ChemoCentryx, Inc.

Good afternoon, and welcome to the Chemocentrics Third Quarter 2020 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session. As a reminder, this conference call will be recorded. I would now like to turn it over to Steve Klass of Burns McLaren. Mr. Klass, please go ahead.

Thank you, Operator. Good afternoon and welcome to the Chemocentrics third quarter 2020 financial results conference call. Earlier this afternoon, the company issued a press release providing an overview of its financial results for the third quarter ended September 30th, 2020. This press release is available on the investor relations section of the company's website at www.chemocentrics.com. Please note there is a slide deck to accompany this call, which can also be found on the company's website. Joining me on the call today is Dr. Thomas Shaw, President and Chief Executive Officer of ChemoCentrics, who will review the company's recent business and clinical progress. Following his comments, Susan Kanaya, Executive Vice President, Chief Financial and Administrative Officer, will provide an overview of the company's financial highlights for the third quarter before turning the call back over to Tom for closing remarks. During today's call, we will be making certain forward-looking statements. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These risks are described in the company's filings made with the Securities and Exchange Commission, including the company's annual report on Form 10-K, filed on March 10, 2020, and quarterly report on Form 10-Q, filed on November 9, 2020. You are cautioned not to place undue reliance on these forward-looking statements, and ChemoCentrics disclaims any obligation to update such statements. In addition, this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, November 9, 2020. ChemoCentrics undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this live conference call. I will now turn the call over to Tom.

