Operator
Good morning. My name is Michelle, and I'm your conference call operator. As a reminder, this call is being recorded. Before we begin, I would like to remind everyone that today's conference call will include 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 candidates and Immunovant's expectations regarding the timing, design and results of its clinical trials, 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, events and uncertainties, assumptions known or unknown, which could cause 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-Q filed with the SEC on August 10, 2023. Joining me on the call this morning is Dr. Peter Salzmann, Chief Executive Officer at Immunovant. Following his prepared remarks, we will open the call up for questions. With that, I would like to turn the call over to Dr. Salzmann.
Peter Salzmann
Thank you, Michelle. Good morning, everyone, and thank you for joining our call. At Immunovant, we are dedicated to enabling normal lives for people with autoimmune diseases. Today, I'm very excited to share new data with you that we believe substantially advances our vision. When we unveiled IMVT-1402, we shared data from cynomolgus monkeys, showing that 1402 matched the IgG reduction of batoclimab but without the albumin reduction or LDL increase seen with batoclimab. We said that we believed these observed differences in monkeys could be attributed to the different binding orientation of 1402 to FcRn as compared to the binding orientation of batoclimab to FcRn.
Both antibodies bind the IgG binding site of FcRn, but with a different 3-dimensional orientation shown on this slide. 1402's orientation is consistent with avoiding steric hindrance of albumin binding to FcRn. Given the prior consistency between cynomolgus monkey data and human data in terms of IgG and albumin across the anti-FcRn class and given the differing crystal structures shown here, we said that we also expected to observe very meaningful differences between 1402 and batoclimab in humans with regard to their impact on albumin and LDL.
So going into this Phase I trial, we had several goals, which I've scored here based on the initial data. First, we wanted to show best-in-class IgG reductions similar to batoclimab. You're going to see that. Second, we wanted to show minimal to no impact on albumin. You're going to see that. Third, we wanted to show minimal to no impact on LDL. You're going to see that. And fourth, we wanted to show all of this could be done with a simple subcutaneous preparation. You're going to see that.
In sharing these data today, we are particularly pleased to be able to share data from the 300-milligram MAD cohort. I'm incredibly proud of our team that was able to pull in this cohort well ahead of schedule. It's a tribute to their energy and capability.
In terms of IgG lowering, 300 milligrams of subcutaneously delivered 1402 demonstrated a mean IgG reduction of 63% after 4 weekly doses in the MAD cohort. The SAD data was exciting too, as 1402 demonstrated rapid and deep IgG reduction in both the 300-milligram and 600-milligram SAD cohorts. The second bullet is also very important. Allow me to read it. Initial 300-milligram MAD data after 4 doses showed a favorable analyte profile of no decrease in albumin and no increase in LDL relative to baseline levels. That's exciting.
Finally, although we believe that the primary axis of differentiation for 1402 will be deeper IgG reduction without analyte changes, we're also excited to be developing 1402 as a simple subcutaneous injection designed to enable patient self-administration.
This Phase I trial is really interesting because in addition to evaluating the overall safety of 1402 at multiple doses, we're also observing whether 1402 lowers IgG without impacting albumin and LDL. Another key aspect of this trial is dose selection since this study is designed to establish our going forward doses.
To achieve the goals on the prior slide, we designed a trial you see on this slide. It is a randomized, double-blind, placebo-controlled study. The IV SAD cohorts are primarily included to accelerate the path to the subcutaneous MAD cohorts. The subcutaneous SAD cohorts give us an early read of IgG, albumin and LDL levels after a single dose of 1402, delivered subcutaneously at 300 milligrams and at 600 milligrams. We expect 300 milligrams and 600 milligrams to be our 2 doses for future studies.
Of course, the MAD cohorts are the most informative because in these cohorts, we can see how 1402 performs with continuous weekly dosing over 4 weeks. This is similar to the MAD design we used for batoclimab, making cross-trial comparisons possible. Finally, I should note that the 1200-milligram IV SAD cohort began a couple of weeks ago, but data is not yet available from that cohort. Similarly, most of the 600-milligram subcu MAD cohort just began dosing this week, and we expect data from this cohort to be available in November.
Let me start with the SAD cohorts. This slide shows the mean IgG percentage change from baseline over time. After a single subcutaneous dose of 1402 at 300 milligrams and 600 milligrams, we observed mean IgG reductions of 37% and 45%, respectively. The IgG reduction following a single dose of 1402 was observed to be as potent or more potent than batoclimab at every time point in the SAD data. Although this comparison is from 2 separate trials, we believe that 1402 can achieve maximum IgG suppression similar to batoclimab.
