Good morning. My name is Daryl, and I will serve as your conference call operator. At this time, all participants are in a listen-only mode. A brief question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this call is being recorded. Joining me on the call today will be Dr. Pete Salzmann, Chief Executive Officer of Immunovant. Before we begin, I would like to remind everyone that today's conference call will include certain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, for example, statements regarding the potential efficacy and safety of Immunovant's product candidate and Immunovant's expectations regarding the timing, design, and results of its clinical trial, including the timing of future data readouts and the announcement of future indications. These forward-looking statements are not guarantees of future performance and are subject to various risks and uncertainties, assumptions known or unknown, which could cause the actual results to vary materially from those indicated or anticipated. For more information, investors are encouraged to review Immunovant's most recent quarterly report on Form 10-K filed with the SEC on June 1st, 2021. I would like to turn the call over to Dr. Pete Salzmann. Thank you, Dr. Salzmann. You may begin. Good morning, everyone. Thank you for joining me on today's conference call to review a corporate update for Immunovant. I appreciate Daryl advising everyone that this presentation contains forward-looking statements for the purposes of safe harbor provisions. As you may be aware, in March of this year, Roivant, our 57% stockholder, amended its 13D to state that it intends to make a proposal to us to acquire the outstanding shares of the company not already owned by Roivant. In response to the filing, our board of directors formed a special committee consisting of independent directors to be prepared to evaluate and negotiate any such proposal from Roivant or other parties. The special committee has retained Centerview Partners as its financial advisor and Wachtell, Lipton, Rosen & Katz as its legal advisor. Moving now to our corporate update. As you recall, in February of this year, we voluntarily paused dosing in our clinical trials for IMVT-1401 due to elevated LDL levels observed in patients treated with 1401. At that time, we shared that we were doing a program-wide review and that we would come back in this quarter to share our findings. We look forward to sharing our insights and our excitement for the future. We learned a lot over the last couple of months. First, we've learned more about patient needs and refined our view of what an ideal anti-FcRn agent should do. I'm going to return to these very important patient insights at the end of the presentation, but suffice to say that the strong IgG lowering observed across a range of 1401 doses matches nicely to patient needs. Second, we've learned a lot about 1401's profile. In addition to covering why we believe the LDL impact of 1401 is manageable, I will also share that our therapeutic window is wider than we anticipated. We're excited to have now seen biological activity across three different disease states. Finally, we've pressed ahead with various clinical development options, and we're looking forward to returning to the clinic in patients later this year or early next year. Let's start by reviewing what we've learned about 1401. In fact, we have four really important findings to share. First, at the doses we're studying, 1401 is more potent than we thought and has a broader therapeutic window. Second, changes in IgG, albumin, and LDL are all tightly linked, and this leads to predictability for individual patients. Third, there's a favorable trade-off between desired changes in IgG and undesired changes in albumin and LDL. Fourth, the changes in LDL appear manageable for several important reasons. Let me now take these concepts one by one. Regarding potency, we observed deeper reductions in IgG with 340 mg and 680 mg when dosed weekly for 12 weeks compared to the reductions we had observed previously during 4-6 weeks of weekly dosing. We now understand that 340 mg is a high dose and 680 mg weekly is a very high dose, while 255 mg weekly also reduced IgG substantially over 12 weeks. In other words, we learned that the therapeutic window of 1401 is broader than we thought. I've also noted the LDL changes at 12 weeks compared to baseline now that we have all the data in from ASCEND GO-2. The 15% change in LDL compared to baseline for the 255 mg dose and a 37% increase in LDL change from baseline for the 340 mg dose. Regarding predictability, we learned that the LDL changes were highly correlated with serum albumin changes and were not correlated with thyroid hormone levels in our study data. Of course, we already understood that IgG and albumin changes were highly correlated, as both reductions are mediated via non-target effect of the Fc receptor. The new learning was that lipid elevations correlated very tightly with albumin changes, and also therefore appeared to represent an on-target effect. Based on the observed correlation between albumin and LDL, plus the lack of an observed correlation between thyroid hormone levels and LDL, the consensus of external expert consultants is that lower serum albumin stimulates hepatic synthesis of albumin in the LDL. In addition to the observed correlations during treatment, we also observed that both albumin and LDL returned to baseline off treatment, which is another important predictability characteristic. Outside of ASCEND GO-2, we observed dose-dependent changes in LDL of a similar magnitude in a healthy subject injection site study in ASCEND-MG and in ASCEND-WAIHA. These observations were based on analyses of stored serum with small numbers. Nevertheless, the pattern appeared quite consistent, and we believe the impact will not differ across indications. New data demonstrated a favorable trade-off between IgG reduction and albumin reduction across the range of doses tested in ASCEND GO-2. Whereas IgG reduction for all three doses clustered near the peak of 1401's IgG reduction, the albumin reduction, and therefore LDL increases, for the three doses did not cluster. The reduction in albumin remained in the normal limits for about half the patients on 340 mg after 12 weeks of dosing. You