Arvinas, Inc. (ARVN) September 2026 Conference Transcript

All right, everybody. I think we'll get started here with our next fireside discussion. So my name is Derek Archilla, one of the Wells Fargo biotech analysts. With us now, we have our Venus from the company. We have Randy Thiel, president and CEO, as well as Angela Cassidy. Chief Scientific Officer. So welcome and thank you so much for coming.

Thank you very much for having us.

So maybe, Randy, I'll turn it over to you. Give us kind of the evolution of our Venus here. A lot of changes, a lot of things going on. So I'll let you take over from there. But just kind of give us the high-level view of the state of the business.

And thank you again for having us. And it is definitely a time of good change for us. I would say maybe four things to start off. So, first of all, it's great that we have a product that's in the market now. So VEP, which we have sold, and another company is now commercializing, is getting to patients and being a company that has invented a technology and then brought the first one all the way through regulatory approval is really rewarding, and we're excited to see that. I think, too, is we're 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 so the conversations that we're having today and this week are very different than we were having you know three months ago now that we have multiple programs which will go through that all have data really coming in the next 15 months or so you know across the pipeline we've got four essentially in the clinic now so ARV 393 is a BCL 60 grader in hematology that program will have its first phase one clinical data by the end of the year the second one I'll highlight is an SBMA program. So Kennedy's disease is a rare disease and we have a program that degrades polyglutamine repeat AR or antigen receptor. That program will have its first phase one clinical data in the first half of next year in both healthy volunteers and in patients with SBMA. ARV-102 is our LARC2 degrader for neurodegeneration relevant for both progressive supranuclear palsy and Parkinson's disease. That's a program that has completed a phase one in Europe, and we've now got a number of regulatory body conversations going on at once across the U.S., Europe, and Japan. And in the middle of that, we'll share some additional biomarker data from the phase one study next month at MDS, so data coming there. And then the fourth program is an HPK1 degrader called 6723. That program is just beginning in the clinic in this current quarter. It's our first IO program, So wouldn't guide to data there yet, but maybe expect by the end of next year or so. But that means that now, as we've turned a bit of a corner from VEP 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's coming. And I would say on the backdrop of that, I would say that since I took over as CEO about six months ago, I've been really clear to say that we will invest and be very careful to invest only where we think our Venice is the right company to do that. and also look for opportunities to partner where it makes sense and I think we've already taken some decisions most specifically around our G 12 D degrader that illustrate that program that will actually have data coming but we've already said we'll only progress if a partner is found to take that forward and then the last thing I would say is from a capital perspective we have our current guidance as cash into the second half of 28 which allows us to get comfortably past all the milestones that we'll talk about today it's a great place to be and as I've taken over leadership this year you know 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 so it's a great time to be to be looking at our Venice and talking about it as we go from you know 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 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, and from a high level, the BCL6 program was one of our first programs that was squarely aimed at an undruggable target, right? So our first historical targets were AR and ER. BCL6 was one that no one had degraded before. So 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 one 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 2012 and 2027 disclosure where we will share data and focus on B cell lymphoma patients both as monotherapy and in combination. So So 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 one dose escalations have not been run in patients with T cell lymphomas. They're generally large basket trials across B cell and T cell. So 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 what are you expecting to receive and at that point you're expecting something like a 35 to 40 percent response rate again if 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 you know hitting that as a target would be would be great to do but we'll look even harder at efficacy as we get into expansion phases and start to expand it at doses. What's really clear in the NHL space is that while there's a lot of competition for bispecifics and CAR T's 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 BCL-6 to kind of confer efficacy and do you need full degradation or is there certain thresholds there?

Yeah, and it's a great place to bring in, Angela, our CSO. Look, at high level, we know we need high amounts of BCL-6 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've looked across high-grade and low-grade, you know, DLBCL models. We've also looked at AITL, which is nodal T follicular helper of the angioplastic type. And we found that, you know, around 90% degradation covers the amount of coverage of the target that we need to impact proliferation and then apoptosis induction within the tumor.

And now you brought up some of the potential combos. I mean, can you talk about how you're thinking about your strategy and development there and what really makes sense and what you would want to produce for kind of as a comprehensive early data set for proof of concept?

