Good afternoon, everyone. Welcome to the Apellis Pharmaceuticals DERBY and OAKS Top Line Phase III Results Conference Call. Today's call is being recorded. At this time, I would like to turn the call over to Meredith Kaya, Senior Vice President of Investor Relations and Strategic Finance at Apellis. Good afternoon. Thank you for joining us today to discuss the top line results from the DERBY and OAKS pivotal phase III studies evaluating pegcetacoplan in patients with geographic atrophy, or GA. For those participating via conference call, we have made the slides available via webcast. A replay of this call will also be available on our website following the call. Before we begin, I would like to point out that we will be making forward-looking statements that are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and our actual results may differ materially. I encourage you to consult the risk factors discussed in our SEC filings for additional detail. On today's call, I am joined by our Chief Executive Officer, Dr. Cedric Francois, who will discuss the phase III DERBY and OAKS results. Our Chief Medical Officer, Dr. Federico Grossi, Chief Financial Officer, Tim Sullivan, and Chief Commercial Officer, Adam Townsend, will join the Q&A section at the end of the call. I'm pleased to turn the call over to Cedric. Thank you, Meredith, and good afternoon to everyone on the call and joining via webcast. As you saw in our press release earlier today, we are announcing top line results from our phase III DERBY and OAKS studies evaluating intravitreal pegcetacoplan, a targeted C3 therapy in adults with GA. We believe that the data from OAKS, DERBY, and our phase II FILLY study provide a compelling and robust data set that supports approval despite the narrow miss in DERBY. We intend to submit an NDA in the U.S. in the first half of 2022. This will be the first NDA ever submitted for this disease. The phase III results show that pegcetacoplan reduced GA lesion growth with a safety profile that exceeded our expectations, and an effect in every other month dosing that is similar to monthly. Further, pegcetacoplan showed an even greater benefit in patients with extrafoveal lesions, underscoring the importance of treating patients early in their disease progression. We believe pegcetacoplan is now positioned to become the first treatment for patients with GA, a devastating disease that is a leading cause of blindness worldwide. We believe this outcome reinforces our leadership position in complement and offers yet more validation of our approach. Geographic atrophy is an advanced form of AMD, which leads to the destruction of the retina and irreversible blindness, and there are no treatments currently available. More than 5 million people worldwide have GA, including 1 million in the U.S. and over 2 million in Europe. Most patients with wet AMD who are undergoing anti-VEGF therapies will inevitably develop atrophy over time. GA severely impairs visual function, independence, and quality of life. It is worth mentioning that lesion growth in GA refers to the continuous loss of photoreceptor cells in the retina, and once retinal cells have died, they cannot grow back. This is why there is an urgent need for a GA treatment that can preserve patients' vision by slowing disease progression. Mechanistically, C3 is the only target in the complement cascade that can control all of the damaging downstream effects of complement activation, which we believe is essential in the treatment of GA. Before we review the data, let me first quickly remind you of the study design. DERBY and OAKS are double-masked, randomized, controlled global phase III studies comparing the efficacy and safety of monthly and every other month intravitreal pegcetacoplan with sham treatment in 1,258 GA patients across more than 200 sites worldwide. The primary efficacy endpoint of both studies is the reduction in growth of GA lesions in the study eye from baseline to month 12, as assessed by fundus autofluorescence. The studies will continue for a total of 24 months, and patients will remain in their randomized masked treatment groups for the duration of the study. At month 24, lesion growth will be assessed again, and secondary functional endpoints will be formally tested. Now let's get into the data. Patients who received pegcetacoplan in OAKS showed a statistically significant reduction in GA lesion growth compared to pooled sham. Monthly treatment resulted in a 22% reduction in lesion growth with a p-value of 0.0003, and every other month treatment resulted in a 16% reduction in lesion growth with a p-value of 0.0052. Pegcetacoplan narrowly missed in DERBY. Monthly treatment with pegcetacoplan reduced lesion growth by 12% with a p-value of 0.0528, with a significance threshold of 0.05. Every other month treatment reduced lesion growth by 11% with a p-value of 0.0750. We are continuing to analyze the data to try to better understand why the data in DERBY looks different from OAKS and our previous FILLY study. In a pre-specified analysis of the combined studies, pegcetacoplan showed a 17% reduction in lesion growth with monthly treatment, with a p-value of less than 0.0001, and a 14% reduction in lesion growth with every other month treatment, with a p-value of 0.0012 compared to sham. The untreated fellow eye analysis further demonstrated the effect of pegcetacoplan in slowing the lesion growth of GA, consistent with what we saw in FILLY. This is a powerful analysis, as it is well established that in bilateral GA, lesion growth progresses at similar rates between the two eyes. Therefore, the underlying growth rate in the untreated fellow eye is a good surrogate for how the disease would have progressed in the study eye in the absence of treatment. The left-hand graph shows that monthly treatment of