Thank you, Steve, and good afternoon to everyone listening. Thank you for joining us on our third quarter 2020 conference call. I am pleased to report to you today that we continue to accomplish the goals that we laid out at the start of this year, despite the subsequent arrival of a global pandemic. As this grim challenge wears on, our deep sympathy goes again to those who have lost loved ones, or who have been otherwise affected by COVID-19. And our admiration and gratitude increases daily for those that are meeting the challenges in the clinic, in the laboratory, and in our community. Our resilience as a society will eventually prove to be the key to victory in this battle. For chemocentrics, we are now at a very important time of accomplishment. a time when we have our very first ever new drug application under review for Avacopan and ankylovasculitis, a time where we have results in hydronitis suprativa that define a clear development and registration path forward, and a time where top-line data will be soon available in a third Avacopan indication as well. So today I will cover in brief three main topics. I will add some clarity and additional insights on the hydranitis superativa, or HS, result, where there is evidence of clinical benefit and a clear, fruitful path forward for Avocopan. I will discuss the accolade trial of Avocopan in C3 glomerulopathy, on which we expect top-line data before the end of this year, and how we propose to look at that trial. And I'll conclude with an update on where we stand on Avocopan and ANCA vasculitis as we approach potential commercialization in 2021. I'll start first by talking about next steps following top-line data we reported very recently at the end of October from the Aurora Phase II Clinical Trial of Avacopan in Hydrolysis Superativa, or HS. HS is a chronic, disabling, painful, disfiguring skin disease described in brief on slide three. The sole FDA-approved drug is viewed as only moderately effective, requires infusions or even injections, but nevertheless accounted for more than a billion dollars in sales for this indication last year. This is a clear sign of the unmet need, indeed some would say desperate need, for innovative new therapies in HS. And yet, is an area that poses questions for many. Yes, even some consternation. It is probably fair to say that this is not an attractive indication to many in the investment community. To this, I respectfully disagree. I would like to explain briefly my conviction for a VACOPAN in this space and that that conviction is high, and clear away some extraneous items that may cloud the opportunity, the view of the opportunity. I'll focus on some simple and emerging concepts on the pathobiology of this disease that helps me see a clear path forward for Avacopan. There is ample independent research demonstrating that complement activation, and in fact, the terminal complement fragment C5A, is implicated in H. sucrativa. Hence, the relevance of Avocopan, since its mechanism of action is designed to stifle the activation of neutrophils via selectively targeting and inactivating the C5A receptor. Aside from other outside reports, we at Chemocentrics also presented data at the recent fifth annual Symposium of Hydronitis Suprativa Advances, or SHFSA, conference, with our colleagues at Stanford University showing evidence for complement dysregulation in the blood and skin of HS patients. All of that is summarized on slide four. Now, the AURORA clinical trial has extended our knowledge as to how Avacopan might benefit HS patients. In fact, in my view, AURORA has given us, so far, the three most important things a Phase II trial can yield. One, we have found an effective dose of Avocopan. Two, we have defined the precise patient population. And three, we have demonstrated safety. Those who seem clearly to benefit from Avocopan are the early Stage III populations. the sickest of the sick, if you will, in HS, for lack of a better term, and those who have virtually no effective treatment options. The Evocopan benefit in this group is evidenced by the data reprised in slide five, a snapshot of the fuller top line data picture that we provided very recently, and the basis of our now clear going forward path in HS. But the key question is this, why Hurley 3? Why is the clinical signal with Evacopan there? What is the opportunity in that group? And what will be required to realize that opportunity? In fact, a major distinction between these most severely afflicted Hurley 3 patients And the far less severe, frequently far less severe, but certainly less severe Hurley 2 and, of course, Hurley 1 patients is the extent of the network of dermal tunnels, also known as sinus tracts or fistulae, that connect the abscesses, nodules, and lesions in the affected areas of the body in HS. In Hurley 3, these tunnels are extensive. And also, there is little to no space among the interconnected skin disruptions that are in evidence on the surface of the body. Thermal tunnels are structures unique to hydronitis suprativa. They have not been identified in any other inflammatory systemic skin disease. And the presence of tunnels is associated with a more aggressive course of Hurley stage 3 disease. Slide six refers to some features of advanced HS that we think are pertinent to Evacopan and its mode of action in hydronitis suprateval. Dermal tunnels are laden with pus. Pus is primarily neutrophils and neutrophil nets or neutrophil extracellular traps that form when activated neutrophils to granulate. In Hurley Stage 3, there is also more tunnel-associated infiltrated proliferative gelatinous mass, or IPGM, which has a distinct active inflammatory set of characteristics. IGPM is an opaque white, reddish, or violet jelly-like material found in the lumen of HS tunnels, and it contains a mixed population of potently, highly pro-inflammatory cells, such as neutrophils and macrophages, cells which I will add and reiterate express the C5A receptor. There is evidence for increased C5 pathway terminal activation products in early stage 3 disease, as the multiple sores, dead neutrophils and pus components, Intensify the cycle of tissue destruction, tissue remodeling, and opening exposure to external environmental pathogens and insults as well. A classical formula for complement activation. We have seen in our own work an exuberance of neutrophils in Hurley 3 skin biopsies, some of which are one example of which is on that same slide. And researchers such as John Frew and colleagues in New York and Sydney have recently published elegant studies, such as in the Clinical and Experimental Dermatology Journal just this September, demonstrating that these sinus tracts and tunnels in Hurley 3 are strongly correlated with a decreased responsiveness to anti-TNF therapy, as well as more rapid loss. of anti-TNF therapeutic effect. We believe that the deactivation and depletion of neutrophils, the reduction of neutrophil nets and other neutrophil activation products occurs as a consequence of a vacupan therapy. Thus, the pus-laden tracts and chambers dry up, much like Lava leaving the magma chambers in a rumbling volcano and the surface manifestations of HS scored clinically by such instruments as high score and IHS4, et cetera, improve. Or to put it another way, I think of a vocal pan in Hurley Stage 3, Hydronitis Suprativa, as the light at the end of the tunnel. Aurora has fulfilled the promise of a Phase II clinical trial, enabling us to identify a clear path forward. Armed with data from Aurora on dose, on patient selection, and on excellent safety, we will discuss the Aurora data with regulatory authorities and we are planning for a pivotal phase 3 child in Hurley stage 3 HS patients. And recall again that these are the sickest of the sick in this disorder for whom treatment options are de minimis. Our plan is to assess Evacopan against placebo at a 12 weeks primary endpoint using the high score as the primary endpoint. Since Frankly, that is the only regulatory path to approval to date. Aurora evidence shows that this should be eminently achievable. We will also include secondary endpoints such as IHS4, et cetera, depending on agency input. We will likely need as few as 100 or 150 patients in each arm in two arms, one study should suffice. You can see from slide seven that Hurley stage three represents a considerable market opportunity for us. Hurley stage three prevalence is estimated anywhere between 35,000 to 60,000 patients in the United States alone. And while preparing for the phase three trial, we plan to file with the FDA for an orphan disease designation just on Hurley stage three enabling a potentially more streamlined path to market. I would invite you to do the math on how many patients would be required to reach $1 billion in the U.S. alone, in hydronidazine supertivo alone, in annual sales using a typical orphan drug price of somewhere between $100,000 and $200,000 per year. There is a clear unmet need. Patients have few treatment options and represent a large underserved population. In summary, evidence confirms that HS represents a huge opportunity for Avacopan, which in our view requires an extremely modest investment when weighed against a striking potential upside of marked returns for patients and investors. Turning now to another potential indication for Avacopan, we expect to release top-line results in the Phase II accolade trial in C3 glomerulopathy, or C3G, before the end of the year. C3G is a potentially life-threatening affliction with no FDA-approved therapy, an overview of which is discussed on slide 8. Our approach to C3G, in my view, has been unique in the industry. Generally, other clinical studies have been small. Single-digit numbers of patients is not uncommon. Frequently, they are open-labeled. And they typically measure only biomarker endpoints, such as proteinuria, serum creatinine, EGFR, and the like. This is not a knock on other studies. It is essentially a necessity of the rare nature of this disease, which is only somewhere between 1,000 and 5,000 people with this affliction in the U.S. at this time. clinical trial subjects are limited. Nevertheless, we took a different route at Chemocentrics. We were determined to do a large, at least for this indication, trial. We designed this trial to be a randomized, controlled, and blinded trial for the primary endpoint period, and we collected and measured kidney biopsy at baseline and at six months to determine the primary endpoint. Slide nine depicts how we went about this. It shows the design of the Accolade trial. I'm sorry. It shows that the design of the Accolade trial, as I mentioned, is