Hey everyone. Welcome to the last day of our healthcare conference, Credit Suisse. My name is Thiago Ferezin. I'm a big tech biotech analyst here at Credit Suisse, and I'm joined today by the Immunovant team. They're going to do a presentation. Feel free to email me any questions, and I will try to work those in towards the end. For now, that's it. I think, Pete, you can take it away.
Super. Thanks, Thiago. Let me just share my screen here. You see that okay?
Yep.
Excellent. Just want to briefly touch on our safe harbor presentation statement. This is on our website. This entire presentation's on our website. I will be making some forward-looking statements under the safe harbor provisions covered here. I encourage you to take a look at these carefully on our website. Sorry. Just getting myself adjusted here. Great. I'm really excited to introduce Immunovant to those of you who are getting to know us for the first time, to review some details about our company, our plans, and our asset for those of you who already know us. Our vision at Immunovant is bold. We are looking to enable normal lives for patients with autoimmune disease. That means making a big difference in their lives, looking for therapies that can really make a difference for patients.
We're going to do that with 1401, which is a fully human monoclonal antibody that inhibits FcRn recycling of IgG. Some unique asset properties allow us to pursue both the best-in-class and first-in-class strategies. We're looking for indications and are already studying indications in both of those categories. We do have some near-term data readouts between now and mid-2021, and a good patent and cash runway that you see reflected here on this slide. There's a little bit more detail in terms of our milestones that gives you a picture of what we're already studying and the fact that we intend to grow our portfolio of indications as we've committed to announcing three new indications by mid-2021.
We have studies going on currently in thyroid eye disease and warm autoimmune hemolytic anemia. We recently reported data in myasthenia gravis and are actively planning to initiate our phase III trial in myasthenia gravis in the first half of next year. For those of you who are a little bit newer to the anti-FcRn space, this is an illustrative list of indications that we may pursue. It's not comprehensive, but it does show some of the indications which are classically associated with autoantibodies or pathogenic IgG. We use those two terms interchangeably, essentially means an IgG antibody that is recognizing a self-protein. Normally, IgG should only recognize proteins that come from outside your body, but if an IgG recognizes one of your self-proteins, then you can end up with a disease condition.
Let's talk a little bit about the biology and then get into the conditions we're studying today. The immune system is made up of both a cellular component and a protein component. The big part of the protein component of your immune system are immunoglobulins. The IgG immunoglobulin on the far left has the longest half-life in your body, and that's because IgG is recycled, which I'll show in a moment, via the Fc receptor. The IgM antibody on the far right, I'll point out for two reasons, is different from IgG. First of all, it is the immunoglobulin which is part of a new immune response. If you're exposed to a pathogen that your body hasn't seen before, a new infection, the initial antibody response will be primarily IgM, and IgM is not impacted by anti-FcRn therapy.
Secondly, the IgM tends to have a different structure and therefore doesn't bind the Fc receptor, and that's what leads to its shorter half-life and not being inhibited by FcRn. Why does IgG have a uniquely long half-life among all proteins and among immunoglobulins? It's shown on this slide. In the lower left-hand corner, you see a light blue antibody schematic. That's an IgG antibody, and when it is engulfed by an endothelial cell, that's a common process. Your body is constantly engulfing small amounts of plasma in order to clean out proteins. Proteins should generally have a short half-life. The IgG antibody you see binding to the Fc receptor, and that binding to that upside-down chair receptor in dark blue prevents the IgG from going to the lysosome where it would be enzymatically degraded. That's the normal process.
There is a pH dependency for a normal IgG, so at the cell surface where the pH is higher, the IgG antibody dissociates from the Fc receptor and is returned to the bloodstream. Inside the endosome, where the pH is lower, the IgG binds tightly to that Fc receptor and is protected from degradation. Our antibody 1401, shown as the purple antibody, binds in the variable region, so not in the Fc region, but in the variable region of the 1401. It binds to the Fc receptor. You can see that schematically in the lower right here. By binding to that Fc receptor, the IgG is prevented then from binding to the Fc receptor. When that happens, your IgG is shuttled to the lysosomes where it's degraded. That's the fundamental biology.
It's really straightforward, and that's one of the nice things about this mechanism. We did a phase I trial to demonstrate this theory played out in people. In that phase I trial, we studied both a subcutaneous dose as well as intravenous dose in the single ascending arms of the trial. Then because we saw very similar activity in the subcutaneous and the IV dose when you compare in equal doses, therefore showing us that there was no penalty in the case of IMVT-1401 for going to a subcutaneous injection, we only advanced the subcutaneous injection into the multiple ascending dose arms of this phase I trial. What we saw was a really nice dose dependency shown most clearly or most simply on the lower right with the multiple ascending dose cohorts.
