Good morning, and welcome to the Connect Biopharma conference call. All participants are now in listen-only mode. There will be a question-and-answer session at the end of this call. If you would like to ask a question, you may press star one on your telephone keypad. Please be advised that this call is being recorded at the company's request, and a replay will be available on the company's website. Attending today's call are Dr. Zheng Wei, Co-founder and CEO; Steven Chan, CFO; Dr. Raul Collazo, VP of Medical Affairs; Dr. Malinda Longphre, VP of Clinical Operations; and Dr. Edward Kerwin, Medical Director, Clinical Research Institute, Allergy and Asthma Center of Southern Oregon. I would now like to turn the call over to Steven Chan, CFO for Connect Biopharma. Please go ahead. Thank you, operator, and thank you all for participating in today's conference call. Before we start, I would like to point out that there is a slide deck that accompanies today's presentation. It can be viewed using the webcast link provided on the investors page of the Connect Biopharma website. Also posted on this webpage is the press release issued earlier today announcing the top-line data of our global phase II-B trial of rademikibart in moderate-to-severe asthma. Before moving on to the presentation, I'll first note that during the course of today's conference call, company management might make forward-looking statements within the meaning of the U.S. federal securities laws regarding future events or performance of the company. Actual events or results could differ materially. We refer you to the documents the company files from time to time with the SEC, specifically the company's most recently filed Form 20-F on April 11, 2023. The company's filings contain and identify important factors that could cause actual results to differ materially from those contained in any forward-looking statements. Please note that the forward-looking statements made during this call are as of today's date, and we undertake no obligation to update them to reflect subsequent events or circumstances, except to the extent required by law. With that, I'll pass the call to Dr. Zheng Wei, our co-founder and CEO. Thank you, Steve. Thank you all for joining us today. Today's reported results from our global clinical trial in asthma come just a few weeks after the positive readout from our China pivotal trial in atopic dermatitis. I'm excited that we have now achieved two significant milestones for Connect, with rademikibart showing strong efficacy in two different indications with a significant market opportunity. Despite the fact that several biologics are currently available for moderate to severe asthma, these treatments can still be improved upon with respect to better management of control of asthma, improved onset of symptom relief, and possible reduced injection burden with IL-4 alpha blockers. With that, let me review the key takeaways for today's presentation on the top-line results from our global phase II trial in patients with moderate to severe persistent asthma, which evaluated rademikibart safety and efficacy over 24 weeks. I'm thrilled to announce that rademikibart, our anti-IL-4 alpha antibody met its primary endpoint of lung function improvement at week 12. They were observed as early as week 1 and were then sustained throughout the 24-week study. Specifically, as you will see in the data shortly, rademikibart 300 mg showed an impressive 189 mL improvement over placebo in a full analysis population, with an exploratory analysis showed an impressive improvement of 308 mL over placebo in patients with baseline eosinophils greater than 300 cells per microliter. With respect to exacerbations, we observed numerical reductions in annualized rates of exacerbation in the treatment group and that rademikibart prolonged time to first exacerbation. While not powered to show significant differences, we're excited by the strong trends in exacerbation data. Beyond the clinically meaningful improvements in lung function, rademikibart improved asthma control in patients, and the improvement was significant and occurred early in treatment and was sustained for the duration of the trial. Lastly, rademikibart continued to be well tolerated, which is consistent with previous trial results, with no new safety signals observed. Together, these results suggest that rademikibart also has a best-in-class potential in asthma and can offer a highly efficacious treatment for moderate to severe asthma. With that, I would like to hand over the call to Raul to take you through the data in detail. Raul? Thanks, Wei. It's my pleasure to review the top-line results from our phase 2 study examining rademikibart in moderate-to-severe persistent asthma. On this slide, we outline our asthma trial design, which we enrolled 322 adult patients, randomized 1:1:1 in three treatment groups. Patients received a loading dose of 600 mg of rademikibart or matched placebo control on day one, followed by either 150 mg or 300 mg of rademikibart Q2 weeks. There were 106 patients in the 150 mg group, shown here in blue, 108 in the 300 mg group in green, and 108 in the placebo group in gray. The treatment period was 24 weeks, with an 8-week follow-up period. The primary endpoint was FEV1 change at baseline at week 12. Additional data included FEV1 at all other time points, data related to asthma exacerbations, as well as patient-reported outcomes, biomarkers, and safety. With respect to inclusion criteria, moderate to severe uncontrolled adult asthma patients were enrolled who were also utilizing a medium- to high-dose inhaled corticosteroid in