Conference Transcript - CUE 2026-09-21

Operator

Good morning, everyone, and welcome to the QBioPharma conference call on the Q221 CSU Phase 2 top-line results. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 11 on your telephone. You will then hear an automated message advising that your hand is raised. I would now like to turn the call over to Agnes Lee, Chief Investor Relations and Communications Officer at QBioPharma. Please go ahead, Agnes.

Agnes Lee, Head of Investor Relations

Good morning, and thank you for joining us today. Before we begin our formal comments, let me remind you that during today's webcast, we will be making forward-looking statements that represent the company's intentions, expectations, or beliefs concerning future events. These statements represent our views as of the state, are subject to risks and uncertainties, and should not be relied upon as representing our views or of any subsequent date in the future. As a reminder, this call is being recorded, and a replay will be made available on the Investors section of Q Biopharmers' website following the conclusion of the event. With me on the call today are Dr. Shaoli Lin, our President and Chief Executive Officer, and Dr. Dominic Borey, our Chief Medical Officer and Head of R&D. Dr. Lynn will open the call and then hand off to Dr. Borey to walk through the study data. Dr. Lynn will then close our prepared remarks and we will take questions. With that, I will now turn the call over to Shelby.

Dr. Shao-Lee Lin, CEO

Thank you, Agnes, and good morning everyone. Thank you for joining us. Today we are reporting results from the Phase II study of Q221 in the Chronic Spontaneous Urticaria, or CSU. We're pleased to share that the study results were positive and that we will be reviewing together those top-line clinical results with you today. The key takeaway is that Q221 met its primary and key secondary endpoints in a manner that reinforces our enthusiasm for the precision-engineered, unique dual mechanism of action of Q221 and its potential to offer clinically meaningful and differentiated benefit in IgE-mediated disease. Slide three summarizes the salient findings from the study. The study demonstrated robust, durable, and dose-responsive clinical effects. The primary endpoint of complete resolution of hives, or HSS7 equals zero, at week 12 was met, with the treatment effect further increasing past the final dose at week 16 to its peak at week 22. The key secondary endpoint of complete response, or UAS7 equals zero, was statistically significant in the high-dose group further supporting the clinically meaningful impact of Q221. These results were achieved in a context of a favorable safety and tolerability profile. Of note, for the Q221 high-dose group, both the complete resolution of hives and the overall complete response persisted for 12 weeks or a full quarter and on the order of five half-lives after the last dose. This was not seen for the lower doses or for omelizumab, despite a comparable dose level, highlighting a fundamental clinical difference consistent with the biological design differences between the two drugs and supporting the concept that Q221 has the potential to be a disease modifying therapy. This marked difference observed off-drug at week 28 relative to omelizumab provides our first clinical evidence supportive of the Q221-engineered dual mechanism of action that includes not only blocking of the IgE-mediated allergic cascade, like omelizumab, but also supports the clinical potential of downregulation of new IGE production, unique to the design of Q221. Additional PK and IGE data are of interest, and while not available today, will be the subject of further modeling analyses and future presentations at upcoming medical meetings. Based on this demonstrated potential for differentiated clinical efficacy in CSU, and the potential to develop a new tool to target disease modification, and the concept of functional cure for IgE-mediated diseases. We are more than excited to now plan both a Phase 2b3 neck study in CSU as well as a Phase 2 study for food allergy. I will now hand the call over to Dominique Borey, our Chief Medical Officer and Head of Research Development. Dominique?