There you can see the 340 milligram cohort and the 680 milligram cohort separating meaningfully in terms of IgG reduction, the 680 milligram cohort achieving a 78% IgG reduction, which is near the top of any IgG reduction reported by anti-FcRns in the class. You can also see that the confidence interval around the reduction in the 680 cohort was tight. You're getting a nice consistent reduction at that higher dose. At the lower dose, the confidence intervals or standard errors are wider, and there's a little bit more variability in that lower dose cohort.
You'll also notice that the fourth dose, which was given on day 21, shown in the red arrow there, the fourth red arrow, did not result in a further reduction in IgG. We believe we've achieved our full reduction of IgG even after three doses, which is nice, and that gave us a confirmation that we're likely at our maximal effect with the 680 dose and gave us confidence in that higher dose. The other thing that gave us confidence in the strength of the 680 milligram subcutaneous dose was the IgG subtype data. There are four different subtypes of IgG, and they bind differently to the Fc receptor and therefore are recycled differently. It's common that the IgG4 subtype is reduced less by some other anti-FcRns. It may bind more tightly to the Fc receptor or have another reason for that observed result.
In the case of 1401, we saw a reduction in IgG4 that was similar to the reduction in the other subclasses and similar to the reduction we saw in the entire pooled IgG analysis. It's important for two reasons. First of all, there are some conditions, including the MuSK-positive subtype of myasthenia gravis, that are mediated by IgG4 autoantibodies. You need to be able to knock down IgG4 well to have a chance at treating those conditions. As I mentioned, IgG4 is typically the more difficult subtype to reduce, this data is also important as another proof point in the strength of our antibody. I'm going to skip through this quickly and show you the actual data. Again, both these slides are on our website, and you can take a look through. The phase I trial was a large phase I trial.
It included 99 healthy subjects, 77 of whom received 1401. I love this chart because it's really just everything there that we saw. It's the kind of chart that I think as an investor you'd want to have access to for any product. What we saw was really just one thing, and that is injection site erythema and swelling. Those two things went together, and really it's based on the volume of the injection because we saw it in the placebo as well. Very importantly, in the middle of the page, you see injection site pain was nearly absent. There were very few cases of injection site pain. This is not an injection that hurts. It is a 2cc injection, so there is a small lump at the injection site that goes away quickly, but it was noticed in the phase I trial.
Otherwise, there's a sort of a smattering of things that you might see across the phase I trial. Importantly, whereas a dose-dependent headache signal was seen with some other anti-FcRns, we did not see a dose-dependent headache signal. In fact, in the high dose cohort, the 680 mg cohort, there were no headaches reported. Great. We're very importantly developing IMVT-1401, not just as a potent inhibitor of FcRn, but also as an inhibitor of FcRn that can be delivered by subcutaneous injection, which is much more convenient for patients and enables chronic dosing for chronic diseases, which is exactly what the patient need is. Why do we have a subcutaneous injection? The inventors of IMVT-1401 undertook a somewhat unique development program when they were selecting their lead antibody.
Generally, antibody development at this stage is focused primarily or even exclusively on which antibody from a family of antibodies binds the target ligand or receptor or interleukin or whatever you're trying to target most tightly. That was certainly a component of the antibody development program completed here. In addition to that, the candidate antibodies were made in small aliquots, and whether or not they were soluble using simple excipients was also a selection criteria. Happily, 1401 was among the most soluble and among the most potent. There wasn't a trade-off where we were forced to choose between a soluble antibody and a potent antibody. 1401 had both of those characteristics, and that enabled 1401 to be, as I like to say, be born sub-Q. It's available in a 160 milligram per ML formulation.
That's the formulation we're using in our trials, and we'll keep that formulation going forward. That's a nice concentration for a human antibody. It can be delivered with a 27 gauge needle. Very nice properties both in terms of the pharmacodynamics and also in terms of the solubility. That leads to this entire profile, which we believe is class-leading. Not only is the pharmacodynamics strong, the pharmacoactivity strong, there's the subcutaneous injection engineered into the antibody, as I mentioned right from the start. There are some other nice features which are important in antibody development in terms of turning off the effector function and reducing immunogenicity with a fully human antibody. Okay. How about some of the diseases we're studying, and I'm going to mention three of them. They're sequenced in the order in which the data was released.
