Vor Biopharma Inc. (VOR) September 2026 Conference Transcript

all right i think we can get started all right great um yeah hi everyone thanks for joining us for the wells fargo healthcare conference my name is sadi rahman i'm one of the biotech analysts here at wells and it's my pleasure to introduce our first session here with vore bio from vore we have the chief commercial officer dallen murray and chief medical officer jeremy sokolov So appreciate you being here. I'm excited to have this discussion. You had a couple of announcements this morning. You also have a very important catalyst coming up in the first half of 2027, which is the Myasthenia Gravis Phase 3 readout. So looking forward to delving into that. Before we get into Q&A, I'll hand it over to you for any opening remarks.

Yeah, well, thank you, Sadia. And thank you for having us. We're excited to be here. And it's just been just over a year since 2.0 has rearranged itself the way we have. And we couldn't be more excited this morning. We've got the announcements that you spoke about, which speaks to a few things. It speaks to the execution that we've been able to generate very rapidly. It speaks to the KOL excitement about this new modality and this new agent. and speaks to the really great people we've been able to bring on board with VOR. So we're happy to be here, and Jeremy's going to walk through the exciting news that we have today. So thank you.

Great. Yeah, thanks. I'll echo Dallin's thanks for the invitation and just kind of take us through some of the events of the last week. So obviously, as Dallin mentioned, VOR 2.0 has only been in existence for about a year, about nine months as an independent clinical development company, And during that time, we've taken over and really rapidly executed on our upstream MG study, our phase three study of teletacicept and myasthenia gravis. We're proud to say that study has completed enrollment. That sets the clock for our 24-week outcome to come in the spring. We're super excited about that imminent event. But even in the meantime, we're doubling down on our confidence on teletacicept in this space. We've announced the plan to start our ocular myasthenia gravis study. Ocular myasthenia gravis is a really important area because it's often a precursor to generalized myasthenia gravis, so it really opens up that space in the totality of the MG market and for patients who have the spectrum of MG from ocular to generalized. We also would be presumably the third, only the third agent in MG and the first upstream mechanism. The other is our FCRNs. Fgartigimod has completed their study, and we believe that Rustigo from UCB is conducting a study as well. However, they are both the same mechanism, FCRNs, for which we think we have a significant advantage, especially as we move upstream in an earlier disease population where we hope to be able to show some degree of disease-modifying effect where we prevent the progression from ocular MG to generalized MG. This is an outcome measure that has not yet been demonstrated. We're still figuring out exactly how to show that. But in the meantime, we're confident we can show a significant benefit for patients with ocular MG in reduction of their symptoms and their morbidity. Finally, we are excited about the AANEM conference, which is upcoming. This is probably the largest neuromuscular conference, certainly in the U.S., and at that we have an oral abstract, which will look at post-hoc data from our China MG study. That China MG study has been published, has been presented both the 24- and 48-week data with significant efficacy, a magnitude of which is relatively unprecedented in the MG space. But what we're really going to be focusing in on here is both the depth, breadth, and durability of that response. And we're also looking now at minimal symptom expression, also known as MSE. And, you know, we're under embargo, but I'll just say that it's really important to how we look at MSE. Any point in time having one day of MSE is probably not what patients want. I think what patients want is to be able to have minimal symptom expression for the duration of their therapeutic window. And so what we'll be looking at here is the durability of MSE. So we're excited to present that data. We think it's important for patients and important to really demonstrate the efficacy of teletazicept in MG.

Great. Congratulations on completing enrollment. That's a major milestone. On the ocular study, is that starting soon? Can you say anything about timelines there?

It'll start in the first half of 27. So we're still working through the build, but we wanted to really double down on our confidence and get it ahead of the MG readout.

Got it. Okay, so let's talk about the MySenior Gravis, the data that you showed in China and how you expect that to translate to the global trial. So in China, we saw a really large effect size, 4.8 points on MG-ADL, very impressive and substantially higher than what we've seen for other approved agents in MG. The expectation here for most is that that would compress in the global trial. So just wanted to talk about why that compression could occur, you know, specifically on the placebo arm, just can you talk about what we saw in China, how that responds compared to like other global trials, and what could be different in a global trial as far as maybe background treatments, anything else that would maybe push that placebo arm higher?