Dr. Dominic Borey, Other

Thank you, Charlie. So let me take a couple of minutes to quickly walk the audience through the science behind Q221. First, reminding ourselves that IgE drives allergic disease by engaging two receptors, the high affinity receptor, shown here on the left, through which IgE and the allergen will trigger degranulation and allergic symptoms, and the low affinity receptor, also known as CD23, shown on the right, which is expressed on the surface of these cells and has an important role 2 as when bound by IgE it triggers a natural negative feedback loop that results in reduced IgE synthesis. On slide 5, Q221 was designed to block IgE binding to the high affinity receptor and in doing so provides potent IgE neutralization or IgE blocking. Q221 high binding affinity for IgE shown here on the left, supports a greater potency at preventing IgE-mediated cell degranulation over omelizumab, as shown on the graph on the right. On slide six, on the flip side, Q221 was also designed to preserve IgE binding to CD23. And this was achieved through selecting binding sites on IgE that are distant from the IgE region that engages CD23, whereas the binding site on IgE for omalizumab and its analog, RPK904, is the same as shown on the right and overlaps with the CD23 binding site and therefore does not allow the drug IgE complexes to bind CD23. On slide seven, as the result of the difference in engineering increasing concentrations of hygiene complex with q221 can bind to the cd23 receptor as shown by the orange curve on the right whereas no binding at all was measured with hygiene complex with omelizumab as shown by the gray triangles On slide eight, the biologic pro-impact of preserved binding to CD23 was demonstrated both at the mRNA and at the protein level where addition of Q221 resulted in a significant reduction in IgE synthesis shown by the orange bar that was not observed for omelizumab in gray bars, indicating that omalizumab, in complex with IgE, cannot block new IgE production. On slide 9, it was therefore very exciting to test the clinical impact of these fundamental biological differences in the context of a phase 2 randomized, double-blind, and placebo-controlled study. A nomadizimab arm was included for comparative efficacy and safety, but no formal statistical testing was planned. The study enrolled participants with moderate to severe chronic spontaneous urticaria or CSU, inadequately controlled with H1 antihistamines, and patients were randomized to either one of Q221 dose groups at one, two, or four milligrams per kilogram administered subcutaneously or to a manizumab at the register of dose or to placebo. All patients received subcutaneous injections every four weeks, and the primary endpoint was assessed at week 12 and measured the rate of complete resolution of HIVE, or HSS7 score of zero. This endpoint leverages an objective assessment of the number of hives, which is carried out by the physician, and achievement requires all clear skin or no hives. The final dose in the study was administered on week 16 for all groups, and after which patients were monitored off-drug for 20 weeks through week 36. Slide 10 shows the subjects' dispositions for the trial. Two subjects were randomized, but not those. One in the four milligrams per kilogram group and one in the omalizumab group. The drop-out rates are in range with expectations for a clinical trial of that duration, further considering the five-month observation period of drugs. This study was analyzed using a modified intent-to-treat approach. The two subjects who were not those were not part of that analysis, but all other subjects were included in the modified intent-to-treat analysis. On slide 11, the baseline characteristics were overall well-balanced across groups. Disease duration ranged approximately for four to six years across groups. and mean baseline urticaria activity score 7 or UAS 7 were in the 28 plus point range indicative of severe disease activity. On slide 12, getting to the results, we are excited to report that the study primary endpoint was met. Complete resolution of highs, HSF 7 equals 0 at week 12, was significantly higher than placebo for all those groups in a dose-responsive manner with a high p-value of less than 0.005 for the high-dose group. On slide 13, the key secondary endpoint of complete response, or UAS7 equals 0, was also met, and the difference versus placebo was statistically significant for the high-dose group. On slide 14, another way to visualize the depth of response is to measure the change from baseline in UAS 7 score at week 12, which was found to be profound and statistically significant across all those groups. On slide 15, this slide captures the depth of response at week 12 by presenting the percent reduction from baseline in uas 7 across various mechanisms although we note that cross-trial comparisons are for illustrative purposes only and should not be interpreted as direct comparison of efficacy across various modalities q221 seems to come closest to providing full control of disease activity on slide 16 if you allow me to shift gears now i want to focus on additional exciting findings arising arising after the week 12 primary endpoints on the middle graph across all q221 dose groups complete resolution of highs continued to increase beyond week 12 and picked at week 22 which is six weeks after the last injection in