I often get a question, which one do I like the best? Which is, of course, a little bit like asking someone which of their children is their most favorite, and you can't really do that, neither with your children or with these indications. They're all exciting for different reasons. I'll talk about thyroid eye disease first, and that is the indication where we released data from a phase IIa proof of concept study in the early part of this year, in March of 2020. This is a summary of the data, which I'll come back to in a second, but let me talk a little bit about thyroid eye disease and then come back to the data, which was really exciting. First of all, what is thyroid eye disease? It's a bulging of the eyeballs associated with Graves' disease.
Graves' is a very common form of hyperthyroidism, primarily hyperthyroidism. Hypothyroidism is relatively easy to diagnose once patients get into a physician. You have patients that have hyperthyroidism. There's a simple test to determine whether it's Graves' disease, a percentage of patients with Graves' hyperthyroidism go on to develop Graves' ophthalmopathy or, as it's more commonly known now, thyroid eye disease. Thyroid eye disease has two phases. There's a proliferative inflammatory phase in the first couple of years. May last up to two or three years, actually. Then there is a longer-term phase, which was originally characterized as static. This graph is from the '50s, actually. It's a classic curve, Rundle's curve. What we're learning now is that this phase of the disease is somewhat active. It's not as active as the initial phase, there's still some disease activity apparent here.
We're learning that from case reports of teprotumumab showing a benefit in patients even in this outer phase, which if the patients were totally fibrotic and inactive, there wouldn't be really an opportunity for any therapy to benefit them. It's likely that patients, even in this outer phase, have some degrees of disease activity that's going to be amenable to a disease-modifying therapy, which is exciting for patients and exciting for our development program. What's the underlying pathophysiology? There is an autoantibody or pathogenic antibody that binds to the thyroid-stimulating hormone receptor, and that is an anabolic receptor. The stimulating antibody drives proliferation of tissue and inflammation via that anabolic receptor. There's a downstream upregulation of the insulin-like growth factor, that's where teprotumumab acts with its anti-insulin growth factor antibody. Upstream TSH receptor stimulation, downstream insulin-like growth factor receptor.
Both of those things leading to proliferation of tissue behind and around the eye. This is not a disease in the eye, it's a disease in tissue around the eye. The existing therapies today, prior to the approval of teprotumumab, were not very good. You had surgery as an option for patients with very severe disease, and corticosteroids are often used, but without tremendous benefit in earlier line patients. You had a lot of patients who really didn't have a good therapy, and the success of teprotumumab in their launch in the United States, I think, demonstrates the degree of unmet need in this patient population, which again, is exciting. How are patients studied? There are three different scores. They're measured relatively simply, actually, which makes this nice from a development standpoint. The primary endpoint from an FDA perspective, this is the most important endpoint for registration.
It's proptosis in the upper part of this slide. It's measured with an exophthalmometer. It's hard to say, but it's actually relatively easy to operate, and that measures the degree of bulging in the eye. There are two other scores which measure things that are very important to patients, and those are, first of all, double vision or the diplopia score. You can read here that there are variations from no double vision all the way up to continuous double vision with some gradations in between. This is something that bothers people a lot, both in their personal and professional life. Double vision when present, it's often present, is an important component of the disease and improving double vision is an important component of the treatment.
There's the clinical activity score, which has to do more with inflammation and pain than bulging of the eye as measured by the exophthalmometer. All three of those are important. What did we see going back here to the summary of our phase IIa open-label proof of concept trial? First of all, we saw IgG reduction, which was as expected. This was primarily a 340 milligram regimen for six weeks. The 65% reduction in IgG was consistent with what we had modeled this regimen would produce. In terms of clinical activity score and proptosis response and double vision, we saw degrees of improvement, which were really encouraging, meaningful to patients, and largely consistent with the data published by teprotumumab at six weeks. Of course, this is a small study, and that trial had 24 weeks for a primary endpoint.
Comparing a six-week open-label to a 24-week trial and looking at the data at six weeks, that needs to be done with caution. I think generally you would look at this information carefully and you'd say it's largely consistent with the six-week data for teprotumumab. On the safety side, importantly, there were no withdrawals due to adverse events. There were no serious adverse events. We actually saw no headaches in this trial either. Again, this is from a tolerability standpoint. We had the subcutaneous injection, which was very well tolerated in this trial, as it had been in the phase I trial. Finally, we have an ongoing study in thyroid eye disease that's much bigger than the proof of concept, this is our ASCEND-GO 2 trial.