a randomized blinded control trial. The original and still core design of Accolade is on this slide. The enrolled subjects, are intended to have high levels of circulating C5b-9 complexes in their blood. This is a stable marker of complement activation down the C5 pathway. These individuals are presumed to have C3G from kidney symptomatology, and then they have to be proven to have active inflammatory C3G by biopsy at baseline. And in fact, this group of high C5b through 9 subjects enrolled at a fairly good rate for such a rare disease, and the group near fully enrolled. They biopsy confirmed at the time of biopsy. So while we do, turning to the now slide 11, there was a second stratum that we added after the start of this trial. And this second stratum was based on the hypothesis that some individuals with actual normal levels of circulating C5B through 9 might also have active C3G and, in fact, might be confirmed as such by kidney biopsy. Interestingly, after many months, indeed years, we now know generally that these normal C5B through 9 individuals do not biopsy confirm as active C3G when they go through the screening. So while we do have some patients in the second stratum, it would take an additional decade or more at this rate to enroll the full complement of this normal peripheral complement stratum. Hence, we will proceed with the data analysis as originally envisioned in the Stats Analysis Plan And we will present data on all patients, both the high and the normal peripheral complement strata, who have passed the 26-week primary endpoint determination. As summarized in slide 11, look for 26-week biopsy-based primary endpoint data from Accolade before the end of the year, accompanied by the traditional biomarkers of such things as proteinuria and EGFR. Turning now to Avocopan and the treatment of ANCA-associated vasculitis, as summarized in slide 12, in Q3, we hit an historic milestone when the FDA notified us in September of their acceptance for review of our new drug application. The FDA set a PDUFA date goal of July 7, 2021. As for the question of an advisory committee, we intend to provide an update following the mid-cycle review meeting of the FDA, and we are preparing for one nevertheless. The FDA's acceptance for review was followed by the announcement just last week of the European Medicine Agency's acceptance for review, known as validation, of the marketing authorization application for Avacopan in ankylobasculitis. with a decision expected in the second half of 2021. As many of you know, the cornerstone of our submission to the regulatory agencies has been the data from the pivotal Phase III Advocate Clinical Trial, which demonstrated statistical superiority of the Abacopan group in sustaining remission at 52 weeks compared to the Prednisone group. The results of the advocate study were presented last month in an oral abstract session during the American Society of Nephrology's Kidney Week 2020 Reimagined meeting. They were presented by the renowned nephrologist David Jane, MD, Professor of Clinical Autoimmunity at the University of Cambridge in England. Dr. Jane's presentation highlighted the potential of Avacopan to offer new hope to patients who suffer from this incurable orphan disease. And just this last Friday, no less an expert than Professor Peter Merkle, MD, the Chief of Rheumatology at the University of Pennsylvania, gave a plenary session on the advocate results at the American College of Rheumatology Convergence 2020 meeting. Professor Merkle delved into many important aspects of the Evacopan data set. including highlighting some important features at both weeks 26 and weeks 52 in the trial result. As Dr. Merkel put it, and I'm alluding now to the next slide in the deck that you can see with the week 26 and 52 data, as Dr. Merkel put it, there are some intriguing findings to explore in the subgroups. Patients who had relapsing disease had even better benefit from Avocopan at 26 and week 52. However, this should not imply that patients with newly diagnosed disease did not benefit from Avocopan because while remission rates with Avocopan in newly diagnosed were about the same as the prednisone group, remember, the patients receiving Avocopan achieved this benefit without receiving daily glucocorticoids and their negative consequences. Similarly, said Professor Merkel, there were findings that patients who were MPO positive received extra benefit, and the patients who received rituximab as background therapy seemed to receive extra benefit as well. One more note on avocopin. It was heartwarming to consider very recently, a newly published case report in the British Medical Journal case reports of a now young lady who had struggled since the age of nine years old with ankylovasculitis for over seven years at the time. As she explained in her own words, after multiple surgeries, loss of most of my sinuses, loss of my left lung, and multiple long-term side effects from medication, I survived. I finally graduated from Toronto Sick Kids Hospital, where she had spent the, as she puts it, the majority of her evenings of her life as a child. I finally graduated from Toronto Sick Kids Hospital and moved to the adult world at Mount Sinai Hospital in Toronto. At this point, she is about 16 years old in her story. At Mount Sinai, she was given a Vakopan on a compassionate use basis. And the case documents that since then, she has been free of relapses for 35 months and counting on continuous dosing of the Vakopan and is on the verge now of getting her degree again. now a woman in her very early 20s. A duration of three years relapse-free with Avacopan is a notable achievement. There has been a growing awareness in the clinical community of the fact that patients in the ADVOCA trial initially treated with Avacopan and Rituximab as a background medication were receiving, in fact, only Avacopan essentially during the last 48 weeks of treatment. following their initial rituximab background medication dose. In this stratum, patients who did not receive rituximab thereafter, that is after the first four weeks, indeed had a sustained remission rate at week 52, as alluded to by Professor Merkel in his presentation, of 71% in the Evacopan group compared with 56% in the same comparator, the prednisone group that had rituximab as background therapy. And by the way, these are all ITT, intent-to-treat analysis numbers. So it's important to note here that we were not setting out in the ADVOCATE trial to test of aquapan as a monotherapy, but it is nonetheless an interesting observation that could have future implications in terms of the duration of therapy and potentially the lack of need for continued immunosuppression in ankylovasculitis. While our regulatory submissions are under review on both sides of the Atlantic, we are building our commercialization infrastructure in preparation for potential launch in the United States, and we are coordinating closely with our partner, VIFOR Pharma, in their preparations ex-U.S. and international markets. And I will remind you that VIFOR would pay us royalties in the teens to mid-20s, that's percentage, on net sales in one aggregate net sale line outside the U.S., as well as potential milestone payments linked to ANCA regulatory events in their territories up to about $75 million. The data presented at ASN and ACR included impressive data from the ADVOCAT trial on Avacopan's ability to preserve kidney function as well, as you know, as measured by estimated glomerular filtration rate, or EGFR, which is a well-known predictor of long-term kidney survival. I'll remind you that in the chart on the right side of slide 12, the Avocopin group is represented in the red line and the active comparator prednisone group by the gray line. The chart shows, again, the sickest tertile of patients, all pre-specified in the analysis, those with an EGFR when they started the trial below 30 mil per minute. In fact, this subgroup had an average EGFR of about 21 mil per minute, evenly balanced between the two groups. That's fairly close to the 15 mil per min rate that would tag someone as a candidate for dialysis. So those people are not that many months away if their current rate of decline continue from being dialysis candidates. However, 52 weeks later, there was an overall improvement in the Avacopan group of nearly 14 mil per min, significantly better than the prednisone standard of care group. The improvement in the Avacopan group increased to nearly, at the end of that trial, 35 mil per minute, effectively moving the average patient from a stage 4 to a stage 3 chronic kidney disease. Really quite a striking improvement. And that really reflects where we may go next with Avacropan. And the next kidney indication we have targeted is lupus nephritis, as alluded to on slide 14. LN shares many key characteristics with ankylovasculitis. It is a complement-mediated disease. poorly controlled with broad immunosuppression, leading to the deterioration of kidney and the risk of progression to end-stage renal disease and transplant. With a prevalence estimated at between 65,000 and 100,000 in the U.S., the clinical and economic burdens of lupus nephritis are indeed severe. We believe the improvement seed with the ADVOCATE trial with Avacopan in terms of EGFR and renal function has the potential to translate to LN and other kidney disease. And we plan to initiate a trial in lupus nephritis in the first half of 2021. Finally, to conclude, looking beyond Evacopan, which has obvious potential to be a pipeline and a drug itself, we are on track to introduce our small molecule, orally administered PD-1, PD-L1 checkpoint inhibitor for cancer into clinical development in the first half of this coming year, 2021. Our preclinical data suggests that CCX559 may be able to penetrate the tumor microenvironment better than antibody-based checkpoint immunotherapies, among other advantages over antibody therapeutics. And CCX559 has, in our view, the potential to be a next-generation cancer treatment used alone or in combination with other oncology therapies. The momentum we have generated in recent quarters is, in my view, only the start of our path to become a fully integrated pharmaceutical enterprise providing novel therapies in critical diseases. Our unique platform has the potential and indeed has generated multiple drug candidates in multiple disease states. We will follow where the science leads us and focus on the areas of greatest promise, greatest need, and greatest opportunity. I will now turn the call over to Susan Kanaya to outline our third quarter 2020 results and our financial strength. Susan?

