Biogen failure in Parkinson's, and we talked about this. But I guess what did we learn from that data set, just about the target in general, but also, again, you had already made the decision to focus on PSP. Parkinson's is more like a flyer in case it hit. But how is that informing PSP development, but also any other future development in neuroinflammatory diseases? Maybe I'll give a very short answer Sure then pass to Angela. The very short answer is it hasn't changed things that much. Heading into that data release, we hadn't heard a lot of conviction that it would be positive, and so when it wasn't, we didn't hear much. I'll be honest. It seemed to meet expectations. But certainly we still see a very strong path forward in PSP and ultimately PD because of the differentiation that we've already seen versus LRRK2 inhibitors. Yeah. ARV-102, based on our preclinical data, there is really no comparison between the level of target engagement that we see in the brain and the level of pathway engagement in terms of phospho-Rab in the endolysosomal system. We are 50-fold more effective at engaging the pathway, which we think is really important. For us, Parkinson's disease was an important step because we know that LRRK2 is increased in that disease relative to the healthy volunteers. We showed degradation in a neurodegenerative population. It was thought that the proteasome was incapacitated. We have now shown that you can employ the ubiquitin proteasome system to degrade LRRK2. Importantly, what we saw was a dose-dependent reduction in some of those really key endolysosomal proteins that are involved in Parkinson's disease, like GPNMB. We also showed a dose-dependent reduction in neuroinflammatory markers like CD68. In October, we will be talking more about a digital biomarker that is a synaptic biomarker of what might happen in the basal ganglia. So we will be looking at eye tracking. This is an app called ASH. So this is amplitude of saccadic hypometria. It is the ability of the eye to track a rapidly moving target. There is a deficit in Parkinson's disease in that measure, and we will show the data that shows that we are seeing unprecedented changes there. We also saw increases in synaptic plasticity measures in the CSF. So two important biomarkers of synaptic plasticity, neuronal pentraxin 2, which has been shown to be a deficit in not only Parkinson's disease by us, but also in terms of tauopathies like Alzheimer's disease and PSP significantly. Cerebellin 4 we are also increasing, which is a prognostic marker of Parkinson's disease. So those are some of the markers that you can expect to see in our data set in October. Got you. So talk to us about PSP and why you guys chose that indication and why you think ARV-102 is maybe best suited to be developed there. Progressive supranuclear palsy, this is a very rapid, devastating disease that's progressively degenerative. We chose PSP because of some biomarker data and genetic data that support LRRK2 elevation as driving increased progression in time to death, but also increased progression in terms of the rating scale within a year. For a company like Arvinas, this enables us to do a very controlled study where we can expect to see functional changes within a year once we recruit all of the patients. Got you. I guess you guys have been running, or are you starting that kind of program and getting it going? As you said, there's some stuff going on in the U.S. and then the EU. Maybe can you walk us through where you are in terms of that and then ultimately, moving this path, moving it forward? Yeah, absolutely. We have completed the phase I studies in Europe in both healthy volunteers and in patients with Parkinson's. So that's the data that we've shared data. That's the patients and healthy volunteers we shared data for at AD/PD, and we'll also show data for at MDS next month. In the wake of that, what the plan had been was to start a phase I-B study in the U.S. and then a phase II registrational study outside the U.S. When we submitted the IND to the U.S. a few months ago, they came back with a clinical hold and asked us not to start that. We hadn't started it. It was a please don't start kind of hold. They asked at the time to see the completed chronic tox data, the full cyno data, the full rat data. What we'd said at that time is that we would complete that by the middle of the summer, and submit that back, which we've done. Now we're engaging with the FDA, but also simultaneous engagements with Europe and Japan. The upside of that is that it allows us to better harmonize the plans across the multiple geographies, which I'll take as a good thing. We announced that the start of the trials then would now be in 2027 instead of 2026, which gives us time again to harmonize those and refine the plans that we will have based on feedback from multiple regulatory agencies. We'll look to provide a bit more of an update on that when those conversations are done. It's a bit premature to do it while they're ongoing. When we do that, we will be able to talk about how those plans have evolved or changed, if they have at all, and then a revised start date. I would not expect to see any change in the plan to go towards patients with PSP first. PD is a longer-term play, and really a focus on getting to a registrational study as soon as possible. Was there anything specifically the agency called out, or was it just because why did they want that data, whereas the EU was a little bit more lenient or accepting? I do not know that I would characterize it as any agency being more lenient or anything like that. It was simply that they asked to see the completed data. Okay. I think it is also fair to say that any time you share data with a regulatory agency, they will have questions about it. So they asked us both to come back with the completed chronic tox data, and then they had a number of other questions about the data that we had already shared. And from the chronic tox perspective, everything looks fine? From a chronic tox perspective, we have submitted that information back to the FDA, so they have everything in their hands now. Then clearly in the engagements that we are having with the other regulatory bodies, they are also seeing the same level