can see from this graph the widespread albumin reduction between the 255 mg dose and the 680 mg dose over a 12-week period. The reductions in albumin on the 255 mg dose were mild. These mild reductions in albumin resulted in small changes in LDL, as shown on the prior slide. Consequently, the larger reductions in albumin for patients on the 680 mg dose resulted in larger increases for these subjects. What have we learned about managing LDL increases? We've learned that we have multiple ways to manage LDL in future clinical trials, and that this should provide good solutions for physicians and patients down the road, assuming approval in different indications. One key lever was customizing the dose for the indication and for the stage of treatment. For indications that require an initial high-dose induction, treatment may begin with a high or very high dose of 1401, 340 mg or 680 mg given weekly. Depending on disease severity and other factors, LDL excursions over the short term during induction might be managed with anti-lipid therapy or might simply be monitored. At the other end of the spectrum, 255 mg weekly is likely to be a standard dose during the maintenance phase of a long-term extension, where the goal is to maximize maintenance of efficacy while minimizing immunosuppression. At 255 mg weekly, we anticipate that albumin and LDL changes will be small for most patients. Recall that the median increase in LDL at the 255 mg dose was 15% at 12 weeks. In the middle of the spectrum, we envision both 255 mg and 340 mg doses achieving a sweet spot of IgG suppression and albumin-LDL changes for many patients. How will physicians handle patients who experience a modest chronic increase in LDL? This market research was designed to test physician response to increases in LDL that are higher than we expect to see for most patients on 255 mg weekly. Physicians were presented with hypothetical product profiles of an anti-FcRn with either no LDL impact or with an LDL impact of 30% or 60%. They estimated their prescribing share for such a product in their practice. We were able to test their prescribing projections across a range of disease severity and across different lines of therapy. This market research showed an increase in LDL of 30% did not really change a neurologist's willing to prescribe an anti-FcRn medication for myasthenia gravis. For example, this group of practicing neurologists anticipated using an anti-FcRn medication for about 27% of their MG patients, with or without an LDL signal of 30%. For very early lines of therapy, there was a slight decrease in projected market share, but generally little change in market share for an LDL increase of 30%, and suggesting very little change for an LDL increase of 15%. In fact, these physicians believe that LDL changes of this magnitude would be readily addressed by a statin or other anti-lipid therapy. When presented with a hypothetical product profile of an anti-FcRn that increased LDL by 50%, they did note that anticipated market share would fall for such a product in this product study, and they believe that some of these patients might be less easy to control with statins or other anti-lipid therapy. Similar research with physicians in other specialties also yielded a comfort with increases in LDL in the 30% range. This next slide is a post-hoc analysis of patients who happened to enter one of our trials already on a statin. We identified five patients in the ASCEND GO-2 trial and three patients in the ASCEND-MG trial who were taking a baseline statin and for whom LDL could be obtained. In ASCEND GO-2, three patients were taking a statin and were randomized to 1401. Two additional patients were taking a statin, then randomized to placebo. All five patients had varying levels of LDL ranging from quite low to moderately elevated. LDL changes during treatment with 1401 for the three patients randomized to active treatment arms were small for these patients. In ASCEND-MG, on the right-hand side of the graph, two patients were taking a statin and were randomized to an active treatment arm, while one patient was taking a statin and randomized to placebo in ASCEND-MG. For the patient who was randomized to 340 mg, LDL actually decreased more than 20%. On the other hand, for the patient randomized to 680 mg and the patient randomized to placebo, LDL increased by about 30%. All of the MG samples are based on post-hoc analysis of stored serum. I should note that for the MG patients, all of the yellow bars show their LDL at the end of the randomized treatment period and don't relate to LDL observations during the open-label extension. The same is true of the thyroid eye disease patients, where the yellow bars all represent a value at the end of treatment. Although this is a very small sample of patients who just happen to be on statin, we find these data to be encouraging and also consistent with experts' views that statins will likely work in this situation. Turning now to warm autoimmune hemolytic anemia. We are encouraged by early findings while also acknowledging the data are very limited. As a reminder, the ASCEND-WAIHA trial is an open-label study in patients with warm autoimmune hemolytic anemia who have failed a prior line of therapy. These patients are often treated with very high-dose steroids to be in disease control. When steroids are tapered, the disease often recurs, and other immunosuppressants are prescribed, though these are not FDA-approved for the treatment of warm autoimmune hemolytic anemia. Patients like this don't spontaneously improve as a general rule. A patient who does improve their hemoglobin by two g/dL on therapy is considered a responder, and that is the primary endpoint for this study. Prior to the pause, we had five patients randomized and dosed in ASCEND-WAIHA. Three patients completed 11 or 12 weeks of dosing. Two other patients completed only two or three weeks of dosing. One of these patients paused dosing due to the program-wide voluntary pause. The other short-duration patient withdrew from the study for a serious adverse event of recurrent ITP in a patient with a history of both ITP and WAIHA. In terms of the patients who completed 11- 12 weeks of open-label therapy, the patient shown here had a strong response and completed 11 weeks of therapy prior to the