Thank you, Tom. Our third quarter 2020 financial results were included in our press release today and are summarized on slide 12. Revenue was $5.1 million for the third quarter compared to $10.6 million in the same period in 2019. Revenue is recognized proportionately based on actual costs incurred as a percentage of total budgeted costs as we complete our performance obligations under our agreements with FIFOR. As such, the revenue decrease was driven by lower costs incurred in 2020 due to the completion of the Evocopan Advocate Phase 3 Pivotal Trial. Research and development expenses were $18.6 million for the third quarter of 2020, compared to $18.1 million for the same period in 2019. The increase in R&D expense was primarily due to professional fees associated with the Avocopan NDA submission for the treatment of ankylovasculitis, and higher research and drug discovery expenses associated with those with the advancement of CCX559, our orally administered small molecule checkpoint inhibitor. These increases were partly offset by lower expenses in 2020 due to the completion of the Avocopan Advocate Phase 3 pivotal trial and the CCX-140 Lumina I Phase II clinical trial. General and administrative expenses were $10.4 million for the third quarter of 2020, compared to $6.1 million for the same period in 2019. The increase from 2019 to 2020 was primarily due to higher employee-related expenses, including those associated with our commercialization planning efforts and higher professional fees. These results produced a net loss for the third quarter of 2020 of $24.1 million, compared to $12.9 million for the same period in 2019. Total shares outstanding at September 30, 2020, were approximately 69.1 million shares. Cash, cash equivalents and investments totaled $485.8 million at September 30, 2020, And we expect to end 2020 with cash investments in excess of $460 million. Tom?