It's a pivotal design phase II-B trial testing three different dosage arms with an emphasis on the two higher doses and comparing all those to placebo. The primary endpoint is that regulatory endpoint that I mentioned, the proptosis responder rate. I don't know if I defined it before, but it's a two-millimeter improvement in the study eye without a worsening in the fellow eye. Often one eye is more affected than the other. There's a little bit of an asymmetric impact often in many patients, so one eye is chosen as the study eye, and the primary endpoint is then done on that study eye. It's the more severe eye. The inclusion criteria are very similar to our own inclusion criteria in our phase II-A trial and also the trial run by Horizon Therapeutics. It's a very similar population.
We selected a 12-week endpoint rather than a 24-week endpoint that was used in the teprotumumab trial. At this point, I think 24 weeks would be too long to keep patients on placebo, particularly in the U.S. where you have an approved therapy. Because the 12-week data was published by Horizon for their phase IIb and their phase III trial, this will ultimately allow a nice comparison across trials. I think 12 weeks is the right duration of therapy, and that's what we selected. Okay, moving on to myasthenia gravis. Again, there's a summary slide that I'm going to skip over for a moment just to introduce briefly myasthenia and our trial design, and then come back to the summary data. In this case, the autoantibody is directed at the neuromuscular junction, the acetylcholine receptor, most commonly in 85% of patients.
Blocking that neuromuscular junction causes voluntary muscles, so the kind of muscles you move under your own will, to be weak. There are a variety of broad-spectrum, older and immunosuppressants that are used in myasthenia gravis, and also IVIG is commonly used, and plasmapheresis is used in crisis situations. This autoantibody-driven nature of the disease, this is maybe the classic autoantibody disease that you learned about in medical school, has borne out in terms of the benefit of anti-FcRn therapy. We saw a very nice and consistent effect in the argenx phase III data, and we replicated in a much smaller trial that same type of impact in our phase II-B trial. What did we see?
We saw a statistically significant separation between improvement in MG-ADL or myasthenia gravis activities of daily living at a 3.8-point improvement in our pooled treatment arms and the placebo arm staying more or less flat. That was exciting. We saw that after 6 weeks of therapy. This is day 42, so a week after the sixth dose. This mean response to MG-ADL is a common way that other trials have reported their data and so allows for some comparison across trials. Another way to look at the data is the percentage of patients who achieve a threshold determined to be clinically important, and for the MG-ADL, the threshold is two points improvement or more is considered to be clinically meaningful. This is another common scale that's reported in other trials, which is the percentage of responders.
We saw in our pooled treatment group, these were patients on both 340 and 680, 60% of patients achieved that MG-ADL response rate, whereas only 20% or one out of five in the placebo arm achieved that in the five patients who were randomized to placebo. That's exciting. The other thing I want to point out is beyond the average improvements, which were impressive and achieved statistical significance, even in this study of 15 patients, we also saw a high rate of deep response. Remember way back at the beginning, I mentioned that our vision is to enable normal lives for patients with autoimmune disease. A two-point improvement is definitely noticeable. It's something that patients and physicians would see as an improvement for patients. Getting back to normal is going to require more than a two-point improvement. It's going to require a multipoint improvement.
For the purposes of this analysis, we're looking at a 6-point improvement in MG-ADL and in QMG. This is a physician assessment. I skipped over the details of it, but you can look through that. Whereas this one, MG-ADL, is how patients are feeling. QMG is a more objective way of measuring the strength that the patients actually have in their muscles. MGC is a composite that has both patient-reported outcomes and physician assessment. Looking at the number of patients who achieved a deep response, none of the patients who were randomized to placebo achieved a deep response, whereas 30%-40% of patients in the treatment arm achieved this deep response is a really meaningful improvement, even after only six weeks of therapy. That's very exciting. You can take a look on our website in terms of some of this summary data.
Again, impressive clinical efficacy over a short period of time. The onset was quick, as we've seen with other trials. This mechanism has been pleasantly shown to be quite quick. That's really important. From a safety and tolerability standpoint, similar to our thyroid eye disease trial, a nice profile. Again, early days, looking good from a safety and tolerability standpoint. I will mention at this point, maybe go back to the beginning for just one second. Right now, what's happening with myasthenia, we have that data in hand. We're actively working with the FDA to finalize our phase III design, which I'm excited about. From a phase III design standpoint, that's an area we get a lot of questions about. I think there's two important elements of any phase III trial.
