Welcome to Kezar Life Sciences 2022 top-line data presentation of the MISSION Phase 2 clinical trial. Today's presentation will be followed by a question and answer session. I would now like to hand the call over to John Fowler, Chief Executive Officer and Co-founder of Kezar Life Sciences. Go ahead, John. Thank you for the introduction, Alex, and good afternoon, everyone. Thank you all for joining us today as we present the top-line data for MISSION, our clinical trial investigating zetomipzomib for the treatment of lupus nephritis. Here are our disclaimers. Now, the second quarter has been very busy for us, having completed not one but two clinical trials. As you read from our press release, we have exciting, positive, and meaningful results to share with you today, so I'm not gonna delay jumping into the MISSION trial data. Here is the outline for the next hour. Kezar just celebrated its seventh birthday, and it's been a true pleasure to work with my dear friend and co-founder, Chris Kirk, on this important journey. Kezar is now over 75 employees strong, and I'm very proud of what we've accomplished with the MISSION trial, but also the infrastructure that we've built that will allow us to successfully execute multiple development programs with zetomipzomib. We also have a very interesting second clinical asset, KZR-261, which is another small molecule with a unique mechanism of action that is currently in a phase 1 clinical trial for the treatment of solid tumors. Underpinning both of our programs is our strong balance sheet, and we're well-positioned to continue planning our next studies for zetomipzomib and invest in our pipeline. I could not be prouder of the team that we've assembled at Kezar. Creative, compassionate, and incredibly hardworking. The global pandemic presented strong headwinds, yet everyone persevered. We wouldn't be here today without our amazing investigators, advisors, and of course, most importantly, the patients who supported this trial. We know it wasn't easy, but your commitment and ability to overcome the challenges of joining a clinical trial during the pandemic were nothing short of heroic. Now, just a few words on the remarkable mechanism of action in our lead program. As many of you know, zetomipzomib is a first-in-class small molecule that inhibits the immunoproteasome. The immunoproteasome, a unique form of the proteasome, is expressed in all three immune effector cell types shown here, and we've demonstrated that inhibiting it has potent anti-inflammatory effects, in part because it acts on all three effector cells simultaneously, resulting in immunomodulation of both innate and adaptive immunity. As a result, there's incredible potential for zetomipzomib to be a meaningful therapy that works via immunomodulation rather than immunosuppression, and that avoids off-target toxicities that can be associated with current therapies. Today is gonna focus on the data from our MISSION study, so sadly, we won't have time to delve into all the remarkable differentiating attributes of zetomipzomib, its incredible specificity and ability to avoid other receptors in the body, or why we think it's a pipeline in a drug for more than 20 potential indications of autoimmune and other immune-mediated diseases. Once again, thank you for joining us today. I will now turn it over to our Chief Medical Officer, Dr. Noreen Roth Henig, who will share the top-line results of the MISSION Phase 2 study with you. At the end, we'll also be joined by our Chief Scientific Officer, Chris Kirk, who will join Noreen and I for the Q&A session. Over to you, Noreen. Thank you, John, and hello to everyone on the line. It is my absolute pleasure to be here with you today and to walk you through the top-line data from the MISSION study. As you will see, the results are quite supportive that zetomipzomib is an active agent and really opens the door to thinking about a shift in the treatment paradigms of the care of patients with lupus nephritis and beyond lupus nephritis into other autoimmune and immune-mediated diseases. The MISSION study to look at zetomipzomib in patients with lupus and lupus nephritis was conducted in two parts. Previously, we shared that MISSION Phase 1b demonstrated safety, tolerability, and preliminary efficacy in patients with lupus with and without lupus nephritis. This slide summarizes the key learnings from the Phase 1b portion. For those of you following the zetomipzomib story, you will recall two patients from the MISSION Phase 1b study who had lupus with manifestations of active lupus nephritis showed a brisk reduction in the protein in their urine while on this early study. Healthy kidneys do not typically leak protein into urine, so a significant amount of protein in the urine, defined by the ratio of urine protein to creatinine or UPCR, is a sign of an inflamed or damaged kidney. Zetomipzomib also reduced important signs and symptoms of non-renal lupus. Before I get to what everyone is waiting for, I want to remind you of some key features of the second part of the MISSION study. The MISSION Phase 2 investigated the use of weekly zetomipzomib in refractory or difficult to treat patients with active lupus nephritis. Despite being on stable background therapy, these patients had unacceptably high levels of protein in their urine. We added zetomipzomib 60 milligrams weekly to their stable therapy. It's important to note that these patients did not receive standard induction therapy as part of this trial. Thus, the only new addition to care is zetomipzomib. Here are the highlights of our top-line results. Zetomipzomib achieved clinically meaningful overall renal response in refractory or hard to treat LN patients. 