Sure. I think there's two things that will push the placebo higher. One is the baseline disease activity. So the patients in China had slightly higher baseline disease activity than has been seen in other global studies. The other is the duration of disease. Many of the patients had a shorter disease duration. And just the fact that none of them had seen any other advanced therapies. They hadn't yet been exposed to biologics such as FCRNs or complement inhibitors. They just weren't available in China at the time. So I think that that might do that. The other thing is, you know, a lot of patients with other treatment options pushes things down the road. And in any immunologic disease and probably any disease, what we see is that as we get to a later line population, we get an increase in the placebo rate. And that's been true of global studies in MG across the board. So we think we'll probably look more like the representative placebo effects we've seen in recent global MG studies, somewhere, you know, in the, you know, two to three range. Now, that could compress your delta for your MGADL, but there's also a strong anticipation that we'll see an increase in the active arm. And if we look at the China data we've seen, there's only a few examples, but in the few examples we've seen of data that went from China to global, what we do see is a lower placebo in China and a higher placebo when we go global, but the delta tends to stay relatively intact because we also see an increase in the active arm as we go globally, probably because the placebo effect is affecting both the placebo arm and the active arm. So the delta tends to remain relatively constant. So we may see a compression. We will see a higher placebo, but we hope that there'll be a roughly proportional increase such that we'll maintain that depth of response we've seen.

And when you referenced the other trial where we've seen like a similar delta with placebo going up, even though placebo went up in a global trial, I guess you're talking about botoclamab.

Botoclamab, yeah. Yeah, Pitoclimab was tested in China, and in China it had a delta of 2, or 1.9. When it went globally, it had a delta of 2. And again, the placebo went up by over a point, the active arm went up by over a point, and the delta was almost exactly the same between China and global. So again, that's just one example. Other examples and other diseases we've seen, you know, Benlista in China had a slightly lower placebo, but the same delta in lupus. We've seen the same with a subgroup of Ionalumab, which is a drug for Sjogren's disease in the China subset. We saw that the placebo was lower in China, the Delta remained the same. So I think that this hopefully is a consistent message that we'll be able to replicate similarly because we really do think that the mechanism lends itself to that double depth of response, though we'll have to wait and see until the data evolves.

I mean, even in China on the teletacizept arm, the improvement in MGA-DL was higher than what we typically see from other agents. It was a 5.7 change from baseline. In other trials, we typically see four to four and a half point improvement. Like, is that something that could actually maybe come down in a global trial? And if you go to maybe a more heterogeneous population or for other reasons, is there any reason to think that that could change?

Any time you move to a more heterogeneous population, you get some degree of dilution. Often it affects the placebo, but I think that MG is a nice indication, and part of the reason why we like it as our first indication, is myasthenia gravis tends to be relatively consistent in its immunology across populations. Diseases like lupus can be very different in Asian, African-American, white, European, in South American populations. MG tends to be very consistent in its immunobiology. So we think that that heterogeneity of the biology shouldn't be as much of a problem. Again, the heterogeneity is more in the cultural interpretation of how people respond to the MG-ADL and the cultural interpretation of how patients report placebo, which is just part of different cultures and how they deal with that. So that's the place where we could see some dilution. But again, our strongest anticipation is that we'll see an increase in the placebo, but hopefully that placebo will carry through to the active arm.

That cultural interpretation piece, is that like, does that affect QMG less possibly? Because with QMG, like it was interesting to me that, you know, maybe it's a more objective measure of response, But you still saw a higher delta there compared to other agents as well, even though placebo was more in line with global trials. So does that give you sort of more confidence that like that more robust efficacy we're seeing with with teletasept is real and could translate in the global trial?

Yeah, there's nothing better than orthogonal validation through a more objective outcome measure. So I think that's exactly right. The QMG was almost spot on, a network meta-analysis done of QMGs across global populations. So the investigators are administering the QMG with the same precision, and the patients are responding with the same level of baseline activity and the same level of response, both in the active and placebo arms. So we think that, again, provides that validation that the dual mechanism for teletacicept really gives the best of both worlds, upstream mechanism and downstream mechanism. And, you know, although I'm hesitant to use the word additive, I think that that's what we're seeing is the additive efficacy of those two mechanisms.

Got it. So a common question that we get on this class and, you know, skepticism of BAPF April's and Myasthenia Gravis and the China data that we've seen from Teletextsup comes from the observation that IgG does not decline as much with BAPF April's as it does with FCRNs. So with BAF April's, we see like 25% to 35% reduction in IgG. FCRNs, we see 60% or more. And with FCRNs, there's some evidence that suggests pushing that even deeper, gets you deeper efficacy. So just wanted to understand how you would address that concern.

