Conference Transcript - CLYM 2026-06-04

Akash Nwari, Analyst — Jefferies

My name is Akash Nwari. I head our farm and biotech efforts on the research side here at Jefferies. And we have Climb Bio, a company that we adjacently track because we cover Jade, and certainly a space where I think there's going to be multiple winners. And I'm really excited to host the management team and also reconnect with Susan, who she and I used to talk about IP with Solaris back in the day, which was a lot of fun. And there's a connection.

Susan Altschuller, CFO

Sweeper technology.

Akash Nwari, Analyst — Jefferies

This is true.

Susan Altschuller, CFO

Soliris to ultimeris.

Akash Nwari, Analyst — Jefferies

That is true. And clearly on to even bigger and better things at CLIMB. So why don't I hand it off to you for intro remarks and we'll get going.

Susan Altschuller, CFO

Yes, so excited to be here with CLIMB. We are a clinical stage company. We have two antibody approaches in renal disease and other autoimmune diseases. Our lead program is our CD19 monoclonal antibody, Budoprutug. Prutug, and that is in development in Phase 2 for PMN, and Phase 1b for ITP and SLE, and we can go through the cadence of readouts there. We just had a spotlight event for Budo in early May, and we presented data showing that with our CD19 antibody, we have the ability to formulate as a sub-Q formulation, which gives us even that much more optionality. So very exciting. More data to come this year and next for Budo. And then our second clinical stage asset is our APRIL-only monoclonal antibody that has the sweeper mechanism, which is pH-dependent binding to APRIL. It's the technology that was used similarly from Zoliris to Ultimeris. And that has the potential to be a best-in-class, next-generation asset in IgA nephropathy. And so we'll go into more detail there. just because I know that Jade had data earlier this week, and it's ERA, so we could start there

Akash Nwari, Analyst — Jefferies

and then talk about Pluto. Absolutely. Yeah, let's start with the anti-April, and I'd love to get your take about, A, the Jade data set, but also really what's kind of broadly going on, I think, in this space, because I think there's certainly a lot of moving parts. But let's hit on this, you know, any thoughts you had on the Jade data set, what they were able to show, and how that may apply to your program as well.

Susan Altschuller, CFO

Yeah, I mean, I would say very validating in terms of the next generation approach and potential value creation that only Climb 116 and Jade have the potential to create. So this, you know, lots of progress and excitement in IGA nephropathy, but this first generation of assets is at best dosed monthly. they're getting to around 50 percent iga reduction and they have some safety liabilities and so we we believe that we and then what jade showed that you can actually win on you know multiple legs of the stool because there's a lot of room left open and in terms of the data uh again you know we think that they showed that they were able to get you know clearly every eight week dosing with modeling get to 12 weeks for you know we think that every two month or every three month dosing is quite compelling for these patients who are diagnosed in their 20s or 30s and they're going to need chronic dosing. So, you know, I think it's a great step forward and there's still a lot of room for both of us to be wildly successful in this very large market.

Akash Nwari, Analyst — Jefferies

Understood. No, and I think that makes sense. And frankly, I think that's a tone that both mentioned teams have struck even pre-ERA, which is always nice to see. Now, maybe I think the, I remember we did some diligence on your program as well when we were looking at ERA. And the thing that we've always kind of, it's difficult to model this, is can you get to, let's say, quarterly dosing with a single subcutaneous injection in maintenance? And that's always really hard because no one seems to give their dose, no one seems to give their actual potency. But that certainly seems like post-AJ data set, something that they're quite confident on being able to deliver. I'm curious for your program as well, again, a higher bar than maybe just initial expectations, but is that a possibility with your