The first is to achieve registration, get the product approved, continue to course on a positive benefit risk, and then to differentiate versus standard of care or versus other assets in the class or both. Our phase III design will be designed to do both of those things. The first point around registration, that's a pretty well-trodden path, I think, right now, given the nice data we saw from argenx and their trial design. Not just the argenx phase III, but some other mechanisms that are maybe not quite as attractive from a patient standpoint but have completed phase III trials. I think we know what the FDA is expecting from a primary efficacy analysis standpoint, which would be a big part of the registration.
In terms of differentiation, the fact that we have two active doses and can deliver the medicine chronically to patients, that gives us a lot of levers to pull to differentiate 1401 in terms of delivering a really strong and durable patient experience over time. Finally, our third indication is warm autoimmune hemolytic anemia. In this condition, the autoantibodies are binding to red blood cells, glycoproteins on the red blood cell surface. Normally, red blood cells, as they age, typical red blood cell life would be about four months or so. When they get to be about four months old, without any antibodies on them, this would be in a normal person, the red blood cells are removed primarily in the spleen.
When a patient has warm autoimmune hemolytic anemia and they have autoantibodies binding to the red blood cells, even younger red blood cells will be removed in the spleen. That destruction of younger red blood cells leads to a situation where the patient's bone marrow can't keep up. They do start producing more red blood cells to make up for the fact that their hemoglobin count is dropping, that their red blood cell count is dropping. The bone marrow can't quite keep up with the destruction, and you end up with patients having anemia and the symptoms of anemia or low blood count, which range from fatigue and weakness to, in more significant circumstances, shortness of breath or even medical problems associated with a lack of oxygenation. This ranges from a moderately impactful disease to a very severe disease, like almost all these other conditions.
They're not mild, there's a lot of unmet need. What do patients have as an option today? On the one hand, high-dose steroids work well. As I've spoken to our investigators around the world, we have investigators for this site in Asia, Europe, and the U.S., and the story's pretty consistent. A patient who reports with warm autoimmune hemolytic anemia can be controlled initially with very high-dose steroids. The challenge for the patient and their treating physician is that those are very high-dose steroids. They're not the kind of dose that a patient can stay on for a long period of time. During the taper process, most patients will have a recurrence of their hemolysis. Steroids work, but they can't be maintained at these really high doses, and that leads to the unmet need. What do people do today?
Often, the steroid is maintained at a moderate dose, at a dose 20, 30, 40 milligrams of prednisone or its equivalent, which is going to have a fair bit of side effects. They may try another immunosuppressant to reduce their steroid dose. They may get intermittent blood transfusions to try to keep up with the hemolysis. There's not really a therapy that can get them anywhere back close to normal, get their hemoglobin up to a high level. Except for splenectomy. Splenectomy does do that in many cases. The challenge with splenectomy are sort of two challenges with taking the spleen out. The first is it's a big surgery that modifies your whole immune system pretty substantially.
The second is that although the spleen does not regrow, the immune tissue that was present in the spleen reforms in other parts of the body, in the liver, and so the effects of splenectomy are not permanent. You end up with, on one hand, a permanent modification of your immune system for fighting disease, and there are patients who've had splenectomy are more susceptible to certain infections. On the other hand, the hemolysis does eventually come back as other parts of the body take up this role of destroying red blood cells. There's not a very satisfactory therapy. rituximab is used, and there are some data that looks decent with rituximab. Of course, that also has a pretty significant impact on the immune system, shutting down B cells for a prolonged period of time, and so there's a desire for new therapies in this area.
We've designed a trial for warm autoimmune hemolytic anemia. It's a proof of concept and takes advantage of the fact that there isn't really a spontaneous improvement in this disease. For patients who would meet these inclusion criteria, meaning they have a hemoglobin below 10, they've not tolerated the steroid taper without their hemolysis coming back, those kind of things. Those kind of patients aren't going to spontaneously remit in any significant number, and therefore, we could trust a proof-of-concept that didn't have a placebo arm as being correct if we see a signal that it's not just a placebo signal. Given that design, we then took another step, and we decided to enroll our high-dose cohort first and the lower dose cohort second.
