Climb Bio, Inc. (CLYM) September 9, 2026 Conference Transcript

Hi, good afternoon, everyone. Thanks for joining us.

My name is Simone Nasrudin, and I'm one of the biotech associates here at Wells Fargo. It's my pleasure to introduce our next company, Climb Bio, and their management team, Dr. Altshuler. So I think it'll be helpful if you can start with an overview of Climb Bio first.

Yes, of course. Happy to. So, Climb Bio, we're focused on developing antibodies for immune-mediated diseases. So, we have two assets. They're kind of co-lead programs. The company started with Budo Prutug, our monoclonal antibody targeting CD19, while the CD19 space in complex modalities like CAR-Ts and TCEs is quite crowded. There's really only up Linza and Budo as naked monoclonals to CD19, and we have a small data set from the phase 1b study in PMN, and now we're in a phase 2 study in PMN, and then a phase 1b in ITP and SLE, and we think there's broad potential for Budo-Futug across immune-mediated diseases. And the targeting of CD19, you're getting across the B-cell lineage from the pro-B-cells, and then you're getting plasmoblasts, which are responsible for the pathogenic autoantibody production. So we feel that that's a pipeline and a product. And then we in-licensed our April-only antibody with a sweeper mechanism of action, which I'll explain, from MabWorks in China. That came in off of one monkey of data, and we generated the NHP data that was presented at ASN last year. And we just last Thursday presented our healthy volunteer data showing a best-in-class 12-week profile for IgA nephropathy with the APRIL asset. So we are moving quickly. We're in a phase 2 study in IGAN patients and working to move to a pivotal hopefully next year. So a lot of activity, and I'm happy to go through, as we go through the program, talk about the catalyst. We have numerous additional data readouts this year and into next.

Yeah, you guys have a lot going on. So I'm going to dive into CLIME 116 and its opportunity to IGAN disease. Do you want to start with the mechanism, the sweeper mechanism, before we get into the data?

So when the company set out to get an asset in the IGAN space, we were April-only believers. First, we didn't believe that BAF was adding to the efficacy profile, but also opened you up to safety liability. And the sweeper mechanism of action for an abundant, soluble ligand like April makes a lot of sense. It's pH-dependent binding to April, and it's the Chugai technology. From back in my day at Alexion, it's the Solaris to Ultimeris. So you have high affinity binding to April extracellularly. It's internalized, and then the APRIL is released and degraded, and the antibody is recycled. So what that does is it's a potentiating effect. You're actually degrading the APRIL, recycling the antibody. So what we're not seeing is TMDD that you see with all the other products in the space, like SIBI, et cetera. And so that is allowing us to have a drug concentration, a nice linear PK profile, free April suppressed over that 12-week dosing interval. And ultimately, the way that the biology works is if you're inhibiting April, then you're inhibiting IgA, GDIGA1, and that ultimately leads to proteinuria reduction and ultimately EGFR stabilization. So, we've focused, like, the first generations in IGAN, at best, are dosed monthly. They have different safety liabilities, and you're getting to 50% IgA reduction. So, we think that with 116, we can win on all three, every 12-week dosing, clean safety profile, and being deeper than 50% IgA reduction.

So getting into the data, did the PK and PD data perform as expected, and how should we think about the translation to IGAM patients with higher APRIL burden at baseline?

Yeah, so it did. It met all our expectations in terms of being able to have a profile where we see that free APRIL suppression over the dosing interval. And I think that the PK profile is nice linear curves, especially when we're over doses at 160 megs and above. We're not seeing any of that, like, deep drop-off that you see with TMD and others. I would say that the PD profile as well with the sweeper, you're seeing deep IGA reduction and a GDIGA reduction, which are better than what we saw with the first-generation assets.

And what level of free April suppression do you need at the end of that 12-week interval, and how do you expect coverage to look like with every 12-week dosing?

Yeah, so with our, so we actually are, we had a concentration of 160 mg per ml, so we had doses of 320 and 480 that we reported in our data set, but we have a high concentration formulation so that we will have a 400 mg maintenance dose going forward. And when you think Think about the goal. You want to have like 90% plus April suppression over that interval because IGA then follows from that a week or two later in terms of the rise. So with our 320 dose, knowing that our go forward will be 400, you had 90% pre-April suppression through 10 weeks and just at like 75% at week 12. We know with repeat dosing, we will have

And then looking into the ADA data and immunogenicity data, how important is it to evaluate the durability of that during the 12-week regimen, and when can we expect an update on that data?