program-wide pause, with an increase in hemoglobin well over 2 g/dL, and this increase was maintained during treatment. Based on expert discussions, total bilirubin is another important biomarker in WAIHA, particularly in the short term, and the improvement in total bilirubin matched the improvement in hemoglobin for this subject. Note also that this patient had failed three rounds of potent immunosuppressants and steroids prior to entry into the ASCEND-WAIHA trial. There was one other patient who had a modest response during 12 weeks of therapy and one patient who did not respond after 12 weeks of therapy. As you know, we had to prematurely terminate our phase II-B study of 1401 in moderate to severe thyroid eye disease due to our unanticipated program-wide medical review. Prematurely discontinuing a study is always difficult, especially for patients and investigators, and in this case more so as only 41 of the projected 77 subjects to be randomized completed the primary efficacy evaluation at week 13, a bit over 50% of those anticipated. Consequently, the question that this study was designed to answer, that is, whether a 12-week course of 1401 improves proptosis, cannot be answered with any certainty. What we do observe is that 1401, in a dose-dependent manner, decreases total IgG and thyroid-stimulating immunoglobulins. From a clinical perspective, the power calculations used to size the study assumed a 45% risk difference in proptosis responder rates for the 680 mg dose compared to placebo. On review of the data from early study visits, when approximately 85% of the enrolled patients were assessed for proptosis response at each visit, it appeared that this risk difference could be achieved with a 680 mg dose and possibly with a 340 mg dose, with no or minimal observed response in the placebo group. Due to the unbalanced randomized design, too few subjects were assessed in the 255 mg group to allow for any meaningful comment. Whether these observed response rates in the 680 mg and 340 mg dose groups would have persisted if the trial had gone to completion is unknown and simply cannot be determined. Efficacy trends in the prospectively defined secondary endpoints were of lesser magnitude, for example, clinical activity score responder rate, or were not evident, for example, improvement in the full dose course. It's important to remember that the study was sized only for assessment of the primary proptosis responder rate and not the secondary endpoints. We believe that the 1401-induced decline in total IgG and thyroid-stimulating immunoglobulin, coupled with the efficacy trends observed at the early visits when most of the enrolled subjects were evaluated to these efficacy parameters, suggest that TED may be another disease where anti-FcRn appears to work. We're continuing to discuss the results with key opinion leaders. Despite our disappointment in the premature discontinuation of the study, we are encouraged by our data review, and we believe that continued investigation of 1401 in this indication may be warranted. We're very much looking forward to discussing potential trial designs with regulatory agencies in the second half of this year. What's next? Where do we go concretely from here? Pending FDA agreement, we plan to return to the clinic and initiate a pivotal MG trial in late 2021 or early 2022, as well as resume our trial in warm autoimmune hemolytic anemia and initiate a phase II trial in TED on a similar timeframe. Beyond these three indications, we plan to initiate clinical studies in two new indications over the next 12 months. We believe one of these could be a pivotal trial. With all this activity, we are very excited that we've consolidated medical and scientific leadership under Dr. Bill Macias. Bill brings over 27 years of pharmaceutical experience to Immunovant, including industry-leading experience in early, mid, and late-stage drug development. Bill's impressive breadth of experience and proven track record of clinical development in numerous therapeutic areas, including immunology, fits very well with the potential of IMVT-1401 across multiple indications. I've had the great pleasure of working with Bill in the past, and as he's come up to speed on our programs over the last weeks, it's been a lot of fun to see him already having a positive impact. Finally, I want to note that based on our existing cash balance as of March 31st, 2021 of $400.1 million, and our current plans as just reviewed, and our timely expectations related to these development programs, we have enough capital to get us into the second half of calendar year 2023. Before opening the line to questions, I want to return to the patient insights we gained. At Immunovant, our vision remains unchanged, normalized for people with autoimmune diseases. This is a high bar and keeps us focused on what is most important. It guides us to really understand what people living with autoimmune diseases need and what tools physicians will require to deliver on those needs. Our recent discussions with thought leaders, advocacy groups, and scientific experts yielded one critical insight to the question: how much IgG suppression do patients with an autoantibody-driven condition need? The answer is almost certainly, it depends. Patients with new-onset disease, patients with flaring disease, and patients with acute conditions generally need a lot of IgG suppression. In fact, when prescribing steroids in these situations, many physicians start with very high doses to quickly gain disease control. On the other hand, patients whose condition is chronic and whose disease activity has come under control will likely need less IgG suppression. Experts agree that maintaining disease control is easier than achieving initial disease control, and they also agree that long-term therapy should target the best efficacy with the least immunosuppression. myasthenic crisis, warm autoimmune hemolytic anemia, and acute rejection following solid organ transplantation are clinical examples where the standard of care begins with high-dose immunosuppression and a rapid and deep IgG lowering. CIDP is another condition where therapy often begins with high doses, in this case, high doses of IVIG. On the other hand, for generalized myasthenia gravis without crisis, treatment doesn't usually