the dose responsive manner more than two-thirds of subjects in the high dose group responded and achieved complete resolution of highs now if we look at the week 28 results this is a time point when patients have been off drugs for 12 weeks this corresponds to approximately five half-life after a last dose for both Q221 and omelizumab, given expected half-life of two to three weeks for these IgG monoclonal antibodies. Let's also note that the formeg per cake dose is, for a 70-kilo patient, the molar equivalent of a 300-milligram zolayer dose. At that week 28 time point, where 60% of Q221 patients are still experiencing complete resolution of hives, only 24% of patients in the omalizumab group are. And this stark contrast cannot be explained only by pharmacokinetics, as residual circulating drug concentrations are likely extremely low to nil for both groups. Rather, we think that this indicates a fundamental difference in biology and provides clinical data indicating that for the q221 dose group there is something different happening which is more than just hygiene neutralization note that a post hoc fisher's exact test was run and found that the difference between q221 and normalizumab was statistically significant on slide 17 to provide further perspective we are providing here this line graph showing the rate over time of HSS7 for the 4 meg per keg Q221 dose group, shown in orange, versus omelizumab and placebo. After the initial injections, there is a rapid clinical impact, and we can then clearly see the curve diverging after the last injection, reaching the maximal difference of week 28, as we previously discussed. This graph clearly shows the sustained high rate of complete highest revolutions throughout the 12 weeks that followed the last injection of Q221. After week 28, both curves are converging again, trending towards the placebo response in the absence of further administration of drugs beyond the week 16 dose. On slide 18, similar to the results seen for HSS7 of zero, a similar pattern of efficacy was seen with the complete response rate for UAS7 equals zero, which was also sustained for over 12 weeks of drug for the high-dose group, again, with the same pattern of marked clinical impact of aromalizumab and supportive of a fundamental difference in biology that is consistent with the differentiated mechanism of action. On slide 19, building on the prior slides, we can start contrasting the features of IgE-targeted therapies. What we think stands out from the week 12 data is that IgE neutralizers like omalizumab or RPT904, which share the same binding epitopes and therefore the same biology of IgE neutralization, they appear to perform closer to Q221 low doses rather than Q221 high dose. Later time point data has not been made publicly available for rats, but again, we are extremely pleased with the different efficacy profiles seen with Q221 over homelizumab at week 28 off-drug, as it supports, you know, fundamental biological differences, which may be directly deriving from Q221 engineering. On slide 20, from the safety standpoint, Q221 was well tolerated. There was no treatment-related serious adverse event, or SAE, and no adverse events of anaxilaxis. Treatment-related adverse events of special interest was limited to one case of grade two injection site reaction. There were two instances of treatment-related adverse events leading to study discontinuation namely one case of worsening urticaria and one instead of insomnia as expected there were no deaths in the study on slide 21 to help place these safety findings in context and because safety considerations will be part of the benefit risk analysis when comparing across different mechanism of action these slides provide a summary of of anticipated side effect profiles for different mechanisms investigated currently in CSU. We believe that Q221 dual MOA should not introduce specific mechanism-related safety that will be different from sole IgE neutralizer, even in the presence of possibly more potent IgE control. And this will be contrasting with the recognized mechanism-related safety findings of other MOAs. We do recognize that broad interest for the field of allergy and IgE-mediated disease results in additional MOAs currently tested at earlier stages of clinical development. We believe that, although still emerging, Q221's potential is already more developed, and we look forward to further characterizing Q221 safety and efficacy profile for IgE-mediated On slide 22, altogether, we are extremely excited to have clinical results in hand that indicate the potential to reach a functional cure for IgE-mediated disease. This did not happen by chance, but may result from the fact that from the very beginning, Q221 was engineered to be different from olizumab and to not only block the high affinity receptor, but do so while preserving the binding to CD23. The preserved capacity of Q221 IgE complexes to bind CD23 results in reduced IgE synthesis at the mRNA and protein level, something that was not seen with amalizumab. And here we now have clinical data strongly supportive of fundamental biological differences between Q221 and Omanizema. We are eager to characterize the PKPD relationship and we'll be presenting these additional results at an upcoming scientific conference. On slide 23 I won't read this final slide but it may be helpful to keep it staying up during the Q&A session.