In the 1402 arms, all time points showed a statistically significant decrease from baseline with p-values less than 0.05. Here, we combine the 2 figures into 1 for easier comparison of the 1402 and batoclimab data. In terms of IgG lowering, we predicted that 300 milligrams of 1402 in purple would be at least as potent as 340 milligrams of batoclimab in light green, and that is what we observed. We also predicted that 600 milligrams of 1402 would be as potent as maximum saturating doses of batoclimab. The batoclimab subcu SAD study didn't test 680 milligrams, but it did test a somewhat higher dose of 765 milligrams. Here, we see that 600 milligrams of 1402 in blue, matched the 765-milligram dose of batoclimab in dark green. Again, this gives us confidence that we can achieve maximum IgG suppression around 80% with 1402.
Albumin data is shown on this slide with a side-by-side comparison to 1402 data on the left, and batoclimab data on the right, whereas batoclimab showed a decrease in albumin in both SAD cohorts, 1402 does not show a decrease in albumin. And the 3 curves for placebo, 300 milligrams and 600 milligrams are basically on top of each other. No albumin data points in the 1402 treatment arms showed a statistically significant decrease from baseline with all p-values well over 0.05.
Consistent with the albumin data, we also observed no impact on LDL in the 2 SAD cohorts of 1402. No LDL value at any time point showed a statistically significant increase with all p-values well over 0.05. No comparison with batoclimab is shown because LDL was not measured in the batoclimab Phase I as this study -- excuse me, as this impact was not anticipated at that time.
Moving on to the MAD cohorts. This slide shows initial results with the 300-milligram cohort through 4 weeks of dosing. As I mentioned earlier, the mean IgG reduction from baseline for the 300-milligram cohort was 63% after 4 weeks of dosing. Similar to the SAD data we just reviewed, the IgG data for this 300-milligram MAD cohort of 1402 looks very similar to the 340-milligram MAD cohort of batoclimab. You'll appreciate that even more on the next slide.
Here, we have overlaid the IgG data from the batoclimab Phase I trial and the initial data from the 1402 Phase I trial. You can see the 300-milligram 1402 cohort in purple, is right on top of the 340-milligram batoclimab cohort in light green throughout the dosing period. As I mentioned earlier, based on these data, we believe that the 600-milligram MAD cohort, which just started dosing, will match the best-in-class IgG lowering of batoclimab 680 shown here in bright green.
The 1402 albumin change from baseline chart is also impressive, showing albumin levels that are mostly above baseline for 300 milligrams of 1402 shown in purple, throughout the dosing period. Note that batoclimab begins to show clear albumin lowering 7 to 10 days into dosing and is peaking 3 to 4 weeks into dosing. So the lack of any decrease in the 1402 arm throughout 4 weeks of dosing is an important observation. This is another very nice chart and not at all surprising given the lack of albumin changes observed in the 300-milligram MAD cohort. After 4 weeks of dosing with 300 milligrams of 1402, the mean LDL change for the group ended below baseline.
Moving on to safety. We included the IV cohorts in our safety analysis. The treatment-emergent adverse events that we observed were mild or moderate with no serious adverse events observed across any arm to date. Also, we are not seeing any patterns where we did observe AEs, whether in 1402 or in placebo groups, they were mostly one-offs, meaning most unique AEs were experienced by 0 or by just 1 participant per group. The exceptions are shown at the bottom of the table. Here we list all AEs that occurred in 2 or more participants in the group.
These 3 treatment-emergent adverse events were actually all more common on a percentage basis in the pooled placebo groups than they were in the pooled 1402 groups. For example, headache was observed in 3 out of 12 or 25% of placebo participants, while it was observed in only 4 out of 40 or 10% of 1402 participants. Catheter site pain refers to pain from the catheter used for blood draws.
Let me share with you my concluding thoughts before we open the call for Q&A. I hope you share our excitement after reviewing these encouraging data this morning. We believe these results strengthen 1402 as a potential best-in-class anti-FcRN. I will note that in the ADAPT-SC study, IV efgartigimod showed a 62.2% reduction in IgG after 4 weekly doses. In the same study, Halozyme-enabled efgartigimod showed a 66.4% reduction in IgG after 4 weekly doses.
Turning back to Immunovant, 680 milligrams of batoclimab has shown IgG reductions of about 80%, which we believe is best-in-class IgG lowering for a simple subcu. Based on the data reviewed today, we believe 600 milligrams of 1402, given weekly will deliver IgG lowering on par with 680 milligrams of batoclimab, enabling the potential for greater efficacy across a range of autoimmune conditions.
We're also excited by the albumin and LDL curves for 1402, which were both observed to be similar to the curves for placebo in all the initial data. This slide highlights the emerging profile of 1402, a potentially best-in-class anti-FcRn and provides the key points all in one place. I also want to remind everyone that we have a composition of matter patent that is pending for 1402, which if granted, is expected to provide coverage into 2043.