Yeah, so we don't have those data yet. We're developing the assay with our partner, MabWorks, to make sure we have that aligned for the Phase III trial. But I will say that when we look at all our data and the individual patient data, we are not seeing any ADA impact, and also one of the things with ADAs that has the reason that people are focused on them is sibaprenlimab targets an epitope on April that causes daisy chaining and high molecular weight complex formation that leads to the ADA formation neutralizing antibodies. We showed in ASN 2025 that we're targeting a different epitope on April, and we don't have that high molecular weight complex formation, so we don't think that that should be an issue going forward. But we're developing the assay, so once we have the data, we will share it.

Okay, and you mentioned that you guys are going with a higher dose for the phase 2 and phase 3. So did you see any tolerability differences with the higher concentration dosing?

No, and from 160 mg per mil to 200 mg per mil, we're not concerned. It was very minimal injection site reactions, so we don't see any difference moving up.

We just are maximizing the concentration that we can deliver

in a single 2 mg injection, because formulation matters in IGAN.

Mm-hmm. And when we're thinking about the relationship between the death of IgA and GD, IgA1 suppression, and the level of protein error reduction achievement in the phase two, how should we think about that? And also, how should we think about, like, the phase three that you guys are already pursuing, too, and the protein error reduction there?

Yeah, so what we've seen, and we've gone back and looked at, again, the data from first generations, as you are increasing GDIGA reduction, you

are also increasing proteinuria reduction.

So there's a real correlation there. And with the CODIGO guidelines changed to you're trying to get patients to 0.3 grams per day versus 0.5 grams per day, because even low levels of proteinuria are causing kidney damage over time. That's what the radar study showed. So we see that, you know, there's going to be a real desire to manage patients to keep the proteinuria levels low, and you get there by having full APRIL suppression over that dosing interval.

How are you guys thinking about long-term immunoglobulin monitoring and infection risk under chronic APRIL inhibition?

Yeah, so we, again, we don't have the BAF component. We saw no hypogammaglobulinemia or even any levels below normal in our study, and again, as we mentioned, we don't have the high molecular weight complex formation, and we think that the profile over the long term with an April-only approach, what we've seen is, you know, very safe profile, And, and no concerns there.

And I know you guys are starting the phase three soon. Or what feedback are you seeking from the FDA on the registrational strategy?

So, so stepping back, so we had our SAD, MAD study in healthy volunteers in Australia. And that's our data set. Our partner MabWorks in China had a parallel healthy volunteer SAD study. And then we are jointly doing a phase two study in IGAN patients. So I think that the totality of those data, and especially given in the IGAM space how readily healthy volunteer data translates into patients, et cetera, so with our data sets together, you know, we think that that should really provide confirmatory support to bring one regimen into a pivotal trial, and again, pending regulatory feedback, that could be next year. So the phase two study that we are doing jointly, we designed it before we had these data. So it's very likely that we're heading to full approval with one-year EGFR, UPCR endpoints. So to make sure that we're getting more patients to target more rapidly and optimizing for that, we decided to have one loading dose, so 800-mig loading dose, so two injections, and then 12 weeks later, the maintenance dose of 400. And when we designed the trial, we didn't know yet what the data would be, so we have a loading dose, and then an eight-week regimen, and then a 12-week regimen. And then we had an optional additional cohort that we will not be going forward with. I think that with the data that we have, we're looking to confirm the 12-week profile that we have in healthies and patients and then move rapidly to a pivotal.

Thanks, Hans. And my last question on the eigenopportunity. So from a commercial perspective, is the larger opportunity in treatment-naive patients or patients who are inaccurately controlled on the first-generation agent?