begin with a high-dose induction. In the case of CIDP and warm autoimmune hemolytic anemia, where symptom control has been achieved for some time, then the goal of treatment switches to tapering immunosuppression and maintaining symptom control. In this phase of the treatment cycle, physicians and patients are striving for a lower effective dose or longer intervals between doses in order to minimize immunosuppression while maintaining clinical benefit. During the maintenance phase of their treatment, patients may also place an even higher premium on a convenient delivery mechanism, such as a simple subcutaneous injection. These insights, which we believe apply to many autoantibody-driven conditions, have important implications for the development of a class-leading anti-FcRn. Specifically, the ability to provide a wide range of IgG suppression with an easy-to-administer subcutaneous delivery device will be key. With that, I want to thank you for your attention, and I'll ask the operator to open the line for questions. Thank you. We'll now be conducting a question-and-answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for your questions. Our first question comes from the line of Robyn Karnauskas with Truist. Please proceed with your questions. Great. Thanks, guys, and thanks for all the color. I'd like to sort of understand the comments at the very end and sort of what all this data that you've shown means for where the most likely uptake will be for your drug. Are you saying that TED will be maybe more challenging because even though you don't have the full practice data, that likely it's a high dose induction so that even though it's an acute therapy generally done with doctors, it sounds like you may need higher doses to see the practice level reduction achieved, maybe high doses, so maybe something to start. I'm trying to understand what you said at the end. Can you help me understand what are the most likely indications that we should be modeling? Do you think that TED's less likely now because you have to use higher doses? For the lower dose amount, what indications do you think will work with that for the 255 mg if that's really the dose that you take forward? The other question I had was, what about less frequent dosing? We know argenx is doing less frequent dosing because you lower IgG and then it slowly comes back. Is that sort of what you're seeing with 255 mg, where you're sort of maintaining lower dose? Could you go even less frequent so you don't see a sustained cholesterol decrease? A couple questions in there. Sorry about that. I'm just trying to figure out how to really value your drug given all the data you've sort of given us today. Yeah. Thanks, Robyn. As always, that's a great set of questions. Let me start with the second one, which is the concept at the end. Really the concept is quite simple, which is that different patients have different needs for IgG suppression. Some are going to need deep IgG suppression. Some are going to need strong IgG suppression. We've shown now that 1401 across a range of doses can deliver both. For those patients who need a deep IgG reduction, and I mentioned a few conditions where that could be the case, the higher doses or very high dose of 1401, 340 mg or 680 mg can provide that. Over a short period of time or when there's a very high unmet need, then the changes in albumin or LDL are less important. On the other hand, there's going to be many patients who are going to be seeking maintenance of disease remission or improvement in symptoms that they've achieved during the acute phase. In speaking with experts across a range of conditions, there's a belief that the degree of IgG suppression needed for that chronic phase will be a little bit less, maybe more in the 50% range instead of the 80% range. What we learned from this data is that our lower dose is 255 mg as an example, potentially 340 mg every other week, as you mentioned, can provide that sweet spot of 60-ish percent IgG reduction with minimal changes in albumin and LDL. That's really the concept at the end, that we've seen 1401's profile is really competitive across a wide range of indications and in both the acute and chronic setting, which is important for a lot of those patients. In terms of thyroid eye disease, what I reviewed there is really the efficacy data is inconclusive because of the study had to be stopped before it was anywhere close to completion, and that makes interpretation very challenging. We are very encouraged by the improvement in biomarkers and an apparent correlation between the biomarkers and clinical impact. At the same time, I want to be transparent that the degree of efficacy which we observed fell a bit short of our expectations. Based on that, we have some ideas for a phase II trial to really optimize who we're studying in thyroid eye disease and where we can deliver a clinical efficacy that's meaningful and competitive, and we plan to start that trial in the second half of this year after discussion with experts and regulators. That was going to be my follow-up question was, in what populations would you go after and what might be the design of a phase II to help us sort of narrow in what the percentage might be for the potential population that might be eligible for your therapy versus TEPEZZA? Yeah, that's a great question and something we're working on. I mean, we do see, I see opportunities on both ends of the spectrum, actually, in patients with a little bit more mild disease and patients who've already, as we've discussed in the past, who've already had a course of TEPEZZA and haven't achieved full remission of their symptoms. Got it. Okay, great. Thank you very much. Thank you, Robyn. Thank you. Our next question comes from the line of Derek Archila with Stifel. Please proceed with your questions. Hey, good morning, everyone, and thanks for taking the questions and thanks for the comprehensive update. Just a couple from us. Just can you give us a sense on your choice to continue in MG given the competitive landscape there? I guess, where do you feel your differentiation is in that indication? For the patients that you provided some data that were on statins and receiving 1401, can you talk about the dose of statins they were on? Were they on the max dose for the statins, or were they