pegcetacoplan reduced lesion growth by 16% compared to the untreated fellow eye. The middle graph shows that every other month treatment of pegcetacoplan reduced lesion growth by 11%. The graph on the right-hand side shows that in the sham group, the lesion in the study eye actually grew faster, by 4%, compared to the lesion in the untreated fellow eye. Between this observation and the fact that the untreated fellow eye may have benefited from treatment in the study eye, the actual treatment effects could have been greater than what is shown in these graphs. As with any study in GA, there is going to be variability in progressiveness of disease. As you can see on this slide, one interesting observation was that the observed data showed that the underlying growth rate in the untreated fellow eye in the monthly pegcetacoplan groups was faster than the untreated fellow eye in the sham groups, by 11% in DERBY and 7% in OAKS at month 12. For every other month, this disparity was less pronounced. We plan to continue to analyze these data further. This slide shows results from a pre-specified analysis in which we then looked at the effect of pegcetacoplan in patients with extrafoveal lesions at baseline. GA typically begins with extrafoveal lesions that later progress into the fovea, with research suggesting that as many as 85% of patients start with lesions outside of the fovea. What we saw in this analysis was that pegcetacoplan showed an even larger effect on lesion growth in patients with extrafoveal lesions, with the effect in every other month treatment similar to that in monthly. Specifically, in the combined studies, pegcetacoplan demonstrated a 26% reduction in GA lesion growth with monthly treatment, with a P value of less than 0.0001, and a 23% reduction in GA lesion growth with every other month treatment, with a P value of 0.0002 compared to sham. We believe pegcetacoplan has the potential to treat GA patients with both foveal and extrafoveal lesions, with an even greater benefit in patients with extrafoveal lesions. This increased effect supports treatment with pegcetacoplan earlier in disease progression. Now moving on to safety. As I mentioned at the beginning, pegcetacoplan demonstrated a favorable safety profile across both studies, exceeding our own expectations. The pooled rate of new onset exudations was 6% of patients in the monthly treatment group, 4.1% in the every other month treatment group, and 2.4% in the sham group. The study design specified that cases of new onset exudations be reported by physicians and confirmed by the reading center. Two cases of confirmed infectious endophthalmitis and one case of suspected infectious endophthalmitis were observed out of a total of 6,331 injections. Two of these patients actually resumed treatment with pegcetacoplan. 13 cases of confirmed intraocular inflammation were also observed in the studies, and importantly, no events of retinal vasculitis or retinal vein occlusion were observed. Additionally, there were no clinically relevant changes in vision for any patients who developed infectious endophthalmitis or intraocular inflammation. We look forward to discussing these results with regulatory authorities worldwide. We expect to submit an NDA for approval in the U.S. in the first half of 2022. We also plan to submit a marketing application for approval in Europe. As we have discussed previously, the EMA has recommended we include the 24-month functional data as part of our submission. From a commercial perspective, we plan to continue the build-out of our ophthalmology commercial and medical affairs teams in advance of this blockbuster opportunity. We have hired marketing and sales leadership in the U.S. and built out our European team and affiliates in Germany and Austria. We plan to share more detailed data from OAKS and DERBY at upcoming meetings this fall. Building on these exciting results, we look forward to advancing our overall ophthalmology franchise. This includes the initiation of a pivotal study of pegcetacoplan in intermediate AMD, which we plan to do in 2022. Intermediate AMD has no approved treatments and represents a significant opportunity to delay or prevent progression to advanced forms of AMD and potentially prevent vision loss. We also remain on track to submit an IND late next year for APL-2006, a potentially best-in-class and next generation therapy for wet AMD that combines the benefits of anti-VEGF with anti-C3 to prevent the development of GA. In summary, pegcetacoplan has the potential to be a transformative treatment for the millions of people with GA who are at risk for blindness, with no treatment options and few opportunities on the horizon. We believe we have a drug that is effective with a strong safety profile and a flexible treatment regimen. All of us at Apellis are committed to bringing pegcetacoplan to GA patients as quickly as possible and advancing our ambition to be number one in the retina. I would like to close by expressing my sincere gratitude to everyone who is participating in the DERBY and OAKS studies. This is a program that is near and dear to our hearts here at Apellis, and without all of you, this milestone would not have been possible. We are especially thankful for all the patients who are participating in these studies. Each of you inspire us every day in our efforts to bring the first treatment option to GA patients. Thank you also to the study investigators and those supporting each of the clinical sites for successfully executing these studies despite the ongoing COVID-19 pandemic. To our amazing team at Apellis, we are so grateful for your unwavering commitment to advancing care for people living with GA and other complement-driven diseases. With that, operator, please open the call for questions. Thank you. We will now open the call