Good morning, and welcome to the Jasper Therapeutics Preliminary Beacon Data Webinar. At this time, all attendees are in a listen-only mode. A question-and-answer session will follow the formal presentations. As a reminder, this call is being recorded, and a replay will be made available on the Jasper website following the conclusion of the event. I'd now like to turn the call over to Alex Gray, Head of Investor Relations at Jasper Therapeutics. Please go ahead, Alex. Thank you, Tora, and thank you for those listening in today. Joining us for the prepared remarks are Ronald Martell, CEO, Dr. Edwin Tucker, CMO, and Dr. Thomas B. Casale, Professor of Medicine and Pediatrics at the University of South Florida Morsani College of Medicine and lead U.S. investigator for the Beacon study. Also on the line is Herb Cross, CFO, who will be available during the Q&A session. Due to other commitments, Dr. Casale will not be available to participate in the Q&A. We will be presenting slides on today's call, which are available via the webinar link and posted to our Investor Relations website. During today's events, we will be making forward-looking statements based on our estimates and assumptions and our current expectations and projections about future events. All statements other than statements of historical fact made during today's call are forward-looking statements. These statements are subject to a number of risks, assumptions, and uncertainties, any of which may be significant, and our actual results may differ materially and adversely from those stated or implied in any forward-looking statements. For a description of risks and factors that could affect our future financial results and business, please refer to the disclosure in the accompanying slides, our most recent forms 10-K and 10-Q, and the reports that we may file on Form 8-K with the Securities and Exchange Commission. All our statements are made as of today, January 8, 2025, based on information currently available to us. We can give no assurance that these statements will prove to be correct, and you should not rely on any forward-looking statements as predictions of future events. We undertake no duty to update any forward-looking statements except as required by law. I'll now hand the call over to Ronald Martell. Ron? Good morning. I'm Ronald Martell, CEO of Jasper Therapeutics. On behalf of my colleagues at Jasper, I'd like to welcome you to our webinar to present preliminary data from our phase 1b/2a BEACON trial evaluating briquilimab in chronic spontaneous urticaria, or CSU. Following the press release we issued earlier this morning. Before handing it over to Ed and Dr. Casale, I'd like to convey our excitement to be presenting our second set of positive clinical data demonstrating the ability of briquilimab to deliver rapid and meaningful clinical benefit to patients suffering from chronic urticaria, following the SPOTLIGHT readout last year. As a reminder, we designed the BEACON trial to elucidate the properties of briquilimab and prosecute an optimal biologic dosing strategy, leveraging the unique attributes of the antibody. The preliminary BEACON data show that briquilimab led to a rapid onset of deep and durable disease control, demonstrated by mean reductions in UAS7 of more than 26 points in the 240-milligram single dose and in both the 120-milligram dose cohorts. We also observed complete responses defined as UAS7 score being reduced to zero at all dose levels of 80 milligrams and above, with dose-dependent increases in the durability of responses and the proportion of patients achieving complete responses, as well as controlled status. Notably, 100% of patients enrolled in the 240-milligram single dose cohort achieved complete responses that were durable through eight weeks post-dosing. As expected, we observed dose-dependent serum tryptase reductions from baseline that were rapid and generally correlated with onset of clinical response. We were also pleased to report that a favorable safety and tolerability profile has been observed at all doses through the 240 milligrams. There have been no dose-limiting toxicities, including following repeat doses longer than 24 weeks, and the rates of treatment-emergent adverse events seen in the briquilimab population were similar to placebo. Importantly, adverse events potentially related to c-Kit blockade, such as hair color changes, taste changes, and neutrophil reductions, were infrequent and transient and were generally limited to low-grade events which resolved on study. We believe the low-grade nature of these events and the resolution of symptoms noted in many cases while on study is clear demonstration of the potential for a favorable safety enabled by optimal biologic dosing. In addition, no instances of anaphylaxis and no discontinuations or dose delays due to possible on-target effects have been reported in the study. While preliminary, we believe these data both strongly support the potential of briquilimab to serve as an important treatment option in CSU, as well as provide positive read-through to the potential of briquilimab in other mast cell diseases. Following remarks from Ed and Dr. Casale, I'll review the next steps and upcoming milestones in the CSU program. I'll now turn it over to Ed. Ed? Thank you, Ron, and good morning, everyone. Before we review the preliminary BEACON results, I'd like to quickly remind the audience of our BEACON trial design and the cohorts from which we'll present the preliminary clinical data today. BEACON is a double-blind, placebo-controlled, multi-ascending dose trial in patients with moderate to severe CSU who are intolerant or refractory to prior omalizumab or antihistamines. As such, this difficult-to-treat patient population represents one of the highest unmet medical needs. Investigative sites were located in the United States and in Europe for the BEACON trial. The BEACON study tested doses ranging from 10 milligrams to 240 milligrams of briquilimab in different dosing intervals. The key assessments of the trial are safety, PK, and efficacy as measured by the UAS7 and UCT. Today's data supports the potential of briquilimab to serve as an important treatment option in CSU, including the favorable safety profile enabled by optimal biologic dosing. An IDMC reviewed the safety data prior to the next ascending dose start in the trial, which enabled the expansion of the higher dose cohorts supported by the safety experience in the preceding cohorts. A higher dose of 360 milligrams single dose was added most