combination with at least one additional reliever or controller. Patients' asthma symptoms were not well controlled, with an Asthma Control Questionnaire score of greater than or equal to 1.5 and at least one documented asthma exacerbation in the previous 12 months. Here we see the patient disposition of the global Phase II-B study. Randomization was well-balanced, with 322 patients randomly assigned to one of the 3 groups. In the full analysis set, there were 108 placebo, 106 patients received rademikibart 150 mg, and 108 in the rademikibart 300 mg group. Discontinuations due to adverse events were low in each group, and COVID-19 logistical issues and site closures had minimal effect on the conduct of the trial, with 91% of placebo patients completing 24 weeks of treatment, 89% in the 150 mg group, and 83% in the 300 mg group. Overall, the number of discontinuations was within the limits of pre-study estimates of 15% attrition over a 24-week period. On the next slide, we can see the ethnic and racial makeup of the trial participants, as well as the geographic distribution of sites and patients in the study. The two largest racial groups were White, comprising about 75% to 80% of the population, and Asian, accounting for roughly 15%. On the right side of this slide, we can see that the majority of clinical sites were located in the United States, with two-thirds of patients coming from this region and another one-third from Europe and Asia. The initial demographics of the asthma population, including age and female representation, aligned with the expected baseline values and were evenly distributed across the trial groups. Importantly, approximately 75% of the patients had baseline eosinophil cell counts of greater than or equal to 150, often indicative of eosinophilic asthma. Additionally, at baseline, FEV1 values averaged approximately 1,900 milliliters, with a percent predicted FEV1 level of around 64% and an ACQ score of 2.7, all indicating a moderate to severe level of asthma severity within this population. Now for the exciting part. Let's talk about some data. First, we'll look at the primary endpoint of pre-bronchodilator FEV1 change from baseline at week 12. In this graph, it is evident that both the low and high doses of rademikibart resulted in significant enhancement in pulmonary lung function among patients. This improvement is supported by a markedly increased FEV1 values. The rademikibart 150 milligram group demonstrated a notable improvement in FEV1 of 235 milliliters over baseline levels at week 12, and an impressive 284 milliliter improvements in the 300 milligram group. When compared to the change from baseline levels in the placebo group, rademikibart group improvements in FEV1 of 140 and 189 mL, respectively, over placebo at week 12 were highly statistically significant. To put these data into context, for individuals with respiratory conditions, even a relatively modest increase in FEV1 of 100 to 150 milliliters can be clinically meaningful for lung function and can lead to noticeable improvements in daily activities, reduce symptoms, and enhance quality of life for some patients. Changes in FEV1 of 235 or 284 milliliters are exciting as a treatment. Now let's look at these improvements in FEV1 over time. These data are very exciting, as they show that the rademikibart treatment, again, with either the low dose of 150 milligrams or the 300 milligram high dose, makes a clinically meaningful difference in lung function as early as one week following treatment. And just as importantly, responses are sustained for the duration of the 24-week study. On this slide, we can see that in the low-dose rademikibart group, 96% of the 24-week improvement and an impressive 195 milliliter difference from placebo is realized by week one in all comers, regardless of eosinophil baseline levels. You can start to see why we're very excited about these data points. On the next slide, if we examine what happens to FEV1 values in patients with high eosinophil counts, even greater changes from baseline levels are realized. On the left side of the slide is shown week 24 data for the full population we just saw on the previous slide. On the right side, we have stratified the patient population by eosinophil level and are presenting data for those who have greater than 300 eosinophil cells per microliter of blood at baseline. Like many other biologics, rademikibart works better in patients with Th2-mediated airway disease. This is not surprising, given the mechanism of action of rademikibart as anti- IL-4 receptor alpha blocker, which plays a role in regulating the differentiation and activation of various immune cells, including the eosinophils. On the next slide, we see improvement effects of rademikibart treatment on the mean percent predicted FEV1 values from baseline to week 12. This value is important because it represents the percent of total breath patients should be able to breathe. In other words, if we take a patient from our placebo group who can breathe at only 61% of their predicted ability based on factors like gender and age, then this person is considered to have moderately obstructed airway, and this is seen in this orange area and may be classified as having moderate to severe asthma. When patients percent predicted FEV1 increases, they move more toward a mildly obstructed airway in the green area and a more mild asthma severity. When we examine the effects of rademikibart treatment on percent predicted FEV1 improvement, both the low dose and the high 300 milligram dose showed improvements at the group level from baseline to week 12, with an 8% improvement over