Dr. Shao-Lee Lin, CEO

And thank you for your attention and now i will hand it back to charlie thank you dominique and thanks to those who have dialed in to be with us today as you can see we are very pleased with the potential that q221 has now demonstrated clinically and which is consistent with its novel precision engineered dual mechanism of action based on these exciting positive results we are working towards the initiation of a phase 2b3 study in CSU, in addition to our planned Phase 2 study in food allergies. I would like to thank the Genesis Life Sciences team for designing and executing a robust Phase 2 trial. I would also like to extend our gratitude to all the patients, investigators, and study staff who participated in this trial and supported the advancement of Q221 for allergic disease. It has been a privilege to be at Q over the past five months and witness all the hard work in progress across our portfolio. And I want to thank the entire Q team for their commitment to our mission to identify and advance transformative therapies designed to enable functional cures across immunologic diseases. We could not do what we love to do without the support of our board, investors, and the patients we strive to serve. With that, I'll open the call for Q&A. Thank you.

Operator

To ask a question at this time, you will need to press star 11 on your telephone and wait for your name to be announced. Please stand by while we compile the Q&A roster. Now, first question coming from the lineup, Murray Raycroft with Jeffrey C. Alanis Nelson.

Speaker 2

Hi, good morning. Congrats on the data update and thanks for taking my questions. For the phase 2b3 CSU study, should we expect a longer dosing interval than the every four-week schedule using the current study? And will you also evaluate additional dose levels? And is there anything additional on timing for when the CSU and food allergy studies could start?

Dr. Shao-Lee Lin, CEO

Yeah. Hey, good morning, Maury, and thanks so much for joining us, and thanks for the question. So, yeah, I think we wanted to indicate with the 2B part of the phase 2B3 that, you know, we're interested in, you know, understanding a little bit more about the PK-IgE and response. And so we're likely, we feel like we have a fantastic dose at this point with monthly dosing that's differentiated. So we'll likely utilize that as an anchor, but nothing's definitive yet. And then we're going to also explore, given the biology that we're seeing, you know, how best to optimize dosing for each indication. And so for CSU, or actually for any indication, for instance. We think that we have something where we can think about fixed dosing. We think based on the profile that we're seeing, there's a potential to think about things like an induction and a maintenance regimen where we're fundamentally modifying some disease biology in the background. We think about this bathtub analogy and, you know, sort of not just emptying the bathtub from blocking or neutralizing IgE, but also turning off the spigot relative to the formation of new IgE. And so one can imagine if you can continue to turn that off better and better over time, that you might reach a point where the interval of dosing now, instead of induction to achieve that time point, becomes a lower dose and less frequent in terms of maintenance. So all of these things, I think we're going to explore, interrogate the data carefully, and determined what the best, you know, sort of approach is to continuing to collect information about this new tool that we have to help patients with IgE-mediated disease. And so that's how we're thinking about it for CSU. From a timing perspective, you know, obviously we think we have something important for patients and we'll move as quickly as we can relative to that. I'd say for food allergy, something completely different. So we think of food allergy as a life-threatening disease, and in the context of thinking about that in that way, you know, we think that this new tool gives us, as Dominique was saying, the potential to approach this from a functional cure perspective, meaning that, you know, we don't want just two-thirds of patients having protection against three peanuts some of the time. We want to get as close as possible to 100 percent of people having 100 percent protection all the time, as close to that as one one can imagine getting. And so we'll approach this sort of new tool, new mechanism, new potential to modify disease in a way that will aggressively pursue that ideal. And, you know, we don't think about this from a convenience perspective. You know, I care less in that instance if it's achievable, whether this is dosed every six months, three months, or even weekly, but really about whether or not I can create an entirely different paradigm for, you know, ourselves and our kids and our families who have this life-threatening condition. So I hope that helps, and thank you for your question.