recently, and we will share that cohort data once it has matured. We plan for further clinical data releases from the BEACON trial in future scientific congresses in 2025. The next slide shows the demographics of the participants enrolled into the BEACON trial. Cohorts were generally well-balanced and were representative of a population with moderate to severe CSU disease, as measured by the UAS7 and UCT at baseline. Age, weight, and gender were typical for participants with CSU. Serum tryptases were within normal range at baseline. As noted earlier, this is a population refractory or intolerant to available treatments representing a CSU population enriched with participants most difficult to treat. Now moving to the efficacy endpoints. Briquilimab demonstrated deep reductions in UAS7 scores at doses of 120 milligrams subcutaneous and above administered every eight weeks or 12 weeks, or when administered as a single dose of 240 milligrams. The reductions in UAS7 observed were clinically meaningful, with several dose regimens showing UAS7 reductions of 25 points or greater from baseline. The left panel shows the 240 milligrams single dose at eight weeks, with a UAS7 reduction of 26.6. The middle panel shows the Q8 dosing schedule for the 80 milligram, 120 milligram, and 180 milligram cohorts at week 12, with a mean UAS7 reduction of 9.3, 27.2, and 13.2, respectively. The right panel shows the Q12 dosing schedule for the 120 milligram and 180 milligram doses at week 16, with UAS7 reductions of 29.8 and 21.7, respectively. Moving to the next slide, this shows the dose-dependent complete responses with CRs achieved in all doses at 80 milligrams and greater. The left panel shows the 240 milligram single dose at eight weeks, with a complete response rate of 100%. The middle panel shows the Q8 dosing schedule for 80 milligrams, 120 milligrams, and 180 milligrams at week 12 for participants with a complete response of 16.7%, 50%, and 28.6%, respectively. On further review, we noted that in this 180-milligram Q8 dose cohort, there were two patients with the potential for having alternative diagnoses. These patients had deep tryptase reductions down to below levels of quantification, and if censored, the CR rate in this cohort would have been 40%. Moving to the next slide, sorry, right panel. The right panel shows the Q12 dosing schedule for the 120 and 180 milligrams at week 16. For those participants, complete response rates were 50% and 57.1%, respectively. Moving to the next slide, participants treated with briquilimab achieved well-controlled disease with a UAS7 of six or less for all dose levels, 80 milligrams and above. The left panel shows the 240-milligram single dose at week eight with well-controlled disease in 100% of participants. The middle panel shows well-controlled rates at week 12 for the 80 milligram, 120 milligram, 180-milligram Q8 regimens and also the 240-milligram single dose regimen of 33%, 75%, 42.9%, 66.7%, respectively. Again, the two patients in the Q8 120-milligram dose who appear to be non-responders and had deep reductions in their serum tryptase, if censored, would yield a well-controlled rate of 60% in the 180-milligram dose cohort. The right panel shows the Q12 dosing schedule for the 120 milligram and 180 milligrams at week 16 for the participants in those two dose cohorts with well-controlled disease at 75% and 57.1%, respectively. When we combine the therapeutic doses of 120 milligram, 180 milligram, and 240 milligram in an aggregate four weeks post-second dose for the serial dosing and after four weeks of the 240 milligrams, we see a combined effect of 52% for complete response and 64% for well-controlled disease. Moving to the next slide, this shows the durability of the 240-milligram dose through 12 weeks. 100% complete response was achieved by week two and was maintained through week eight. Well-controlled disease was achieved as early as week one, with 66% maintaining disease through week 12. This slide shows substantial UAS7 reductions over time for the 120 milligram and 180-milligram Q8 and 240 single dose regimens. Onset of UAS7 reductions was observed as early as week one across all dose levels. Subsequent doses drove deeper reductions in UAS7, including all patients reaching UAS7 of zero in the 120-milligram Q8 cohort. The 120 Q12 and the 180 milligram Q12 week cohorts showed similar patterns as the Q8 week cohorts through eight weeks. The next slide shows the reduction in serum tryptase in relation to briquilimab administration. Serum tryptase, being a marker of mast cell biology, showed rapid decline after dosing, consistent with the rapid clinical responses seen in the UAS scores after dosing with briquilimab. In these analyses, tryptase levels below levels of quantification were imputed to half of the LLOQ value. There was a clear dose response for both tryptase reductions and the durability of those tryptase reductions. Of note, tryptase levels below the level of quantification were reported at week one in six out of seven participants, 86%, in the 180-milligram Q8W cohort. All patients in the 240-milligram single dose cohort reached the lower limit of quantification at week one and stayed below that level through four weeks, with deep suppression through eight weeks. Moving to the preliminary PK results, we see an early Cmax consistent with the rapid clinical responses and serum tryptase reductions described earlier. Our PK results are consistent with prior briquilimab trials, including our healthy volunteer studies. At the 240-milligram dose, we see the Tmax is four to seven days, and the approximate half-life of the drug is nine days. Based on initial PK modeling, no accumulation is anticipated for a 240-milligram Q8 week dosing schedule. Preliminary data indicate a 34% incidence of antidrug antibodies, and these had no clinically meaningful effect on briquilimab PK in CSU patients. Now moving to safety, briquilimab was well tolerated and demonstrated a favorable safety profile through doses of 240 milligrams. These data include all safety follow-up for cohorts one through six, representing greater than 24 weeks of exposure for the 10 through 180-milligram doses and 12 weeks for the 240-milligram doses as of the data cut of 31st of December 2024. We continue to accumulate additional safety data at higher doses, and we'll report these at a later time. As the table shows, there was no dose-limiting toxicities reported. Treatment emergent adverse events were of a similar rate in both the briquilimab and the placebo