placebo with the 150 milligram low dose and a 9% improvement with the higher dose. This 9% improvement for the group moves more people from the moderately obstructed orange range into the mildly obstructed range in green and moves patients into a more mild to moderate range of asthma severity. Equally exciting for us is the changes that we're seeing in patient-reported outcomes, and on this slide, we present the change from baseline data for the asthma control questionnaire. We started to see numerical separations again as early as week 1, with statistical distances occurring from week 2 going forward. At week 24, the change from baseline for the low dose group is 1.17 and 1.09 for the high dose group versus 0.76 for the placebo. This is a difference of 0.41, 0.33, respectively, for each group. So what about exacerbations? The next slide demonstrates some exciting trends in reduction in exacerbations. Although this phase 2 study was not powered to detect differences in exacerbations, the fact that's corroborated by our patient population that had just over one exacerbation in the last 12 months prior to screening. Nonetheless, even with a low number of exacerbations, rademikibart prolonged the time the first severe asthma exacerbation was seen on the left side of this slide, where both treatment groups are trending towards separation from placebo. Additionally, when we examine the annualized exacerbation rate for the population, it was noted that the exacerbation rate was cut in half with rademikibart treatment from 0.56 exacerbations per year to 0.24 or 0.3 exacerbations per year for the low and high dose groups, respectively. As you can see from the numbers below the graph, overall exacerbations were low in this study. Considering that we did not enrich for previous exacerbations and that baseline exacerbations were minimal, these data are quite exciting as those strong trends are encouraging for phase III trials going forward. While we need to be cautious when comparing across trials, we wanted to put some of the lung function data into perspective for you. This slide compares published phase III data from several biologic asthma medications with FDA approvals in the last 10 years with the current WW02 global trial data that we revealed today. In order to make the comparisons as similar as possible, we use pre-bronchodilator FEV1 adjusted for baseline, since, according to the American Thoracic and European Respiratory Societies, this endpoint has been carefully standardized and is a measurement that allows comparison of the study population with most other studies. On the left side of the slide, we look at the full analysis population for several biologic programs and see that rademikibart at 300 milligrams gets a greater improvement in change from baseline FEV1 when adjusted for placebo rates. Similarly, when the population is enriched for patients with eosinophil counts greater than 300 at baseline, rademikibart continues to show greater improvement in change from baseline FEV1 values than other biologic programs with approved asthma indications. Additionally, these rademikibart data are demonstrated early at week 12 compared to later time points for many other programs, and rademikibart's 24-week data are slightly improved from week 12, as we were shown earlier. The next slide demonstrates these differences in the form of a table with more information around each study and each asthma program. It is clear to see from the red box why we're excited to share these data with you and the healthcare community, as we see early responses after only 1 week and lung function improvement is impressive in the full population as well as the eosinophil-enriched population when compared to other FDA-approved biologic medications for the treatment of moderate-to-severe asthma. Now turning our attention to safety data. When looking at the safety across both the high and low doses, rademikibart continued to be well tolerated, with no apparent new safety signals, with treatment out to 24 weeks in patients with asthma. There were few serious adverse events reported to be related to study drug, and the rates of serious adverse events were similar across groups. Discontinuation rates were low throughout the study period, as were hospitalizations and ER visits due to asthma exacerbations. Overall, the AE profile appears consistent with previous rademikibart trials. With that, I'll hand the call back to Wei for closing remarks. ... Thank you, Raul. To conclude today's presentation, similarly to what we reported a few weeks ago, rademikibart has now shown for the second indication, its best-in-class potential as the next generation anti-IL-4 alpha antibody. Rademikibart met its primary endpoint with robust significance, showing an improvement of up to 190 milliliters over placebo in FEV1 at week 12. The improvements were seen as early as week 1, when other biologics showed partial improvement starting at week 2 or 4. Also, the improvements achieved were sustained through week 24. These improvements were even more pronounced when we stratified the data based on baseline eosinophil level, showing over 300 milliliters of improvement in FEV1 over placebo in patients with the eosinophil count greater or equal to 300 cells per microliter. Furthermore, rademikibart led to an approximately 9% increase in mean percent predicted FEV1, meaning that patients that were previously considered to have moderate airway obstruction now have a mild obstruction. When it comes to exacerbations, we saw numerical improvement in annualized exacerbation rate and that rademikibart prolonged the time to first