In closing, we are very excited about the initial data we reviewed today. We're also very excited about the many attractive potential indications with 22 different indications being studied across the anti-FcRn class. This breadth of indications and the strength of IgG as a biomarker, both topics that we've been speaking about for a long time, make the data we reviewed today all the more important. With that, let's open the call for Q&A.
Operator
[Operator Instructions] Our first question comes from Derek Archila with Wells Fargo.
Derek Archila
Great. Congrats on the data well done. Just 2 questions from us. So maybe just discuss your reasoning to test the 1,200 mg fixed dose in the SAD. If I recall, I believe that was originally an optional dose. So that would be great to know. And then just in terms of the 600 mg performing better than the 765 mg batoclimab dose in the SAD, I guess, would you expect now in the MAD trial to perhaps get greater than 80% IgG reduction? I guess what's possible? And I know you just kind of compare to the other [indiscernible] space, but -- how does that compare to things beyond VYVGART and some of the other full-length antibodies?
Peter Salzmann
Yes. Thanks for those questions, Derek. So with regard to the 1200-milligram SAD IV cohort, that's done to really round out our PK/PD models and help to answer some of the points you raised in your second question. That's really the only purpose for that cohort.
The second question is interesting. We're pretty convinced that 680 milligrams of batoclimab is maximally saturating the Fc receptor and therefore, yielding the maximum amount of IgG reduction that can be delivered via this mechanism. That's consistent with what can be achieved with very, very high doses of nipocalimab given IV for example. So the 765-milligram dose of batoclimab would be equivalent, obviously, to the 680-milligram of -- dose of batoclimab. We don't see in the data we have that going above 680 of batoclimab would yield greater than 80% IgG reductions.
So with all that said, we also believe that 600 is going to be fully saturating and that the, again, a fully saturating IgG reduction that we expect is around 80%. I think those curves are probably pretty close, even though there are a couple of time points where one is a little higher than the other.
Derek Archila
Excellent. Thanks for the questions and congrats again.
Peter Salzmann
Thanks, Derek.
Operator
Our next question comes from Yasmeen Rahimi with Piper Sandler.
Yasmeen Rahimi
Congratulations, great data, extremely well done on the execution. A few clarification questions. Team, could you maybe comment on sort of the variability of the air bars and IgG reduction along the SAD and the MAD and whether it came in as expected or whether it was consistent with other studies. Any sort of commentary around variability in these measures would be helpful.
And then second question is, is there any assumptions like thank you for predicting the 600th MAD dose group, but is there any room that you could I guess what are the assumption that something could go wrong and it doesn't show 80% reduction? Like, I guess, how confident can we be for the prediction of the 600 mg dose group. That would be really helpful.
And then the third question that I think a lot of investors have is sort of thoughts around which indications you're interested and what -- when you hope to disclose sort of the next steps post the full MAD data in November. And thank you for allowing me to ask all these questions.
Peter Salzmann
No problem. Thanks, Yas. So starting with the variability, I think, Yas, what kind of variability are we seeing. So across the data set, we saw albumin had a standard deviation of plus or minus 5, IgG by the way, had a standard deviation of plus or minus 6. And LDL was plus or minus 16. As we said prior to this data release, the albumin value is really the most important one, and that's because we believe the albumin data is most derisking since the LDL changes seen with batoclimab happen because of the albumin changes. So with the flat albumin curve through 4 weeks of dosing in the 300-milligram 1402 MAD with variability -- observed variability of just plus or minus 5%. We have a lot of confidence in the data.
With regard to the 600-milligram data and how confident we are that, that will saturate the receptor and yield maximum IgG reduction. We're very confident on that based on a couple of things. The translation of 340 to 680, that's based on -- we have a lot of PK/PD models for batoclimab that gives us confidence in being able to predict where batoclimab sits along the saturation curve. We used that model as well as preclinical binding affinity of 1402 that is a little bit higher to correctly predict that 300 would be the same as 340. And so doubling 300 will run up the curve to 600, obviously, just in the same way that 340 runs up the curve to 680. 680 is probably a little -- be a little bit on the flat part of the curve. What I mean by that is even a dose a little less than 680 of batoclimab would likely be saturating and deliver 80% IgG reduction.
So several different points that we can use to triangulate to give us confidence that 600 will be the maximum dose -- sorry, will yield the maximum IgG reduction. And then finally, what indications do we plan to pursue. So gosh, there's so many good ones, right? And our strategy is really to kind of attack maybe there's 3 different types of indications that we're excited about. In spite of 22 indications being studied, we still have some of the first and some of ours are still first-in-class and 1 there that we have a proof of concept that you know about with batoclimab is Graves' disease and we're expecting data for that later this year. If that data is positive, I think Graves' disease is a really nice opportunity for 1402. And we've talked about that one pretty extensively before.