Well, thank you, Susan. To summarize, as you can see in slide 13, we are forging ahead with our lead candidate at Evacopan in three distinct orphan diseases, each of which has a market opportunity in the hundreds of millions of dollars and beyond. The FDA is reviewing our NDA for Avacopan and ankylovasculitis, and the European Medicines Agency is reviewing the MAA. We plan to conduct a pivotal phase three trial of Avacopan in severe hydronitis sugrativa patients following the clear signals we saw in the Aurora data and to make an orphan drug application for early stage three disease in H.S. We expect to report top-line data from our accolade trial of Avacopan and C3 glomerulopathy before the end of the year. And we face the prospect of another banner year for chemocentrics in 2021, perhaps our most significant one yet with the potential FDA approval for Avacopan and acovasculitis with a PDUFA date set for July of this coming year and the MAA approval expected in the second half of 2021. the potential launch of Avacopan in ankylobasculitis, and the next cycle of pipeline advancements, which begins with two more clinical programs, an orally administered checkpoint inhibitor of the PD-1, PD-L1 pathway, CCX559, and Avacopan in lupus nephritis. Frankly, we have the funding to accomplish all of this, and we see this virtuous cycle repeating in the future. given our unique discovery platform, which has the proven potential to produce multiple drug candidates for multiple diseases. Ladies and gentlemen, in my view, hemocentrics has never been stronger than now. And with that, I will turn the call back over to the operator, and we will look forward to your questions. Operator?

