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Intrinsic Value is all-important and is the only logical way to evaluate the relative attractiveness of investments and businesses.
Intrinsic Value is all-important and is the only logical way to evaluate the relative attractiveness of investments and businesses.
Good morning. My name is Melissa 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 [Operator Instructions]. 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, among other things, statements regarding Immunovant’s plan to initiate two Phase 3 clinical trials for batoclimab in TED in the second half of calendar year 2022, with an expected topline data readout in the first half of calendar year 2025, and its plan to initiate a Phase 3 clinical trial in MG by the end of June 2022 with an expected readout in the second half of calendar year 2024; Immunovant’s plans to develop batoclimab across a broad range of autoimmune indications; the potential efficacy and safety of Immunovant’s product candidate; Immunovant’s expectations regarding the timing, design and results of its clinical trials, including the timing of future data readouts; and the announcement of additional indications, and whether if approved batoclimab will be successfully distributed, marketed, and commercialized.
All forward-looking statements are based on estimates and assumptions by Immunovant’s management that although Immunovant believes to be reasonable, are inherently uncertain. All forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those that Immunovant expects. For more information, investors are encouraged to review Immunovant’s annual report on Form 10K for the year ended March 31, 2022, filed with the SEC on June 8, 2022, and Immunovant’s subsequent filings with the SEC. Any forward-looking statement speaks only as of the date on which it was made, and Immunovant undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events, or otherwise.
Now I would like to turn the call over to Dr. Pete Salzmann. Thank you. Dr. Salzmann, please go ahead.
Thank you Melissa. And thanks to everyone for joining the call today. I’m very excited to share that Immunovant recently achieved alignment with the FDA Division of Ophthalmology to move forward with a pivotal program in thyroid eye disease or TED. This is a big milestone for Immunovant, and we now plan to initiate two placebo controlled Phase 3 trials for TED in the second half of 2022. We expect to have topline data for these trials in the first half of 2025.
TED is the second pivotal program we have announced for batoclimab, and represents a first in class program with an exciting market opportunity. As we heard from physicians, and as we discussed at our R&D day this past March, there has been a paradigm shift in the treatment of TED. As many of you know, the FDA approved teprotumumab in January of 2020, which is now the only FDA approved treatment option for thyroid eye disease.
When new medications are approved for a disease with high unmet need and a historical lack of innovation, then some patients who are already under the care of a physician can rapidly gain access to the new medication. In addition, these types of approvals raise awareness of the disease among other patients, who may not yet be under the care of a physician or specialist. The growing patient awareness also impacts physician decision making and the market expands. We have seen this unfold in thyroid eye disease.
The market opportunity continues to grow, as the awareness of the disease continues to expand. We believe this will be the case for quite a while, similar to the steady market growth experienced in other immunology markets after the first big innovation. At the same time, the TED market has some very unique features. The disease itself is heterogeneous and therefore lends itself to complementary mechanisms of action. Fixed duration of dosing, specified in the FDA labels for TED, also supports the development of new and complementary mechanisms of action. The net result is what we believe to be an exciting opportunity for patients and for batoclimab.
Today I will introduce our TED Phase 3 clinical design and focus on the important points of differentiation for batoclimab in thyroid eye disease. I’ll start by reviewing some of the fundamental biology for how batoclimab may work in TED and why we believe that TSH receptor auto antibodies are key drivers of Graves hyperthyroidism and of TED.
In the top row of the figure, anti TSH receptor auto antibodies circulate in the body and bind to the TSH receptor. In the rightmost figure, the autoantibody is binding to a TSH receptor in the thyroid gland. This activates the thyroid follicle, increasing cellular metabolism and the release of thyroid related hormones. Of course this is not the end of the story, since TSH receptor antibodies can circulate in the blood and bind to other target cells that also express the TSH receptor.
In the middle figure, the auto antibodies are shown binding to the TSH receptor in the periorbital space, where they activate orbital fibroblasts. This leads to proliferation of the periorbital tissue and differentiation of these fibroblasts. In the absence of batoclimab, anti TSHR antibodies are recycled back into the blood by the FT receptor and endothelial cells. They remain present to recirculate and reengage receptors throughout the body.