Looking at this emerging profile for 1402, which we believe is heading to best-in-class. If you have the best-in-class asset, and that allows you to go after the best indications based on a belief that the share market will ultimately be driven by the best-in-class profile of an asset, not so much the launch order in these indications. And there's a whole variety of really good indications as defined by largest addressable market, most unmet need and highest probability of technical success. And then we have some emerging indications that are really interesting.
The J&J just reported a lot of data from their proof-of-concept study in rheumatoid arthritis, which I find to be very encouraging. They had consistent signs of efficacy across many different clinical parameters. They achieved that with only a 58% reduction in IgG and -- so -- and they showed a correlation between depth of IgG reduction, depth of ACPA, I should say, reduction, which is 1 of the pathogenic IgGs in clinical response, even though that ACPA only was driven down by about 30% for nipocalimab, we believe we can get higher levels of IgG reduction, obviously. And therefore, drive that clinical efficacy potentially higher in RA. So there's some other indications that are emerging that are really exciting. So a lot to think through now that we've got this data.
Operator
Our next question comes from Robyn Karnauskas with Truist Securities.
Robyn Karnauskas
And congrats on the quality of the data. Your presentation was really well done. I guess a few questions. How do you decide what indications to go for in financing those? Because obviously, you can run 1 million trials at once and be competitive. How do you decide like where you go and what choices you make and where to capitalize your spend?
And second, I'm glad you brought up the RA data. Given nipocalimab is not probably at the highest dose it could be, do you -- how do you comp that to 1402? And where you think you can go for RA?
Peter Salzmann
Yes. Thanks for the questions, Robyn. So we -- I mentioned in response to Yas' question kind of how we're thinking about indications broadly and how there are so many that are exciting. Your question kind of follows up on that, which is how do we prioritize which ones to start with. And I think there's a whole variety of factors to consider there that have to do with both the best indications are always going to rise to the top. So that's going to be probably the most important thing. And that's -- there's no -- each indication is a little different on a different dimension. Some are more commercially attractive. Some have a higher probability of technical success. Some are a little bit easier to execute. So we'll be looking at all that to basically decide which are our favorite few to start with.
And then in terms of RA, specifically, again, in 1 of the abstracts that Johnson submitted to ACR, which is on the website now, they report this 58% reduction in total IgG with about a 30% reduction in ACPA, and they state in the conclusion that ACPA reduction correlated with clinical remission, not just clinical response, but remission. These patients were pretty sick. They were -- there had to be at least a minimum of 1 TNF failure, but probably they had many that were more than 1 TNF failure. So to get to a clinical remission in that population over 12 weeks, even with only a 58% IgG reduction. And I know it wasn't statistically significant, but they're small numbers. I think that's really impressive.
Where could we get going to 80% IgG reduction, well, -- there's not enough data in RA to know for sure. But if we look across many, many other indications where deeper IgG reduction led to meaningfully more clinical response, we think we can do better on all of the percentages that they reported in terms of like ACR 2050/70 should we decide to pursue RA. So that's definitely one that will be in consideration.
Robyn Karnauskas
Pete, 1 follow-up question for you. So when you think about catalyst, you mentioned Graves'. But when do you think you could articulate when we get the indications you're going after? So we understand we can model it better. I mean I think a lot of clients are looking at MG, but they're way ahead. So like how do we think about when you disclose what indications you're going after, so we can better model your company and the opportunities?
Peter Salzmann
Yes. Great question, Robyn. And there's always a tension between granular transparency and indication selection and the strategic value of waiting until the last minute to disclose an indication. And the last minute is usually defined by -- when you're posting it on clinicaltrials.gov. And generally, the strategic advantage outweighs everything else. So I think we will disclose the indications probably as they're just about ready to go for 1402 on a case-by-case basis. .
Robyn Karnauskas
Okay. Congrats and great job in the presentation. Very clean. Thank you, I appreciate it.
Operator
Our next question comes from Samantha Semenkow with Citi.
Samantha Semenkow
And let me add my congratulations on the data, very well done. I wonder if you can maybe just talk about your next steps with FDA. I know you have an open [indiscernible]. Do you think you'll be able to take this data directly into patients in the U.S. with the safety database you have or will you have to do any bridging work? Just curious on your thoughts there.
Peter Salzmann
Yes. Thanks for the question, Sam. So first, we're going to finish the Phase I trial. We have another cohort to complete. It's just started the 600-milligram MAD cohorts and then that data needs to be all locked and clean so that we can use it for regulatory interactions. But in terms of bridging, there's not really a bridging concept between data from Western countries at least, Europe, New Zealand, Australia, Canada, U.S. That data is essentially equally valid from an FDA perspective. So we'll take this data to the FDA. And in terms of which division, that depends on the indications that rise to the top. And different divisions have responsibility for different indications. So as we make our indication prioritization decisions, and that will define which divisions with -- at the FDA that we'll be going to next year.