Oh, I think that it's both. This is a space where nephrologists have had nothing to give their patients, and now there's recognition that these disease-modifying therapies are really going to be game-changing for patients in this space. We think there's around 200,000 IGAN patients in the U.S. alone. This is a $20 billion plus market. The first generations at best are monthly dosing. They have some safety liability, and they're at 50% IgA reduction. Yes, you're seeing EGFR stabilization, but there are subsets of patients that are not getting to target. And so our goal is to get more patients to target and have that safe profile with 12-week dosing. And so we see that as patients are going to be monitored based on their UPCR. If they are not responding, they're going to switch. But if you're a new patient, the biology of April is very established and validated, and we expect switching to a best-in-class or starting with a best-in-class profile after the first generation have kind of established the market and grown it.

So commenting on the best-in-class profile, outside of dosing advantages and, I guess, the deeper April suppression that you guys are pursuing, are there any other attributes that you think you can differentiate here from the first gens?

Yeah, I think that the focus is the safety aspect, no hypogamma globulinemia, long-term infection risk, especially patients who are in their 20s and 30s when they're diagnosed, so the infection liability is a question over the long term. And so for us, it's really about that deeper, the full April suppression gets you that deeper IGA and GDI-GA reduction. And so I think that the results that we showed both in IGA and GDI-GA were really compelling to KOLs. And so if we replicate this profile, that's very differentiated across those three pillars of safety, efficacy, and convenience. Okay.

And with the lack of efficacy, seeing what like the dual BATH and APRIL inhibition in IGANS, does this influence where you see the greatest expansion opportunities for Climb 116?

Well, so with a best-in-class APRIL asset, we are now making sure that we explore where else we might bring this. I know people have talked about SIPI going into Sjogren's, and we're looking at, you know, which disease states and areas would we want to move forward with now that we, you know, once we confirm the profile in patients, want to make sure that we're, there's lots of diseases where an April asset is going to have potential, so we're exploring that now. We want to move quickly. Yeah, makes sense.

I guess switching gears to Budo-Proutignal, which component of the profile is most important for driving deep and durable B-cell depletion, and how relevant is that differentiation in tissue components where traditional anti-CD20 therapies may underperform?

Yeah, so maybe just stepping back, like when we think about our portfolio, there's a really nice synergy across, you know, April and where we're at in IGAN. And then with CD19, we really think it's the Goldilocks target for PMN. And so we've got this, you know, the renal disease across both. And I'll go, the reason I bring that up is that povitacicept is being studied in PMN. We don't think that that is the best approach or profile in PMN

versus a CD19 approach.

So CD19 is IgG4-mediated disease. The plasma blasts are what is responsible for the pathogenic autoantibody production. It's in 75% of patients, it's PLA2R. And so with CD19, you're getting across the B-cell lineage through the plasma blasts, A little bit of the plasma cells, but you are not depleting the long-lived plasma cells that are required for vaccine-based immunity, and so we do, so, and with the CD20s, they are not getting the plasma blast, and, you know, they're bringing things down, but they're dosed every six months, so, and at best in PMN, the complete renal response, obinutuzumab just had their data at ERA in June, and at 18 months and two years, it looked just the Same as rituximab, 36% complete renal response. And what we had in our five patients of phase 1B data was a 60% complete renal response, you know, full B cell depletion, PLA2R seronegativity, and the complete renal response in three of the five patients.

So we think that profile is incredibly compelling and

in line with current standard of care, which is rituximab. And if you were given a CD20 and you haven't responded, are you going to go with another CD20 or are you going to go with a CD19 approach, which, you know, fundamentally is getting to the underlying disease pathophysiology. So that's the approach with PMN. Now, when talking about, like, the April baths there, you're damping things down, and you're going to have chronic dosing, and it's monthly at best. And so in our Phase I-B study, we had follow-up data for four of those patients, and three of the four didn't need any additional immunosuppression after just two doses of BUDO, two weeks apart, and then six months later. They didn't need any additional immunosuppression for three years. So the question is, as we dose up, are you getting more patients to have, you know, getting to target and having a treatment-free interval? So that's the approach there and how we think to maximize. And then with Budo, just the approach was, again, PMN makes a lot of sense, and we had the original data. We're in phase two there. But then we wanted to say, you know, this is a potential pipeline in a drug, and you see with a Blinza, once you know the dose, you can go right into pivotal trials. So we, PMN gives us our renal dose. There's a very strong rationale.