exacerbations. When we looked at patient-reported outcomes, rademikibart significantly improved patient-reported asthma control, with significant improvement starting at week 2 and continuing through week 24. In terms of safety, rademikibart was generally well tolerated in patients with moderate to severe asthma. As for next steps, these results indicate further clinical development is warranted, and that we plan to discuss these results with the FDA in an end-of-phase II meeting. With this, I'd like to ask Dr. Edward Kerwin to provide some observations on the data reported today. Dr. Kerwin, thank you for joining us today. Yes, thank you very much, Wei, and all who are attending. Yes, so what I'd like to say is that asthma continues to be a very prevalent atopic-driven disease, what we call a T2 disease, and it's one of the diseases that is becoming more common as time goes by in industrialized countries. We, there is a knowledge that some 15% of asthma patients just can't be well controlled and stay uncontrolled even when they're on conventional therapies. And that's why new targeted therapies like rademikibart look very promising. Rademikibart actually blocks early-stage cytokines in asthmatic T2 inflammation, and it specifically blocks both the IL-4 and IL-13 receptors, and that mechanism looks very promising. So this, these phase II-B study results really could not be more exciting. The primary endpoint of airflow improvement or FEV1 improvement was met with high levels of statistical significance. And as you've seen from the graphs, the change took place within about a week of starting dosing, which really is quite gratifying. The improvements in FEV1 were confirmed by similar improvements in daily peak flow and daily FEV1. And also, you've seen the ACQ-6 scores improve, which is, that's a real goal for us, is to get asthma patients feeling better control in their day-to-day activities and their lives. And then the trend toward improvements in exacerbations is exactly what we like to see with these new targeted therapies to help asthma. It, although this study was not the right kind of study to show a statistical improvement in asthma exacerbations, certainly it's our goal to prevent these steroid burst exacerbations. Finally, I'll just say the safety data continues to look quite good with rademikibart, with no real concerning adverse events found. So I find these Phase II-B data quite exciting, and it shows a potential for a new medicine that could even be best in class to treat uncontrolled asthma. So thank you very much, Wei, and I'll turn it back to you. Well, thank you, Dr. Kerwin, for the insightful remarks. So with that, let me hand this back to the operator for Q&A. Thank you. Ladies and gentlemen, the floor is now open for questions. If you would like to ask a question, please press star one on your telephone keypad at this time. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. Today's first question is coming from Thomas Smith of Leerink Partners. Please go ahead. Hi, this is Matt Sarnecki on for Tom Smith. Congrats on the positive data. We have a couple questions. So first, how's the patient population in this study compared to other late-stage trials in asthma? And focusing on the improvement on exacerbation rates, how are these results compared to dupilumab or other approved treatments? ... Thank you so much for the question. Yeah, so, let me just start briefly, and then we have, Raúl or Malinda, to provide some information as well. You know, the way I look at this is that this is really a well conducted study with patient population in terms of geographical distributions and race. It's really where it should be with two-thirds of patients enrolled in the U.S. and include Asia as well as Europe. And so if you also look at what we just presented, or Raul just presented with demographic information, as far as the FEV1 at baselines and other parameters, this is where you want to be. So I think it's a typical well-rounded study of this type in moderate to severe and persistent asthma. So let me maybe turn this over to Raul to provide additional information. Raul? Yeah. So, thanks for the question. You know, in terms of the exacerbations, you asked how this trial is different than other trials. You know, I would say that the largest difference in this particular trial is a Phase II-B trial versus Phase III, where the primary endpoint would be the rates of exacerbation. You know, we were looking at FEV1 as a primary endpoint, so we did not enrich the patient population for exacerbations. In this trial, in the 12 months previous to enrollment, the patients only had to have one documented asthma exacerbation. In many of the Phase III trials, that's usually two exacerbations or more. When you look at some of the Phase III trials, you'll see that those trials at baseline have about three exacerbations in the previous 12 months before enrollment. So that's really the difference. When you start to look at the actual data, and you start to see the trends of exacerbations being cut in half, with the treatment groups, I think that's very similar to what you're going to see when you go back and look at the Phase III trials with dupilumab as well. Yeah. Thank you, Raul. And just to add, just to add a little bit more to what Raul just said, it's actually pretty well documented. And there's a, there's a very good publications from our scientists from Sanofi, looking at the degree of exacerbation reduction based on the number of exacerbations of patients in the previous year before enrolling the study. And there is a, there's a good correlation. So in asthma, as an endpoint