Operator
Our next question comes from Sam Slutsky with LifeSci Capital.
Samuel Slutsky
Congrats on the update. Just 2 for me. I guess, as it relates to the development and CIDP, just how are you thinking about the path forward for batoclimab versus 1402, depending on the scenarios for the initial CIDP data next year?
Peter Salzmann
Yes. Thanks for that question, Sam. So when we launched the CIDP indication, we launched that with a lot of optionality. You probably remember those discussions. It has sort of a proof of concept built into the pivotal IIb design in the sense that the period 1 is testing 2 doses. And our hypothesis at the time was that Argenx would likely succeed in CIDP as they have and that there would likely be some additional room for efficacy based on some patients in the randomized withdrawal period relapsing, which we also saw.
Then the third thing we hypothesized is that 680 of batoclimab would outperform 340 of batoclimab in our period 1. So that we won't know until the first part of next year. But with all -- if all those things are true, then there's a compelling argument to be made to develop CIDP with 1402 through to registration versus batoclimab. So I think that's the way we're trending with regard to our CIDP program.
Samuel Slutsky
Got it. And then I guess on MG, obviously, batoclimab has the advantage versus currently marketed FcRns that it could be self-administered versus healthcare administered for the currently approved products. Obviously, it has the LDL signal whereas 1402 doesn't. I guess does it make sense to study both in MG? And kind of what's the physician feedback been on batoclimab post Argenx and ROSA approval since they're healthcare administered?
Peter Salzmann
Yes, great question. So the -- you mentioned 1 of the key differentiators that we believe our batoclimab program offers in myasthenia gravis, which is the simple subcu that we believe will ultimately lead to the ability for patients to self administer. But the more important differentiator is the deeper IgG reduction, which batoclimab can also achieve although for a shorter period of time than 1402, we'll likely be able to achieve it based on the analyte changes.
Given the induction and maintenance paradigm in myasthenia gravis, then that shorter period of deeper IgG reduction, which is built into our -- the period 1 of our MG study, which has an induction maintenance design, is very attractive to physicians. I was at an investigator meeting for some of our -- a bunch of our clinical trial sites for myasthenia last week, and there's just a lot of enthusiasm for the trial design. It really resonates with neurologists to start with the more potent dose and then after for those patients who will achieve a good response, they have the opportunity to titrate down their dose. So we're really excited about what batoclimab can do for patients with myasthenia gravis. And you're right that there will be some patients, particularly in the long-term extension, who may have a modest increase in their LDL and that may require anti-lipid therapy in some cases, but with the potential for additional efficacy and the potential for a better route of administration, we still see that program as really differentiated.
All that said, myasthenia is a really important indication for the anti-FcRn class. So I also wouldn't rule out that we'd eventually do a myasthenia study with 1402. But our short-term plans are to take batoclimab through the registration for myasthenia.
Operator
Our next question comes from Thomas Smith with Leerink Partners.
Thomas Smith
Let me add my congrats on the data. Just 2 quick clarification questions on my end. I guess, first, can you share any color on what you saw with the single-dose IV cohorts on albumin and LDL and particularly with the higher doses you explored there? And then secondly, you mentioned, I guess just a follow-up on your comments, Pete. You mentioned your standard aviation for LDL was plus or minus 16. Can you just comment on where that falls relative to your expectations and within the context of the assay variability?
Peter Salzmann
Yes. Yes. Thanks, Tom. So the -- we didn't show the IV cohorts because they basically look just like the subcu cohorts, and we had enough SAD data in the presentation we thought already. We do expect the IV cohorts to provide some additional insight to us in terms of IgG reduction, and that's competitively sensitive since some companies are struggling to move from IV to subcu. But in terms of albumin and LDL, there wasn't anything interesting in the IV cohorts.
And then what was your second question, Tom? Sorry, I missed it. I didn't write it down.
Thomas Smith
And then, yes, it was just -- you mentioned the LDL standard deviation was plus or minus 16.
Peter Salzmann
Yes, variability. Thanks. Sorry about that. Yes. So as I mentioned in response to Yas, I think the most important thing is that the observed variability for albumin was just as we predicted, plus or minus 5%. That's really the analyte of most interest here because any LDL changes that we observed with batoclimab relate to changes in albumin that's not an independent signal. The albumin was relatively easy for us to estimate the variability in advance of the trial because we have so much albumin data with batoclimab because all of our batoclimab trials had multiple albumin measurements all along the way. Because that wasn't true for LDL. LDL wasn't measured in our Phase I trial for batoclimab. It wasn't measured in the MG trial. It was measured infrequently in the TED IIb trial. So we just had many fewer data points on LDL. And there's not that much in the literature. We found literature estimating LDL variability anywhere between 10% and 16%.