So FCRNs obviously mechanistically lower IgG. That's what they do and it's all they do. so there's going to be a directly proportional decrease in the pathologic antibodies as your total IgG so a 60% reduction in total IgG is roughly a 60% reduction in pathologic IgG now the first challenge is that doesn't reduce IgA and IgM and those have pathologic antibodies as well and so that's a cap on the efficacy bar for for that mechanism but I think with our mechanism what's unique is that we do see a 30% reduction in total immunoglobulin, but across multiple diseases, we see double that reduction in pathologic immunoglobulin where we measure it. So in lupus, we see a roughly 70% reduction in double-stranded DNA, even in the context of exactly 30% reduction in total IgG, or roughly 30% reduction in total IgG. Similarly, in myasthenia Gravis in a mechanistic study, they showed roughly somewhere around a 60% reduction in myasthenia in anti-acetylcholine receptor antibodies, the pathologic IgG, again in the context of a 30% reduction in total IgG. So we think that there's the ability to more robustly and more, I don't want to say specifically, but relatively selectively reduce the pathologic IgG. And it does that because autoreactive B cells tend to be highly dependent on BATH for their survival. So when you starve the system of BATH, you end up with a preferential reduction in autoreactive B cells and a relative sparing of your homeostatic protective B cells. We think this is an opportunity, not a liability. And I think, you know, if you look at the data, it also supports that. And what's really nice now, and again, you know, we're happy that Uplizna is now approved for MG. People are using and getting experience. And again, very minimal relative reduction in total IgG, but still some degree of efficacy if delayed and perhaps not as robust as we might have hoped. But I think that speaks to the fact that when we move upstream, we're able to affect the pathobiology of the disease without significantly lowering the total humoral immunity.

With APLISNA, I mean, the IgG lowering there is only about 10%, right? Do you think that also gets to, because we're seeing meaningful efficacy despite that. So do you think like pathogenic antibodies are still being depleted to around that 60% level or maybe like other B cell actions are driving efficacy as well?

Yeah, I think it's a combination of that. I think there's definitely a reduction in pathologic antibodies. The degree to which is something I'm not aware, but I would guess that it's less than you get with a BATH-APRIL inhibitor. We think of Uplizna as BATH. We think of APRIL as FCRN. So I think that combination of upstream and downstream reduction in autoantibodies is really what's getting you that depth of response. The other thing is that there probably are antibody-independent mechanisms that drive the pathology of most autoimmune diseases. MG has always been thought to be one of those prototypic antibody-driven immune diseases, right? It responds to FCRNs. It responds to IVIG. It responds to plasmapheresis. But I think what that data tells us from Uplizna is that at least to some extent, the ability to decrease your B-cell hyperactivity, those autoreactive hyperactive B-cells, is able to abrogate the disease. So I think that by combining that upstream mechanism of B-cell inhibition and the downstream mechanism of deep antibody depletion, there really is the opportunity for additive efficacy. So we get the best of Uplizna, and we get the best of other mechanisms with deeper immunoglobulin depletion.

Yeah, and I think the kinetics, if you look at the kinetics of IgG depletion with Uplizna and the efficacy curve, it kind of tracks a little bit. So that makes sense, what you're saying about deeper IgG reduction and then the B-cell efficacy as well. So back to the question about translatability of China data into the global trials. Are there any differences in trial design, like patient mix or background therapy, between the China and global studies that you think could contribute to a different outcome in the global trial?

For the most part, the studies are very similar. I think the one thing that is different is the background therapies. We do allow prior exposure to biologic therapies, including FCRNs and complement inhibitors. Now, the number of patients is relatively small. We think it's the sweet spot where we have, you know, enough patients that we'll be able to draw numerical conclusions about the ability to respond to teletasticept in the setting of prior FCRN or complement inadequate response. But, you know, again, it would take a lot of those patients to dilute the any effect size. So that's always a risk, is that when you go to a more heavily pretreated population, you can reduce your effect size relative to a naive population. So that's the only one that might be different.

And as far as just trial conduct in general, like, you know, concerns about any issues in Remagen studies versus, like, in, you know, your global trial, we do have data from Remagen and IGAN that's very consistent with other BATFAPRILs and global trials, right? Maybe can you talk about that and how that makes you comfortable with, like, the operational aspects of the China trial?