We also then started a phase 1b in ITP to

get a non-renal dose, and it's a great disease to assess because you see the B cell depletion, platelet response. But we've said that we wouldn't go forward in ITP with a pivotal unless we were really seeing a substantial differentiation in durable platelet response, which right now, with all the current therapies available, is around 20%. So we'd need to see something far above that. And we did see that in the 250-mig cohort that we presented at EHA. And by year end, we'll have the data in ITP at the 500 and 1,000-mig cohorts.

Okay, I guess piggybacking off the ITP comment there, the 20% is what you need to see to advance.

No, 20% is what, like, all the agents in the space, the BTK, the sick inhibitors, you're only getting about a 20% durable platelet response. We saw well over 50% durable platelet response in that small and 250-mig cohort, which is why we're looking forward to putting forth the 500 and 1,000 data by year end.

With that data by your end, I guess, what exactly are you looking for beyond what you already showed to advance the program forward, and how do you envision the chronic maintenance dosing or periodic disease resets?

Yeah, so again, small ends in the phase 1b study, so we want to see those data were incredibly compelling. Do they hold up as we have a more larger end, more heterogeneous population of patients? But seeing something like we saw much greater than 50% is really compelling. I think that, again, with the Phase 1B trial, we were dosing patients, and we had an option to redose. I think that's where the pivotal would end up. If we ended up justifying going there, you'd want to make sure that we'd see, is it chronic dosing, or are you, again, getting that reset for some patients over time, depending on the data?

Okay, and I know you already touched upon PMN, but can you, like, elaborate more on that opportunity, and how should we think about the expected remission rates as you move into a broader, more severe patient population?

Yeah, so it's around 75,000 patients in the U.S. We do think there's nothing approved. We do think that with the Gizaiva data and Roche, you know, going forward in the market, that there's going to be more and more awareness and rising interest. It's not like IGAN, where patients are largely asymptomatic and diagnosed young. They're heavily proteinuric. They have a lot of water on them, and so we think that this is a disease that really needs disease-modifying treatment, and so, again, complete renal response is the aligned endpoint that FDA is looking for, and if we're able to recapitulate what we showed, Which was, you know, OB was around 36%, and we had 60% in that phase 1B data. But what we will do in a larger patient population is characterize baseline characteristics, how much proteinuria is on. And that's also, the five patients of data we had were, three were at 100 mg, two were at 200. Incredibly compelling. But again, we want to see, do we dose up in a more heterogeneous population where there might be some more patients that start out with a higher level of proteinuria?

I guess, what would be the ideal baseline populations, and how many?

I think that the goal is to have a broad range of the refractory patient population. So we want to, I mean, I think that this is not a subset, really. Around 30% of patients will spontaneously go into remission within, like, six months, but the rest of the patients we think would be eligible for a disease-modifying therapy like BUDO.

Okay. Moving on to, like, the SLE opportunity now, what can we expect to learn from that upcoming data set? You can talk more about, like, the opportunity there as well in your plans, and when will the program reach, like, clearly therapeutic exposure levels?

Yes, so that's a great question. So when we were designing kind of the strategy to characterize BUDO, So PMN makes sense, renal disease, ITP, hematologic disease, and then lupus. There's a strong rationale there, but we think of our study as more of a, or two studies more as a translational experiment, just knowing that it's a very different beast to go into a pivotal trial in SLE, more heterogeneous population, probably 2,000 patient study, and And more subjective end points. So we see that. So we started a global study, but FDA requires you to start at Mabel doses in SLE. So the data we'll have for BUDO and SLE this year will be a single dose at 100 mg. So we'll be looking at B cell depletion, etc. there. I think that's interesting, but more we have a parallel study in SLE in China that we started where you can start at therapeutic doses. So that will come next year, and we'll be able to, if we see real potential in SLE, that's something we think that's more of a partnership opportunity versus something that we as CLIMBio can execute on our own. So I think that we, you know, there's clear potential there, but we just recognize the cost and challenges associated in such a broader indication, and so would need to see really strong data to underwrite a pivotal there.

What are some of the benchmarks, I guess, for the data?

Well, so with the data that we have this year in terms of just looking at the B cell depletion, I think that that's where the focus for us, I think, in this space is really the PMN data set that we have in the fourth quarter and the ITP data set. I think it's next year we're at the therapeutic doses where you can look at additional endpoints other than just the B cell depletion.