21 patients enrolled, and 17 completed the study through end of treatment at week 25, which is the defined time for the primary endpoint. Of those 17 evaluable patients with active lupus nephritis, 11 of 17 or a full 65% achieved a 50% or greater reduction in proteinuria within six months. This is a strong, clinically meaningful, and rapid response, and it occurred without the addition of induction therapy. Six of 17 patients not only reduced their proteinuria by 50% or more, but the UPCR fell to 0.5 or less and achieved a complete renal response. In the month following treatment, this response deepened, suggesting that the kidneys continue to heal in the absence of inflammation. The clinically meaningful reductions in UPCR were achieved with less prednisone than what the patient started on, as well as stable doses of background immunosuppressive therapies. Also important to the care of patients with lupus nephritis, we observed reductions in other manifestations of lupus disease activity and improvements in key biomarkers, suggesting that zetomipzomib as a potent inhibitor of the immunoproteasome could be a meaningful therapy for patients with lupus, systemic lupus erythematosus. Now that you've seen the upshot of the MISSION trial, let me walk you through how we got there. This slide outlines the study schema for MISSION Phase 2, an open-label trial to evaluate the efficacy and safety of zetomipzomib in patients with active lupus nephritis. Our target enrollment was 20, and we enrolled 21 patients. These patients had active LN, histologic Class III or IV, ± Class V, and a UPCR greater than one, indicative of active nephritis. They received zetomipzomib 60 milligrams subcutaneously once weekly for 24 weeks. The first dose received was 30 milligrams, which we found is an important way to tolerize patients and mitigate some adverse events described in earlier trials. End of treatment was assessed at week 25, one week following the last dose. There is also an additional 12 weeks safety assessment, which is the period between end of treatment and end of study. Today, we are sharing the top-line results, which includes all patients who achieved the end of treatment milestone at week 25. MISSION Phase 2 remains an active study with some patients still yet to complete the 12-week safety assessment phase. One key difference between the MISSION study and recently published interventional trials in LN is that patients did not receive standard induction therapy with IV corticosteroids, cyclophosphamide, or high-dose MMF at the start of this study. Zetomipzomib was added to whatever stable medications the patient was on, and we documented the addition of zetomipzomib as the only change in therapy. In addition, we did not have a protocol-mandated taper of glucocorticoids, but at their discretion, investigators were encouraged to lower the doses of prednisone or equivalent, as well as any doses of other background therapies if the patients were improved and able to reduce their steroid use. Now, let's look at endpoints. The primary endpoint was the number of patients with greater than or equal to 50% reduction in UPCR after 24 weeks of zetomipzomib treatment compared to baseline. Clinically meaningful secondary endpoints were patients who received a complete renal response and partial renal response. Our protocol definitions are shown here. For the purpose of defining partial renal response, we use the definition of greater than 50% reduction in UPCR and a change in absolute UPCR is the more conservative of the definitions. This is also the overall renal response rate and our primary endpoint. Preservation of the estimated glomerular filtration rate and no use of prohibited medications is also part of this definition. For a complete renal response, patients had to have a UPCR less than or equal to 0.5, as well as prednisone use less than 10 milligrams per day. When we get to the study results, you will see the overall response rate and the complete renal response rate. As you can see here, we enrolled 21 very typical patients with lupus nephritis. The study population is mostly young women with the mean age of 35 years who have suffered with lupus and lupus nephritis for a long time. The patients were diagnosed with lupus for approximately eight years and lupus nephritis for a mean of approximately three years. A mean baseline of UPCR of 2.6 indicates these patients had significant