Jade Biosciences, Inc. (JBIO) September 14, 2026 Conference Transcript

Good afternoon everyone, welcome back. Thanks for joining us to have a conversation with Jay Bile. With us today is CEO Tom Froelich and CFO Brad Dames. So I guess Tom, both of you, welcome. And Tom, I guess to kick off, for the investor new to your story, could you give us an overview you on what Jade is and how is your guys' Chinook background as well as the partnership with Paragon to shape your strategy there.

Yeah, absolutely. And first of all, just thanks Arthur for hosting us here at the conference. It's been a great couple of days. So thanks to you and the whole H.C. Wainwright team. So at Jade, we're a company focused on developing best-in-class therapeutics for autoimmune disease. We have three assets in our pipeline that, as you mentioned, we have licensed from paragon and work with them on the discovery process there i'm sure everyone's familiar with paragon they're able to develop extremely high affinity binding antibodies and have a particular expertise in half-life extension should i let's kind of go okay i'll just use this um half-life extension technology and the difference between the or the combination of that potency and the half-life extension just allow to have really best-in-class therapeutics Our lead program is Jade 101. It's an anti-April in development for IgA nephropathy. We reported a positive phase one data a few months ago showing very deep and pronounced reductions in IgA, which is the key biomarker that would predict clinical activity. so feel very confident about having best in class clinical activity with the asset and those iga reductions were suppressed for for 12 weeks which gives us confidence in getting acute 12-week dosing interval for for maintenance so really moving forward with that asset currently in phase two looking to read out that phase two study in 2027 and we're also moving very quickly towards initiating a pivotal trial uh anticipate initiating that study in the first half of 2027 j201 is an anti-bath receptor uh that's an a few cost related effector function enhanced bath r uh very exciting because it has a dual mechanism of action in b cell depletion one it can drop b cells in circulation very quickly but also it blocks baff signaling uh to starve those b cells from that pro-stimulatory signal and so we're very excited by that has applicability across a number of different autoimmune diseases that agents currently in a phase one study in rheumatoid arthritis patients and reading out next year as well in 2027. The third program is J301 which we recently disclosed it's going after dermatomyositis it's an interferon beta antibody anti-interferon beta. Dermatomyositis is an area of high unmet need with symptoms in the neuromuscular and also skin components. We're following in the footsteps of a compound called Dazu Kaibart which is currently at Pfizer. It's another interferon beta asset showing very promising phase 2 data showing good activity not only on the total improvement score which is the the primary endpoint but also on skin uh really best in disease activity on on skin uh they're currently in a phase three study reading out next year uh we believe we have the opportunity to positively differentiate from tazu kybert because it's uh has low bioavailability and is dosed iv uh and with j301 we can capture the activity but uh go sub q to have a big advantage um so super exciting pipeline uh underpinned by by strong financial position and then as you mentioned as well a lot of our team actually come from chinook where we all work together so have a lot of experience

developing drugs together particularly in iga nephropathy and really have great capabilities to push these programs forward at speed awesome uh thanks tom so maybe let's stick to the eigen and the one-on-one for a bit uh i guess we all know there's a couple of uh new eigen drugs will be on the market by the end of the year um so my question like for you guys is like why are you guys thinking making eye gain as a leading asset and what you think um the uh at the end of the day when one-on-one will be available uh how the market landscape look like yeah so we we're working on iginefrapity at chinook uh as as you mentioned uh but we had a

couple of long-held beliefs and thought there was some actually some unfinished business there. The long-held beliefs were one, IgA nephropathy is a very large market opportunity, almost 170,000 patients diagnosed in the U.S. More than half of those, 60 to 75 percent, are at high risk of disease progression as defined by higher levels of proteinuria and really believe that they need therapy but 50 of them will progress to end stage disease within 10 years of diagnosis so so a huge unmet need there we've also had a long-held belief that the anti-april the selective anti-april mechanism of action will be the dominant class because it does reduce pathogenic iga reduces proteinuria and can stabilize kidney disease function so we believe that's going to be the predominant foundational therapy for patients and then within the class we think there's room for improvement that's why we developed jade 101 to be extremely potent and long acting to be able to fully capture all of the efficacy available to the mechanism and do that in the most convenient format for patients these patients are typically diagnosed very young in their second or third decade of life but have a high lifetime risk of progression so need lifelong therapy so giving them something that is going to be convenient and have a low treatment burden is going to be very very important i see so uh you guys reported a positive phase one data uh early um this year so could you work the newer investor how the data overview for for that yeah um yeah happy to talk