populations. There was a single serious treatment emergent adverse event, which was a COFAR grade 2 hypersensitivity reaction, which led to the sole discontinuation, which is shown in the table. There was a single grade 3 event of neutropenia, which was deemed by the investigator to be unrelated to briquilimab due to the patient having a prior history of idiopathic neutropenia and thrombocytopenia. This slide reflects the safety observations possibly related to c-Kit blockade, which were infrequent and generally limited to low-grade events. The majority of events resolved during repeat doses and did not result in discontinuations or dose delays. The hair color change reporting rates observed were similar in the active and the placebo groups. There were no reports of skin discoloration in the active arm for more than 24 weeks of follow-up in multiple cohorts. Mild low-grade transient taste change and a hypogeusia occurred in six participants following first dose, four of which resolved prior to subsequent dose, one of whom reported recurrence at second dose, which also resolved. The median time to resolution of these events was 31 days. Mild taste change was described as a reduction of salt, bitter, or umami taste. Neutrophil reductions or neutropenia, as reported by the investigators, are shown in the table. One grade 3 neutropenia was observed, deemed by the investigator not to be treatment-related, as described earlier. The remaining events were all grade 1 and resolved prior to subsequent dosing, with no association of these events with fever nor infection. This slide shows the observed neutrophil counts from week 16 for the 120-milligram Q8 week, the 180 Q8 week, and the 240 single dose cohorts. As you can see, there is a predictable reduction observed, which did not deepen on serial dosing, and the mean values remain within the normal limits in all cohorts. More importantly, one can see the neutrophil count recoveries in the weeks prior to next dose. In summary, preliminary BEACON study results demonstrate that briquilimab achieved rapid, deep, and durable responses in moderate to severe CSU patients in five dosing regimens presented today. It is remarkable that these results are in a population that is refractory to all approved CSU treatments, including omalizumab. In terms of efficacy, briquilimab administered subcutaneously demonstrated rapid onset of effect with clinical responses as early as one week post-dose. Multiple dosing regimens showed mean UAS decreases of more than 25 points, with responses as deep as a 29-point reduction. Complete responses were seen in all dose cohorts at 80 milligrams and higher, with 100% CRs in the 240-milligram cohort occurring by week two and durable to eight weeks. Importantly, repeat dosing showed deepening clinical responses across multiple dose cohorts. Rapid dose-dependent tryptase reductions correlated with early onset of clinical response, with reduction to the lower limits of quantification observed in multiple dose cohorts. Briquilimab was safe and well tolerated in the study, and adverse events were potentially related to c-Kit, were mild, transient, low in frequency, and did not result in any dose delays or discontinuations. A single discontinuation due to an adverse event was observed. The deep and durable efficacy and favorable safety data collected to date support the commencement of a registrational program in CSU expected to start in 2025. These data, along with additional data from the BEACON study, will complete optimal biologic dose selection. Data to support the final dose selection for the registrational program will be generated in the ongoing 240 and 360 single dose cohorts, which we will be expanding, with the addition of two new BEACON cohorts evaluating 240-milligram Q8 week regimen and a cohort which will examine the 240-milligram induction dose, followed by a 180-milligram Q8 dosing regimen, and also the BEACON and SPOTLIGHT open-label extension study enrolling patients at the 180-milligram Q8 dosing regimen. We look forward to commencing our registrational program. Before concluding, I would like to thank the investigators and patients that participated in the BEACON study, along with their families and caregivers. It is now my pleasure to hand over to Professor Thomas B. Casale, Professor of Medicine and Pediatrics at the University of South Florida Morsani College of Medicine, our lead PI in the U.S. for the BEACON study. Thank you. Thank you, Ed, for that excellent presentation on the initial results of the BEACON study. It's a very exciting study on novel treatment for patients with moderate to severe chronic spontaneous urticaria. Why is it important that we do treatments? We do treatments because this is a disease that causes a very significant impairment on quality of life. It produces hives and itchiness that take patients from everyday activities, takes patients away from being able to sleep at night, and in some cases, even affects their relationships, their ability to work, to go to school, and to interact with others. You can only imagine how embarrassing it might be if you had hives on your body and you're trying to go out and socialize or go to work or school. Because of that, there's a number of patients that have not only this impairment of quality of life, but associated mental health issues, including depression and a higher risk of suicide, which fortunately can be modified by treatments. We know that there's about 1.4 million patients in the United States, Germany, France, Italy, Spain, and the U.K. that have moderate to severe chronic spontaneous urticaria. We also know that about half of these patients do not respond well to standard treatment with either licensed doses or up to four times the licensed doses of antihistamines. We do have another biologic anti-IgE molecule that has been a significant breakthrough for a number of patients. However, there are many patients that still don't respond, that still have impairment in their quality of life. Having another therapeutic option, I think, is extremely important. Could I have the next slide? In thinking about this disease, we mentioned that not everybody does respond to omalizumab. As Ed pointed out, the patients enrolled in these studies were actually failures, could not respond well to either high doses of antihistamines or omalizumab with significant improvement of their hives. What causes hives? What causes hives are mast cells. Mast cells present in the body are degranulated or release their mediators to a number of different