renal disease, especially considering these patients were already on a steroid plus at least one immunosuppressive agent. The mean dose of prednisone or prednisone equivalent was almost 20 milligrams per day. These patients were cared for with well-accepted maintenance therapies of MMF, hydroxychloroquine, or azathioprine, in addition to oral corticosteroids. As you can see, by definition, these patients were refractory to best care because they continued to have signs of active lupus nephritis. Now, let's look at patient disposition. We enrolled 21 patients, each represented by a bar here. 17 patients completed the study through week 25. Four patients exited the study early. There were generally no difference in the profile of the patients who exited the study early from those who remained through to the end. There was also no singular cause for patients exiting the study. One left due to an unrelated serious adverse event at week 18, and the other three left prior to week 13 due to related but not serious adverse events. Our rate of completion exceeded our expectations, given that the study was conducted during the COVID pandemic. Let's move on to results. The zetomipzomib achieved an overall renal response of 65% and a complete renal response in 35% of patients at week 25. This is a very clinically meaningful result. The bar to the right is week 25, where 11 of 17 or 64.7% of patients experienced a greater or equal to 50% reduction in their UPCR. A complete renal response was achieved in six of 17 patients. If you look to the bar at the left, you can see that the reduction in proteinuria could be seen as early as week 13. 10 of 17 patients had experienced a greater or equal to 50% reduction in their UPCR, with 4 of those patients achieving a complete renal response. If you look across this slide, you see that the reduction in proteinuria deepens with time and more patients achieve a clinically significant renal response. Next, I'm going to share with you results at week 29, four weeks following discontinuation of zetomipzomib. As a way of background, in preclinical studies and in earlier clinical studies, we noticed two important properties of zetomipzomib. One, unlike many treatments for lupus nephritis, there is not an immediate rebound of proteinuria when the drug is discontinued. Two, the benefit we observe as reduction in proteinuria is the result of decreased inflammation and a measurable form of healing once inflammation is quieted down. Now look to the right at week 29. You see further reductions. What happened in this study when zetomipzomib was discontinued? As you can see, complete renal responses are maintained, and additional overall renal response occurred. At the far right of the slide, you see week 29 data measured four weeks post-treatment with zetomipzomib from all 17 subjects. At week 29, 16 of 17 patients, or 94%, achieved a 50% or greater reduction in proteinuria, and the six patients with a CRR maintained this benefit. This graph further illustrates the deepening of the response as many patients who had also achieved a greater than 50% reduction continued to lower their UPCR. At the end of study, which will occur in July, we will analyze the full data set from the 12-week safety follow-up period between end of treatment and end of study and share our observations with you later in the year. For those of you familiar with our interim results presented in November, we labeled 1 patient as having no response at week 25. Interestingly, with additional time by week 29, this patient experienced a reduction of UPCR by greater than 50%. Again, this is consistent with the idea that once inflammation is quieted down, kidney healing begins, and the result of the healing is reduced proteinuria. The slide you've been staring at for a little bit here is another way of looking at the mean and median reductions in UPCR. As you can see, it goes down steadily over the 24 weeks and including the week 29. There's a deepening of the response. As you can see, the median UPCR decreases steadily such that at week 25 it is below one, and at week 29 it's actually below 0.5. As you can see, the box plots also really tighten up, suggesting that the variability in the UPCR is going down as patients are healing. This is quite a remarkable response with just six months of therapy in a patient group refractory to standard of care therapies. Now, the reductions in proteinuria occurred with less than half the baseline corticosteroid use. In our protocol, investigators were encouraged to taper glucocorticoids if they felt their patients were doing well, but it was not protocol mandated. With the addition of zetomipzomib, many investigators proceeded to lower the dose of corticosteroids. The net result was a mean dose that is 53% of starting doses. The International Society of Nephrology recommends a dose of 7.5 milligrams daily or less for maintenance, and the difficult to treat patients enrolled in this study were not able to achieve that with their usual care prior to entering into the study as their baseline