So this variability falls within that range. But the most important thing is the albumin variability, which is plus or minus 5%, and that gives us a lot of confidence.
Thomas Smith
Got it. That's super helpful. And if I could just sneak in 1 other clarifying question. Just wondering if you could provide any additional color on the one AE-related discontinuation in the 300 mg cohort?
Peter Salzmann
Right. That person had a mild AE that was not deemed related to study drug. It was an event -- it was a preexisting condition that was mild and flared up, but just led them to discontinue the trial. Again, not related to study drug.
Thomas Smith
Got it. Super helpful. Congrats again on the data.
Peter Salzmann
Yes. Thanks, Tom.
Operator
Our next question comes from Yatin Suneja with Guggenheim.
Yatin Suneja
Nice results today. Just a question on the regulatory part. Do we know if there is a regulatory path forward where you might be able to switch 1402 without running a pivotal study -- just curious if there is any precedent? Is that something you could do or you plan to do? Or you would have to sort of run a pivotal study with 1402 in the indication where that already ahead?
Peter Salzmann
Thanks, Yatin, for that question. Yes, our assumption is that anywhere we seek to get 1402 approved in the U.S., we will need to run a registration trial with 1402. That said, there are some interesting pathways, including the model-informed drug discovery pathway that the FDA just recently released some initial guidance on and has been a big topic of conversation, which provides some interesting opportunities for leveraging data from a first-generation asset where you have a good biomarker for second generation asset, and that pretty much exactly describes the situation here with anti-FcRn, batoclimab and 1402. But at the end of the day, I do expect that any indication where we want to get approval from the FDA in the U.S. will require a registrational program. Again, that program could be a little bit optimized with the MIDD pathway, but you're going to need a registrational study for sure.
Yatin Suneja
Got it. Very good. Just 1 more. So if we look at the assay, the 300-milligram, it matches, especially if you look at the IgG reduction, it matches the 765 batoclimab, but in the MAD 300 is sort of more closer to 340. And what would be the possible explanation there?
Peter Salzmann
Yes. Thanks, Yatin. I think the primary explanation from that situation is that you just have a lot more variability after a single dose. And even in the MAD, you do see a little bit steeper, at the very beginning, drop with the 300. But I think if you look at the totality of the data from the 300 again, just sort of right on top of the 340-milligram of batoclimab in the MAD. And the MAD curves are more reliable as a specific estimate of what you're going to see with continuous dosing since obviously you have continuous dosing there. So I think that's just a little bit of a fluke of variability in the SAD data.
Operator
Our next question comes from Jason Gerberry of Bank of America.
Jason Gerberry
So firstly for me, and apologies if I missed this, but just curious in lieu of today's data, how you're thinking about this optional 450 mg dose in the MAD. If I recall, this could give you an option to have a single prefilled syringe as your high dose option. And so just wondering if you're thinking about exploring that and what is sort of the minimal IgG reduction you need to see for that to become your preferred high dose?
And then secondly, if you can just comment, are there any meaningful differences in baseline albumin levels in this versus batoclimab Phase I studies. I know that other sponsors sometimes have come in low baseline and that can kind of skew the percentages. So just curious if you can comment on that?
Peter Salzmann
Yes, Jason, great question. And you noticed a difference between our prior trial schematic and this one because we've now advanced as we have more data in terms of our thinking. So you're right. We previously had listed that we had optional cohorts at either 150 or 450. And those were put in the protocol as optional cohorts in the case that the 300-milligram 1402 performed a lot, yielded much deeper IgG reduction than we predicted. That's not the case. So 300-milligram did what we predicted, which was it matched 340 mg. Those 450 mg and 150 mg cohorts were kind of in the unlikely case that we had much deeper IgG reduction with 1402 because you never know, we want to be ready for that, then we could test the lower doses.
So at this point, we believe 300 milligrams of batoclimab will be our sort of standard dose that yields sort of a standard degree of IgG reduction of around 65% and 600 mg will be the high dose. So we're not planning on doing the 450 mg or 150 mg cohort.
And then your second question, Jason?
Jason Gerberry
Yes, it was on the baseline albumin levels, this versus batoclimab studies?
Peter Salzmann
We didn't see any, there was nothing remarkable about that. This study done in New Zealand has a pretty unskewed population. It was a similar population to what you typically see in a healthy volunteer study. So nothing remarkable about baseline characteristics.
Operator
Our next question comes from Louise Chen with Cantor.
Unknown Analyst
This is Wayne on for Louise. Congrats on the data. So there are 2 of us. First is now that you have some 1402 data, are there any batoclimab indications that would be better suited for 1402 and then the second question is, have you ever considered like a collaboration or partnership for your anti-FcRn assets?