So we're incredibly comfortable with teletacep as a molecule. I think benchmarking exactly, as you suggested, Sadia, the IGAN is an objective outcome measure. It's, you know, proteinuria measured in a lab. And what we see is that, you know, when dosed appropriately, we can get every bit of the same efficacy and perhaps a little bit more than any other Bafepril inhibitor. So benchmarking molecule-to-molecule teletacicept is potentially best-in-class potency as an FCRN inhibitor using IGAN as the benchmark. The other thing it speaks to is the ability of Remagen and the China investigators to execute at a clean global level. The placebo wasn't elevated, you know, not that you'd expect such with a hard outcome measure like proteinuria, But just the fact they were able to execute a study which basically benchmarked almost precisely to other optimized FCRNs tells us that teletacicept is not a fluke China mechanism. It's a mechanism that translates globally.

And even the EGFR stabilization that they showed, I think some people might have been skeptical now of seeing the EGFR is stabilized with these April and...

Well, this actually is a very interesting point. So, you know, we are not currently entering into IGAN, but I think that, you know, people have this debate of whether BAF adds anything to APRIL in IGAN. And, you know, at least when you look at the proteinuria reduction and GDIG reduction, it's probably almost entirely driven by APRIL in that early portion of the disease effect. But one thing that people ignore is the fact that not all BAF-Aprils are exactly the same in the sense that the ratio of BAF to April is quite different. So teletacicept is slightly heavier for BAF. It's two to one potency for BAF to April. And what that means is that when we dose to April, which is what most people do, you dose to April because if you overdose on April, you'll end up with hypogammal globulinemia. And if you underdose on April, you might leave some efficacy on the table, especially early. But when we dose to April, we're slightly overdosing on BATH, and that's okay. As Ben Lista taught us, 1 mg per kg, 10 mg per kg, minimal increase in efficacy, no change in safety. So you can hit your BATH side quite hard and not end up with any toxicity, whereas if you overdose on April, you'll end up with hypogammal globulinemia. So again, when we dose to April, we're giving a much heavier dose of BATH than other BATH-April inhibitors, or certainly than any April inhibitor. And we think what that's going to do is going to really remodulate that upstream B-cell repertoire. And we'd like to think that might be part of the reason why you saw that stabilization in EGFR in the China population that wasn't seen in the global population at 38 weeks. Now, also, just to be transparent, patients in China tend to have slightly worse IGAN. so they have slightly more rapid progression, so that might have also been a reason why they were able to show that. But nonetheless, the mechanism was the first and only to show in their first part of their study, GFR stabilization, really showing the benchmark efficacy of teletacicept relative to the other BAT-favorols in the class.

Compared to povitacicept, they're running a phase 2 trial that could also read out in the first half of next year. um how should we view read through and maybe talk about like the difference in ratio of targeting bath in april there and like what that might mean for dose selection for povy yeah we're worried not because of the competition we're worried because they might read out negative and we don't want that negative read through because again they don't hit bath very hard when they dose to april they may also end up with hypogammaglobulinemia especially at their higher dose because of the amount of April they're using.

And again, it's simple PKPD. If you dose to effect, you can overdose if you try to go too far. So we're encouraged by the fact that they're following in our tracks. They're confident that the Bath-April mechanism was important to MG. We have a three-ish year head start, so that gives us a significant confidence in our ability to deliver, and Dallin can speak more to that. But I think that from a mechanistic perspective, we think that their read-through shouldn't be completely direct. If they work well, we know we'll work well. If they have challenges, I don't think any challenges that that molecule would have would directly read through to teletacicept because, again, they're underdosing on BAF most likely when they dose to April. And if they end up with overshooting on April, we've already had about 3,000 patients dosed with teletacicept, and we haven't seen any safe and hypogamma globulinemia signal when dosed appropriately. We can get hypogamma globulinemia, but we don't dose that far. And I think that the breadth of patients treated with teletacicept really gives us a very good exposure response relationship such that we can avoid hypogamma.

And we think that three-year head start is very significant. You only need to look at the MG market to see Argenix had far less than a three-year head start in terms of the FCR class, and yet they've had incredible success and really built a real beachhead in the disease, and that's what we hope to do.

Got it. Just on the hypogamma point, you know, with the class, we do see pretty similar IgG reduction out to, let's say, one year or two years, right? And, like, IgG continues to decline, I think.