of information. Got it. But no new signals or anything that you have seen from the earlier talks? Well, I cannot comment on what is in the chronic tox data we have not released. But maybe suffice it to say that we feel good about when we get through the different discussions with the regulatory bodies, that we will have a path forward to move towards registration in PSP. Got you. Yeah. In terms of PSP, just maybe walk us through the current treatment landscape. It seems like there's more of a dearth of options there. Where this could really play a role, and as you think about these trials, where's the best place to intervene in these patients from an enrollment perspective, and how important will that be in the trials? It's a great question, and of course, there are no disease-modifying therapies in PSP, as you mentioned. It is a tauopathy, so going after tau is a reasonable approach. This is the one Novartis is taking with their antisense currently in their phase III. It's an intrathecal antisense oligonucleotide that reduces about 20% of pathologic tau. Our goal is to actually really take it from multiple perspectives with LRRK2, where we would be impacting the endolysosomal turnover and impacting tau. Also impacting cGAS and other pathways like neuroinflammation, and we've seen CD68 change. This is a major microglial marker that indicates that the pathologic process is now at play. So if we can modulate that and improve synaptic plasticity, that would be the goal with one molecule. So we think it would play well in the space, even with a tau antisense. Got you. Okay. Just in terms of the enrollment of patients, so where in the spectrum would these PSP patients generally sit? Yeah. That's a great question. Usually, by the time they're diagnosed, their disease has probably progressed enough that you can actually tell that they have the disease. It's hard to say exactly where they are in the progression. There are several digital approaches that lead to earlier diagnostics, like speech and other markers that are being used now, which we think is very interesting. I meant to mention there's another progranulin pathway modulator that appears to have just received accelerated approval. Playing into this endolysosomal process. Gotcha Which might be interesting too. The timelines here mostly, just remind us, we could be at develop by next year, is that fair? Yeah. Presume that we'll, at least the way I think of it, is that to get through the regulatory discussions in this fall, and then to begin the trial next year. Got you. Okay. Maybe moving along to some of the other, kind of earlier pipelines. SBMA and Kennedy's disease, maybe just give us a little bit of background there and why you chose that program to move forward. Yeah. Kennedy's disease, also known as spinal and bulbar muscular atrophy, is a slow progressing but devastating neuromuscular disorder. We know that it's caused by the accumulation of a version of androgen receptor, polyglutamine repeat androgen receptor in muscle. It is an X-linked disease, so typically only men will get it. But the interesting thing about it is that we know it's driven by polyglutamine or polyQ AR is what I'll call it. This is a situation where the target that we've chosen is not some upstream or indirect cause of the disease. The target of the degrader is actually the disease-causing target itself. We've got some really interesting data from preclinical mouse models showing that if we degrade even 50% of the polyQ AR, we actually see a full recovery of endurance and strength in the mouse models that we have. It's an unusually tight linkage between the target we're degrading and the disease itself. That's one where we've got the program in phase I right now. The first part of the phase I is in healthy volunteers. We will also be enrolling patients with SBMA towards the tail end of the phase I study, and we'll have data for that program in the first half of next year. I think that beyond that, what a lot of the conversation will be around is, how can we come up with a way to get to an accelerated approval that doesn't require us to wait for the full functional rating scale data for patients with the disease, since, as I said, it's a relatively slow progressing disease. I think the next step after the phase I is likely to be moving it straight into a registrational trial. That'll require some work with the agencies to figure out exactly what the path will be, what the biomarkers are that we might look at. But it's unlike some neuro and neuromuscular diseases. Because of that tight linkage between the target and the disease, we think that the phase I data, despite being focused on safety, PK, and PD, that PD marking is going to be unusually predictive of our, I think, potential for success in treating that disease. Can you talk to the biomarkers other than just looking at the actual protein versus that would kind of be predictive or at least, what sort of linkage is there to some of those functional biomarkers? What are we talking in terms of the progression? How long of a trial would you really need to actually run to actually see that improvement on the function points? I can just say in our preclinical models, we've seen nice changes in muscle energetic markers as well as structural markers for the muscle. MRI is a good muscle integrity measure. Then other functional endpoints that look like they're more measuring the lower body extremity functions. There's an alternate SBMA rating scale that's been developed that appears to be more sensitive than the scales that were used previously. You're still looking at a slow progressing disease that changes within 18 months pretty dramatically. Where do you, going back to the previous question too, but where do you think you need to enroll in the spectrum, so to get these patients maybe on the cusp of starting to progress? How well known is that in terms of the different stages in the progression? Yeah, Derek, it's a really good question because in the field of neurology, if there are no treatments prescribed, patients tend not to get diagnosed because there's no advantage really. We think something like this would be really important. You're going to get the whole scale. Our goal is to intervene reasonably