dose was closer to 20 milligrams per day. Despite their long history of prednisone use, by week 13 the mean dose was half that at approximately 10 milligrams per day, and by week 25 at the end of treatment period the mean prednisone dose was 9.1 milligrams per day. Four weeks following discontinuation of zetomipzomib, further decrease in prednisone occurred, and the mean prednisone dose was 8.6 milligrams per day. Other background medications remained stable as well, and although none were discontinued. Now we also want to ensure that the overall function of the kidney is maintained. Here you see what I consider to be the most boring slide in our entire presentation, and I mean boring in the very best way. All subjects maintained their eGFR, a measure of overall kidney function during the course of the study. Let's look outside the kidneys to signs and symptoms of systemic lupus erythematosus, not just the manifestation of lupus nephritis. Here too, you will see a reduction of SLE disease activity. We use seven different instruments to look at other symptoms of active lupus. There is a nice reduction in disease activity across all seven scores, including the SLEDAI-2K, physician and patient assessments of disease activity, and the HAQ pain scale. More meaningful than any of these these scores taken in isolation is the fact that they all move in the same direction and tell the same story. Patients are just feeling better, which is much more important to patients than reductions in proteinuria. It also suggests that zetomipzomib has the potential to be used to care for all manifestations of lupus. In addition to signs and symptoms of lupus, we looked at key biomarkers of lupus and lupus nephritis activity. Again, all indices are moving in the direction of reduced inflammation. Of 12 patients with abnormal anti-double stranded DNA at baseline, 10 improved, and of those, five normalized at end of treatment. Complement, which can be low in patients with active lupus nephritis and lupus, moved toward normal in patients who had low levels at study entry. Importantly, we found no negative changes in serum markers. There was also no change in cell counts consistent with absence of immunosuppression. This finding encourages us that zetomipzomib may be able to be used chronically without the need for monitoring. Let's move on to safety. We included all 21 enrolled patients in our safety analysis. With increasing experience with zetomipzomib, our safety and tolerability profile continues to be favorable. Treatment emergent adverse events were generally mild to moderate, less than grade two, consistent with previous reports. We continue to observe that patients can experience a constellation of symptoms with initiation of zetomipzomib that attenuates or completely goes away with repeated administrations. These symptoms can include an injection site reaction, pyrexia, headache or nausea with or without vomiting. While at least one of these symptoms was experienced by most patients, they generally did not lead to study discontinuation and patients continued to use the drug. In early studies, there was concern raised about zetomipzomib provoking vomiting. In the MISSION Phase 2, with over 440 doses of zetomipzomib administered, the per dose rate of vomiting was approximately 3%. We anticipate that in the future, when patients are self-injecting zetomipzomib at home, these symptoms will become even more manageable. Injection site reactions continue to be the one adverse event that patients are likely to report at any time during the study. We believe that these are due to a direct effect of immunoproteasome inhibition. There is no evidence of immunologic or vasculitic reactions. Now, since the interim analysis presented in November, there have been no additional serious adverse events. Let me review those for you. In the middle panel, you see the two patients with serious adverse events that were previously reported. One patient experienced three serious AEs, including worsening pulmonary arterial hypertension, acute kidney injury, and a urinary tract infection. These were deemed unrelated to zetomipzomib, but the patient was exited from the study for additional care. One patient experienced a severe migraine headache that was attributed to study drug administration. This patient temporarily held doses and then resumed treatment, successfully completed the study and did have a greater than 50% reduction in UPCR by week 25. On the right-hand side of the slide, we list the reasons for early termination from the study. One is related to the previously mentioned SAE of worsening pulmonary arterial hypertension. One was reported in November as unrelated and believed to be due to the burden of the trial participation during COVID. However, it is now attributed to an injection site reaction and considered related. One patient who received two doses in eight weeks reported asthenia, which means a generalized malaise and feeling badly, and the last patient to terminate early reported an increased reticulocyte or red blood