for questions. If you would like to ask a question, you will need to press star one on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question will come from Anupam Rama with JP Morgan. Please go ahead. Hey, guys. Thanks so much for taking the question. When you think about the results for DERBY and OAKS on GA lesion size growth, in particular in the monthly arm, what are the couple factors that you could attribute to why there was a big difference here, and were the baseline between the two trial relatively similar? What confidence do you have that U.S. and OUS regulators would be comfortable with sort of a pooled analysis in terms of regulatory? Thanks so much. Yeah. Thank you so much, Anupam. Look, we have much more work to do, of course, to look at the differences between these trials and trying to understand why there was a difference between OAKS and DERBY. What I would like to point out here, which I think is really important and will help us in the submission strategy that we have, is that in 2015, we made a commitment to study this very complex disease of geographic atrophy with consistency. In FILLY, in DERBY, and in OAKS, we studied the exact same patient population. We analyzed it in the same way. We did the imaging in the same way. That consistency provides a data set where, quite frankly, if you put everything together, the narrow miss in DERBY can become contextualized. When you run a couple of phase III clinical trials, you will always get some differences, and this is one of those examples where, of course, it didn't go the way we wanted to in DERBY, but where all the remainder of the data support our hypothesis. What that is related to, we're not going to comment on now, but we'll see later. For the U.S. and the ex-U.S. submission, we feel very comfortable and confident, again, based on the data that we have. In the U.S., the lesion growth is the primary endpoint that matters. In Europe, as you know, at 24 months, we will look at the correlation with functional endpoint. It's important to note there that for the functional endpoints, only a directional change is required. That's in summary. Thanks so much for taking our question. Thank you, Anupam. Thank you. Our next question will come from Madhu Kumar with Goldman Sachs. Please go ahead. Hey, thanks for taking our question. Following up on the question around timing of data. Is there a data cut between 12 months and 24 months where you can look at DERBY and OAKS to see whether additional separation is achieved on GA lesion growth to see whether DERBY does change over time to crossing that statistically significant threshold? How should we think about future cuts from this data? Is it really just 12 and 24? Is there anything in between? How should we think about that? Thank you, Madhu. Next time point is 24 months. That's the next data cut. These patients are continuing to be enrolled, continue to be followed. There's nothing between now and the 24-month time point. I think your question is referring also to the increased effect that we saw in FILLY. That is something that we continue to be very interested in and that we will have a better chance to evaluate when we get to that time point. Okay. Following from the earlier commentary around functional endpoints, in some of the upcoming presentations through the fall, will there be any kind of discussion of? Functional endpoints like visual acuity or other kind of features of visual function that are being assessed in DERBY OAKS? Yeah. Thank you, Madhu. The functional endpoints that are relevant and important in geographic atrophy are microperimetry and reading speed. Those we have in the statistical analysis plan and will be analyzed on a pooled basis at 24 months. That is not something on which we will present in the fall. Other ones, like visual acuity, which looks at the foveal vision, et cetera, all of that should come earlier. Okay, great. Thank you. You're welcome. Thank you. Our next question will come from Umer Raffat with Evercore. Please go ahead. Hi, guys. Thanks for taking my questions. I had a couple here, if I may. First, Cedric, as I look at OAKS, and I'm trying to eyeball the curves over time, so this is not precise, but it looks like the benefit in the first study, OAKS, is around 20%+ at six months, and it's in that same ballpark at 12 months as well. Again, the lead-in sizes expand. Is that consistent with how you guys see it? I'm trying to then compare that with DERBY, and it shows far tighter effect size at six months versus 12 months. Just trying to think through that. Secondly, COVID impact, if you could quantify if DERBY had a higher impact or more modeling went into DERBY from missed doses or COVID impact. Finally, what is your understanding of sort of spread of patients with a GA baseline lesion size above 14 or super high, and did that matter or not matter in phase III? Thank you very much. Thank you, Umer. As it relates to OAKS and DERBY over the course of 12 months, again, kind of the top line is what it is, right? At 12 months, we definitely do not see the increased effect that we saw in FILLY, and we'll have to look over the next 12 months whether that materializes or not. That's something to look forward to, but for which at this point in time, we don't have really a way to assess that sufficiently yet, neither in OAKS or in DERBY. As it relates to the impact from COVID-19, whether that would be more in DERBY or in OAKS. Look, running phase III clinical trials in the middle of a pandemic is, of course, a very complicated affair, and we had very dedicated patients, very dedicated physicians, and we are super happy with the quality of the data and how everything came together. Whether there was a different impact from COVID on these two studies, that is very hard to tell at this point in time. There