Speaker 2

Yeah, all makes sense. Great perspective there. And one other specific question on the data. Yeah, you reported change from baseline in UAS7, which appeared fairly similar across the 2-to-1 dose groups in omelizumab. How did HSS7 change from baseline compare across the treatment arms, and are you seeing a similar pattern there as well?

Dr. Shao-Lee Lin, CEO

Yeah, the patterns that we've seen across the endpoints have been very similar, which has been comforting to us from a robustness of the signal that we're seeing. So, you know, and we chose the change from baseline percent to compare with others because, you know, there are some studies that have placebo and some don't and some have active preparators and others don't. And this was the best way to have an internal sort of, you know, give an arm to itself comparison within the context of its own study.

Speaker 2

Got it. Makes sense. Thanks for taking my questions.

Dr. Shao-Lee Lin, CEO

Thank you so much, Maury.

Operator

Thank you. And our next question in queue coming from the line is Mayank Mantani with the Riley Securities. Your line is now open.

Speaker 7

Good morning, team. Thanks for taking our questions, and congrats on the spectacular data here. So on the response building for six weeks after the last dose, which was not a phenomenon for amelizumab, is there anything in the diary data that separates continued deepening in existing responders from maybe new responders converting late. I was obviously interested in that because a neutralizer with long half-life can only hold an effect, whereas your mechanism maybe can have that depth of response coming in late, if you could talk to that.

Dr. Shao-Lee Lin, CEO

Yeah, Mayank. Thank you for that. You know, so I think maybe the best place to see that is in the line graph or in the bar chart before that. And I know we're not, you know, sort of synchronized in terms of projecting, so I'll have to ask you, the audience, to go to those slides yourselves. But the bottom line is all of these representations are actually for complete resolution of. So resolution of hives is what we've shown the line graph for. And so there's no, you know, sort of deepening of response beyond the zero, right? And so the percentage just tells you the percentage of individuals that achieve that complete resolution of, in this case, hives response. So we are definitely getting that. And if you look at the, you know, what we think is particularly amazing about the line graph is what I'm looking at currently is you start to see the separation by week eight. You see the space between the gray line and the orange line, which is Zolaire versus the four milligram group. And that area under the curve is really quite striking. If you follow the gray line, which is omelizumab from the last dose, which is week 16, sort of, and follow your eye down to the week 30 time point and extend that line, you can really see how that continues to degrade towards the placebo line. There was maybe one subject that sort of even off drug at that period of time spontaneously improved, which happens in this disease state and certainly happens with small numbers. But you can see how that's degrading towards placebo, which you expect five months off of drug. What was surprising was the durability of the four milligram group off of drug. Again, as Dominique pointed out, you know, sort of same milligram dose level, therefore same molarity because they're both monoclonal antibodies, same sort of number of half-lives off of drugs, which is like four to five, so the drug itself should really be gone. And yet the effect is still there. And so it tells us that there's something fundamentally different in terms of the biological effect that's happening in those outer weeks between omelizumab and 221. And for us, given that 221 was engineered specifically with a second mechanism, you know, our assumption at this point is that that's that second mechanism in terms of synthesis of new IgE that's kicking in. And one can imagine then, for instance, that over time, if you are in fact, you know, effective against, again, turning that spigot off that, you know, and decreasing free IgE over time, that that may actually cross zero at some juncture and modify the way that you approach the dosing of the disease itself as well. So you can think about mechanistically things like total IgE and receptor engagement on the effector cells or the high affinity receptor, really downregulating those receptors and making those effector cells more quiescent over time. And then you can think about also turning off the synthesis of new IgE and reaching some sort of steady state that fundamentally is disease modifying for these patients. And so that's what we're going to explore, you know, at a bare minimum, purely clinically, all of the scientific hypothesizing aside, the bottom line is that we We have a remarkable clinical difference here that we think is meaningful for patients and pointing to the fact that this molecule is providing a new tool by which we can approach, you know, getting more for each of these patient types.