on lower mid-range doses? Thanks. Hey, thanks, Derek. Those are some really good questions. With regard to myasthenia, I think competitiveness in myasthenia will be similar to competitiveness in many other indications that'll be driven by efficacy, safety, and tolerability. In myasthenia, in particular, something we talked about back in August when we released our results is I think that in addition to the responder rate, the other percentage that's maybe equally or even more important is the deep responder rate. Remember, we talked about those patients who didn't just have a 2-point improvement in their MG-ADL, but had a 6, 7, 10-point improvement in their MG-ADL. Those patients have a tremendously different quality of life with treatment than they had during the moment of the trial. Although our trial was too small to conclusively validate a link between deeper IgG reductions and those deep clinical responses, I think that link is pretty logical and was also suggested in the nipocalimab data. This gets to the point that Robyn asked me about as well, which is the concept at the end there, because sometimes you need a deep reduction, sometimes you need a strong reduction. For patients who really are looking to achieve a big change in their symptom control, we think we have maybe the best shot of achieving that given the deep IgG reductions we can deliver. As we've also discussed in the past, as patients move into a long-term extension or in the clinical setting, move into a chronic maintenance phase, we believe that many of those patients will be able to taper down to lesser levels of IgG suppression. As they do that with 1401, then the albumin and LDL changes become much less significant. The changes in albumin and LDL that they might experience in short term, in the front end, are probably a reasonable trade-off for a deep improvement in clinical symptoms. As they move into chronic phase, those adverse events either go away or become much less important in their magnitude. In terms of the statins, there were a range of statins, but they were mid-range statins. Several of the patients were on atorvastatin 20 mg. One was on CRESTOR at 5 mg or 10 mg. They weren't super high doses, but they weren't low doses either. One person was on, at least one or maybe two were on atorvastatin 40 mg. None of them were on atorvastatin at 80 mg. They were mid-range. You saw even the LDLs coming into the trial on the statins varied. Some were had their LDL at 100 or less. Others, even with the statin therapy, were more in the 150- 160, 170 range at baseline. Got it. Thanks. Thank you. Our next question comes from the line of Yatin Suneja with Guggenheim Partners. Please proceed with your questions. Hey, guys. Thank you for taking my question. Just a couple from me. Number one, do you have to do more dosing work? Do you have to establish even a lower dose before you move into pivotal or other studies? The second question is on the TED study. You were pretty excited about the seven patient data that you had generated in the past, but we're not really hearing that same level of excitement now that you have 40 patients. Give us a little bit more sentiment into the TED data. Thanks, Yatin. Those are two excellent questions. I'm really glad you asked both of them actually, because on the first one, we do not believe that additional dose-finding studies are on a critical path. We may do some dose finding in the context of a phase II trial in a disease population where we can correlate that with biomarkers or potentially in a phase I setting where we could examine concomitant anti-lipid therapy or things like that. Those studies are not on a critical path to returning to the clinic in disease populations. The reason we believe that is that the PK/PD models for 1401, and probably for anti-FcRn agents in general, are really quite predictable. We've shown a very tight correlation between IgG and albumin, and albumin and LDL. Now having data from three different doses and to some extent different intervals because we do have every other week dosing in the open label extension of the MG trial. We had every other week dosing in our healthy injection site study completed recently. All that data allows us to build much more robust computer models of PK/PD than we had in the past. Those again, they show a nice range of IgG reduction as well as impact on albumin and LDL. That allows us to go back to the agency with trial designs that we feel confident in, that will test a range of doses, which will have a meaningful difference in terms of their effect on those parameters. Got it. Go ahead, Yatin. No, you go. Sorry. Okay. One more question I have is on the Roivant offer. Can you maybe also talk about how that is going to play out? Who decides the price? They are the majority holder. Can they force a transaction? Are you also running a proper process where you are engaging other parties who might be interested in the asset? Right. Thanks for that question. As with any M&A transaction, and in particular in an M&A transaction with the majority shareholder, there are many specific regulations governing how that process works. I shared on the first slide, which I've sort of put back up here on the webcast, if you're following along and I'm controlling, really the important parameters, which is that in response to Roivant's amended 13D, our board of directors formed a special committee consisting of independent directors and that special committee, their charge is to be prepared to evaluate and negotiate any proposal that could come from Roivant or any other party. That special committee has engaged Centerview Partners as their financial advisor and Wachtell, Lipton, Rosen & Katz as a legal advisor. The machinery is all in place. Given the really tight regulations around these types of situations, I can't comment on anything else about the process or the activities of the special committee. Yeah, you asked about TED. I didn't answer that question yet. I think it's an important question. We were absolutely very excited about the data that we presented from the seven patients in the open label trial. There are elements of this phase II-B trial that are exciting as well, including at the early time points where we had improvements in proptosis that were of a similar magnitude to what