Note that, beside the TSH receptor, the insulin growth factor 1 receptor, shown on this slide in blue and adjacent to the TSH receptor, also plays a role in the pathophysiology of the disease. Once an autoantibody binds to the TSH receptor, there is crosstalk between the TSH and the IGF-1 receptors, and the engagement of both receptors leads to activation of intracellular pathways linked to the clinical signs and symptoms of TED. So this crosstalk between the TSH receptor and the IGF-1 receptor appears to be crucial in the pathophysiology of the disease.
As most of you likely know, batoclimab reduces circulating IgG by binding to the FT receptor and inhibiting FcRn mediated recycling of IgG that normally takes place in endothelial cells. I’ll review some data later in the presentation regarding batoclimab’s observed impact on anti-TSHR antibodies in TED patients from a prior study. Although proptosis is a prominent and important feature of thyroid eye disease, TED is actually a heterogeneous condition. Indeed patients experience a variety of symptoms.
This slide includes pictures of two different people with thyroid eye disease that together provide an example of how TED can vary patient to patient. Both people in these photos have proptosis, but the degree of inflammatory changes differs between them. The patient in the top panel has much more eyelid edema and conjunctival redness than the patient in the bottom panel. This symptom heterogeneity is common in TED. We also found that, even with treatment, patients with active TED report making substantial lifestyle modifications. Based on our market research, 80% of participants reported making moderate or major lifestyle modifications despite ongoing systemic therapy to which they were responding.
The patients we surveyed were between 30 and 60 years old, reflecting a prime working age range consistent with the TED population. In fact, the impact on work life was highlighted as particularly challenging, as participants reported difficulty working on electronic devices, difficulty driving, and challenges engaging in social situations. When we asked participants to rank their most important treatment goal, there was not a single top treatment goal shared across the patient population. Rather, the most important goal varied, patient to patient.
While improving proptosis by 2 millimeters or more is clinically significant and very important, there are symptoms other than proptosis that can be an even higher priority for certain patients. We believe it’s possible that medications with different mechanisms of action will address different symptoms in different ways, and can therefore be complementary in the treatment paradigm.
As I mentioned in my opening comments, teprotumumab has made a meaningful impact on the treatment of TED since its launch in early 2020. The launch has probably improved diagnosis rates in TED, and has certainly reframed the urgency to treat, compared to the historic watch and wait approach that was frequently applied. This sort of post-launch market development is common for a disease that hasn’t had any innovation in a long time.
In addition to this favorable market growth, which we expect to continue, the TED market also has some unique features centered around the fixed duration of dosing specified in the FDA label. Fixed duration of dosing is uncommon in immunology but common in ophthalmology. In fact we believe that FDA labels for TED will continue to specify a dosing duration defined by the length of the controlled period of the clinical trial. This is important because the dosing duration specified in the label may be insufficient for many patients.
As noted here in the OPTIC 48-week off-treatment follow-up period, 44% of Tepezza patients who were proptosis responders at week 24 in OPTIC were not proptosis responders at week 72, highlighting an opportunity for additional treatment. We believe this opportunity is ideally suited for a new mechanism of action, not only because reimbursement is often strictly limited to the frequency and duration specified in the FDA label, but also because TED is a heterogeneous disease that is likely amenable to complementary mechanisms of action. Such complementary treatment, in series, will of course be longer, and so a simple subcutaneous route of administration becomes even more important, at least for one of the medications.
So what is the bottom line? How many TED patients do we believe could benefit from a therapy with a new mechanism of action? We estimate this total addressable population in the U.S. to be between 8,000 and 18,000 patients annually. Assuming success in our pivotal program and product approval, we anticipate some patients would be treated first with batoclimab. When comparing potential product profiles, many patients and physicians in our market research selected a profile like the one batoclimab may have, for patients on the moderate side of the moderate to severe active TED spectrum.
A product given by a simple subcutaneous injection, without hearing loss issues and with solid proptosis efficacy, even if a bit less than Tepezza on this dimension, is attractive as initial therapy for patients on the moderate end of the moderate to severe spectrum. This group makes up about half of the potential addressable market for a new mechanism of action.
The second logical group is made up of patients who respond well to Tepezza but have some residual symptoms at the end of their 24 week course of treatment, or who relapse at some point off-treatment. This group also makes up about half of the potential addressable market for a new mechanism of action. Collectively, we believe 8,000 to 18,000 patients in the United States could be candidates for treatment with batoclimab, and this may even be complementary to Tepezza’s growth. So we see this as a very exciting market that is really just beginning to show its full potential.