factors, some of which we're just beginning to learn about in the pathogenesis of urticaria. Nonetheless, once the mast cell fires and releases chemicals and mediators like histamine, and that's why antihistamines do work in some patients, but also leukotrienes, prostaglandins, and a number of cytokines that continually drive this inflammation and itchiness, that's a real problem. Briquilimab blocks c-Kit signaling, which is critical for mast cell to continue a viable path in inducing urticaria. Briquilimab may lead to depletion of mast cells. And of course, if you get rid of that target cell that releases the mediators and chemicals and causes individuals to have symptoms, you could effectively treat patients with urticaria regardless of the cause or regardless of the particular trigger that might make them worse. So the preliminary BEACON efficacy results show a very large and clinically meaningful decline in UAS7 score. UAS7 is a measure of the severity of urticaria. And when you look at the response in the BEACON study, you could see a very dramatic and rapid decrease in urticaria scores. And very importantly, for those of us that treat urticaria, is a high percentage of patients either have complete remission or complete response, or they have a reduction in urticaria symptoms that is considered to be under reasonable control. So what does that mean? That means that that patient no longer has the signs and symptoms of urticaria that can affect their daily lives and impair them in doing daily activities and sleep. So important to that is that this drug also appears to work very rapidly. So if you have a patient that has urticaria and they come to see you in the clinic, they're miserable. And what they want is they want relief, but they want it now. They want it yesterday. So having a treatment that not only is very highly effective, but rapidly effective, and works in patients that did not respond to our currently FDA and EMA approved therapies for urticaria, that's a significant plus. Now, as in any disease state, you're always, when you see a patient, thinking about what's best for that patient in regards to picking the best therapy, but also balancing that with any potential adverse consequences from that therapy. And the preliminary BEACON safety results show a very low incidence of adverse events. And these adverse events were nothing that were of concern. That is, there was no significant or serious adverse events. So in summary, it appears that briquilimab could be the next important new therapy for the management of this very significant disease. And it's clear to me that it's an exciting time to be able to trial this drug to lead to hopefully approval for the million-plus patients that we manage globally with chronic spontaneous urticaria. So thank you again for allowing me to give my perspective. I'm going to turn it back over to Ron now. Thank you, Dr. Casale. As I noted earlier, we are extremely encouraged by the preliminary results of the BEACON study in CSU. Rapid, deep, and durable efficacy was observed in the study, including disease control as early as one week following the initial dose, complete responses at 12 weeks in doses as low as 80 milligrams, and durable complete responses out to eight weeks achieved in 100% of the patients in the 240-milligram single dose cohort. The favorable safety profile also underscores the potential of an optimal biologic dosing strategy to allow for the recovery of other c-Kit-expressing cells beyond mast cells. Based on these data, we plan to commence a registrational program in the second half of 2025 with a phase II-B portion to finalize dose selection for the phase III studies. The data collected to date support advancing a 240-milligram dose into the registrational program. Ultimately, doses and dosing regimens that we will advance into the program will be further informed by the data from the open-label extension study enrolling BEACON patients at the 180-mg Q8 week dose level, as well as the data from the three BEACON cohorts yet to read out, the 360-mg single dose cohort, in addition to the planned cohorts evaluating 240-mg Q8 weekly and 180-mg weekly after a 240-mg induction dose. Results of these cohorts are expected by mid-year 2025, and we'll support a well-informed, data-driven decision in consultation with regulatory authorities regarding which doses and regimens to bring forward. Beyond CSU, we believe these data support the potential of briquilimab to serve as an important treatment option in a large number of mast cell-driven diseases with significant unmet medical need impacting tens of millions of patients. In addition to our programs in CSU and CIndU, Jasper is currently conducting a clinical study in patients with asthma where we believe briquilimab could have impact across respiratory diseases driven by mast cells. Beyond our ongoing studies, we believe briquilimab has franchise potential in additional mast cell diseases, including food allergy and other dermatological, respiratory, and gastrointestinal diseases. Finally, I will briefly review our upcoming milestones before opening up for Q&A. As noted, we are planning to report data from all cohorts in the BEACON trial as well as the SPOTLIGHT trial by mid-year. We expect to commence a pivotal program in CSU in 2025. We look forward to presenting additional data from the BEACON study at AAAAI in February. We are currently enrolling patients in the ATESIAN challenge study evaluating briquilimab in allergic asthma, and we expect to report initial data from the study in the second half of the year. Before opening the line for questions, I'd like to note that due to other commitments, Dr. Thomas B. Casale is unable to join for Q&A. Operator, could you please open the line? Great. Thank you, Ron. So at this time, we will be conducting a question-and-answer session with our speakers. Please hold for a brief moment while we pull for questions. So our first question comes from Yaron Werber at Cowen. Please go ahead, Yaron. Great. Thanks for doing the call and the data. This is really useful. So maybe just a couple of questions for me. As you think about doses from here on, as you're going to wrap up the dosing that you're doing, it sounds like 240 milligram and above is going to be the Q8-week dose, and you're still going to look at the 180-mg Q8-week with the 240 milligram loading dose. Do you have a sense how many doses are you planning on taking into the phase II-B, and how long would it take to do that upfront sort of dose finding before