Yes, sir. And ladies and gentlemen, if you would like to ask a question, press star 1 on your telephone. Again, if you would like to ask a question, press star 1 on your telephone. And just a reminder, we will limit our questions over to two questions per participant. For our first question, we have from Joseph Schwartz from the SVB Lear Rink. Joseph, your line is open.

Hi, I'm Julie Dialing in for Joe. Thank you for taking our questions. My first one is on HF. So thank you for the introduction on possible differences between Hurley stage 3 patients and Mildred patients. And my question is, to your knowledge, how homogeneous are the dermal tunnels in HF patients and Hurley stage 3? And how easy or difficult do you think it will be to identify these patients in stage 3?

Well, I do agree that the dermal tunnels, and I think this would be a widely held view, Look, dermal tunnels are extremely prevalent in Hurley stage 3. Yes, they occur in Hurley stage 2, but far greater in 3. They are not always perfectly easy to identify, but by the time someone is in a Hurley stage 3 condition, again, with very little normal skin space between the overt lesions on the surface of the body, I think that it is fairly certain that Hurley 3 stage diagnosis is is made with the inclusion of these dermal sinuses in mind. So just as the way that the net is cast in HERLE3, you are going to capture more dermal tunnels. Now, the question about would we be better off to see if we could devise a method actually looking for tunneling, I think there is some pretty good literature on this recently. I've really been impressed, again, with a kind of new wave of thinking around HSC I mentioned Dr. Frew and his colleagues at Rockefeller and in Sydney. There are others as well. Dr. Prenz in Europe has done some interesting work with his colleagues. You know, it's harder to actually say let's include a certain number of tunnels or a certain width of tunnels. I think that's just not the nature of the beast yet. But these are far from scarred over vessels, frankly. I think there's a lot more going on. Why are these dermal tracts so filled with neutrophils, dead and dying, so filled with pus, so filled with these infiltrative proliferative masses? There's a lot more activity going there than we may have thought even two or three years ago. So I'm pretty convinced that crude as the Hurley designations are, that we will capture a more severe disease with Hurley 3 diagnosis and And de facto, we're going to capture a lot more tunnels. I think that's going to be to an advantage for avocopan. And by the way, you know, there has been analysis that adalimumab, again, with more tunnels corresponding roughly with severity in HER3, but more tunnels means less efficacy. Adalimumab seems to be better with the less severe patients. So I think there's a super important niche for avocopan. And I do believe that crude as our methodology is now, with both Hurley 3 and, yes, high score, but FDA insists on it so far, we're in a great position to capture the signals that we need to capture. And I think other emerging science will help us define that as we go along. But we're certainly going to be mindful of it as we design this Phase 3 and think about inclusion-exclusion criteria.