Yeah, and this is definitely one where, you know, the landscape's changing rapidly and what's really clear is the most important thing for us to show is first some good solid monotherapy activity and some solid combination therapy activity. So that feels like the bottleneck that we have to get to first. Over the longer time frame, the way we think about it is monotherapy in later line opportunities and combinations in earlier line opportunities. So if we look just at DLBCL, there's 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's 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. that we've started in combination with GLOFI, have a supply agreement with Roche to do that, and that's 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's a monotherapy late line opportunity where patients as I said roughly get served with the 35 to 40 percent response rate but there's really no clear standard of care and on the AITL side as well there's an opportunity in the first line perhaps there to combine with chemo whereas on the on the DLBCL side maybe it's an ultimate goal to try to displace chemo from the first line so I know that's there's a lot of potential opportunities there it's not too specific on where we will go again we've got to show good monotherapy activity good combo activity I think with multiple agents and then we'll get a little more clear about where we'd 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 you know because it's dose ranging right so like well you know how many are we really gonna see maybe at these effective doses where are you starting in terms of like you know from the animal studies and the translation issue we are we already at therapeutic level doses so yeah walk us through all that because these data sets can be kind of not not say messy but like yeah we just want to make sure we're looking at the right data set and look at the benchmark we should be yeah that is a great question and reminds me to say that as we started this phase one study it was quickly clear that we were dosing quite a ways below the predicted efficacious range so that actually is one of the reasons that we've said that will focus the initial update on T cell

patients because we know based on the modeling that we did pre clinically that the level of exposure we were reaching in the early cohorts, we were not expecting to be efficacious for DLBCL. So 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. And 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. So imagine, you know, in terms of the data coming at the end of the year, for patients that we have, again, across pre-efficacious and efficacious range, this 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 DL-BCL patients in the update for next year as mono and combo. what sort of responses should we be focused on like is there like a benchmark 20 percent 30 like what what should be classified as like good data well you know as i said in in t-cell patients there's really no first uh sorry phase one trials to look at that will run specifically those patients and so we're looking at what a patient would typically get in second line aitl again these are going to be patients that are pretty heavily pre-treated but something if you're on you know in the market you'd be looking for something like a 35 or 40 response right again you know I think that the long-term play here is clearly as a combination yeah so 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 like what we should be expecting from a safety perspective and ultimately like is there really any reason to think that there's any issues with degrading you know meaningfully bcl6 for for long periods of time maybe the best way to answer that is what our preclinical data would have predicted for safety yeah so we we did look at um you know cytopenias in general and we do have a very nice margin relative to those so i would say that um you know 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 in this population well when when we say this population we're ultimately looking as monotherapy lateline 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 and so from the phase one it's important to see that we can dose to a efficacious range without any untoward effects as we've looked at other therapies that have come already and had some clinical data while hitting BCL-6. 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 talks, eosinophilia was the one that was predicted that we should look for, so we'll certainly look for that. But overall, we want something that's going to be combinable with bispecifics and with other therapies.

Excellent. So 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, you know, 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 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 so so we are thinking about this much more as a proof of concept getting getting the data out there making sure that investigators are highly aware that we have clearly reached an efficacious exposure to help you know drive continued interest and making sure that as we head into the multiple combinations that we'll want to run that we're able to do that in a in an efficient way so you know we have so

basically T cell data you know T cell indications this year next year more folks on B cell how do you think about the development path for both of these you know basically if we figure out you've got good activity would you do a monotherapy late line or would you just want to run the early line combos what's kind of the development path do you see for for both of these we would anticipate late line monotherapies right so certainly those are not the biggest commercial opportunities as compared to the earlier line combinations but they are areas of incredibly high on met need especially for patients with t-cell lymphomas so getting getting the drug to market sooner even in a population that's relatively smaller and they're not tiny but they're smaller than the earlier

line therapies both allows the allows patients to benefit sooner but also it makes a lot easier to run ultimate combination studies with a bunch of other agents too so we definitely see value in exploring the drug in late line monotherapy even as we're simultaneously pushing towards earlier lines and combination when would those decisions to kind of be made is that a 2027 event in terms of understanding that yeah yeah yeah yes gotcha Maybe shift gears to 102.

So, you know, LARC-2 degrader, you guys are looking at PSP. We did see, you know, the Biogen failure in Parkinson's, and we kind of talked about this. But, you know, I guess what did we learn from that data set just about the target in general? But also, again, you had already kind of made the decision to focus on PSP. Parkinson's is more kind of like a flyer in case it hit. But, you know, like how is that kind of informing PSP development, but also, you know, any other future development in kind of neuroinflammatory diseases?