Now I’d like to briefly review our clinical development with TED to date. The data on this slide is from a cell-based assay that looks specifically at those auto antibodies which stimulate the TSH receptor, not just those antibodies that bind to it. This is important because some auto antibodies bind the receptor but they don’t stimulate it, and it’s really only the stimulatory antibodies that are important to the pathophysiology of TED.
The primary graph shows the dose dependent decreases in stimulatory auto antibodies that were observed with 12 weeks of dosing, and the gradual recovery of auto antibodies after the dosing period. Data in the table on the right side of the slide shows the percentage of subjects in each group whose stimulatory auto antibodies came down into the normal range, based on the cell based functional assay.
The upper limit normal in this assay is 140, and getting below 140 indicates a seroconversion where the level of stimulatory auto antibodies is no longer considered different than what is observed in control serum. So over a 12 week period, the observed level of seroconversion was highest in the 680 milligram arm. This was one of several data points leading to our final study design, that includes an initial 12 weeks of dosing with 680 milligrams delivered subcutaneously.
This slide shows exploratory proptosis data from the same study. As a reminder, the data on this slide is from week six of our TED Phase 2b trial. Although the primary endpoint for this prematurely terminated trial was not significant at week 12, we selected week 6 for this post-hoc analysis because it represents the latest time point with the largest amount of patient data available prior to dosing being stopped due to the voluntary pause. At this early time point at week 6, the observed proptosis response rate was numerically higher at the higher dosages. Again, all treatment was weekly by subcutaneous injection.
This slide shows CT scan data that I find very intriguing. CT scans were done in a few centers, and were interpreted by a specialized central reader. This graph shows data for all subjects who had a baseline CT and who also had an end of treatment CT scan after completing 12 weeks of dosing. As you can see on the Y axes, the bars show percent change from baseline in total extraocular muscle volume.
Looking at week 12 CT scan data on this slide, we observe a suggestion of a dose dependent effect on muscle volume, with a 30% reduction of total muscle volume observed in the 680 milligram batoclimab group. We observed numerically smaller decreases in other batoclimab groups, while placebo subjects increased slightly on average. Of course these are exploratory endpoints in a small number of patients. At the same time, the readings were done by a blinded central reader, and this is the complete CT data set from the trial.
Overall, we believe that data from our prior TED trials are very encouraging for our pivotal development program in batoclimab in thyroid eye disease. We also believe that these data suggest that higher levels of IgG suppression may be required initially, and that leads to our trial design. Whereas our 340 milligram weekly dose provides IgG lowering typical of other anti-FcRns development, our 680 milligram weekly dose has consistently shown IgG reduction around 80% with subcutaneous dosing, something unique to batoclimab within the anti FcRn class. This initial 12 week dosing period with 680 milligrams adds differentiation beyond even first in class.
As the ophthalmology division of the FDA has provided guidance that two pivotal trials are required for new medications in TED, we’ve designed two identical studies to run in parallel. We expect to enroll approximately 100 subjects for each trial with two to one randomization to either batoclimab or to placebo for a 24 week treatment period. Subjects randomized to the batoclimab arm will receive 680 milligrams of batoclimab delivered weekly for the first 12 weeks, followed by 340 milligrams of batoclimab delivered weekly for the next 12 weeks.
The key inclusion criteria are similar to other pivotal programs in TED, and the primary efficacy endpoint will be measured as proptosis responders at week 24 versus placebo, where responders are defined as a ≥2 millimeter reduction from baseline in proptosis in the study eye without deterioration in the fallow eye. As I mentioned previously, this design takes advantage of batoclimab’s specific attributes namely the deep IgG reduction and simple subcutaneous route of administration. We plan to initiate these Phase 3 trials in TED in the second half of calendar year 2022, and expect to have topline data from both trials in the first half of 2025.
Finally, here’s a review of our overall development program for batoclimab. We plan to initiate our Phase 3 myasthenia gravis trial later this month, and as a reminder this Phase 3 MG trial represents our first pivotal program with batoclimab, with topline data expected in the second half of calendar year 2024. Building on our progress in MG and TED, we plan to engage with the hematology division of the FDA to discuss development for warm autoimmune hemolytic anemia. We also expect to announce two new indications as previously committed by August of 2022.