Speaker 7

Thank you. That was very thorough. And I think the IDE data also will help as that becomes available. i was just maybe my follow-up was is um uh do you have baseline ige data uh didn't say that you can see that in the in the table and was also asking that in context of uh you know csu of the the the range is very narrow in the 100 sort of range but the food allergies the baseline ids can be much higher so if you could maybe comment on uh how you're thinking of you know what the induction maintenance paradigm. Some of it, I know you commented, but what high dose levels you could go there just because of, you know, where you're starting with your IGE levels and how is the data here inform how you kind of progress in CSU versus food allergy?

Dr. Shao-Lee Lin, CEO

Yes. Thank you for that, Mayank. I mean, I think we're very excited to be able to provide specific IGE, PK, you know, you know, PK response data and modeling associated with that and how we're thinking about that relative to each of these disease states, as we said, at a future scientific meeting. And that's not us being coy, to be clear. We have the clinical data at this juncture. We definitely wanted to, you know, make good with our promise to provide data by the end of the third quarter, which is what we are delighted to be able to do at this time. and those data otherwise are just not available at this juncture. But the way I think about this, and obviously it would be a tremendous grand slam to have both of those pieces together today and tell you the other piece of the story. But the way I think about this, certainly as a clinician and a drug developer, is if I had the bioassay data today, I would be asking myself, yes, but is it clinically relevant? What does it really mean clinically? And that's really ultimately the takeaway. And I think that we're incredibly fortunate to have very clear clinical data, despite the relatively small numbers. I mean, it's a phase two trial. It's not tiny, but it's also not massive. And to get the kind of clarity across endpoints, the kind of statistical significance that we're seeing with these numbers, we're very pleased by. We think it's very clean and very consistent. And it's telling us that there's something different. And we can argue about what that thing might be, but we think the most likely, you know, Occam's razor and all, we think it's most likely the thing that it was engineered to do. And so, you know, more to come there.

Speaker 7

Makes a lot of sense. And if I could, final, final question. On ADA formation, anything on tolerability, on immunogenicity, if you could comment, because that obviously is relevant as you develop this in sub-Q format, and I know there was one patient in your phase one that had a nausea headache. Just clarify if you've not seen any of that. Thanks again for the new question.

Dr. Shao-Lee Lin, CEO

Yeah, and I apologize, Mayank. I didn't quite hear the first part of your question, but I'll go ahead and address the second part, which is from a safety perspective, we feel very, very good about the profile. You saw the table with all the zeros all over it. There hasn't been anything. And that subject in the phase one, I think it stated clearly in the supplemental as well, it was not deemed to be related to study drug, if I recall correctly.

Speaker 7

Sorry, the first part was about ADA or any immunogenicity comments.

Dr. Shao-Lee Lin, CEO

Yeah, I mean, like PK, like IgE, ADAs are also things that are, these are things that require assays to be run. And, you know, with typical studies, and this is not specific for this particular study, you know, we'll batch them at the end so that they're all run at the same time, which eliminates some variability associated with them and some noise. And so they typically come after the clinical data. And that's what you're seeing here. Thank you.

Operator

Our next question, Q&AQ coming from Delaina, Dev Prasad with Lucid Capital Markets, your line is now open.