are certainly geographical differences. You line that with timing, et cetera. It's possible, but at this point in time, we cannot really comment on that. For now, however, we do not believe that, for example, the missed injections had an impact on the readout of the studies. Your last question as it relates to the lesion size, that is a further analysis that will follow in the months to come, whether that had any effect or not. Thank you, and congratulations, everyone. Thank you so much, Umer. Thank you. Our next question will come from Phil Nadeau with Cowen and Company. Please go ahead. Good afternoon, thanks for taking our questions. I guess first, in your prior interactions with the FDA, has this scenario been contemplated where we have one positive study, one study that just missed the positive pool data? Has the FDA indicated to you in your prior discussions how they would deal with such a package? The short answer to that question is no. It is worth mentioning that we have three prospective, randomized, and well-controlled studies, right? We have OAKS with high statistical significance on monthly and every other month. We have FILLY with the same, and then of course, DERBY with a narrow miss. I think it's again, the consistency between the patient populations, the consistency that we applied to the imaging and to the analysis that we think makes this a very robust data package. Great. Second question, again, trying to grapple with the different data between DERBY and OAKS. Were there differences in foveal versus extrafoveal lesions between the arms or the trials? In both studies, we saw that differentiation between extrafoveal and foveal. The pre-specified analysis was on the pooled studies. We believe that this is a real signal and presents an opportunity to treat patients earlier in the course of the disease. I guess what I'm wondering is it does seem like the effect size on extrafoveal is a bit bigger than foveal. Were there more extrafoveal patients in one study versus the other? The distribution between extrafoveal and foveal was more or less the same between the two studies. Great. Last question, just on the 13 cases of inflammation, can you remind us how many of those were previously disclosed and came from the initial manufacturing lot versus how many were treated with subsequent lots of pegcetacoplan? Only six patients in this entire study were treated with that lot that had the cases of inflammation in the beginning. They are included in the full intent to treat or the mITT and are part of the inflammation cases as described here. Perfect. Thanks for taking our questions. Thank you so much, Phil. Thank you. Our next question will come from Steven Seedhouse with Raymond James. Please go ahead. Great. Thanks so much for taking the question. A couple quick ones for me. First, just wondering if you could maybe comment on the lack of a dose response, particularly in the pooled data and what you make of that. Then I'm also curious in the patients that had CNV, could you comment on how many of those received anti-VEGF treatment and remained on pegcetacoplan versus how many actually just discontinued pegcetacoplan? I guess I'll stop there. Thanks. Thank you so much, Steve. The lack of dose response is really something that we see kind of marginal differences, right, across the studies. Something where it definitely is not something that is pronounced, and where we truly believe that with every other month doses, we get the majority of the effect that we see with monthly, which provides a unique opportunity for patients to have a more convenient dosing regimen. Mechanistically, of course, that will require more work, but we're very excited about what that means for patients. As it relates to the CNV treatments, the majority of the patients that had exudation, as reported in the study, went on anti-VEGF treatment, and the majority of these patients continued to be on pegcetacoplan. Okay. Apologies if I missed it, but could you just comment on the inflammatory events? How are those distributed between the arms in the studies? Thank you. Yeah. All of the inflammatory events were in the treatment arms because it is important to note that in the sham control, there is no physical injection that takes place, right? It is really the investigator taps the eye but does not actually physically introduce a needle. The inflammatory events that are reported here are in the active arms. Okay. Do you know between monthly and every other month how they're distributed, or? I don't believe that we have that available yet, but that will follow. Thanks so much for the questions. Thank you so much. Thank you. Our next question will come from Justin Kim with Oppenheimer. Please go ahead. Hi. Good afternoon. Thanks for taking the questions. It's encouraging to see some of the hypotheses around exudation rates in FILLY align with the findings in DERBY and OAKS. Just wondering, appreciating the data are still early, was there any observed timing of onset that differed between the treatment arms? The short answer to your question, Justin, is no. I think you touch on something really interesting and which I believe is the hidden gem of these studies, right. It's the initial thing is, oh, my God, there was an arrow missing in DERBY. What does that mean? Is the effect size something that is commensurate with the clinical benefit that we need? It's important to go back to how we went into these phase III clinical studies, right. We were hoping to have a treatment for monthly dosing in these patients, in these older individuals, with the possibility that there would be an overhang of exudations and ultimately the notion that there would be a risk versus benefit equation that a retinal specialist would have to go through before treating these patients. What we came out