Beyond MG and TED, we’re planning to initiate a pivotal trial in one more indication in 2022, bringing the total to three pivotal trials expected to be initiated in calendar year 2022. This development plan reflects the enthusiasm our team has for the anti-FcRn space in general and for batoclimab in particular.
Thank you so much for your time, and with that I’d like to open it up for questions.
Thank you. At this time we’ll be conducting a question-and-answer session. [Operator Instructions] Our first question comes from the line of Robyn Karnauskas with Truist Securities. Please proceed with your question.
Great. Thank you for taking my question. First, can you talk a little bit about, in your market research, about, I think you mentioned in the beginning that for the moderate patients, the patients that has a similar profile to Tepezza, which I think you’re seeing around [indiscernible] and the 83% for the primary endpoint, that you could see a use as a first line therapy, but what sort of market research was done around and thoughts around why you choose one product over the other and what would make a patient or a doctor do that?
Then second question is, for follow up do you expect that the FDA will give you a similar label? I assume that you say it’ll be around six months. Do you think there’s any flexibility there, anything like that? Thanks.
Thanks, Robyn, for those questions, I appreciate it. So for the first question with regards to market research, just to go into a little bit more detail there, the market research we conducted, it was relatively recently conducted so it was in the U.S.. It was after the launch of Tepezza, and patients in the market research had active thyroid eye disease across the spectrum from moderate to severe, and they were on systemic therapy with either steroids or Tepezza with about an even split in terms of medication between both of those groups.
They all actually reported, 100% of them reported improvement in their symptoms, but 80% of them, as I mentioned reported that they were still making moderate or even more than moderate lifestyle modifications, in spite of improvements with therapy. Then there was a section of the market research where we asked them to consider product profiles. So for Tepezza the product profile was just equivalent to the FDA approved label. For batoclimab, the profile included what I mentioned, so subcutaneous route of administration, a proptosis efficacy that was a little bit less than Tepezza and the lack of any hearing loss as an assumption in that product profile.
When comparing those two product profiles, different people chose different things, and across the spectrum actually some people chose the Tepezza profile. Some people chose the batoclimab profile. But there were more people on the moderate side of the spectrum who tended towards the batoclimab profile. And I think that’s consistent with just treatments of a lot of conditions where, when someone has a very -- they’re very, very severely impacted, then the outstanding efficacy that Tepezza has demonstrated is probably going to lead to that being the first choice, in spite of any adverse events.
On the other hand, for someone who is impacted, for sure, but a little bit more moderate, they’re more drawn to a profile that provides efficacy but with potentially less safety issues and no irreversible safety issues. So that was how that split came out. The subcutaneous route of administration also played a pretty big role, I have to say, in spite of the fact that these were people who were being treated with a systemic course of therapy and were aware that the total duration of therapy was only six months.
To that point, with regard to the label, our interactions with the division of ophthalmology strongly suggest that they have a really standard approach to development programs in TED, and are likely to have a very standard approach to labeling. So I think the key tenets of the Tepezza label will be reflected in any other product that’s approved for thyroid eye disease that has a similar program, meaning a 24 week placebo controlled program.
Got it, and just as a follow up, do you think you’ll be allowed to have patients that have previously been on Tepezza? Will there be a washout period? And also I was going to ask you just around the guidance for 2025 data, given the shorter timeframe for the trial, like what is your assumption for enrolment? Seems slower, given that there’s more awareness of the disease.
Right. So in terms of the timing for the trial, our enrolment assumptions for these two trials, which would be run in parallel, is sort of halfway between the actual experience of the two Tepezza trials for their first trial and the second trial. The second trial was obviously faster. They had sites up and running, and the first trial was positive. So those two things, I think, were an accelerator for the second trial compared to the first one. So we took a position sort of down the middle.
There’s no question that the approval of Tepezza has generated additional awareness, and we do expect to enroll patients in the U.S., in spite of Tepezza being on the market. But there will be a little bit -- there’s always more competition when you have an approved product, which is true for now at least only in the U.S. That leads a little bit to the first question, which was, will we include patients who were previously treated with Tepezza? We will not, for the pivotal program.