you start the phase III? And then maybe the second question, on just that grade 2 hypersensitivity, can you give us any more information about that patient? Did that patient stay outpatient the whole time? How fast did they resolve? Any information you can give would be useful. Thank you. Good morning, Yaron. Thank you for your questions. Before I turn it over to Ed, yes, the 240 milligram will certainly be a backbone in the registrational study. The question will be, is that 240 milligram Q8 or 240 milligram followed by 180 milligram? The data that we'll be generating this year will inform that. We would anticipate that we'd likely have two doses in that phase II-B portion of the registrational program, and the data that we're generating could inform that as well, or will inform that. I think one of the interesting questions is also the 180 milligram Q8, as Ed noted earlier. In fact, we had really robust data from the 180 milligram Q8 week, but we'll also be evaluating the 240 milligram followed by the 180 milligram, with, again, our objective here is to not just optimize this drug for the efficacy, but it's optimizing for both safety and efficacy. And I think to your last point, from a timing standpoint, that if we initiate this phase II-B portion of the study in the second half of this year, it still would likely put us only 12-ish months behind in this arena, given that we would then only be taking one dose regimen forward into the phase III portion of the registrational study. Ed, I'll turn it over to you. Yeah, thanks, Ron. Thanks, Yaron, for the question. Yeah, so I think that what the BEACON provides is a great deal of clinical data at various different doses and dosing regimens. And so that will inform, as Ron mentioned, the potential doses that we take through into the phase II-B. And we also elaborated on both our dose expansions and also the additional dose cohorts. So I think that we'll have a rich dataset to inform the phase II-B, and the expectation is that we would take a single dosing regimen into our phase III study. With regards to your second question, Yaron, the hypersensitivity case was a COFAR grade 2. We use COFAR, which is the Consortium for Food Allergy Research, as our grading system for hypersensitivity cases. And that was a grade 2 because it involved a single organ system, which was essentially skin manifestations. Those occurred after first dose and occurred about three hours to four hours after administration. The patient was observed and made a full recovery. Great. Thank you for the questions, Yaron. Our next question comes from Gavin Clark-Gartner at Evercore. Please go ahead, Gavin. Good morning, guys. Thanks for taking the questions. First, just on safety, how did the safety look at each dose level, specifically on neutropenia? And what was the rationale to not break out the safety table by dose level? Yeah, thanks, Gavin. Good morning. Yeah, I think that we're very pleased with our safety profile. And as you saw, the numbers are quite small. And so trying to infer any sort of dose relationship with small numbers is very, very challenging at this stage. So we do not see a clear dose concern or an increase in adverse events as we ascend the doses. We'll continue to observe those in our ongoing and future trials. And with regards to the neutrophils, could you repeat the question again, please, Gavin? Oh, I was just wondering how the neutropenia broke out by dose level? Yeah, so we saw neutrophil reductions in a number of the cohorts, including cohort 5, which was the idiopathic neutropenia case, which we presented in the table. We also had a single patient in the cohort 6, that's the 240 milligrams. That was a grade 1, and their value was 1,666, so just under the lower limit normal. It was transient and recovered on next assessment. Got it. That's helpful. And just thinking ahead to the full BEACON study data, which I believe you said you'll be presenting mid-year, can you just clarify how many additional patients will be included? So at the 240 and 360 doses, but I think more importantly, how large are those two additional cohorts that you're adding? Yeah, thanks again, Gavin. So the additional cohorts, the 240 Q8 and the 240 induction followed by 180 Q8, we'll be adding four additional patients randomized three to one in the same convention in our BEACON trial. That adds an additional eight in the, sorry, eight in each of those cohorts, that's 16 patients. We're also expanding the single dose cohorts by the addition of four patients in each of those dose cohorts as well. When that data is available, we'll be presenting later in the year. All right, great. Thanks so much for the details. Thanks, Gavin. Thank you for the questions, Gavin. Our next question comes from Greg Renza at RBC. Please go ahead, Greg. Great. Good morning, Ron and team. Thanks for the detailed presentation this morning and the data. Ron, just circling back to dosing and the go-forward and as you expand the trial, as you've discussed, certainly the 240-mg and the induction, as well as the Q8W. Just curious, have you given any thought of exploring maybe more frequent dosing, perhaps with the 120 or 180 every four weeks, maybe even after higher induction doses? Just walk us through the implications of tweaking the frequency a little bit. Thanks. Sure. Good morning, Greg. Well, certainly, again, we are very pleased by what we observed in the 240 with 100% complete response at week eight and durability of the well-controlled through week 12 in two of the three patients from that cohort, combined with the safety profile, as Ed stated, at that 240 dose level. There was only one mild and transient neutropenia. And as you saw on the neutrophil graph, the neutrophils all recovered before eight weeks. So it gives us real confidence in our ability to dose 240 as a Q8 week dose schedule. And I think then that combined with the data that you observed in the longitudinal chart with the 120 dose, that even dosing that at either Q8 weeks or Q12, we observed a deepening response on each subsequent dose at the 120 level. And if you were to go back and to look at that chart, those patients had the durability of their response through at least the first four weeks or six weeks. So the 120 certainly could be a four to six-week dose regimen as well. And we think also, if you remember back to the SPOTLIGHT study and what we observed in the SPOTLIGHT study, that we had complete responses in SPOTLIGHT at the 120 milligram dose level also that were durable through six weeks in the