Aoife Brennan, CEO

program as well? Sub-Q maintenance on quarterly. Yeah, I think, you know, what we have set out as the target product profile, which Susan alluded to, is we kind of take it in a tiered perspective. So I think first we look at safety and I think, you know, April has been, you know, very good safety tolerability profile. So I think, you know, we expect no issues there. And then I think the second piece is efficacy. And obviously this is a very young patient population. You want to ensure that they're not moving to dialysis or ultimately kidney failure would need a transplant. So I think we're going to want to ensure that we hit that efficacy bar. And, you know, I think that was set with the first generation agents. And I think we're looking to, could you potentially improve beyond that. And I think our NHP data suggests that there is the potential there. So I think we're going to want to ensure that we maximize efficacy. And that's looking at April suppression as well as IGA suppression and healthy volunteers over the dosing interval. And then I think that third tier is dosing and convenience, which we completely agree is, you know, in this particular patient population, really critical. This is a young patient group. You know, they have busy lives we want to make sure they stay on therapy and that they're compliant over is which is going to be a lifetime of therapy so obviously if you're able to improve that dose frequency I think that's going to be critically important and so I think we'll look at all of those parameters but with you know the sweeper technology we really feel that there's the potential to you know not only extend the half-life with the LALA mutation that we have but also with the sweeper show you know enhanced effects over time on the PD parameters that are really going to lead to a more improved clinical profile.

Susan Altschuller, CFO

And to just directly answer your question, like, is, you know, every eight week or every 12 week maintenance a possibility, that remains the possibility for us.

Akash Nwari, Analyst — Jefferies

Now, I think the other thing, you're absolutely right, in terms of when we look at your non-human primate data, you have similar potency, at least it looks like that, to CIVI. but the sweeper kicks in on the tail right and i think that's quite important so certainly i think as you get to steady state drop that that i think effect will amplify if anything else the question also becomes i think when you talk to let's say our friends at biohaven or you know we cover our genics and you know they'll be like a view of look i don't know we can get better depth reduction or if it even really matters because egfr is kind of your downstream thing it might be a little more forgiving but we will try to improve on onset of effect right um uh and so like you can do that with a degrader you can do that with a sweeper uh that we at least see with the data from argenics i'm curious with your product profile as well i don't i mean this certainly the non-human primate data suggests you get the depth and tail effect of a sweeper technology but do you think you're going to get the same onset of effect that you could see as well. So, for example, that not only do you get to, let's say, 70% IgA reduction, but that can

Aoife Brennan, CEO

happen, let's say, in a month. Yeah, I think with the degraders, I think their profile is really that very rapid onset. And I think Biohaven has even talked about onset within hours. You know, I think we believe that the April mechanism works, you know, fairly quickly when you think about a chronic condition. I mean, you're looking at April nadir's in the four-week timeframe, you're seeing reductions within weeks. And then the IgA follows closely thereafter. So I think it's for, you know, this disease population still a fairly rapid onset of effect as you think about, you know, those biomarkers that will ultimately impact the proteinuria and EGFR. You know, is there a world in which a patient comes in with, you know, very elevated proteinuria where you need that very rapid onset? You know, I think maybe that's more the area where a degrader could play. But for, you know, a chronic therapy for a lifelong condition, we think anti-April is a great approach. And Akash, an interesting thing, you know, I think everybody, you know, has focused

Susan Altschuller, CFO

on EGFR, but there was the recent NKF and FDA summit at the end of April. And really, it seems like the renal division is going strong in this highlight of the FDA right now. And so I think that there's just growing recognition that proteinuria lowering and keeping it low below the 0.3 is translating into EGFR stabilization. And so we do get questions. I think that the question is, it's not just about the median, it's can you get more patients to target over the long term as well. So I think that just there's evolving. Yeah. I mean, certainly if

Akash Nwari, Analyst — Jefferies

you look at the SIBI data and you do the stratification, whether it's on weight, whether it's on ADAs, I think, to your point, getting everyone right shifting the curve on exposure in and of itself, I think, could have, you know, a more consistency in response. I think that's absolutely right. Now, you know, one of the things that I find quite fascinating is I don't think we know enough about apobiology. And I have, you know, and Manoj is on my team, who's much smarter than me, who's told me I'm wrong. But I have this kind of theory when I look at, for example, the VOR data. And, you know, I get it. You're not going to replicate in GMG that MG-ADL placebo response. I get it. But there's a durability of response and a depth of response. And it's not a particularly good B-cell drop, right? I look at the VOR molecule as good anti-April and then not as potent in terms of BAF. And yet there's a dose response. And so part of me, and then I cover argenics. We've learned, looking at FCRNs, a really nice, tight relationship between IgG reduction and MGADL response. That curve doesn't work when you get 20% IgG reduction with the vor molecule with the depth of MGADL response they get. So to me, I almost think, hey, April's doing more than we realize. And then when you look at the biology, if you suppress anti-April, you also make BCMA functionally silent. So there's stuff going on here that I don't think we all fully understand i'm curious what your team's view is in terms of where april can work and where can it not right um do you do you think you know april inhibition alone can actually be much more dramatic than maybe the traditional kind of dogma right now i think that i mean there's a