Our goal with the pivotal program is to have as close to an apples to apples comparison, with regard to the patient population, as Tepezza had in theirs. So that’s the rationale for having naïve patients in our pivotal trial. That could be an opportunity for a future Phase 4 trial or something like that, but for the Phase 3 trial it will be patients who are naïve to any biologic therapy.
Okay great. Thank you.
Yeah, you’re welcome.
Thank you. Our next question comes from the line of Derek Archila with Wells Fargo. Please proceed with your question.
Hey, good morning and thanks for taking the questions and thanks for the update. Just a couple from us, different track though. I mean, I just wanted to get your thoughts, Pete, on the recent kind of failure in wAIHA from fostamatinib and how that might kind of enter your thinking about moving forward in wAIHA with batoclimab and thinking about the opportunity there.
Then second question, just on the cash guidance out to 2025, does that assume that you have cash through the top line TED data? Thanks.
Great questions, Derek. I’ll answer the second one first. Yes. That’s the easy answer, easy and direct answer. The first question is very interesting, and that call’s happening, I guess, in parallel to this one. I did have a chance to review the press release, which had a fair amount of information this morning. And as I’m sure you saw, there is a big variation in the placebo response rate by geography, whereas the response rate for fostamatinib by geography was relatively similar.
Why might that be? I think, in any trial in immunology where there’s a potential to use non-steroid immunosuppressant therapy, which was allowed, I think at least one of them was allowed in the Phase 2 trial, the protocol for which has been published, I’m not totally sure about the Phase 3 trial, but I would guess there might be a similarity there.
Non-steroid immunosuppressants, as you know, one of their big limitations is they take a long time to work. That’s a big limitation clinically. It’s also something that can cause issues in clinical trials if you have someone in the placebo arm whose non-steroid immunosuppressant therapy is just kicking in midway through the trial.
This is an area where we’ve gotten a lot of nuanced feedback from investigators across our clinical trials, particularly the ones that have a longer duration, but it actually applies everywhere where these medications are used. So it’s possible that that might explain it. The placebo response rate that they saw in Eastern Europe or in some of those geographies, seems much higher than again, what hematologists are telling us, one would expect in a true placebo arm. So then you wonder if the concomitant medications are kicking in and causing a compounding there.
Okay, I guess, and how does that kind of like factor into your thoughts about going into wAIHA now that maybe that competitor is not there, versus the undisclosed indications?
Yes, yes, yes. Well, I mean I think the first thing is to make sure the trial design is really carefully done to the point that I was just making. In terms of wAIHA, with or without fostamatinib, we’re really excited about this opportunity, because there’s just been a lack of innovation in wAIHA. The therapies that are mostly used are steroids actually even more so than non-steroids, at least within the major markets, moderate doses of prednisone with occasional blood transfusions, which is really just not a very satisfactory long term solution unless with a targeted therapy.
Even if fostamatinib had reported positive results this morning, I mean it is an oral therapy but the GI side effects, I think, may be limiting for chronic use. So, this is -- I’m not sure it changes a lot. Our thinking is centered around what batoclimab can do, which we believe could be pretty exciting in wAIHA.
Got it. Thanks for the questions.
Yeah.
Thank you. Our next question comes from the line of Thomas Smith with SVB Securities. Please proceed with your question.
Hey guys. Good morning. Thanks for taking the questions. Just a couple on the plans in TED, can you give us a little bit more visibility into some of the regulatory dialogue and achieving alignment here with FDA? Like were there any discussions around the need for a lipid management program in TED? And I guess, where did you guys settle on that?
Great question, Tom, thanks for asking. We will apply the same identical safety and monitoring program to the TED clinical trial as we have previously discussed for MG, the same narrow exclusion criteria for people who have a baseline LDL greater than 190 or who have existing cardiovascular disease and have an LDL greater than 160. As with the myasthenia trial, should a patient come into the trial on a statin, that’s fine, and we would expect that there’ll be some patients who have controlled hyperlipidemia on a statin, just based on the broad prevalence of that in the population, and that’s not a problem.
However, there won’t be any statin use initiated during the clinical trial, and there won’t be any unblinding due to LDL excursion. So the discussion was straightforward and similar to the one with the neuro division for our MG program.
Okay, got it. That makes sense. Then, maybe following up on Robyn’s question on the targeted patient enrolment, you’ve highlighted the potential role in patients with maybe less severe disease, more on the moderate end of the moderate to severe spectrum. Is there anything specific in the inclusion/exclusion criteria for these Phase 3 studies that could drive maybe greater enrolment of a more moderate patient population on the disease severity spectrum?