SPOTLIGHT study. So thereby confirming that the 120 dose is absolutely a viable dose at a four to six-week dosing schedule. I think once we conclude the dosing of 240 as a Q8 week and a 240 induction followed by the 180, that will really inform us about what a subsequent dose might look like here. Great. That's helpful. And maybe just back onto the safety side, and it was helpful to hear Dr. Casale's view on the balance. And maybe for Ed, just double-clicking a bit on the taste effect, how inhibiting do you think that is? And as you get up to 240, maybe just double-click a bit on what you saw in these six patients. And as you pointed to that resolution, how impactful is that 30-day mark that you identified with those four patients? Thanks again, guys. Yeah, thanks, Greg. Good to hear from you. I think with regards to the taste changes, not unexpected. We did see that in our healthy volunteers at the highest doses. And what we saw in the BEACON study was transient, very mild effects, salt and umami in particular. And patients had a transient event, which recovered before dosing, and no discontinuation. So these patients can really stay on drug. It does not appear to be a tolerability issue. And I think that we'll look forward to looking at subsequent doses and also higher doses to see if we still see that signal. So we think this is very manageable, as Professor Casale mentioned. And we do not feel that this will impact the experience of the patients. Greg, I think it's also important to note as it relates to the hypogeusia, is that this taste change, it's not, let's say, relevant like the Paxlovid. So these patients are not aware on a day-to-day basis, if you will. They're not walking around with a certain taste in their mouth. It's a reduction in that taste. Patients really only noticed it when questioned on this. We'll keep an eye on this moving forward. Great. Thanks for the questions, Greg. Our next question comes from Ben Burnett at Stifel. Please go ahead, Ben. Hey, great. Thank you so much. I guess first, just a high-level question regarding sort of the competitive landscape. As you look at these data, and it feels like there's going to be a fair bit of further exploration with the 240-mg dose going forward. But as you look at these data, what are you seeing as emerging as sort of the key differentiating features for briquilimab relative to the landscape of therapies that are out there? Certainly. So from an efficacy standpoint, these efficacy data stand up to those comparable to the only other antibody in the space, which is superior to all of the other drugs that have been in development and really set the standard for efficacy. So these are comparable and potentially better. I think that the other important piece here is the attributes of briquilimab and the potency, the CMAX, the time to CMAX, and the half-life of the drug lead us to be able to optimize it for both safety and efficacy, where the other antibody that's in development has really just been optimized for efficacy. And we think we have an opportunity to not only have a good, but potentially best-in-class drug here. Yeah, and I would also add as well, we'll take a look holistically at our efficacy, safety, and also dosing schedules for convenience for patients. What I mentioned in the presentation was that this is an omalizumab experience. These patients are refractory to all available and approved therapies. So we feel that both the safety and efficacy in patients who have essentially failed all available therapies is a huge plus for briquilimab. And it bodes very well for a broader population of patients, not only those that are omalizumab experienced and failed omalizumab patients, but also a broader population of patients as well who are omalizumab naive. And we'd like to explore that in our registrational program. Okay, that's great. And I was wondering if you could also speak to some of the variability in the efficacy data that you're seeing. It looks like you're seeing a pretty clear dose response on tryptase. But on other metrics, the 120-mg arm outperformed the 180-mg arm. And you touched on this in the call, but any more color you can provide here? I mean, I guess, is this just noise given the tryptase data? Yeah, thanks, Ben. I alluded to this in my presentation that we did see, I think, fantastic dose responses from a biology perspective. And we also looked at our PK. So everything behaved. But we saw two patients that potentially have an alternative diagnosis. And in small numbers in these cohorts, it can significantly impact the rates, as we showed, for well-controlled and complete responses. So I layered in some comments around the censoring of those two patients because actually, I think probably at least two of those patients may have an alternative diagnosis. And that potentially could be an urticarial vasculitis patient or two. So we're going to take a look a little bit more deeply at this, but I think that's why it skewed the 180 a little bit. And we'll have further 180 milligram experience in the ongoing trials, but also all patients in the BEACON study have the opportunity to roll over into the open label extension with that 180 milligram QA. So we'll get a lot more data in there to shore up that data for the future. Okay, that's great. Thanks very much. Thanks for the questions, Ben. Our next question comes from Pete Stavropoulos at Cantor Fitzgerald. Please go ahead, Pete. Good morning, Ron and Ed. Thank you for the detailed presentation and for taking our questions. I believe the skin biopsies were optional. We're curious if you have sufficient samples across the dosing cohorts to sort of determine the depth of mast cell depletion and repopulation kinetics so that it can be tied back to clinical response, and have you seen that data to help determine the new dosing cohorts or based on clinical observations? Yeah, thanks, Pete. Good morning. We did achieve consent. These patients volunteered for skin biopsies. We have not processed that, as you can imagine. This is the preliminary data. So we'll look forward to processing that data and then present that at a later conference. The two patients that were on 180 milligrams that may have been misdiagnosed, did you have skin biopsies from them by some chance to help determine? We don't know that at the moment, but we'll certainly be following up on that. Okay. And one question on the phase II-B, just a little bit more detail about size, duration, and would you be waiting for a 52-week endpoint to start the phase III or a 12-week