It continues to trend down even past one, two years. so just curious like how you are thinking about monitoring for hypogamma differences between agents even though broadly igg reduction looks similar yeah again on average ig looks the same there's always going to be variability in populations again if anything the china population should should have a slightly higher risk for hypogamma because they're a slightly smaller population in terms of bmi but we don't see it so again across the igan study the MG study at both the 240 milligrams, as well as the lupus RA and Sjogren studies at 160 milligrams, nobody had to stop for hypogammal globulinemia during the 3,000 observed patients. And then even in the open-label extensions out to a full year, there was no evidence of hypogammal globulinemia followed, you know, every month to every three months, depending on the stage of the study. And then in the real-world studies, you know, this drug's been approved in China, for six years across lupus, where patients do tend to get hypogamma. And patients are just not stopping. So if you look at the real world experience, it doesn't seem to be a big challenge. And I think it's a testament to the early dose ranging and a little bit of luck in how that balance of Baph-April came about with the molecular engineering.

And in our global study, we're following the patients out in the open-label extension for a full year, and then Jeremy has extended it beyond that. So we'll be generating good long-term data on both safety and efficacy because we believe both in the safety long-term but also the durability and that increasing magnitude over time.

Got it. Just to be clear on povitacicept on the readout, like, you think it could be negative maybe at the lower dose, but on the higher dose, do you think they're hitting BATH enough, but we might see those safety signals pop up?

It's hard to speculate. Again, the question is, where do they have enough BAF to really get a depth of response that mimics teletazacept? And that's an answer I just don't know. But mechanistically, we're hopeful that we offer something different in the sense that by hitting BAF heavily and APRIL to the adequate extent, we get that additivity of upstream and downstream mechanisms versus a drug which has a much more APRIL-dominant mechanism, which may under-address that upstream mechanism that we think is, quite frankly, contributing not just to the depth of response, but that breadth of response and that durability. So how many patients get a change of five in their MGADL? And more importantly, as Dallin alluded to, how many patients get better at 24 weeks and continue to get better between 24, 48, 100 weeks?

And Dallin, just commercially, can you talk about how differentiated this would be bringing that depth of response, even if it's similar to FCNs, because of that durability piece and then also the dosing and convenience side?

Yeah. Well, the gold standard for efficacy is the MG-ADL in the market. And so if we come close to replicating the Chinese data, you're looking at a drug that's double the efficacy of the entire rest of the field. So it would be very differentiating. And, you know, as we've said before, this is not, though it's a rare market, it's not a one-time therapy. So the bar for physicians changing their patients out, if there's a better therapy, is pretty low. So we think just on the MG-ADL delta alone, as you asked, it's very, very significant efficacy difference. Now, as we've talked about, we believe we have efficacy differences beyond the MG-ADL delta. We were talking about the durability, and that's one thing that as Jeremy and I got out, started meeting the KOLs, They were excited about the MG-ADL, but almost more excited about the fact that the patients continue to get better in that second six months. And we can see from the Uplizna launch that despite a pretty modest efficacy at 24 weeks, you can see an increasing efficacy in the second six months for them. And despite what many doctors describe as disappointing primary efficacy, Uplizna's launch has been pretty good, and they have taken a lot of first-line business, and it just demonstrates what we believe is this unmet need in the market and a real strong excitement about targeting upstream and durability. So that's the second of our efficacy advantages. And then the third one, Jeremy alluded to it, is that the FCRNs target IgG, and IgG alone and there's emerging data coming out of Yale and other labs showing that there's IgA and IgM and that about a third of the patients roughly have IgA and IgM involvement. And so what we're seeing in the China data that we hope to replicate in the global data is a breadth of response that is also best in disease in that 100% of patients are getting at least some kind of modest response on the MG-ADL, like a response of two or three or greater, and that's pretty significant. And actually, that actually might even be the biggest of all three of our advantages, because if you think about it from a physician and patient standpoint, if there's a higher percentage, you're going to have even some kind of a modest response versus, you know, if you're getting close to 100% of some kind of response versus, you know, two-thirds having a response, it's a really good reason to start with a therapy that gives you a better chance for some kind of response. So we actually think we're going to win on three elements of efficacy. All of the focus has been on MG-ADL to date, but the durability and what we're calling the breadth of response we think are also going to be big advantages. Got it. can you talk about the dosing volume in in my senior gravis and whether there's room to concentrate the formulation it yeah it's a low-volume injection we will be launching with the current formulation which is two shots once a week but the team is moving very rapidly and executing well on a higher concentration formulation that'll get us to one pre-filled syringe once a week and we're going to move from that as rapidly as we can into an auto-injector. So we're moving as fast as we can. It won't be day one of launch, but we're continuing to develop that.

Got it.

We actually have the high concentration formulation. We're now just doing the CMC work on the devices and that will be, it's in the device. It just takes time for stability. So we'll have it, but it'll be a little after launch, unfortunately.