Okay, great. Thank you. And then for AAV, I was just wondering, how does your intriguing advocate subgroup analysis data at weeks 26 and 52 potentially impact your regulatory path? Do you see it possibly impacting how physicians could use a VACUPON or your label? I was just wondering what your view was on the possible impact.

Well, you know, I hate to even presume to think about what the agency might think or say and certainly don't want to, you know, think to discuss any discussions with them until those are all done. But let me put it this way. Look, fundamentally, this is the longest randomized trial ever done in ankylovasculitis, right? The randomized blinded trial, 52 weeks continuous dosing and following. Look, that's not been done before. So we've got the biggest data set by six months. That's important because it informs a lot of discussions. So without thinking yet about what the agency may or may not say, they'll look at the data in their own way, obviously, but the data kind of speak for themselves. What I will tell you this, it sounds like we're already informing new discussions in the physician community because the fact of the matter is, If you have evidence that the hardest people to treat, the anti-MPO relapses are notoriously difficult to treat. The MPA diagnosis, which goes along more or less with MPO positivity, really difficult to get a handle on, especially with relapses. But fundamentally, I think the more subtle and for me the more profound point is that My goodness, when you look at the fact that Avocopan not only had a really just a general improvement in relapse risk, reducing relapse risk by some 54%, and those were two charts shown in these meetings as Kaplan-Meier graphs where Avocopan was clearly advantageous in the population. And part of that comes from that really interesting advantage that Avocopan has with when given with rituximab as background therapy versus daily prednisone with rituximab as background therapy. 71% still in remission at week 52 versus 56% with the prednisone group. The important point here is we ran this trial according to rituximab's label at the time, and it was fully enrolled under the old rituximab label, which was You don't give Rituximab except for that first course of therapy. That's four weekly infusions based by a week. So they get it for four weeks. You don't top them up after that under the original label. This data, some people have criticized us for that, like we had a choice to begin with, which we didn't. But in fact, the more enlightened discussions that I've heard, especially recently, are no, the data actually show you don't need to keep immunosuppressing people with Rituximab. That's a large N, 107 people per group were following. They didn't get Ritux. They're totally matched except for prednisone versus Evacopan. They didn't get any additional Rituximab. So Evacopan was kind of monotherapy, right? They didn't get azathioprine or anything else after the Ritux. And people are really, really markedly in remission at the end of 52 weeks. So that's an important discussion to have. So I don't know how that will play out. And again, I don't want to make too much or too little of that observation, but I think it's compelling, and I think it's starting to inform some new discussions.

Okay, thank you very much.

Again, participants, just a reminder, we will limit two questions per participant. And for our next question, it's from Steve Seedhouse from Raymond James. Steve, your line is open.

Hey, good afternoon. Thanks for the question. I have one very quick one, and then... part two of the question. The first one is just I want to get your updated current thoughts on pricing this drug in the ankylovasculitis market. And then, Tom, given your confidence that you just highlighted nicely in Avacopan as a potential maintenance therapy to prevent relapse even without rituximab, I'm curious about your view of using Avacopan in patients that are just currently in remission, so not in a post induction setting, but just using it outright to prevent relapse. Is it a study that you would ever consider doing, and is there a reason to believe that that would be effective if you would or could do such a study? Thanks.

Thank you, Steve. You know, I was impressed by some of the research done by one of your other eminent colleagues in your community, the analyst community, and she mentioned to me