cell count. Last but not least, what we are not seeing is also important to us. We found no opportunistic infections, laboratory abnormalities, or suppression of immune cell lines. This is consistent with our findings in other studies so far and supports the potential for immunomodulatory action of zetomipzomib, with no off-target immunosuppressive effects observed. In a difficult to treat patient population, the patients with active lupus nephritis, zetomipzomib 60 milligrams subcutaneously weekly achieved its primary endpoint of reducing proteinuria by greater than 50% or more and overall renal response of 65%. By week 25, 35% of patients achieved a complete renal response. This therapeutic effect was achieved without induction therapy and in fact occurred with less prednisone and stable background therapies. The reduction in proteinuria deepens even after discontinuation of zetomipzomib in most patients, consistent with an interruption of inflammation and kidneys able to heal itself. Zetomipzomib appears to control more than just the lupus nephritis. Patients just feel better. The safety and tolerability profile remains quite favorable and consistent with an agent which is immunomodulatory rather than immunosuppressive, and which does not have any recognized off-target effects. The use of a step-up dose of 30 milligrams appears to tolerize patients, and thus patients were able to take zetomipzomib for six months consecutively. We are very encouraged by these results and excited to move quickly to our next studies. With the results of this study in hand, we are eager to advance into late phase trials. Let's talk a little bit about that. While we did include difficult to treat patients in the MISSION study, going forward, we will be positioning zetomipzomib as earlier therapy for all patients with LN and possibly systemic lupus erythematosus. When we think about zetomipzomib, a first-in-class inhibitor of the immunoproteasome, we of course, are excited by the results of this trial. We also look at the many favorable attributes which position it well as a meaningful and useful therapy for the treatment of lupus nephritis, as well as potentially many other autoimmune diseases. Here we list some, but not all of these attributes, including immunomodulation rather than immunosuppression, a short half-life, no off-target effects, no teratogenicity in preclinical studies, which is important for women of childbearing potential, no predicted drug-drug interactions, an overall favorable safety and tolerability profile, no need for monitoring, and benefit across multiple organ systems. What's next? Zetomipzomib is well-positioned for use as a chronic therapy for the treatment of lupus nephritis. Back in November, with the interim data in hand, we began working on our registration program. While we still need to complete MISSION, which will happen later this summer, we can make considerable progress toward the next studies. We will consult with the regulatory authorities here and across the globe, and we are excited to push ahead. Our goal is to design an efficacy trial that has the best opportunity to demonstrate the unique attributes of zetomipzomib, a truly differentiated therapy. Zetomipzomib has the potential to be both steroid-sparing and be used without induction therapy, both which would be an important benefit to patients. Thinking of the future, because there is positive impact on extra-renal manifestations of systemic lupus, it is possible to imagine that zetomipzomib could be the cornerstone of therapy for all patients with lupus. We also recognize that the autoimmune diseases we are interested in affect young people who are trying to work and care for their families while dealing with their disease. As such, we will be commencing educational initiatives and programs to help reduce the burden of participation in clinical trials. We will provide fuller guidance by the end of the year. Like John, I also want to extend my sincere gratitude to the investigators and patients who participated in MISSION. It's a great community to work with, and we are excited to continue to pursue better therapies for patients with lupus nephritis. Thank you so much for joining our call today. I will now be joined again by John and by Chris for final remarks, followed by a question and answer period. Thanks so much, Noreen. We've reached the conclusion of today's event, but at Kezar, we're not done. The results we just shared with you today give us the unequivocal confidence to move ahead in the late development of zetomipzomib, and we look forward to providing updates by the end of this year, as Noreen said, following completion of the MISSION trial and conversations with regulatory authorities. Without further ado, we're happy to move into question and answer, and I'll turn it to you, operator. Thank you. We will now go into the question and answer portion of today's webcast. In order to be mindful of time, please try to limit yourself to one question each. To ask a question, please use the Raise Hand feature in Zoom. Our