Mm-hmm. And just one difference between the China trial and the global study. In China, the drug was administered in clinic, and in the global study, you have a mix of in-clinic and at-home administration. Can you just elaborate on that mix in the global trial and which one could be reflected in the label at the start?

The label will reflect both because we have done the option so we'll have we'll have both in the label is the anticipation obviously to be determined but that's the anticipation we do find that patients who get injected in the clinic tend to have more smooth injections patients who injected home when they had any sort of an injection site pain or reaction we bring them back retrain them and they tend to do very well so we think that that the the China population had us probably had a slightly lower injection site reaction rate because they had clinic administration but that said you know we're also fairly confident that we can get patients who want to treat themselves at home to be well

trained to treat themselves at home in an effective way and that's where you see the market going is having that flexibility for patients to be able to dose it at home and we think that's critical one of the things we talk a lot about the differentiation versus the current therapies But the biggest opportunity in MG is the fact that only about 20 to 30 percent of the patients have even gotten biologics. So there's still a huge opportunity for that market to grow. And I think one of the big ways it can grow is allowing more flexibility for patients to dose at home. Because a lot of the patients that we're going to find as we grow the market are in areas that it's not going to be easy to get into the big MG centers to get their weekly injections. So allowing them to dose at home is going to be an important advantage when we go into the market.

Got it. We only have a couple of minutes left, but I do want to touch on Sjogren's. Just, you know, talk about what we had the Inalumab data somewhat recently. And just talk about, like, the placebo response in that trial, how you're trying to manage placebo response in your trial.

Yeah, we think the most important thing that really drives placebo is the S-Di efficiency of conducting the S-Di scoring. And we think, again, we don't know. One of the challenges that they may have met was a lot of new investigators who didn't have experience with the S-Di. So when you look at the baseline S-Di, it was probably slightly higher and slightly exaggerated, not by any conscious effort, just because of new investigators eager to get patients into a study of a drug that's really critical, a disease that's really critical to treat. As they got better at the S-Di over time, there was probably some degree of increased precision, which may have increased both the response in the placebo as well as the active. So we think the most important thing that we've done is getting as many experienced investigators as possible. Again, they had, you know, 600 patients in their study. They had to have three times as many sites as we did. We were able to pick up a lot of those sites from the Inalimab study, as well as people who have experienced with nipicalumab or other concluding studies to come over to our trial. And we think that that gives us a much better precision, which will give less regression to the mean in terms of the placebo response. So will there be a higher placebo than China? Absolutely. Will there be a placebo as high as ionalamab? We're fairly confident we'll be able to control for that. And as far as powering of the study, is it adequately powered for an effect size like we saw with ionolimab or yeah well it's it's not powered for a 1.1 directly we have about an 80 power for a 1.5 change but we have a 96 power for a 2 to 2.5 change and we really think that quite frankly we need that we need that to make any difference the minimal clinically important difference for Sjogren's for the S-dye is probably in the range of three some people would lower that to two or two and a half given the given the complexity of the s die and the and the unmet need in Sjogren's so we're powering for the minimal clinically important difference that we feel would be clinically meaningful so we're well powered for that and we're slightly overpowered we're dramatically overpowered if we get anything that looks like the China data just on dosing and Sjogren's it's a lower dose than what was used in the IGAN and my gravis trials and that's that was selected based on Remagen's dose finding work in China how confident are you that that dose will provide sufficient exposure in a Western population yeah at least if you look at the population PK analysis from China BMI is not a significant variable in terms of exposure nor in terms of efficacy at the exposure response so we're pretty confident that we have adequately addressed the the target again it covers enough bath because we think bath is a slightly more dominant mechanism in Sjogren's but it also covers enough April as you can see from the immunoglobulin reductions of you know well over well over 25 30 25 30 percent starting with they start with very high immunoglobulins and in Sjogren's that's part of the disease pathology. So we're fairly confident that we've got an effective dose, and we're not going to be going over, and we're enthusiastic to see the results. I'll just make a plug. The great thing about Sjogren's is we took over MG with not a lot of patients after about a year and a half of the study. We've been in Sjogren's for about six months, and we've already basically kept, not capped out, but we've almost reached our goal for U.S. enrollment. It just shows the enthusiasm for Sjogren's across the population as well as the impact we're having in influencing the the community the Sjogren's community which we think is critical mm-hmm great well unfortunately we're out of time so I'll end there but thank you both thank you for joining us I really appreciate it thank you for the invitation