Okay. And I know you guys are working on the SC formulation for BUDO. Can you talk more about your progress there? And I guess what indication would be the most likely initial opportunity for that formulation? And do you think the SC administration would help you meaningfully expand use beyond academic centers?

Yeah, we, so again, we were able, the differentiation we have versus up Linza, we have higher affinity to CD19, enhanced ADCC, and we have, we showed in May at our Budo Spotlight event that we were able to equivalently deplete B cells with a sub-Q formulation and an IV. But what, in healthy volunteers, you can't fully deplete a patient, the volunteers in these cells. So now we need to go into a patient study, likely a basket study, to further characterize what that profile looks like.

Is it more Ocrevus-like or Cosimpta-like?

And we would not wait for the sub-Q formulation to move into a pivotal in any indication, you know, if we were justified to go forward in PMN or ITP. We know that we could do a bridging study for that with LAUNCH, but we think that the sub-Q formulation is just going to provide a lot of additional optionality for us, not a differentiated indication strategy.

And I guess stepping back now on just BUDO in general compared to the other B-cell diseases and opportunities there, Where do you expect the biggest advantage to emerge between BUDO and, like, rituximab and B-cell-mediated diseases?

Yeah, I mean, I think that, again, it's about targeting the plasma blast and having the broader coverage across B-cells.

One of the things that, and another

thing that we talk about in dosing up is, like, obinutuzumab, they've been able to show, like, you are able to deplete B-cells in the tissue as well as in the periphery. So that's another aspect of Budo.

As we dose up, are you able to see more of that reset?

I think that one of the tailwinds for Budo and that aha moment is that there's just a Linza and Budo in the naked monoclonal, and you're not worried about the CRS risk that a TCE or a CAR-T would have. So you think about the community nephrologist being much more comfortable prescribing a naked monoclonal antibody approach to the broad swath of patients where you'd be reserving the higher risk modalities for only the most severe patients.

Is there a specific patient population where you think BUDO could become the preferred anti-CD19 therapy?

Well, I mean, we think in PMN, definitely. I mean, I think that the, again, the CD19 had been overlooked because CD20 is just expressed in greater abundance, and I think that the, now that we are, like, the oblinza uptake and kind of really seeing where there's potential, we think that the CD19 naked monoclonal in these B-cell mediated disease is going to be a preferred mechanism. And that's why we want to make sure that we, that's why we have the coverage across the different indications for BUDO, because we know that we can go into additional indications once we've got that right dose.

Speaking of the PNN opportunity, what's the biggest remaining clinical risk there? And do you think that, like, years later, if it works out, would it primarily be used in patients with persistent disease?

I mean, so these patients, as I said, like, I think, you know, there's the spontaneous remission, but then you've got 70% of patients that are going to need a chronic treatment to control their disease. And so in PMN, there is, again, just rituximab and obinopituzumab, the CD20s. And there are other approaches, but we do think that the CD19 monoclonal approach, where you're dosed every six months and there may be an opportunity for a treatment-free disease I think in terms of kind of the risk, the data that we will present in the fourth quarter where we have the 200 milligram, 15 patients from that first cohort, if we can recapitulate the original data, I think that will be very de-risking, people seeing that we have a drug here, and same with the ITP data later in the year. So I don't think that there's any one watch out. It's just, are we able to see and replicate what we did in a smaller patient population and a broader, more heterogeneous population? But the biology is very well understood and validated for both these assets.

How much of Budo's potential value depends on demonstrating superiority versus existing B-cell depletion versus simply just offering a more convenient, durable alternative?

Well, I think that, like, again, with what you're seeing, like, in PMN is at 18 months, two years, obinutuzumab had, you know, 36 percent. So that's not a great response rate. And so I don't think you have to be better because it's just if you aren't responding and you have a different mechanism, patients will switch to that. But we do think that the CD19 approach should also provide Better efficacy.

And just piggybacking off your prior comments on the dosing, I guess, what are the key dose response questions you're trying to answer when you go from like a phase two to phase three?