Maybe I'll give a very short answer in the past 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 LARP2 inhibitors. Yeah.

And, you know, BIV-122, based on our preclinical data, there's really no comparison between the level of target engagement that we see in the brain and the level of pathway engagement in terms of phosphorab and the end of lysosomal system. We're 50-fold more effective at engaging the pathway, which we think is really important. and you know 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 so you know it was thought that the proteasome was incapacitated we've now shown that you can employ the ubiquitin proteasome to degrade LRRK2 and importantly what we saw was a dose dependent you know 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 and then in october we'll be talking more about a digital biomarker that is a synaptic biomarker of what might happen in the basal ganglia so we'll be looking at eye tracking this is an app called ash so this is amplitude of saccadic hypometria it's the ability of the eye to track a rapidly moving target and that's there's a deficit in Parkinson's disease in that measure and we'll show the data that shows that we're seeing unprecedented changes there and then 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. And then cerebellum 4 were 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.

Gotcha. So talk to us about PSP and why you guys chose that indication and why you think 102 is maybe best suited to be developed there.

So progressive supranuclear palsy, this is a very rapid, devastating disease that's progressively degenerative. And so we chose PSP because of some biomarker data and genetic data that support LARC-2 elevation as driving increased progression in time to death, but also increased progression in terms of the rating scale within a year. So for a company like Arvinus, this enables us to do a very, you know, controlled study where we can expect to see functional changes within a year once we recruit all of the patients.

So I guess, you know, you guys have been running, or are you starting that kind of program and getting it going? So as you said, there's some stuff going on in the U.S. and then the EU. So maybe can you walk us through where you are in terms of that and then ultimately, you know, moving it forward?

Yeah, absolutely. So we have completed the phase one 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 share data for at ADPD and we'll also show data for MDS next month. In the wake of that, what the plan had been was to start a phase 1B study in the US and then a phase 2 registrational study outside the US in the when we submitted the IND to the US a few months ago they came back with a clinical hold and asked us not to start that so we hadn't started it was it was a please don't start kind of hold and asked they asked at the time to see the completed chronic tox data the full Sinnoh data the full rat data so 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. And so now we're engaging with the FDA, but also simultaneous engagements with Europe and Japan. And 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 and so 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 but the but when we do that we'll be able to talk about how those plans have evolved or changed if they have at all and then a revised start date but the plan i wouldn't 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 I was there anything specifically the agency kind of called out or was it just because you know look why did they want that data whereas the EU is a little bit more lenient or I think it's I don't know that I would characterize it as the as any agency being more lenient or anything like that it was simply that they asked to see the completed data okay and then I think it's also fair to say that anytime 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'd already shared.

And from a chronic tox perspective, it looks fine.

From a chronic tox perspective, we've submitted that information back to the FDA, so they have everything in their hands now. And then clearly in the engagements that we're having with the other regulatory bodies, they're also seeing the same level of information.

But like no new signals or anything that you've from like the earlier talks.

Well, yeah, I mean, I can't comment on what's in the chrono-tox data. We haven't 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.

And in terms of PSP, just maybe walk us through kind of the current treatment landscape, and it seems like there's more of a dearth of options there, but where this could really play a role, and where, as you think about these trials, where's the best place to intervene in these patients like from an enrollment perspective and how important will that be in the trials it's a great question and of course you know there are no disease modifying therapies in PSP as you mentioned it is a tau opathy so act so going after tau is a reasonable approach this is the one Novartis is taking with their antisense currently in their phase three it's an intrathecal antisense oligonucleotide that reduces about 20% of pathologic tau um our goal is to actually you know really take it from multiple perspectives perspectives with lark 2 where we would be impacting the endolysosomal turnover and impacting tau and also impacting c gas and other pathways like you know neuroinflammation and we've seen cd68 change. This is a major microglial marker that indicates, you know, 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.

Gotcha. Okay. And then just in terms of like the enrollment of patients, like so where in the spectrum with these PSP patients generally?