Dev Prasad, Analyst — Lucid Capital Markets

Hi, congrats on the update and the data and thank you for taking our question. I have a couple of questions. One is if we look at week 12, the 4 and 2 mg per kilogram dose are nearly identical at 54% and 53% for HSS7, but they're substantially different at B28, at 60% and 31%. How do you interpret that pattern pharmacologically? Does it suggest 4 mg per kg crosses and exposure threshold required for durable expression or is it just accumulation? And one question on plan phase 2B3 design. Are you aiming to demonstrate superiority over placebo or omelidumab or both? Thank you.

Dr. Shao-Lee Lin, CEO

Yeah, no, great question. And maybe I'll take the second question first, which is, are we planning to design a head-to-head trial, I think is what you're asking us. And I think that's to be determined. Well, you know, I think we had shared previously that we, based on the phase one data and what we were seeing relative to, you know, a single IV dose really having a very prolonged effect on suppressing IgE below limit of quantification that, you know, we were especially interested in this molecule and its potential in food allergy because it's such a strictly IgE mediated disease. So it seemed like the perfect place for something like this. We now feel sort of doubly excited about food allergy as a result of that. We'd also always stated that CSU is a more complex disease, has lots of potential mechanistic aspects that are involved in the disease state. And so how much more we would get with better IgE coverage was an unknown. and we would commit to CSU if it had the potential to be differentiated. I think that what we're seeing with these data we feel again very clean, very consistent, those responses statistically significant and the line graph really kind of says that all in terms of the difference between those curves you know not just at one point but across the experience of what these patients are achieving and then and then a durability 12 weeks thereafter. So with these data we're committed to the phase 2b 3 for CSU some of the things as as I you know sort of shared with more earlier as well is in terms of exactly what those those levels will be and whether or not run an active comparator in a head-to-head fashion I think is TBD as well and yeah maybe to you or to you the first part of your question about the the differences of potential differences between the the two meg per keg and the four meg per keg dose and so you're you're correct that there is a there is a slight difference at week 22 but that may not be where it's the most relevant to look

Dr. Dominic Borey, Other

at it i think we uh we we we can agree for example when when we look at site 16 that these two dose levels seem to behave somehow similarly at week 12 and and but maybe with some slight separation at week 22, what we think is really relevant is to look at week 28, you know, after those. And that's where maybe we start unmasking this second mechanism by the fact that we are at the four meg per cake dose, you know, really seem to have done something in excess of the two meg per cake.

Dr. Shao-Lee Lin, CEO

And maybe to add on to that, you know, just to reiterate that that that isn't an exposure issue, because, again, these are antibodies that are, you know, have a regular monoclonal antibody half-life of two to three weeks. And so we're four to five half-lives out at week 28. We don't expect a lot of drug around. So it's less about an exposure issue in our minds and more likely a biological threshold of effect. And, you know, we obviously are biased, given, again, the design of the molecule, to have one explanation for all of this, which is, you know, we know we were designed to turn off, to have the potential to continue to utilize the natural mechanism to dampen new IgE synthesis. We think as the total IgE complexes are formed, as they stabilize as a total IgE complex, we have the benefit not only of, you know, sopping up the IgE, preventing it from binding to the high affinity receptor, but also utilizing that complex to, you know, be a high IgE state, if you will, and dampen new IgE production. And it's not, you know, sort of unreasonable to think that that has a threshold associated with it. So very excited for CSU patients, we think for food allergy patients, and then, frankly, the CSU study being a complex disease and having this kind of effect gives us enthusiasm for other disease states like atopic dermatitis, allergic asthma, et cetera. So, you know, sort of more to come as we continue to explore the biology and think about our study designs moving forward.

Dev Prasad, Analyst — Lucid Capital Markets

Great. Thank you.

Dr. Shao-Lee Lin, CEO

Thank you, Dev. really appreciate it.

Operator

Thank you. And there appears to be no more questions in the Q&A Q at this time. Ladies and gentlemen, this doesn't include today's conference call. Thank you all for your participation, and you may now disconnect.