So for our phase two study in PMN, we actually, so we designed it so that we're enrolling patients that are PLA2R positive, because again, that's like 75% of the patients. And the reason we're doing that is we have 15 patient cohorts at 200, at 600, and 1,000 milligrams. And we don't want to have to wait for the proteinuria data from the highest dose cohort to make a go-forward decision and go into the pivotal. So we can base that off the PLA-2R data. But we will have all comers for the pivotal trial.

And speaking of the PLA-2R data, how are you thinking about the relationship between the anti-PLA-2R reduction and the ventral clinical remission and PMN?

Yeah, they're very correlated. I mean, actually, the parasol group is exploring PLA2R as a surrogate endpoint. I mean, the complete renal response at either 52 or 72 weeks is the approved endpoint now, and we'll be looking at PLA2R levels, of course. But I think that it's an interesting approach, and it will be helpful in surrogate and measuring.

But again, 25% of patients, their PMN is driven by a different autoantibody,

which, again, CD19 will address. But using that as the surrogate for all PMN trials going forward, not sure.

It seems like you guys have, like, PNM pretty, like, planned out. But I'm thinking for, like, given the complexity of SLE, how are you guys thinking about the eventual positioning there with positioning GUDO against the CD20-directed therapies and other targeted biologics?

That's why we say it's more of a translational experiment right now. We really would have to see quite compelling data from that China study to say, okay, we're going to partner this and go into a much broader population, and I think that we will have the totality of the data we have for Budo next year will really let us know kind of where else we want to take it and where we as Climbio, like the PMN pivotal, ITP pivotal, less than 150 patients, that's completely within our capability to execute and deliver. SLD is just a totally different ballgame.

Makes sense. So going into more corporate questions now, with multiple data sets expected by year-end, how are you guys thinking about capital allocation across 116 and Buda as both programs mature?

Yeah, no, it's a great question. So we ended Q2 with $239 million and our runway goes into the second half of 2028. We raised $110 million in a pipe at the end of April. And the reason we did that is we wanted to be able to move with expediency, knowing that we, and I'll talk through the catalysts that we have next, but we are now, the funding through the first half of 2028 is inclusive of CMC and Pivotal startup and execution spend for 116 in IGAN and for Budo in PMN. So we wanted to make sure that we could move expediently no matter what, but yes, to run a pivotal in IGAN, we would want to bolster the balance sheet to get through full approval, but I think we're in a very strong position. Talking through the catalyst, so we just, we had our, in May, we had our BUDO spotlight where we announced the sub-Q data. Last Thursday, we announced our, the top-line data from our healthy volunteer study for 116. Then in the fourth quarter at a medical meeting, we and our partner MabWorks will have additional data from our healthy volunteer studies, and we will also have our 200 milligram cohort of BUDO and PMN. Then we'll be SLE, and then by year end, the ITP data. And then our ongoing IGAN phase 2 study, we will have data coming out from that probably every two to three months. And, you know, with regulatory feedback, we could be in a pivotal next year. But we've said the phase 2 IGAN data will be in the first half of next year. So, and then also the VUDO 600 and 1,000 milligram cohorts and more SLE data. So, it doesn't stop in 26. It keeps going into 27, but it's really a joy to have two assets being explored in so many indications.

So, what would a global IGAN phase three program cost, and at what point would you guys consider, like, partnering?

I don't think that that's something that we would need to partner. That is a $150 million or so study, something that we, with our partner MabWorks in China, can readily execute. And we think that that's a real asset, our partnership, just because, and also in China, the standard of care in IGAN is very similar to that in the U.S. There's not a genetic reason that you'd see variability. So we feel very confident about our ability to execute a pivotal, and again, and that's, it's only three or four hundred patients. It's not the 2,000 patients SLE study.

Makes sense. And I guess my last question with the minute we have left, what is the biggest thing that you think investors are missing about ClownBio today, and what's the success look like three to five years from now?

Yeah, so there's a lot of things. I think that when you look at our, you know, where our valuation is relative to competitors, and we have two phase two assets, I think that there's just been a disconnect. And I think part of the challenge is getting folks, we have so much going on, we have two antibodies, multiple indications. So really just getting the story out and the clarity about the potential in each is really the piece for us. Five years from now, we think that we're going to be experts in the renal space and broader autoimmune disease, and we think we have that potential pipeline and a product with both of our assets.

Sounds good. Thank you so much. Thanks so much.