Peter Salzmann
Thanks, Wayne. So in terms of our batoclimab studies, the -- as I mentioned earlier, Graves, we have a proof of concept running with batoclimab and data expected later this year. If that data is positive, then we would anticipate future development in Graves to be done with 1402. And then I previously addressed another question, our plan for CIDP and myasthenia gravis, and that just leaves our Thyroid Eye Disease Program. That's a fixed-duration therapy program, 6 months of fixed duration therapy. And so for 6 months of fixed duration therapy, the incremental advantage of 1402 versus batoclimab is less. So we plan to continue TED with batoclimab.
In terms of collaboration or maybe more broadly, how do we maximize this amazing opportunity. I think we're going to look at every different possibility to maximize the potential of 1402, starting with our Plan A, which is what we've done in the past, which is to raise capital in the equity markets and then use that to develop the indications ourselves. Thanks for the questions.
Operator
Our next question comes from Alex Thomson with Stifel.
Alexander Thompson
I guess for CIDP, I wonder if you could talk a little bit about what the functional path forward would be post proof of concept with batoclimab transitioning into 1402 study there. And then for subcu in particular, is there a path forward to potentially having a high dose be a single injection there at all with formulation or something like that. But again, congrats on the data.
Peter Salzmann
Thanks for those questions, Alex. So I think for CIDP, there's a lot of different options. But most fundamentally, similar to my answer to Yatin, which was a little bit more general. Assuming that we -- our registration program for CIDP is with 1402, which is what I said we're probably trending towards -- that we need a registrational study with 1402. How we can support that package, make that package most efficient by taking advantage of batoclimab, we have a lot of different -- a lot of different ideas there, not the least of which is we have a lot of experience now, a lot more experience than we had a year ago, running CIDP trials and working with investigators around the world.
In terms of the injection presentation for 1402, our base case assumption is that it will be the same as batoclimab. So we have the standard dose in a single injection, a 2 cc injection with a 27-gauge needle. And that will be adequate for many people in many different indications. And then we can provide maximum IgG suppression with 2 injections, two 2 cc injections similar to the way we do it in induction phase for batoclimab. At this point, the data so far in the Phase I trial does not suggest that you could get to saturating levels of IgG suppression with a single 2 cc syringe.
Operator
Our next question comes from Douglas Tsao with H.C. Wainwright.
Douglas Tsao
Congrats on the data. Pete, maybe you talked a little bit about how you're thinking about some of the indications ongoing in development in terms of batoclimab versus 1402. I'm just curious -- at this point, are there new indications that you would pursue with batoclimab? Or should we think about now those efforts largely being focused on 1402?
Peter Salzmann
Yes. Thanks for the question, Doug. I think that our primary focus in the near and medium term is likely to be in terms of new indications is likely to be 1402 primarily.
Operator
Our next question comes from Yaron Werber with TD Cowen.
Yaron Werber
Great. Congrats as well. I think in the past, you've talked about having potentially a best-in-class profile, but also potentially having a few indications where you might just be able to be first-in-class with 1402. There's obviously multiple indications, including several that are not being developed yet by the competition. I don't want you to necessarily trump things here, but -- any sense you can give us which indications you think you can potentially have a fast path to market with?
Peter Salzmann
Yes. Thanks for the question, Yaron. I mean I think the 1 that we can talk about because it's already been talked about is Graves' disease. We talk a little bit about how we selected that, and that would be a process that we would use to find other potentially first-in-class indications and maybe not necessary much find them, but end up prioritizing them because I think the 6 or 7 or 8 indications that could well be studied with an anti-FcRn that are not currently in anyone's portfolio of announced indications, those probably aren't a secret to anyone and Graves' wouldn't have been a secret, I don't think before we announced it.
But what led us to have the conviction to start studying Graves, it was really 2 things, and these are probably the most -- 2 most important things for us, which is our assessment of the probability of technical success, even without any anti-FcRn data. And then secondly, our assessment of the unmet medical need. So in terms of the first assessment, there's no data in Graves yet with anti-FcRn. But it's a classic autoantibody condition. And so that gave us a lot of conviction. We also had some hints in our TED IIb trial that I've mentioned on prior calls.
For other indications that involve different components of the immune system, the assessment would be a little bit different, but the basic idea is can we triangulate to a conviction on probability of technical success that's moderate even without any anti-FcRn data. And I think the answer is yes for some remaining indications. And the second question is equally important, which is our direct assessment of how much unmet need there. And this is something I think that we probably had an assessment that's different than others, and it will come into focus in a positive way for us.