through that arthur yeah so i think if you take a step back tom was mentioning there's really like two things that we were trying to solve for with j101 when the drug was initially invented one you want to have really high binding affinity to april and then two you want to have an extended half lift so that's why the yte modification in the fc but on point one we have a novel epitope that was designed for ultra high binding affinity to april so it's a femtomolar binder it's about 750 fold more potent instead of from the map in terms of its binding affinity to april about 2 000 fold more potent than ziga chi bar and what we wanted to show in the phase one data set was was deep IGA reduction. So our target was to get to what the initial, so let's call them the first gen B-cell modulators such as sidroprimumab and popetazicep showed at their higher doses that they weren't able to take forward for various reasons, which was roughly in the high 50s to 60% range of IGA reductions. So we're very glad to see that we're actually able to get to 70% IGA reductions in our 700 milligram dose, which is our induction dose. And in our pharmacodynamic modeling, where we basically created a virtual IGAN patient population leveraged off of primarily the CIVIT-FERILMAP integrator review. So taking JADE-101 attributes, such as pharmacokinetic profile across all doses, and then taking all the geographic disposition from IGAN patients, different body weights, showing 500 simulated clinical trials so we can sustain those IGA reductions at deeper than 70% with a single sub-Q maintenance dose of 350 milligrams. So we're able to get to a Q12-week maintenance dose based on our Phase I healthy volunteer data. And because this mechanism is so well-behaved, IGA reductions at early time points are very well correlated with UPCR reductions at week 36, which, as you know, has been historically the accelerated approval endpoints. I'm really encouraged by that overall. uh so from a and from a half-life extension standpoint we're able to show almost a three-fold increase from the uh first-gen citiprilimab uh human half-life uh and then almost a nine-fold increase uh over povitacis in terms of uh its half-life and then tom was talking about the selective anti-april moa we feel very strongly that that is uh leading to all of the efficacy and again after all it's a plasma cell mediated disease but importantly we're able to show a very clean safety profile consistent with the selective anti april moa at doses all the way up to 1400 milligrams so really encouraged by the overall data set in terms of getting best in class iga

reductions showing that we're able to do that for a q12 extended dosing interval and then showing the clean safety profile of the april moa uh thanks very much all right you pretty much answer my follow-up question so so i guess uh let's getting a little bit more active here so we will know climb by also drop their data and early this month um so i guess two questions so what's your overtake on the data and i believe they decided to go taking 800 dose plus 400 maintenance dose uh forward like as a as a go uh regimen forward right so do you think did that go deep

the ig reduction for that for their drug so i think we'll have to see it's really hard for us to speculate on on their go forward regiment without seeing the data i think we are looking forward to asn whether to present more follow-up data on the higher doses they they had in in the phase one um one thing we did notice with the first generation of assets of anti april's like cibiprinlimab and zigakai bart um is when in their single ascending doses when they increase the dose to to very high levels that are kind of multiples of what you see in their phase three in commercial doses uh that they weren't really punching through a plateau in iga reduction so cibiprinlimab had a 50 to 55 percent reduction in iga even when they went up to 12 mg per kg iv in the single ascending dose uh they weren't breaking through what what what you kind of see is sort of that that plateau we haven't seen that yet with the climb data um their 320 mg dose was was quite similar to their 480 or their two times 320 we didn't see a deepening of effect but you know the caveat there was early time points and probably need to to see a little bit more i think what we find extremely encouraging though as brad was pointing out uh is that with jade 101 and we think it's really driven by the potency as you are seeing those extremely deep reductions in iga kind of high 60 approaching 70 with a 700 make uh cohort uh where we are getting to these really deep profound reductions in iga at early time points uh which can be sustained with 12-week dosing which we think gives us the chance for best-in-disease activity.

Sure. So another aspect for their data overview there, they claim this seems like there's no TMDD for their drug. But J. Wang Wang has a similar to SAV, they still have a little bit of TMDD there. So, but with a very high potency.

So my question is, in your view, what's the pro and cons for for a high affinity antibody with tmdd versus uh relative low affinity with without tmdd so what's your guys thinking yeah we think that the most important thing in iga nephropathy and sort of says it in the name is is driving down those those iga levels to very profound levels um and doing that in in a time course that that allows you to see good effects on proteinuria and then eGFR stabilization at fairly early time points that gives that clinician and the patient kind of that really the feeling that the medication is working and you're going to get to those Kdigo targets which is below 0.5 grams a day and understand if you're going to achieve those with a medication in a reasonable time frame. And we really do think it's the potency that's driving that ability to get to those deep IgA reductions um and so there's there's a great advantage there um with jade 101 with a dosing format that uh or the dosing regimen that we're taking forward there's a 700 milligram induction dose uh which gets you kind of well above that tmdd range and then you start your maintenance dosing at week four with 350 mgs uh and then every 12 weeks thereafter um so you can really make sure that those iga reductions are are staying down uh over time uh so we don't think there's a big penalty to to having that potency i see um so i guess they're wrong already in the