study, you definitely want to have, you know, over two and up to three exacerbations per year. In this particular study, I believe we are, we are basically one exacerbation. It has to do with the fact that, you know, during the pandemic, these, you know, many of the triggers that cause exacerbations were not there when people stay home and have less exercise, et cetera. But, probably this is where perhaps Dr. Kerwin can provide additional insight as well. Yes. Well, I would agree with what Wei and Raul have said. The trial population here was well selected for phase IIb. They all had had one exacerbation in the last year, but it was not as severe a population as in some trials. But even with baseline FEV1 63%, baseline ACQ about 2.7 and 1.2 exacerbations a year, nevertheless, in this fairly small study, almost all of the designated primary and secondary endpoints were met. And so this is impressive data. Dupilumab, in its week 12 FEV1 data, showed about 140 mL improvement in FEV1, but rademikibart is showing up to 189 mL improvement with a 300 milligram dose. So I feel the study population was well selected. It's remarkable that good results were seen even though it was conducted during the pandemic. Yeah. And just, you know, scientifically, this is very interesting because, if you look at the more kind of T2 type Th2 subpopulation in our study that Raúl just presented, in looking at the eosinophil counts over 300 cells/μL, you know, the FEV1 improvement, it's just, you know, well over 300 mL over baseline. That's just extraordinary. So I think that, you know, this, this trial really provides us with good information on designing, you know, phase III studies with different endpoints. So I hope that that- Got it. Have you answered the question? Yeah, that's very useful color. On the Phase III, the potential Phase III development, do you plan to secure a partner before initiating a trial? So, you know, we continue to have our discussions with- ... potential partners on this asset. And, you know, it includes different indications now. So, you know, we just have impressive data just a few weeks ago from the Q2W, Q4W dosing in the atopic dermatitis, which showed equally impressive efficacious in their study. And this one will look at high dose and low dose. So in terms of business development and plans for phase III, I think the first step for us is to, you know, start a process of having a discussion with the FDA. And then, you know, the planning for future study and BD discussion can go simultaneously, right? With this impressive data set that we have with this and AD, I think we've opened up many opportunities in this different area of activities. Got it. I have one last question for Dr. Kerwin. So like in your practice and with the availability of dupilumab, like what's the current unmet need in asthma treatment, and how can rademikibart potentially fill the gap and fit into the current treatment paradigm? Well, thank you again for asking that question. Yes. You know, we, as I explained briefly earlier, for whatever reason, as our society's gotten more industrialized, allergic atopic diseases, which not only include asthma but allergic rhinitis, atopic dermatitis, eosinophilic colitis, and sinusitis, these diseases seem to be becoming more and more common. And I, I sort of explained earlier that even with conventional treatments like inhaled corticosteroids and LABAs, not every patient really gets great control. So I, I do find it very exciting that new biologics, that target cytokines active in T2 inflammation, look to be showing surprising amount of efficacy, and a great degree of safety in patient populations. Now, dupilumab is dosed every two weeks, which can be cumbersome, but these medicines are well-designed for patients to administer at home. And rademikibart seems to be as effective, at least at this stage of studies, as any of the biologics that have come out for asthma. There's at least six biologics, you know, approved for asthma at this time. So I, I feel we are in a world where patients don't only have asthma or only have atopic dermatitis, but they might have food allergies, choking from eosinophilic esophagitis. And the ability of this kind of, you know, every two week or even potentially every four week injected therapy to improve the whole patient and to keep them out of the hospital, and prevent these systemic steroid exacerbations, I think it's quite promising. These kind of treatments do need to become globally available. That would be very exciting, and of course, they, we would be excited if they could be given a little less often than every two weeks, but those data still will have to be found. So I, I feel, this new rademikibart data are really some of the best data we've seen for asthma biologics, and that's in a crowded area. There are, you know, quite a number of biologics for asthma, but rademikibart, excuse me, looks like it may be one of the most efficacious. That's very helpful. Thank you so much. That's it from us. Thank you. At this time, I would like to turn the floor back over to Dr. Zheng Wei for closing comments. Thank you. Again, thank you all for joining today's call, and we want to thank our team, the clinical development team, and the doctors and patients who participated in this program. We thank you for all the efforts that generate this very exciting data set that we reported today. We look forward to providing future updates and have a great day. Ladies and gentlemen, thank you for your participation. This concludes today's event. You may disconnect your lines or log off the webcast at this time and enjoy the rest of your day.