first question comes from Derek Archila with Wells Fargo. Derek, please unmute yourself and ask your question. Hey, guys. Congrats on the data. Very well done. Just, you know, one major question, then maybe one quick follow-up. On the first question, maybe can you just put into context, today's data relative to voclosporin's? Obviously, you highlighted some of the differences in the patient populations, but that would be helpful. Noreen, just your last comments there in terms of, like, the next steps in lupus nephritis. I guess, what would that trial look like? Would that be a traditional induction type therapy, or would you look to do this similar kind of indolent lupus nephritis patients, a trial in that population? Thanks. Great. Thanks for the questions, Derek. You know, when we look at the results that we achieved in this trial and compare it across the recently approved and published trials of voclosporin as well as, Benlysta and Gazyva, we are very, very pleased with our results because essentially we achieved very, very similar results as voclosporin, but did so without any induction therapy. That's both a benefit for patients, and it's also a clear sign of the potency of zetomipzomib, we believe. With respect to our next trials, we are looking to show off zetomipzomib to the best of our ability, and we do believe that can be achieved without induction therapy. However, it will require a discussion with regulators since induction therapy has been a portion of recent approvals. Time will tell what our next studies will actually look like, but we do believe that if we can't get there in one step, we will eventually get there in more than one step to show that we can use zetomipzomib without induction. Excellent. Thank you, and congrats again. Thank you. Our next question comes from Matt Phipps from William Blair. Matthew, please unmute yourself and ask your question. Hey, guys. Congrats. I mean, awesome to see data get that much better even from a strong interim. Wondering how many patients actually achieved a PRR? Then also, you know, with the median UPCR getting below 0.5, it seems like there, you know, must have been some other reason why you didn't almost have more CRRs, just given the criteria, maybe it was another factor. Yeah. Thanks for the question. We report out the overall renal response rate and the complete renal response, and so by definition, the delta between the two is the partial renal response. You can go through and calculate that at each week. As mentioned, we used our conservative definition of the partial renal response of a greater or equal to 50% reduction in UPCR, so it all works out. That is very conservative, and actually there were some patients that had a meaningful absolute reduction in UPCR that didn't quite make the 50%. We didn't count them at week 25, but almost all of them crossed the line by week 29, which is what you saw. Now, with respect to the complete renal response, you're exactly on point. The definition of a complete renal response included not just the reduction of UPCR to less than or equal to 0.5, but also patients had to be on a prednisone dose of less than or equal to 10 mg per day, as well as stable eGFR and prohibited medications. What we did find is that some of the patients did have a UPCR less than 0.5, but did not fully achieve a prednisone dose less than 10 mg per day. Even if they had come down from their original dose, they were not counted as a CRR. Got it. If If I could just one quick safety question. On that patient with the reticulocyte increase, did they have anemia or, you know, what may that be treatment-related? Have you seen any of that in the prior SLE study? Yeah. It's a great question because often patients with autoimmune disease such as lupus and lupus nephritis will have anemia, and this patient did have kind of an acute anemia in the run-up to the study. With addition of zetomipzomib, the reticulocyte increase, which overall would usually be considered a positive thing, but the investigator and the patient chose to exit the study. Great. Thanks so much, and congrats again. Thank you. Our next question comes from Philip Nadeau from Cowen. Philip, please unmute yourself and ask your question. Hi, good afternoon. Let us add our congratulations on great data. One question on data then a follow-up on the future studies. In terms of the patients at baseline, you mentioned they had to be on stable doses of prednisone. For how long was the patients on average on those doses of prednisone? In kind of similar, how long were patients' UPCR stable at baseline? I think what question we're likely to get in the future is whether there's a waxing and waning component to the disease. What would be a placebo rate for this patient population? Yeah. Sorry, go ahead. Sorry. No, it's a great question. We documented medication stability for greater than three months for all patients, but in actuality, most of these patients were on their therapies for many more months to years. Great. Then the follow-up on the clinical trial is you mentioned, I