Yeah, so 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. So it's, you know, it's hard to say exactly where they are in the progression. There are several, you know, digital approaches that lead to earlier diagnostics, um you know like speech and other markers that are being used now um which we think is is very interesting um there's another and i meant to mention there's another progranulin pathway modulator that appears to have just received accelerated approval so playing into this endolysisomal process which might be interesting too so the timelines here are mostly just remind so we could be developed by next year is that yeah yeah presume that will 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 gotcha okay um so maybe move on to some of the other you know kind of earlier pipelines so spma and kennedy disease maybe just give us a little bit of background there and why you chose that program to move forward yeah kennedy's disease uh also known as a spinal and bulbar muscular atrophy is a slow progressing but devastating neuromuscular disorder so we know that it's caused by the accumulation of version of antigen receptor polyglutamine repeat antigen receptor in muscle it is an excellent disease so only typically only men will get it but the interesting thing about it is that we know it's driven by polyglutamine or polyq AR was what I'll call it and so this is a situation where the target that we've chosen is not some upstream or indirect cause of the disease the the target of the degrader is actually the disease-causing target itself. So we've got some really interesting data from preclinical mouse models showing that if we degrade even 50% of the poly-Q AR, we actually see a full recovery of endurance and strength in the mouse models that we have. So it's an unusually tight linkage between the target we're degrading and the disease itself. So that's one where we've got the program in phase one right now. The first part of the phase one is in healthy volunteers. years we will also be enrolling patients with SBMA towards the tail end of the of the phase one 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 but But so I think the next step after the phase one is likely to be moving straight into a registrational trial, but it'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 one 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.

I mean, can you talk to the biomarkers other than just, you know, looking at the actual protein that would kind of be predictive or at least what sort of linkage is there to some of those functional biomarkers? And what are we talking in terms of, like, the progression? Like, how long of a trial would you really need to actually run to actually see that improvement on the function at one point?

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. And so MRI is a good muscle integrity measure. And then other functional endpoints that look like they're more measuring the lower body extremity functions. So there's an alternate SBMA rating scale that's been developed that appears to be more sensitive than the scales that were used previously. but you're still looking at a slow progressing disease that changes you know within 18 months you know pretty dramatically and like where do you like going back to kind of the previous question too but like where do you think you need to kind of enroll in the spectrum so to kind of get these patients maybe on the cusp of starting to progress um and and is and 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, you know, get diagnosed because there's no advantage, really. So we think, you know, 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 and then you know they're also going to have to you know be able to have reasonable functionality so that the tests can be completed within the day so so you think so so data next year so do you think like we'd have a good idea of what the path is and agreement on biomarkers you know by the end of next year we were just talking about this earlier look I think 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 one data so being able to look at as we talked about safety and tolerability of course you know 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 so the phase one's ongoing now it feels like we need to wait till you know maybe the middle of next year to have those conversations which to me feels like a path by the end of the year it's kind of rough speaking but we want to make sure we have enough to go on and then ideally you know 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 the you know the good and bad news is that there's a lot 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 so there's been a lot of energy behind you know trying to take a leadership position and identifying biomarkers and really you know understanding the disease and how we might be able to affect it gotcha and And then maybe last one, HPK1, just your thoughts on that program.

And again, I think this one's 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'll say a little and Angela can dive in. HPK1 is our first IO target. So HPK1 is not a novel target to industry. There's 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's a checkpoint inhibitor that's active not just at, say, the effector T-cell activity level, but throughout the activation of the immune system. So 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, and just briefly to add, you know, not only are we reducing the suppressive effect on the T cell, we're also reinvigorating the tumor microenvironment from the standpoint of the myeloid compartment, which is really important. And we've been able to show this in seven different ICI models that were significantly impacting and remodeling the tumor microenvironment, in addition to recruiting the T cells. And so we're seeing a massive interferon response, which is great.

Gotcha.

So it's very different as an oral molecule in the space.

So maybe to take it home here, so a lot more focus on the pipeline. you've got a lot of different kind of data updates and then you know 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 kind of a protac and the greater platform kind of capable of and you had you know said earlier Randy that some of these you may take yourself some of them you may partner so you know having done a big partnership in the past you know how are you evaluating that you know this time around yeah I think it's and I'm glad you brought up the what else can we do because we 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 our Venice to be the ones that are investing and there will be a number of programs where there's a monotherapy path and a combination path there will be programs where BCL six being example where to really maximize the value of the program it's going to need a whole lot of combinations over time now we certainly I would love to be in a position where their early data we have give us the ability to do that but I would also be happy to you know be in a situation where we're supplying 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 the ability to raise and continue you know and on the continue front look we are famous for making protact degraders but that is not all that you know we have in store right so 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 in 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'll leave it there. Thank you so much.