early, where folks will have to be ambulatory and walk a certain amount of time and score at a certain level on the two minute walk test, let's say, or the six minute walk test. Then they're also going to have to be able to have reasonable functionality so that the test can be completed within the day. So endurance. Data next year. Do you think we would have a good idea of what the path is and agreement on biomarkers and stuff by the end of next year? We were just talking about this earlier. Look, I think by the end of next year is probably a good timeline because what we would want to be able to do is go back to the agencies with a clear plan. To have a clear plan, we kind of need the phase I data. Being able to look at, as we talked about, safety and tolerability, of course, first and foremost, the degradation of AR, other exploratory biomarkers. We would want to be able to go back to the agencies and propose a path that has enough meat behind it that they can respond to it. The phase I is ongoing now. It feels like we need to wait till maybe the middle of next year to have those conversations, which to me feels like a path by the end of the year. It is kind of rough speaking, but we want to make sure we have enough to go on. Ideally, if we could get to a point where we could be running a trial for accelerated approval and then follow that with a confirmatory study, that might be the right way to go. But we have some work to do to get there. The good and bad news is that there are a lot of patients, despite it being a rare disease, who are in a lot of activity in the space, a lot of good advocacy in the space. There has been a lot of energy behind trying to take a leadership position in identifying biomarkers and really understanding the disease and how we might be able to affect it. Got you. Then maybe last one, HPK1, just your thoughts on that program. Again, I think this one is the earliest, so we probably won't get a lot of data near term. But just kind of the advantage there and just your thoughts on the overall opportunity. Yeah. Maybe as typical, I will say a little, and Angela can dive in. HPK1 is our first IO target, right? HPK1 is not a novel target to industry. There has been a couple others that are out there. We think that having a degrader in this space versus an inhibitor will provide a substantial advantage. But the idea behind HPK1 more broadly is that it is a checkpoint inhibitor that is active not just at, say, the effector T- cell activity level, but throughout the activation of the immune system. The idea is that by hitting HPK1, not only can we affect its entire function, not just the kinase function, but we can recruit the immune system to help as an IO therapy is supposed to do to get responses in solid tumors. Yeah. Just briefly to add, not only are we reducing the suppressive effect on the T- cell, we are also reinvigorating the tumor microenvironment from the standpoint of the myeloid compartment, which is really important. We have been able to show this in seven different ICI models that we are significantly impacting and remodeling the tumor microenvironment, in addition to recruiting the T- cells. We are seeing a massive interferon response, which is great. Got you. It is very different as an oral molecule in the space. Yeah. So maybe to take it home here, so a lot more focus on the pipeline. You've got a lot of different data updates and then subsequent regulatory updates. These things may go into registrational trials fairly quickly for a fair amount of these programs, which is exciting. What else is your PROTAC and the degrader platform capable of? You had said earlier, Randy, that some of these you may take yourself, some of them you may partner. So having done a big partnership in the past, how are you evaluating that this time around? Yeah. I'm glad you brought up the what else can we do because there's certainly a lot more. I think that as we think about the partnerships, it's what I said at the start, which is where does it make sense for Arvinas to be the ones that are investing? There will be a number of programs where there's a monotherapy path and a combination path. There will be programs where, BCL6 being an example, where to really maximize the value of the program, it's going to need a whole lot of combinations over time. Now, I would love to be in a position where the early data we have give us the ability to do that, but I would also be happy to be in a situation where we're supplying ARV-393 to other companies to run trials with. I think that if I look at programs in terms of their profile and their ability to drive near-term interest for the company versus being longer term plays, sometimes the longer term plays can be places that make sense to have a partner come in and help out with as well, because they also tend to be more expensive, although not always in the case of like an SBMA, which is a rare disease. So I think we think about it pretty holistically, but always keeping in mind that it is important for us to make sure that we have places where we are keeping the wholly owned programs to continue to drive value and ability to raise and continue. On the continue front, look, we are famous for making PROTAC degraders, but that is not all that we have in store, right? We've gotten involved over the years in other ways to take degradation forward, other forms of induced proximity, maybe a little early to talk about at this point. But we certainly anticipate Angela's shop and research has shown itself to be highly productive in terms of an ability to bring programs into the clinic. I would say more programs than we probably will be able to afford to take forward on our own, but that doesn't just mean an opportunity for partnerships on clinical assets. That could also mean partnerships around research that would allow us to do more than we can currently do. As any small company, we've got to prioritize the clinical programs, and so it'll be important to find ways to keep the engine running and create more opportunities for us and other partners to have impact for patients. Excellent. Well, Randy, Angela, I think we will leave it there. Thank you so much. Thank you, Derek. Thank you very much. Great. Thanks for coming out. Thanks.