phase two and uh and the guidance for for next year for data so for for the data readout what what's what's the expectation we should put out yeah so it's uh yeah so it's a 30 patients uh open label phase two pretty consistent with what you've seen with some of the prior igan trials we dose our first patient in uh may just before we uh disclose the phase phase one data um enrolling in in multiple sites to be pretty you know representative of a global igan population um it is a small study right so i think it's tough to put exactly what you know a success looks like obviously you want to be in sort of the zip code of what the first generation uh agents showed in terms of proteinuria um but we have guided that we'll have data in uh in 2027 so as we get closer to that we'll start narrowing the guidance around you know what what quarter that'll that'll be but yeah really excited to have that uh have that readout and then um while that trial is going on we have also got it we'll initiate the phase three in the first half of 20 2027 so really trying to move j101 to get to market as quickly as we possibly can i see so i think you guys take a kind of right to take a risk of initiative phase three uh before kind of phase two data fully out um have you guys interact with the uh fda in regarding the design of phase three so there was a uh national kidney foundation meeting back in the in the spring so basically the fda called this consortium uh that consisted of uh doctors regulators sponsors including us patients to talk about novel uh designs for phase three trials acknowledging that it's you know not ethical to have patients on placebo for two years as has been the case in the first gens it seemed that they were coming out uh leading to a you know a year to a year or so for for a primary uh primary endpoint um depending on the on the mechanism so we know that the b cell modulators have shown to be relatively safe so feel pretty good that it'll be a much shorter duration trial than the two-year trial um as we have our own interactions uh we'll you know we'll update the street on those but feel again very good about the initiation of the first half of 2027. Awesome.

And another aspect is you guys decide taking both QA week and Q12 week together into the pivotal trial. I guess what's maybe help out here a little bit, like what's the rationale and what's the, what if the QA week is really good?

What's that going to be happen for your strategy for the q12 week yeah so so i think that would be kind of a big surprise to us because when we do look at the pkpd modeling um it does look like the q12 week dose will maintain the same levels of iga suppression uh as the q8 week dose so our expectation is actually to have very little differentiation between the doses um and our intention is to commercialize the the q12 week dose and and have that as the predominant dose on on the market the reason why we have those two doses in the phase three design is as brad points out we're not waiting for the phase two data because it would take actually quite a bit of information to try to differentiate between the two if if at all but we do believe because we're moving forward so quickly there may be a global regulatory expectation that we have some dose range finding in in in the studies which we won't have from the phase two at that point because we're moving so quickly so we're kind of preemptively putting that in there to be able to make sure we're addressing those concerns and allow quick initiation of that study we don't think there's really a big penalty there either or a cost to including the two dose arms just because we now know from the the first generation of agents kind of what the assumption should be around the placebo group drop in terms of egfr

and also what the the treatment effect size should be from the active groups and so we know how to power the study for for the number of patients and it's actually probably more powered around the safety database rather than an efficacy size so including the two dose arms actually isn't that much bigger than just having a single dose arm going forward I see that makes sense so maybe let's shift the gear a little bit here I know you have another two in the pipeline 201 and 301 maybe we get 201 first so um the data is next year you guys haven't decided indication yet right uh my question is what kind of data could i give you a very clear guidance to

making a pick of the in terms of indication one yeah so as mentioned in the introduction we're following in the footsteps of another baff receptor antibody inalumab that's currently at novartis they they've run six different phase threes and have positive shogren's data what was really interesting in that shogren's data is they ran two dose arms a q4 week and then a q12 week arm where the q4 week was superior in terms of efficacy to the q12 week so they're moving forward with the q4 we think the reason that was more effective was that through that q4 week dose with ionalumab they likely had nearly full receptor occupancy for for that whole period where they lost it after q4 and they were just dependent more on on b cell depletion for that q12 week so we think receptor occupancy is really the thing to focus on um so we'll be able to look at our our phase one which we're moving forward in rheumatoid arthritis patients to really understand not only the safety tolerability pk but also what that receptor occupancy time point is and understand are we extending that duration that will give us the opportunity potentially to have kind of better efficacy because there's more complete receptor occupancy coverage but then also a longer duration of action which will obviously be beneficial for patients i see and for 301 i believe you guys had the presentation at the upcoming edv so what kind of data we should pay attention from there yeah that'll be your typical characterization preclinical characterization we'll have some non-human primate data as mentioned in the the opening the introduction to get an antibody to the the muscle you actually need pretty high sea trough concentrations because the gradient to get in the muscle is pretty difficult and we also know that Dazukaibar has low bioavailability so we'll present just a comparison to Dazukaibar and HP is looking at pretty standard things like their binding affinity to interferon beta plus half-life or in the monkey

correct okay awesome um so i guess i saved the mouse for the for the best so um so brad can you remind me the the cache position in the wrong way what's included what's not included yes we have 461 million as of uh our most recent filing as of june 30th uh we've got runway into q4 2028 so that supports a really accelerated development timeline for jade 101 uh for j201 um as you mentioned you know we haven't we haven't um uh decided on the exact go forward indications but we also want to be cognizant of our capital allocation like j201 is one of those programs that you could go after you know half a dozen indications like novartis is obviously we're not going to do that so we've embedded a couple of different phase twos in that assumption for runway and then for j301 it assumes again let's say an ambitious development plan but um as tom as tom was uh was mentioning so we'll go in the we'll go and have the volunteers in j301 in q4 and we'll have data from uh from that program in 2027 as well as data from jade 101 in phase two and j201 in the uh ra study in phase one awesome thanks thanks man uh really I appreciate it.

Thank you, Arthur. Appreciate the time.