That gives us an ability to get to the what's likely to be the best benefit-risk data sooner because that high-dose cohort will enroll first. At the same time generates a low-dose cohort, which will be interesting for us and for regulators in final decision-making around phase III. Using the same trial infrastructure, having gone through the work of getting the trial in place, then using that same trial machinery to generate a low-dose cohort we thought was valuable as well. The primary endpoint is hemoglobin responder rate. It's defined as patients who achieve a two gram per deciliter improvement in their hemoglobin and an ending hemoglobin greater than 10. That's a pretty standard and simple endpoint that will now allow us to get, I think, in a relatively simple study, a good sense for the effect of anti-FcRn therapy in warm autoimmune hemolytic anemia.
That's what I have. I know it's kind of a whirlwind of topics, but I wanted to make sure I gave a taste of both our underlying biology, our strategic goals, which I'll come back to here and maybe just end on that slide again, having shown you that we've got a really exciting antibody from a feature standpoint with the IgG reduction and the ability to deliver it right from the start in clinical trials via subcutaneous injection. That allows us to go for both best-in-class and first-in-class indications. We are, I should mention, the only anti-FcRn so far studying thyroid eye disease. Given the excitement of that class, we might see another competitor there at some point, but we're first in class in thyroid eye disease, and we believe we can have a best-in-class solution in warm autoimmune hemolytic anemia and myasthenia gravis.
Great. That's perfect. Thanks a lot for your time. I do have one question that I received, and that's mostly related to the ASCEND-GO 2 expectations. With longer dosing, you saw there with the Horizon study, you did see an increase in proptosis responder rate and all of the biomarkers are tracking in the right direction here. Would you expect to see the same kind of behavior with an FcRn asset? How does that play with the evolution and the biology of the disease, and what expectations should be for the ASCEND-GO 2 study?
Yeah, great question. I think it's not at all surprising for those who aren't as familiar with the data from the teprotumumab trial. They saw essentially the same thing in both. They did a phase II-B and a phase III that were pretty similar. You saw a nice improvement in the first six weeks, then a pretty good improvement from six - 12 weeks also. From 12 - 24 weeks, there was some additional improvement, but you began to flatten out a little bit. The biggest improvement, the biggest sort of slope of the improvement, was in the first 12 weeks. I think that makes a ton of sense, actually, when you look at the biology, because you have, as I mentioned, this simulation of the TSH receptor causing an anabolic process leading to proliferation. Maybe even more so than inflammation, you get proliferation.
That means growth of tissue. Stopping that process, whether by removing the anti-TSHR antibody or hitting the downstream part of the pathway with the insulin-like growth factor, it's going to take a little bit of time for that tissue to regress. There's tissue behind the eye, fatty tissue that has grown larger, and it's a small space. That's why the eyes are bulging out. The other anabolic effect, proliferative effect that happens in this disease is some edema of the extraocular muscles. There are small muscles behind your eye that allow it to move, and when they get swollen, then that can also cause the proptosis and double vision and other symptoms. It's not at all surprising to me that it's going to take a little bit of time. That it's not going to be within a week or two that that's going to just go away.
The tissue has to shrink back, and so I'm not surprised by that. Similarly, on the back end, this process I mentioned as described initially by Brambell in the '50s was kind of the active phase and the static phase. I think there's more overlap here in the Venn diagram between active and static, and we're starting to see that patients probably have some degree of smoldering in this part of the disease state as well. That speaks to me to the need for a more chronic therapy than just six months. teprotumumab is indicated for six months of therapy based on their trial design, which was probably due to having an intravenous infusion and wanting to have a shorter period of time where patients had to have that intravenous infusion.
I think one of the questions you asked was our expectations on our phase IIB trial versus the IIA. We do have a longer treatment duration. We also have a higher dose. I would expect our IIB trial, certainly at 12 weeks, to be better than our IIA trial at six weeks. One, because of that longer period of dosing and the period of time where the tissue can shrink back is going to be longer. In addition, we have a dosage arm that is 680 milligrams for the entire 12 weeks. In the IIA trial, as I mentioned, this was primarily a 340 arm. I think it's on here. They had a loading dose of 680 milligrams for two doses, but then they got four doses of 340, and the 65% IgG reduction was similar to what we saw with straight 340.
The difference is you achieve it sort of a week faster by having that loading dose of 680. The fact that we have a higher dose arm and longer treatment should yield more improvement by 12 weeks in the ASCEND-GO 2 than we saw at six weeks in the ASCEND-GO 1.
Perfect. That makes a lot of sense. I guess we can leave it at that. I appreciate the time for the presentation. Thanks for joining us. I'm sure the management team. I'm also happy to follow up with investors if there are any questions. For now, just have a good rest of your day. All right?
Thanks, Thiago.