we saw in the phase II-A trial. We definitely don't have definitive data from this trial because it stopped early and it was unblinded and people are at different stages of finishing their treatment and all those complications of a failed trial when you have to unexpectedly unblind it. Nevertheless, there's more data in this phase II-B trial than in the phase II-A trial, and the data that we do have doesn't suggest as strong of a magnitude of impact as we were hoping for based on the phase II-A trial. That makes us want to ensure that any future study is in the right population where we can really demonstrate not just a statistically significant impact, but a really clinically and also a commercially significant impact. Thank you. Our next question comes from the line of Danielle Brill with Raymond James. Please proceed with your questions. Danielle, could you check if you're on mute, please? Hi, guys. Can you hear me? Sorry about that. Yes, please. I do now. For the question. Great. I just wanted to first clarify that the magnitude of LDL impact was in fact consistent across all indications, and then curious if you have any thoughts as to why competitor programs with similar albumin impacts haven't reported similar findings? Pete, the new IgG reduction data you presented looks slightly different from the phase I data in healthy volunteers. I believe the magnitude of IgG reduction you saw with the 340 mg was in line with what you're reporting here for 255 mg. Just curious how many patients are included in this data set, and what gives you confidence that what you're seeing here in the low dose is actually real? Thank you. Yeah, those are really good questions, Danielle. Thanks for that. With regard to the consistency of the LDL findings across indications, the degree, the magnitude of change, and the correlation with dose and albumin reduction was consistent across all the indications. Caveated slightly by the fact that we're dealing with small numbers and that when we looked in the other indications or in the healthy subject study, which was an injection site study, those were post-hoc analyses. They weren't pre-specified. They were run on stored serum. Cholesterol is a pretty standard test, but it's not as standard to run cholesterol on stored serum. We need to view those slightly cautiously. When we ran stored serum on the thyroid eye disease patients, it was very consistent with the cholesterol findings that had been specified and run prospectively. All those things triangulated to give us a sense that the change in LDL in terms of magnitude was really similar across all the indications. The other thing that bolstered that, which we were a little surprised, is that we just didn't find any correlation between thyroid hormone levels and LDL. There's a well-described relationship between those two in general, but in our data, we were not observing that correlation. We're pretty confident of this consistency across indications in terms of LDL impact and the difference in terms of degree of LDL change by dose and by degree of albumin change. In terms of the magnitude of the IgG changes, I think these are generally consistent with what we've seen before, but a little bit deeper at the later time points. I have the slide up right now, which shows the IgG curve, and you can see with the 340 mg arm and to some extent with the 680 mg arm, there's just a little bit of additional reduction that you get after six weeks. We saw that also in the albumin curves, which were a little deeper for 680 mg and 340 mg at 12 weeks compared to 680 mg. Those both being on target effects, both being consistent across two different biomarkers, give us confidence that these are good estimates of the degree of IgG suppression that we would see with the different doses. As I mentioned, those computer simulation models that we've been building allow us also to estimate the IgG reduction that we might see with different dosages or different dosage frequencies. That's really helpful in picking the best dose going forward. Thank you. Our next question comes from the line of Thomas Smith with SVB Leerink. Please proceed with your questions. Hey, guys. Good morning. Thanks for the updates and for taking the questions. Appreciate some of the early market research you presented, Pete. Did you conduct any market research that contemplated the presence of multiple FcRn agents in the marketplace? If so, what was that feedback? Then just in terms of how you think about study timing, can you help us understand some of the outstanding gate factors to getting these clinical studies going again later this year? Absolutely. Thanks, Tom. Great questions. We did do a lot more market research than I'm showing here. I picked what I thought was maybe one of the most important themes. We double-clicked on that theme in ways as you described. That was interesting, having physicians choose different profiles. We did see that the benefit of a simple subcutaneous injection format can counteract the disadvantage of a modest change in LDL, recognizing that the modest change in LDL wasn't perceived as that big of a disadvantage, actually. For physicians, I showed the neuronal data. We did similar work with different specialties and pretty much across the board, when you're looking at changes of 30% or so in LDL, we didn't ask actually about less than that. They really didn't view that as something that would significantly impact their prescribing at the margin. It was something they have to address and may start a statin here and there, but they have a lot of patients on statin. When you're at that 30% rate, it's just one of many factors that they consider, and I think they'll go back to the efficacy they're achieving and the points I was making within myasthenia and the ability to achieve deeper responders and things like that are going to be the real drivers. In terms of timeline to getting back in the clinic, for myasthenia, each study is a little bit different. For myasthenia, we had a very productive end-of-phase II meeting with the FDA back in January, just prior to the voluntary pause in our program across all the trials. Based on that, we gained good alignment with the FDA on a design for MG and then many other features of the pivotal trial. We believe most of those will be able to carry