No. In fact, it’s probably a little bit the opposite, in the sense that there’s a floor of a clinical activity score 4, which is common, versus dropping it to a 3 or something like that. So the population is really the same. It’s the moderate to severe population. Often people who are enrolled in clinical trials just generally are a little bit more severe. That’s totally fine. I mean we expect to have good efficacy in the more severe group on that moderate to severe spectrum. What I was discussing really related more just kind of to clinical decision making.
If you have two different products, they have a different profile, and you have a spectrum of patients, physicians will generally pick sort of a sub profile of patients that they prefer for one product, and a sub profile of the other. That’s just kind of natural.
The moderate to severe TED patient, that’s a large and heterogeneous pool, so I think it’s actually going to be relatively straightforward for a physician to make a decision, that works for each of them clinically, to decide where they would use batoclimab first, where they would use Tepezza first, assuming batoclimab’s approved. I think in the end of the day, many patients will end up getting both, which is what I meant by a complementary therapy given in series.
And the question then is which one do you get first, and I outlined our thinking in terms of how those decisions will be made, but individual clinicians will probably vary in their decisions there.
Okay. Got it, that makes sense. Then just maybe lastly on enrolment, there are a few other programs out there that could also be enrolling later stage studies in TED. Just as you think about kind of the geographical and regional enrolment, I know you mentioned, Pete, that you expect to get some patients from the U.S., but do you have a sense for kind of regional breakdown between the U.S. and Canada versus Western Europe versus Eastern Europe at this point?
I don’t have detailed projections by country yet, but we do expect all regions to be important. And that was true in our previous 2b trial, and we’re looking to be as expansive as possible in all of our pivotal trials, to ensure that, anywhere there’s a good clinical trial site, that we have an opportunity to tap into that pool of potential patients, given the competing trials across a lot of rare diseases. So that’s definitely something we’re looking at just generally.
Okay. Got it, makes sense. All right thanks Pete, appreciate you taking the questions.
Yeah, thank you Tom.
Thank you. Our next question comes from the line of Douglas Tsao with H.C. Wainwright. Please proceed with your question.
Hi, good morning. Thanks for taking the questions. Just maybe, Pete, in terms of that work that you did that sort of suggests that there are sort of that moderate patients might get some more traction as first line therapy. I’m just curious from -- I think you mentioned tolerability as a key attribute for batoclimab in terms of its tracking. So I’m just curious what the relative tolerability. Is there anything in particular that came out in terms of the market research? Any particular tolerability issues that were appealing to physicians?
Right. So that’s a great question, Doug, I appreciate you asking it. So, both with patients [ph], we did highlight, in the potential product profiles that we were testing that, in the batoclimab profile, there could be changes in LDL and that some physicians may choose to monitor, even though there’s not monitoring in the trial that leads to unblinding, in the clinical setting, that could be the case. That didn’t seem to be something which led to any negative perception with regard to decision making on the part of physicians or preference on the part of patients.
Outside of the blood monitoring, which for these types of patients with thyroid eye disease, is done regularly anyway because many of them have -- they’re [indiscernible] in the trial, but many of them are being treated to maintain their euthyroid state, so they’re used to getting blood draws for thyroid function levels. Outside of the blood draws that may be required, the anti-FcRn class as a whole and batoclimab specifically has been generally well tolerated. So some of the adverse events that have been reported consistently for Tepezza, for some people are a trade-off, particularly when they have another option. So that was kind of how the decision making went in that market research.
Okay great, and then just, do you anticipate you’ll have the MG Phase 3 completed; do you anticipate needing additional sort of safety expansion data to potentially file in TED?
Yeah, so all these -- every division has slightly unique but generally similar requirements for safety exposures. So we work with each division to understand them. The good news is that, consistently across the FDA, safety exposures can be pooled. So having patients being studied in different indications, those safety exposures that we’ll have for example in TED outside of -- for our TED BLA, patients in the MG program can be submitted and vice versa. So that’s helpful, in terms of meeting the safety database requirements.