We spent a fair amount of time -- a lot of time actually talking to endocrinologists and even talking to people with Graves' disease to really appreciate that while there are many people who are well served with the existing cheap oral generic antithyroid drugs, there's also another large group that is not well served by those medications and is not excited about radio ablation or surgery, which are basically the only other 2 options. So I think what led us to Graves' was really a deeper look at the patient experience, and that's an approach we'll take to other indications we're thinking about where you could potentially be first-in-class.
Operator
Our next question comes from David Risinger with Leerink.
David Risinger
So just to follow on, on Graves, could you please add some additional color on the trial design, key study considerations? And then also, could you please comment on the potential commercial overlap of Graves' with thyroid eye disease. .
Peter Salzmann
Thanks, David. 2 great questions. So in terms of the current trial, it's really designed to give us an estimation of the effect size and effect size to do what. The effect size to take people who are insufficient responders to an antithyroid drug as defined by they are still hyperthyroid in spite of antithyroid drug therapy. So they're an insufficient responder, they're hyperthyroid and convert them to being euthyroid, which means normalize their thyroid hormone levels. That's essentially the definition of hyperthyroidism, you have high T3, T4 high thyroid hormones and you normalize them and then you don't have hyperthyroidism anymore. So it's a nice condition from the standpoint of the biomarker is also the clinical endpoint.
Since there -- as I mentioned in the last question, there isn't any FcRn data in Graves', then estimating that effect size, this is an important part of the work you need to do prior to running a pivotal trial. There's some other things we'll learn from that trial that are important as well. In terms of the overlap with TED and Graves, actually, 1 of the things that drove us to Graves where the advisory boards that we are running with physicians for thyroid eye disease, where they kept bringing up the idea that while thyroid eye disease is a really exciting indication for an anti-FcRn, Graves is as well.
Patients with Graves are obviously the ones who get thyroid eye disease. Graves patients tend to be predominantly managed by endocrinologists, whereas patients with thyroid eye disease are managed by both endocrinologists and ophthalmologists or more specifically often oculoplastic surgeons. So having an anti-FcRn, even if it's 2 different FcRn to ultimately treat thyroid eye disease and Graves provides a lot of kind of commercial and promotional synergy down the road. So that's a consideration for why we signed these 2 indications attractive.
Operator
Our next question comes from Brian Cheng with JPMorgan.
Unknown Analyst
One question that we often get is whether IgG reduction, deeper IgG reduction will drive better responses. And the balancing act of driving deeper reduction and potential infection risk. So what is your latest view on those 2 key pushbacks that we're hearing and especially on the back of today's data.
Peter Salzmann
Brian, thanks for those questions. They're both really good and important. So deeper IgG reduction has been shown to correlate with more clinical response, essentially everywhere that anyone has looked with any amount of data. So if you look at all of the MG trials that have a difference in IgG reduction, Argenx data has been interrogated and published in this regard, the large Phase II study with nipocalimab, Momenta published a strong correlation between depth of IgG reduction and decrease in MG-ADL, our small IIA study in MG showed the same thing. The UCB data in ITP, where they had a Phase II trial with many different doses, a much wider range of doses than they've studied elsewhere show the correlation between depth of IgG reduction and improvement in platelets.
Our thyroid eye disease IIb trial, which had 3 doses plus placebo, so 4 different levels, including the null level of placebo pretty much every parameter correlated with dose and depth of IgG reduction. And so in the Pemphigus data from Argenx as well had some -- they had some different doses in their Pemphigus trial. Typically, they've just studied 1 dose, but their Pemphigus trial had different -- had multiple doses, and you saw a correlation with depth of IgG response and now the Johnson data in RA. So just time after time after time, you see this correlation between depth of IgG reduction and clinical response.
Second point I'd make is I don't think it's a surprise. The idea that you get a strong clinical response with 50% or 60% IgG reduction, you get a better clinical response with 80% IgG reduction. I don't think that's surprising. So you have a sort of a non-surprising hypothesis supported by a lot of data. Given the severity of a lot of these conditions from a clinical standpoint, then the ability to get incremental efficacy is going to be highly valued by many patients, and all physicians. Any individual patient can make -- can and should make a personal trade-off on risk benefit, and that gets to your second question, FcRn is a very selective and targeted immunosuppressant, but it's still an immunosuppressant.
So you're likely to have higher rates of infection with deeper IgG reduction. But that's in the context of a mechanism that's really been pretty safe to date across all of the various trials that have been run now. So I think there'll be a risk-benefit calculation, but the ability to offer -- even offer that opportunity for patients to go for deeper, more potent IgG reduction and then have data whether if there is an increased infection risk or not and to characterize that, that will all be important data that we can generate in our trials that have multiple doses and deliver to physicians, which they're excited about.
So net-net, I see a really, really big opportunity for deeper IgG reduction to be a positive differentiator across this class.
Operator
This does conclude the question-and-answer session. Thank you for your participation. You may now disconnect. Everyone, have a great day.
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