forward into the actual pivotal trial that we're planning. As we're finishing up our computer modeling, that'll allow us to come forward with a dosing recommendation, and then work with experts to develop cholesterol monitoring guidelines and things like that, which will be pretty straightforward. That's what we need to do there with regard to myasthenia. Warm autoimmune hemolytic anemia, that trial is more or less paused. Since it was an open-label trial, it didn't have to be terminated like the thyroid disease trial. That one we're looking forward to starting back up on a similar timeframe with roughly the same existing protocol, just the addition of the monitoring for LDL. Of course, for both trials, we've gotten a lot of data over the last couple of months, we need to lock that data, add it to an updated investigator brochure, and share that with the FDA as well. Thyroid eye disease, because that trial had to be stopped because of the unblinding, there we'll be proposing a new design. There'll likely be a phase II design. That's all work that's at the top of our priority list right at the moment. Okay, great. Thanks. Maybe just one other clarifying question. You provided some really good color just on the albumin reduction seen at 680 mg and 340 mg. I guess, can you clarify, did any of the patients who received the 255 mg dose fall below the lower limit of normal regarding albumin? In the 255 mg dose, we have such a small number that I'm not sure it's useful to provide the individual patient's level data. The average right in the middle there was quite well above the lower limit of normal of 3.5. The average was 4. We're confident that patients on 255 mg, when we have a large population, they're not going to have issues related to albumin and the LDL changes that they'll have as a group are going to be low and manageable. You do see that with the 340 mg dose, the average patient's right on the line there. In the 340 mg arm, there were patients who fell obviously below the lower limit of normal. In the 680 mg group, the averages are already pretty low. It's a point I made during the presentation, but I'll just make it again, which is that the difference in albumin reduction by dose is large. There are PK/PD modelers talk about albumin being on the steep part of the curve, and what that means is as you reduce the dose, you have a big change in the reduction in albumin. Whereas IgG is on the flat part of the curve, so as you reduce the dose, you don't have as much loss in IgG suppression. This really makes the 255 mg dose a very favorable dose. For many patients, the 340 mg will be a favorable dose because there's individual variability patient to patient. For some people, for some individuals, the 340 mg performs like the 255 mg in others. Between those doses, that's a really nice set of options I had on the slide here with the different dosage options. The 255 mg and the 340 mg, we think, will provide a really nice balance of IgG su pression with minimal changes in albumin and lipids for most patients taking those two doses together. Got it. Okay. Thanks, Pete. Appreciate the call. Yeah. No problem, Tom. Thank you. Our next questions come from the line of Brian Skorney with Baird. Please proceed with your questions. Hey, good morning. Thanks for taking the question. My one question is really on just kind of the thoughts on your plans for lipid management. Has there been any thought to basically starting patients on statins at baseline, or is it purely interventional? If you're kind of thinking about it as a purely interventional basis, maybe in terms of the MG phase III study, how do you ensure study conduct and that patients aren't being unblinded, provided that one would expect to see LDL increases probably more heavily in the treatment arm than placebo? Thanks. Yeah, a couple of really great questions there, Brian. First of all, with regard to our approach to lipid management, first and foremost, it's to get people for longer-term dosing in the sweet spot where most of them aren't going to have more than a modest increase. Some of those modest increases are going to occur on a background of a relatively low LDL to start with. We're not thinking that we're going to need to start everybody on a statin or something like that, but rather have, for the few patients that fall outside of the normal guideline, they may have a statin started at the discretion of their physician. There might be some rough guidelines, and that can translate through ultimately to the label where many other products that have a similarly modest change in LDL have a note in the adverse events, warnings, precautions section warning of lab abnormalities that cholesterol increases can happen, and a recommendation that the physician manage those according to regular guidelines. In the short-term studies where we may be using higher doses and those may result in a change in not just LDL, but albumin, we have several things in place to ensure that there is not unblinding, including having separate physicians or healthcare professionals who do the medical monitoring versus those who do the clinical assessment. There's some standard things we can do there. We've done that even in the prior trials because albumin can be unblinding, but it was important to have a physician involved in the treatment of the patient to understand where the albumin was at any given point. There's that. We don't think that in the short term, patients are going to need to start statins during the blinded treatment period or something like that might add an extra level of unblinding complexity. That's our thought with regard to MG and more generally in terms of statin management. Great. Thanks, Pete. Yeah, no problem, Brian. Thank you. Our next question comes from the line of Sam Slutsky with LifeSci Capital. Please proceed with your question. Hey, good morning, everyone. Thanks for the questions. I just first building on Brian's question a second ago. The 15% or so increase in LDL at the 255 mg dose, just help us understand the clinical significance of this as it relates to needing an intervention? Right. That's a great question, Sam, and it ultimately comes down a lot to the absolute level, more so than the percentage level. At the population level, the percentages are important to get a