time point? And will you be focusing in on Xolair experienced patients or all comers? Yeah, thanks, Pete. I think from a phase II study design, we'll clearly be in dialogue with the regulatory agencies, but our go-to here would be a phase II adaptive design where we would assess doses and dosing regimens in that trial and then move a dose into our phase III program. Pete, we would look to enroll both omalizumab-naive and omalizumab-experienced patients in that study. Okay. Thank you again for the presentation and taking our questions. Thanks for the questions, Pete. Our next question comes from Jay Olson at Oppenheimer. Please go ahead, Jay. Oh, hey, guys. Congrats on the results, and thanks for providing this update. Can you talk about the placebo response observed in the BEACON study, especially in the Xolair refractory patient group? It seems like the placebo response also may have deepened over time. So are there any strategies you may pursue to mitigate the potential placebo response in your registrational trial? And then I have a follow-on question if I could. Yeah, thanks, Jay. Good morning. Yes, we did not adjust our results for rescue medications. Certainly, the placebo cohorts through the study did receive additional rescue medications, as you could anticipate, and so I think we can really interpret the improvement in the placebo as a result of the initiation of the rescue meds in the placebo cohorts. Okay, great. Thank you. And then can you elaborate on the other potential indications that you'd like to pursue with briquilimab, especially as you optimize the profile in CSU? What are you seeing that makes you most excited about some of the other indications you mentioned? Food allergy, other derm and respiratory mast cell-driven diseases? Good morning, Jay. So yes, we're very encouraged by these data at multiple dose levels here. So I think that as we think about additional indications, the first one would potentially be in asthma, broader patient populations in asthma. And should asthma be successful, then you might imagine COPD being a viable option as well. And given the safety profile that we observed here and what we think we can do with an optimum biologic dosing and giving the other c-Kit presenting cells a drug-free interval, we think that that broadens our opportunity to go after additional diseases like maybe food allergies or diseases like that as well. Super helpful. Congrats again on the progress. Thanks for taking the questions. Thank you, Jay. Yes, thanks for the questions, Jay. Our next question comes from Matthew Phipps at William Blair. Please go ahead. Good morning. Thanks, team, for taking my questions. I was just wondering if you could help me understand the N or the kind of sample size between slides 7 and 8. There's a couple just a little bit of difference in particular, like the 120 -mg and 180-mg groups. I know, Edwin, you mentioned two patients in the 180-mg Q8 maybe not being true CSU patients. Is that the only difference between the 5 and 7 and the kind of the N there? Or is there something else? No, thanks, Matt. No, we presented the data, including those two patients who I think probably have alternative diagnoses. With regards to the differences in the Ns, that represents missing data that was not available for this presentation, and so we took a conservative imputation for missing data, which is a last observation carry forward, and so that accounts for the differences in the different numbers on the cohorts. Thanks, Edwin. And similarly, for that last observation carry forward imputation, I mean, you also had a patient who discontinued, sounds like, fairly early at the 180-mg dose. Did that kind of negatively impact, I guess, this number, or was that patient excluded? No, the patient's included. And yes, again, we're conservative and transparent in how we present the data. So yes, thank you for raising that one. Okay, and last question, I guess. I understand small patient numbers at the 240-mg group, but can you give us any sense of how many of those three patients had hair color change? The concern being that if this, I mean, obviously, this level had great efficacy, but if you're redosing at that level, maybe you get cumulation of kind of the on-target AEs over time. So can you give us any sense of kind of the on-target AEs at the 240-mg level? I know you already touched on neutropenia, but some of the others. Yeah, thanks, Matt. We've not seen any hair color change in the 240-milligram cohort. Okay. Great. Thanks, guys. Thank you for the questions. Our next question comes from Justin Zelin at BTIG. Please go ahead, Justin. Thanks for taking our questions. I wanted to ask about the grade three neutropenia event, if you could give us a little bit more color on that patient and how it was deemed unrelated and whether a patient with a similar background would be included in the study moving forward. Yeah, thanks, Justin. Yeah, this patient came into the study, met all the inclusion/exclusion criteria. Our entry criteria for neutrophils is 2,000. So this patient came into the study just slightly above that. And then we noted this grade 3 adverse event where the patient had a neutrophil count of about 980, which obviously we inquired further to the investigator. On deeper look at the patient's prior history, he had a two to three-year history of low normal neutrophil counts with no other clinical sequelae. This was labeled by the PI as idiopathic neutropenia and thrombocytopenia. And so the patient has now received several doses and has not had any associated fevers nor infections from their original grade 3 neutropenia and continues in the study without sequelae. Understood. And maybe just any efforts to mitigate the differential diagnosis during screening moving forward, if you have any strategies to ensure that the patients have urticaria? Yeah, I mean, it's certainly a challenge for ensuring that all patients included in a clinical study are our target population. Now, we are subject to small numbers in these cohorts, and so one or two patients can certainly have a dramatic effect on your study. As we move through into our registrational program, those studies will be much larger and so can accommodate single and small numbers of patients who may not actually have the appropriate diagnosis. Sometimes this happens, and we talk to our KOLs, that diagnosis can be a misdiagnosis for CSU. It rarely happens, but in a patient population that is refractory to omalizumab, I think we've probably enriched for that potential to occur