think you suggested the possibility of maybe doing more than one additional study. Would you consider doing two registrational trials, one with an induction regimen and one without the induction regimen? I can see where the induction regimen would be helpful because it would give physicians an apples-to-apples comparison against the other data in the field. Yeah. We are considering multiple scenarios, and exactly what you described is one of them, where we would do one study with induction and one without. Great. Thanks for taking our questions, and congrats again on the data. Thank you very much. Our next question comes from Maury Raycroft from Jefferies. Maury, please unmute yourself and ask your question. Hi, I'll add my congrats to the update. It was a great data. Wondering if you can talk more about the relationship between efficacy and steroid tapering over time, how efficacy and tapering kinetics compare to other studies in this space, and how meaningful are these kinetics data to KOLs? Yeah, it's a great question. I think, very importantly, just as a reminder, we didn't mandate a prednisone taper in this protocol, although we are very likely to do so in the future. You rely on the investigators' impressions of how the patients are doing if they can take away a therapy that patients have grown accustomed to. We were very, very pleased with the overall reduction. What we noticed when we looked across the board is that there are some investigators who never touched the prednisone dose and others that actually tapered prednisone to very low doses. Even though we're reporting a 53% reduction, there are patients that actually went much lower, almost to off prednisone even. I think that that's actually quite noteworthy because patients hate corticosteroids, and physicians hate it because of all of the off-target effects. To be able to achieve this in a relatively short period of time with just the addition of zetomipzomib, it really speaks volumes to having an agent that is potentially steroid-sparing, and that is something that we look forward to demonstrating more robustly in future trials 'cause that would be a huge win for both patients and clinicians. Okay, thanks for taking my question. Our next question comes from Catherine Novack from JonesTrading. Catherine, please unmute yourself and ask your question. Hi. Thanks for taking my question. I guess just one on the rapidity of response. I'm curious if you can speak to this, you know, versus LUPKYNIS and Benlysta or induction therapy even for that matter, and how the 13-25 week CRR might be differentiating? Another great question. Usually induction therapy, especially the high-dose IV steroid portion of it, is often attributed with kind of a more rapid reduction in UPCR, but that's still measured in the three to six month range. The fact that we achieved a very brisk and robust reduction in proteinuria in the same period of time without prednisone is quite meaningful or without high-dose IV prednisone or corticosteroids. That's very meaningful. If you recall the recently approved agents, LUPKYNIS works the most quickly. Others take one to two years to actually measure a benefit. Even if you look at the treatment effect with LUPKYNIS, their placebo group had achieved an almost 50% rate of response. What they saw in terms of their CRRs was you know, about 15% more on top of that as a treatment effect. Again, we find this very notably different, because there was no induction therapy and our results were just as strong and just as brisk. Our final question comes from Mitchell Kapoor from H.C. Wainwright. Mitchell, please unmute yourself and ask your question. Hi, everyone. Thanks for taking the questions. Just wanted to ask about the follow-up in the summer with more patients. Could you just kind of talk about the expectations there and, you know, specifically what you could imagine the expectations would be for minimally acceptable ORR and CRR there? Potentially even in a larger study, if you could just talk about the evolution of data and how you see it. Yeah. It's a great question. I think it is important to set expectations about this because remember, this is a 12-week period where patients are no longer receiving zetomipzomib. We may continue to see deepening of the response, but we also may learn a lot about the kinetics of a response and then recrudescence of inflammation. Over the next 12 weeks in that safety period, we may see patients continue to get better, and we may see patients begin to rebound. We would expect both because they're no longer receiving zetomipzomib. We may actually also learn something about the way the drug works based on those kinetics and who is more likely to have proteinuria return versus others. Thank you very much. There are no further questions. All right. Well, thanks, all of our covering analysts for your thoughtful questions. Really appreciate it and for everyone who dialed in, for taking the time today to review these exciting data sets with us. Appreciate your time and wish you a great day. Thanks, everyone.