Susan Altschuller, CFO

possibility where you know i think that on the april bath and the bath side of uh the equation for IGAN, we're not seeing any real benefit, you know, and it has the safety liability. When we think about where we will take 116 beyond IGAN, you know, clearly there's a rationale for Sjogren's and other indications. But I think that, you know, right now our focus is preliminarily on generating these data, getting into an IGAN pivotal moving forward. And the nice thing is that with the ongoing studies in April biology being, you know, better understood, we can actually, you know, make fast decisions following on from where others are going to say where else we would expand into.

Akash Nwari, Analyst — Jefferies

Would there ever be appetite to, let's say, take this into mycebio gravis? Or no, because you feel like it's very tightly correlated with IgG reduction.

Aoife Brennan, CEO

I think, you know, we would look and explore where we think April biology would have the And I think you kind of hit on, as we look at even our NHP data, you saw dramatic effects in IgA and IgM, less so in IgG. And I think for IGAN, that works perfectly. So other IgM-driven diseases, I think, would certainly be on the table. I think something that's primarily IgG-driven, I'm not sure you get the reduction with April

Akash Nwari, Analyst — Jefferies

Well, both companies disagree with me. But I will say, IgM seems to have a role in CIDP and GMG as well. But, understood. um now when we kind of step back we're going to get a few more data sets including we cover vertex we get the full poby data and um i'm i'm curious like your understanding of what the fda needs for monitoring requirements right so uh cibi got approved i don't think people appreciate this there were eight cases of hypogam mild with that if you look at their multidisciplinary so it's not like anti-April doesn't show that. They did not have a monitoring requirement. Looking at Vertex's commentary, I think externally, they've been very clear, like, yeah, we have some cases of hypogam, but we're not having serious infections. Ergo, we file for accelerated approval. We're very excited about the data. We think it should be supportive for a broad-based approval without monitoring requirements. You've had interactions with the FDA, and this is kind of a nebulous issue. How do you think about whether you have a monitoring requirement or not? and what is the bar is it the infections or is it the hypogam itself i think i mean it's it's

Susan Altschuller, CFO

challenging you can't speak for the conversations they've had because we also don't have a bath component um but i think that uh the the question that we have and that when we're talking to kols in particular is more of the long-term risk yeah and so i that's the question of the trade-off imbalance because you might not be seeing it but you know over a couple years and these are young healthy patients does it open them up so i actually haven't you know we haven't had major discussions on monitoring with you know our approach but i i could see it going either way because it's theoretical more than you know actual yeah i mean like for the record i think at 80 mix

Akash Nwari, Analyst — Jefferies

per cake we think there's a really nice safety profile with povy but trying to get more information here so um now uh i think maybe just lastly uh you mentioned you know consistency of exposure um you know when you look at city and we can talk about the ada's but then we can also talk about the fact that it's sub-q and there's probably some limit in terms of what they can fit into an auto injector do you feel like there is actually room to improve you know upcr you know i think like the street whether it's scientific or not it's a different question it's probably not scientific but if let's say let's say a company had a six handle versus something in the 50, I think people would be like, oh, okay, that is differentiated. You know, do you think that there is actually room left on the table in terms of UPCR improvement that POVY couldn't test because they were limited by BAP inhibition, they couldn't hammer April up, and then SIBI couldn't because,

Aoife Brennan, CEO

again, they were limited by their dose or ADAs? Yeah, I think if you look at the SIBI phase two, you know, it does show that there's room for improvement there. So they, you know, the middle dose, their 4 mg per kg, which is roughly equivalent to their 400 fixed dose. You know, they saw, you know, April sort of creep back up within the dosing interval. When you look at the IgA reductions and the proteinuria reductions, they weren't as great as they were with the 8 mg per kg dose. And so I think they showed more dramatic IgA reductions. They showed greater proteinuria reductions, which I think importantly, what we believe is that it got more patients to target at that higher dose. And so I think the ability to dose up and even, you know, over time get a little bit more protein re-reduction, you might see within the spread because you're looking at medians. The spread and getting more patients to that target level, I think is going to become critically important as more agents become available. And I think that's the benefit of if you can do just a bit more, you could probably get more of those patients.