in our study. In the future studies, we'll continue with our inclusion/exclusion criteria, and I think we can maintain a population of CSU patients that is representative of the broad population in the community. Great. Thank you for the questions, Justin. Our next question comes from Emily Bodnar at H.C. Wainwright. Please go ahead, Emily. Morning. Thanks for taking the questions. I guess maybe if you could just set some expectations for what you would be hoping to see with the new 240-mg doses to kind of decide which dose to move forward with? Thank you. Yeah, thanks, Emily. I think as a clinician in development, we always want more data. And I think that what we have today and what we've shown could potentially move us into the registrational program. But having additional data informs our final dose selections into that phase II-B and, as I mentioned earlier, the potential for an adaptive design moving to phase III. So I think the more data we have, the happier I'll be. But certainly, we feel that with the data we have in hand today from an efficacy and safety perspective, we're certainly informed around the attributes of briquilimab and how it delivers efficacy and maintains a safety profile in patients with CSU. I think the interesting question, Emily, is we were 100% complete response through eight weeks with tryptase, as you saw, below the lower limits of quantification with that dose, with no significant impact to the neutrophils. And as Ed pointed out earlier, we didn't see any grading in that population and one grade one neutropenia with a very minimal drop in their neutrophils. So that's really encouraging that if we dosed 240 on a Q8-week basis, could we, in fact, enhance the efficacy without exacerbating the safety from what's been seen with the other antibody in this space? Thank you. Thanks for the questions, Emily. Our next question comes from Silvan Türkcan at JMP Securities. Please go ahead, Silvan. Yeah, good morning and congrats on that data. And thanks for taking my questions. Maybe if you can walk me through the details of the Tryptase, serum Tryptase reductions on slide 12. I've noticed that the 120-milligram and the 180-milligram is pooled. Does that pool mean eight-week and 12-week regimen or not? If you help me square that up and if you can maybe comment on how 12-week would look versus eight weeks. And then I have a follow-up. Yeah, thanks, Sylvan. Good morning. Yes, we pooled the 120s and the 180s because essentially it's a first dose presentation for those two cohorts, which just increases the N for those two cohorts. And the redosing, one would anticipate to see significant reductions in tryptase on redosing as well. With regards to separating out the 12-week dosing regimen, we still see rapid reduction in tryptase on first dose. And we anticipate seeing rapid reduction on second dose with tryptase reductions down to LLOQ. We simply presented today the eight weeks to show the rapid onset in all those cohorts. And we combined those two to give a bit more N. Yeah, that makes perfect sense. And then if you help me understand on the previous slide, slide 11, we have the UAS7 scores, and maybe that ties into a previous question. But you mentioned that the two patients that were potentially misdiagnosed in the 180-milligram dose cohort, they certainly may have had an impact on complete response and well managed. But here, it looks like even the UAS7 score 180 underperforms 120. If you can just help us understand how those two lines look like in terms of noise or what you're thinking around and if there's a real difference between the two or not. Thank you. Yeah, thanks, Sylvan. I think you're absolutely right. I think when we conducted a sensitivity analysis on that slide 11, and certainly when you remove the two responders, two non-responders, the lines drop precipitously in the 180-milligram line, which we're showing here in green on slide 11. So we're assured that there is a clear signal with the 180 and a dose response through 80 through the 240-milligram cohort. Great. Thank you. Thank you so much for taking my questions. Thank you for the questions, Sylvan. Our next question comes from Etzer Darout at BMO. Please go ahead, Etzer. Great. Thanks for taking a question. I just was curious as to sort of a clarification on the two patients with the alternative diagnosis. Was that specifically at the Q8W? And just trying to understand sort of the exposure efficacy relationship at the Q12W for the 180-mg dose. If you could just clarify that for me, Ed. Thank you. Yeah, thanks, Etzer. Yeah, we've communicated the two non-responders in the Q8-week 180-milligram cohorts as an example of really trying to elucidate why the 180-milligram showed deep clinical responses in some patients and then others did not, so that sort of raised our suspicions that we may have one or two patients in there. So when we went back and looked at the past medical histories and the preceding information on these patients, they probably don't have the profile of a typical CSU patient, and so when we pulled that data out in our sensitivity analysis, it was very clear that they'd had a very negative influence on the results for the 180-milligram Q8-week cohort. Got it. Thank you. And in the Q12W, any impact there on sort of any sort of alternative diagnosis? We're just trying to understand that exposure efficacy. Again, it seems with the 120 outperforming 180. And if there were sort of any commentary you could make around the Q12W cohort of patients? Yeah. Again, I think we're hostage to small Ns. And certainly, we'll be taking a look at the 180 Q12 week similarly for ensuring diagnosis. As I mentioned earlier, this is an enriched population of patients who are refractory to approved therapies. And so we potentially have brought patients in who potentially may have been misdiagnosed. That's certainly something which we discussed with all our KOLs. And that was certainly something that person pointed to immediately on seeing the 180 data, particularly when we see the biological effects with the tryptase going down to below LLOQ. Great. No, thank you for the updates today. Thank you for the questions, Etzer. So this concludes our Q&A session for today. I'll now turn it back over to Ron for closing remarks. We'd like to thank everyone for participating in the call today. We're very excited about these data and the clear path forward for us to be able to move to a registrational trial and look forward to updating you on the company and on the BEACON trial as we move forward.