sense for the magnitude of the issue and 15% is a low magnitude versus something like 60%, where if that were chronic, if you're using that in a large population chronically and at a 60% increase, you definitely have to have a broad-based program. At 15%, as I was describing to Brian, we don't think that we're going to need a broad-based, prescriptive anti-lipid regimen. How will physicians make decisions about individual patients? They'll make those primarily based on the absolute LDL of that patient. If you look at the slide that has the statin, a few patients who are on statins, which I have up now, I'm just looking in the middle here, there's a patient who was randomized to 255 mg, and you can see that they had an LDL of about 90. This person didn't change their LDL on therapy with 1401 and also with a background statin. If they had gone up 10% or 15% on a background of 90, the physician's unlikely to be doing anything. They're going from 90 to 105 or something. You see the patient on the far right who was randomized to 340 mg. They came in on a statin, more like about a baseline of about 170. That person, even before they had an increase of 7%, probably needed their statin dose increased or their lipid management optimized. When you're looking at these relatively small single digits or teen increases in LDL, the decision-making is going to be much more based on the absolutes, and that's probably their sense of variability. The patients who start higher may need intervention almost regardless of 1401 than people who are lower won't. That's just one more factor why we think it's not going to have to be a large anti- lipid component to our trials. Okay. I guess based on the data you have then, I was expecting it to be a smaller percentage of patients who might need that. I guess it differs as well by indication a bit. Right. Yeah, there's some difference, obviously, in the age and the population, in terms of risk factors. If you look across a broad swath of autoimmune diseases, as we're doing as we prioritize our next indications, some of them are younger patients with few cardiac risk factors. Some are a little bit older with more cardiac risk factors. There will be differences indication to indication. Okay. Lastly, too, just on the kinetics of the increase, what time points did you start to see this show up and this differed at all by dose level in terms of at what time point you saw the increases? Yeah, we have very thin data there. Most of the data, the really solid data, comes from the thyroid eye disease trial where cholesterol was prospectively measured at zero, 12, and 20 weeks, and we saw the data that you're familiar with now. The percentages that we're reporting today are a little bit lower as we've gotten more data in and ensured that it was all accurate. What happened between zero and 12 weeks? We did have some patients who had some intermediate time points where we could look at stored serum, and the increase was mostly apparent in the first six weeks or so. They went up to where they were going to go in about six weeks and then were generally stable there. Similarly, when they came off therapy or went to every other week in the MG open label trial, the LDL dropped over a similarly relatively rapid timeframe. Okay. All that's based on small data. It triangulates pretty well, but I'm not showing it here because it's just small data and each patient's a little bit different. Got it. Okay. Thank you. Our next question comes from the line of Douglas Tsao with H.C. Wainwright. Please proceed with your questions. Good morning. Thanks for taking the questions. Just trying to confirm your comments. Do you think, just given the sort of magnitude of effect that you anticipate seeing, you don't expect to have a need to put patients on statins during the blinded portion of the study? Correct. Okay. In terms of afterwards, in the sort of open label, in the extension period where patients would potentially need to be put onto statin therapy, will there be sort of a prescribed protocol, or will that largely be left up to physicians in terms of management? Thank you. Yeah, that's a great question, Doug. I can imagine there'll be a little bit of both, depending on the trial and the disease population and some other factors. I think one of the things that came out of the market research with physicians is that they are very interested to have some data. I showed some very anecdotal data today that we found very interesting, and physicians are going to want to know what happens when I prescribe a statin to a patient treated with 1401 whose cholesterol has gone up a bit, or who's at more risk of cardiovascular risk, and they're wanting to keep their LDL lower. I think we'll probably have some designs where we are a little bit prescriptive, which will allow us to create sort of some predefined data sets to answer some specific scientific questions that will help clinicians understand how to treat their patients. I think there will also be other trials where we will leave it to physician management and judgment, and that will also create a different type of data that'll be useful. I imagine that we'll end up with both designs over time. Okay, great. Thank you. I was talking about the long-term extension there in those two examples. Okay, there are no further questions at this time. I'd like to hand the call back over to Pete Salzmann for any closing comments. Thanks for that. I really appreciate everybody's attention and just a lot of great questions. We have completed, as I reviewed today, a pretty extensive review of our program, looking at data from a lot of different trials. We're excited by what we see. We see a lot of potential for 1401, given its broad therapeutic window and given the insight that the LDL signal that we have seen is modest at the doses where most patients will be treated and should be manageable for the vast majority of patients. Based on those learnings, we're excited to get back into the clinic, and we've got a team that's working hard to get that done, and I look forward to more discussions with all of you about our future plans and the indications we'll be announcing in the future. Thanks, everyone. Thank you for your participation. This does conclude today's teleconference. You may disconnect your lines at this time.