Susan Altschuller, CFO

Well, and Codaigo updated the guidelines that you're targeting 0.3 grams versus 0.5 grams because showing that even the low levels of proteinuria are imparting kidney damage over the long term. So we do think that there's room there.

Akash Nwari, Analyst — Jefferies

Now, maybe stepping back, again, there seems like a lot of different disease states where anti-arribal can work. And you might not be first in eigen, sure. But I think there's how you guys develop this drug. and I think this is going to be a relevant conversation even for Budo as well, sometimes it's the drug, but it's also really the strategy and the approach, right? So when you think about how you're going to develop this asset versus how your peers think about this class of drugs, how do you plan to stand out? And are there indications where you're confident you can actually be first in class?

Susan Altschuller, CFO

Well, I think that the standing out and how we're going to progress, I think that what is underappreciated about our path forward is our collaboration with our partner, MadWorks, in China. So we have our healthy, sad, mad study going on in Australia. They have a parallel study in China with sad and healthies and mad in IGAN patients. So we do think that that's going to provide us with more data, more dose-ranging data, et cetera. And when we do our spotlight event later in the summer, we'll disclose MabWorks plans, our plans, and then how we go forward together. But we do think that that's an asset in terms of being able to accelerate the development process.

Akash Nwari, Analyst — Jefferies

I know in China you often have these academic-sponsored studies, you know, or you can do basket approach trials. I mean, I think that's something that, you know, we've seen our GenX tap into as well. Is that potentially avenues that, again, are available in China that may not be available in Australia or the United States?

Aoife Brennan, CEO

Yeah, I think potentially. I think, you know, as Susan said, I think our focus at the moment is really on IGAN and shoring up that development path there. And I think coming as sort of that next generation, a lot is known about the biology. So we can focus on those differentiating parameters. Like we're already thinking about what would be our presentation at launch and what is optimal. So I think you can do a lot of optimization, um, to, to make, make sure you're in a really good position at launch, which when you're, you know, first and paving the way and learning about the biology and what's possible, perhaps you don't have the foresight to be able to do yet.

Akash Nwari, Analyst — Jefferies

Now, um, wait, has it already happened yet? It's happening. It's happening. Like I'm like, okay, I'm not that good. Um, okay. So it's happening. You guys are going to give modeling data. Like, what are you going to give at ERA? Have you already given it? Yeah, yeah, yeah. But, okay, so what should we get at ERA versus, you know, it sounds like there's going to be another data disclosure as we get to maybe ASN. So help us understand, and maybe not, like, what's getting drop one?

Aoife Brennan, CEO

Yeah, so I think tomorrow is our presentation at ERA. And from the abstract, you can see what we're going to share is translational modeling from the NHP data to healthy volunteers, and the basis on which we designed our phase one approach. So you'll also get the design and doses that we're looking at in phase one, and also what our partner is evaluating. So I think you'll get a really fulsome picture of our phase one strategy. And we'll also have some of the initial safety data from the ongoing studies. Okay. So it'll be a first piece and then what the data that everyone is more eagerly anticipating is that PKPD data which we've said will be later in the

Susan Altschuller, CFO

summer. Okay, understood. And then and then you mentioned you know ASN like you know that that's the other major kidney you know meeting in the second half of the year. There is potential for us and for MabWorks to have additional data disclosed this year but we haven't we haven't you know yeah laid out that