Okay. Then just one final one. I think you indicated that, one, you expect to initiate an additional pivotal trial by year end, potentially one from the two indications that haven’t been disclosed. I mean, how are you thinking about sort of that risk reward in terms of going into indications in pivotal study where you haven’t necessarily done as much clinical work previously?
Right. That’s a great question, Doug. The decision on whether to go directly into a pivotal trial or a pre-pivotal trial, that’s in some ways -- the second question, an important question but the second question. The first most important question we ask ourselves is what are the indications we want to develop, which is maybe stating the obvious. There we’re looking at the degree of unmet need, the size of the patient population we think is addressable for a new therapy. And then the probability of technical success that you highlighted in your question.
When we’re thinking about the probability of technical success, we consider not only our own data but also data from anti-FcRns, since they’re such a good biomarker, obviously, for anti-FcRn development programs. So then having selected a pool of indications and we have a leading list that’s long and reasonably prioritized beyond the three that we’ve disclosed, then the next question is whether to go straight to pivotal, which is great for long term value creation, because you get faster to BLA, or whether to do a pre-pivotal trial and that has a potential [ph] of generating some additional catalyst data but also, for certain indications, has the chance of advancing our scientific understanding and making our pivotal program stronger.
I think ultimately, having a really, really strong result in your pivotal trial, that’s the most important thing, if you can avoid an issue like what Rigel’s announcing this morning, by having your inclusion/exclusion criteria a little bit more optimized, then that’s going to be desirable. For some of the indications, there is a little bit less scientific information, [technical difficulty] to do approach [ph], and that be the most value creating.
So the most important thing is which indication, and the second most important thing whether it’s pivotals or pre-pivotal.
Okay, great. Thank you so much.
You’re welcome.
Thank you. Our next question comes from the line of Yatin Suneja with Guggenheim Securities. Please proceed with your question.
Hey, this is Evan [ph] on for Yatin. Thanks for taking our questions. Two quick ones for me. First, can you remind us what the bar is for TED? And second, what gives you confidence to move forward in TED, given some of the prior mixed results that you’ve seen?
Yeah, great questions, Evan. So I think the bar for efficacy is equal to or greater than what you see with steroids. And the steroid data is not as robustly characterized as Tepezza data, obviously, which had two very well controlled pivotal trials. But generally steroids have an efficacy on proptosis response of around 50%. So I think anything between the steroid and the Tepezza result is where the efficacy bar lies for a new medication with a strong tolerability profile like we believe batoclimab will have. Our confidence really comes from triangulating a lot of information.
So our 2b trial, we had to pause it midstream, which made the data difficult to interpret. We had a lot of patients who had a varying degree of exposure throughout the trial. So rather than looking at it as you would evaluate a pivotal trial, where you first look at the primary endpoint, is it statistically significant, and then which gate the secondaries hit, we looked at it more as you would look at a proof-of-concept trial, where you triangulate a lot of the information to see if there’s consistency across various clinical scores and biomarkers, and whether there is dose response.
I think that’s one of the most important things when making a decision for a proof-of-concept. Because if you see inverse dose response or something like that, then you wonder if the results that you’re seeing in a smaller trial are spurious. Across a lot of biomarkers and radiologic markers and clinical parameters, we saw that we observed a dose response, as I highlighted a little bit in the slides today, and even in more detail at our R&D day. So that gives us a strong conviction that we have an effect here and that we’re likely to hit the bar that I outlined in terms of efficacy.
Got it. Thanks. Maybe if I could, just one quick follow up. For that post hoc proptosis data, what proportion of the total patient number in each arm is included in that analysis?
That’s a tricky question to answer, because what do you put in the denominator? You put everybody who was ever randomized, everybody who finished the week 12, there were some people that got to 11 weeks and not 12 weeks. So I think just generally there is about half as many people that got to week 6 as to the later, say week 11 or week 12. So it’s a smaller number of people, sort of half to two thirds, depending on what you put in the denominator.
Got it. Thanks Pete. Very helpful.
Yes, no problem.
Thank you. Ladies and gentlemen, that concludes our question-and-answer session; I’ll turn the floor back to Dr. Salzmann for any final comments.
Thanks Melissa. Thanks again everyone for joining us this morning. We’re really excited by this unique first-in-class opportunity in TED. I appreciate very much the opportunity to discuss it with you all this morning. Good bye.
Thank you. This concludes today’s conference. You may disconnect your lines at this time, thank you for your participation.