Akash Nwari, Analyst — Jefferies

plan yeah right but we wouldn't be surprised okay um now uh it's also tricky have you guys disclosed the doses you're taking that's tomorrow okay yes i'm gonna disclose the doses not surprising but um so maybe intent is the question right like because you know with jade too they're like hey we're thinking about this level of exposure there's one dose which is going to be much higher and that's more of a safety test um what are the doses that you're taking in terms of let's say relative like what you anticipate your induction dose to be and what you anticipate your maintenance dose to be are any of those doses getting tested um in the back half of this year and then are there other exposures that you're pointing investors to that you're going to be

Aoife Brennan, CEO

observing yeah i think what you know we saw was in the nhp data we looked at six mix per keg and 30 mg per kg, and, you know, we've said that we thought that 6 mg per kg was really in that, like, clinically relevant range. We tested 30, ultimately, to push a dose and to look at a dose that was equivalent to a higher dose that SIVI looked at in their NHP studies. And I think we saw, you know, a better profile with our 6 mg per kg relative to SIVI, which we've shared. And so then we kind of projected out into phase 1 what that range would look like to give us some safety coverage um both lower and higher and also give us a really robust data set upon which to model and yeah you know importantly our our phase one also has a mad component so we'll able we'll be able to model some accumulation and and the like as we think about repeat dosing

Akash Nwari, Analyst — Jefferies

understood um all right that's enough on april let's hit on budo um but hey let's susan for you like kind of the same question because look we've seen um some i can comment on some we can't present gilead about or now that's a good example there's a lot of bcma cd3s out there right but gilead bought that company partially because i think it's a strategy it's the approach it's the way that they're thinking about modulating autoimmune diseases and i think that sometimes differentiates just as much as the products themselves do as well you guys are in a similar situation no one's everyone's heard of c19 at this point um but what is your approach what is your strategy that you think is different that will really start to stand out yeah i mean so

Susan Altschuller, CFO

at our budo spotlight i mean and this is i underwrote joining climb on budo alone um yeah because there's there has been so much interest on cd19 with the car t's or tce's and it's almost like we went to the complex modalities where you're at risk for crs or icans and you're going to be treated at the academic center where the beauty of a naked monoclonal antibody approach to CD19 is that the community nephrologist can dose the patient or a hematologist can dose the patient. Uplinza is a great analog for uptake, you know, of a CD19 antibody. You know, we know that we have the sub-Q formulation that's differentiating and, you know, we're going into different indications. But I think that for us, and that's why the data that we had at the low dose for BUDO in five patients in the phase 1b proof of concept, really were compelling even at those low doses. But as you dose up, are you getting more durability of response, etc.? And the nice thing with an antibody is you can re-dose it. And one thing stepping back, in the five patients of data where we saw a complete B cell response, PLA2R seronegativity, and we had 60% complete renal response. That study, again, was stopped early, but we were able to have follow-up data on four of those patients, and three of the four didn't need any additional immunosuppression after just those initial doses of BUDO for three years. So the question is, with an antibody approach that's safe, you know, for some patients, do you have a treatment-free interval can it be a reset but i think also just the the the safety profile of budo and the the just the antibody approach is so much more amenable and it's it's kind of funny to me that

Akash Nwari, Analyst — Jefferies

we kind of skipped over that that's a really good point um and certainly i think the aplenza story uh is proving that out um so just to hit on one of these uh fc then on the safety so um on fc alone like there's levels of b cell reduction right we've got rituxan which again gets you peripheral reduction but it doesn't get into the spleen and the lymph nodes very famously like it doesn't get that level there's the car t's and the things that kind of really get there when you think about budo have you shown the ability to completely deplete the spleen like right like is the whole pitch we're not giving up anything by you know not having a cd3 in fact we're getting the exact same level of b cell reduction that's the question and that's why we're going to be

Susan Altschuller, CFO

dosing up to see but i think that what we we've already generated um a high sensitivity b cell assay where we can assess 0.4 cells per microliter and so you know we really do think you need to fully deplete the b cells to have that reset and so the question is in you know in what portion of patients and how many can you get there so that's kind of the experiment you know but do you have to get to that level with an antibody approach that you do with a CAR-T not necessarily but you know we're that's why we're dosing up and exploring any lessons you learned from

Akash Nwari, Analyst — Jefferies

uplinza with the cd19 depleter um is did you see was there an upper limit there that you know it got it got to a certain point but it couldn't really get to a CAR-T level I don't so uplinza

Susan Altschuller, CFO

is not i mean that's it's a cd19 it's it's b cell depleter just like ours but and um but they they went for nmosd i mean this was the horizon drug from viala bio and there it wasn't like they optimized for what we're trying to optimize to see as you dose up is this an immune reset approach i mean with nmosd if you have as you know if you have a flare like you could be

Akash Nwari, Analyst — Jefferies

debilitated completely so I think that the premise was always chronic like rituxan to be honest yeah

Susan Altschuller, CFO

but I think that with yeah and so then the other piece versus rituxan is that we're with the cd19 approach you're getting the plasma blast but you're preserving the long-lived plasma cells which is really that kind of why it's the goldilocks target we like to say for the antibody

Akash Nwari, Analyst — Jefferies

approach in diseases like can you talk a bit a it's like the dosing but what have you optimized with the molecule that is maybe different than Implenza.

Susan Altschuller, CFO

So picomolar affinity to CD19, enhanced ADCC, and we don't know why Implenza doesn't have a sub-Q formulation. We know it was assessed back in the day, but they don't. So that and indication strategy have been kind of the clear differentiators.

Akash Nwari, Analyst — Jefferies

It doesn't get talked about enough, but I think you're onto something that's quite important, which is, again, you're on these autoimmune conditions. And it's like, I think it's on a, you know, to get on IVIG chronically, probably not ideal and also just exhausting your T cells. But that's theoretical. Can you, is there any data points you can point to us where it's like, look, but maybe it's an oncology with the CD3s where you feel like there is a debilitating impact of chronic kind of T cell exhaustion?

Susan Altschuller, CFO

Hmm. I mean, I think, like, we're, like, our approach is harnessing the NK cell approach, and I think that that's why we think, you know, like, I think with the CD3 and the T cell approach, that's why I think the promise, or the promise of TCEs was you'd have CAR-T-like efficacy, but the safety of an antibody, and it's kind of not, we're not necessarily seeing that. And so the question is, like, can you get very good efficacy with the antibody approach? Could you get CAR-T-like efficacy at the right doses? And one of the other pieces you asked about the spleen, it's hard to get biopsy data, but we have a, so lupus nephritis, sorry, in SLE we have a parallel study we opened in China because in the U.S. you have to start at subtherapeutic doses. And we'll be trying to get biopsy data from LN patients in that study. We don't think it's necessary, but we do want to answer that question for ourselves.

Akash Nwari, Analyst — Jefferies

Now, maybe just last as we wrap up here, in terms of are there any combination approaches with, you know, BUDO and the anti-April that you're thinking about? Or really, no, they're two distinct molecules, two distinct profiles. That's not really what we're, you know, our long-term approach. We just have to ask what we're excited about. Because I'm hearing this theme of combination is going to become increasingly important. We're very convinced Argenix is going to be actually a combination story over the next few years.

Susan Altschuller, CFO

I think we think combinations are going to come, but is it like complement in April? So we see that as being a trend going forward, definitely. We haven't really contemplated a BUDO plus, you know, Just also, like, the dosing paradigm is different in terms of kind of the, you know, being able to target CD19, deplete the B cells, and you're dosed every six months versus – that's why we don't think that the CD38 or BCMA approaches are the right approaches, particularly for PMN.

Akash Nwari, Analyst — Jefferies

Can you expand on that a bit?

Susan Altschuller, CFO

Yeah, so in terms of the, like, again, the Goldilocks target, you're depleting the plasma blasts, but you're preserving the long-lived plasma cells so that you...

Akash Nwari, Analyst — Jefferies

Yeah, you don't have to get revaccinated.

Susan Altschuller, CFO

Yes, exactly.

Akash Nwari, Analyst — Jefferies

That makes sense. We are out of time. This is a great conversation. Not surprising at all. I really do appreciate your attendance, and thanks so much. Looking forward to tomorrow, because I knew the ERA is well.

Susan Altschuller, CFO

And the rest of the year.

Akash Nwari, Analyst — Jefferies

And the rest of the year. Thank you. Thank you.