with here is a drug product that we believe can be given every other month with efficacy, and where the safety kind of almost completely removes the risk, right? Where on top of that, when you look at patients with extra fovea lesions, which is 85% of the patients before they get into the fovea, right, the effect size is 26% on monthly and 23% on every other month. That is at the end of the day why we are really excited. We believe that there's absolutely a path to approval here in the U.S., in Europe, and we believe that the product profile of this drug is actually really, really good for patients. That is something that we believe ultimately will materialize. Okay. Got it. Great. Just maybe just a clarification question. If I recall, one of the studies assessed microperimetry. Am I correct? Can you remind us which study that would be? That is in the OAKS study. Okay, great. Thank you. Thank you, Justin. Thank you. Our next question will come from Colleen Kusy with Baird. Please go ahead. Hi. Thanks so much for taking our questions. On the comparison of the untreated fellow eye, as you pointed out, the difference in the monthly arm for DERBY is there's a faster growth rate in the untreated eye. Do you have a sense of what could be driving that? Any sort of imbalance? Yeah. Colleen, it's really, really tempting to go there and come up with all types of hypotheses. We're going to be looking much more into that in the months to come. What I do think is important and important to bear in mind here, right, is that the physicians, by protocol, were instructed to treat the worst eye in terms of vision. Therefore, it's not a surprise that in the sham control arm, the fellow eye is actually slower moving than the study eye, right? To see that inverted and see that consistent with contralateral or with the, sorry, the every other month and the monthly groups, again, is another stamp in the direction where we want it to go. It is also very similar to what we saw in FILLY, again, on the similar, same patient population. Great. That makes sense. Thank you. Could you I guess, have you talked to the FDA about, or have you considered filing in specifically GA with extra foveal, or would you pursue a broad approval? Thank you, Colleen. This was a study that was designed and run to treat all patients with GA, regardless of where the location of the atrophy takes place, right? In this pre-specified analysis, we were specifically interested in knowing whether there would be a differential effect on these early patients. Again, the reason why we stress it in the top line and why we think it's important is because when you have a newly diagnosed patient with GA sitting with a retinal specialist, right, you can tell that patient, "This is what the data tells us you could gain in terms of benefit." We have the opportunity probably to do this every two months instead of monthly, right, in a way that's safe. That is why we pointed out as something important, the study was run on all patients with GA. Great. Thank you for taking our questions. Thank you. Thank you. Our next question will come from Tazeen Ahmad with Bank of America. Please go ahead. Hi, guys. Good afternoon. Thanks for taking my questions. You did have pretty impressive safety profile as it relates to exudation rates, and thanks for clarifying what they were. To drill a little bit deeper, can you confirm whether those exudation rates that are in the press release are rates that are similar between the two studies? I think those were the combined rates. Then I have a couple of follow-ups. Yeah. They were of course, not identical, but close enough for us to report it as we did. These are consistent numbers across the two studies. Okay, great. Then just to clarify for the two studies, can you say today whether or not those had meaningfully different dropout rates and/or whether the number of missed doses was meaningfully different between the two? I mean, the one thing that's standing out for me as I look at the data is that you had one study where both the every month and every other month arm performed well. Heading into this readout, frankly, I think most people were expecting that the every other month arm would just not perform. It looks like there seems to have been pretty good compliance in at least one of the two studies. If you don't have that information now, I'm just curious when would we be able to see that? Thanks. Thank you, Tazeen. Details on these will follow in the months to come at the conferences as we dive deeper into the data. For now, I can tell you that dropouts rates and differences between missed doses, we believe do not account for the differences that we see here. I think at the end of the day, something accounts for this. I want to, again, kind of point you in the direction of the fact that we have not two, but three well-controlled studies, in which in one we narrowly missed and with high statistical significance in the other two, which makes us believe that we have a solid path to approval. Okay, thanks. You're welcome. Thank you. Our next question will come from Alethia Young with Cantor Fitzgerald. Please go ahead. Hey, guys. Thanks for taking my question. A couple. One, I might heard this, but can you guys clarify if you're going to try to file on both the monthly and every other month arm in the study, especially when we think about, like, in light of this pooled analysis? Just can you give us a little bit of perspective about how you think doctors will think about 1 trial working, 1 trial not, then you have the phase II that did work as well. How do you think that's going to come together for them as well? My third question is just do you think the protocol differences for the exudative events actually helped in DERBY and OAKS? Okay. Thank you so much, Alethia. Well, as it relates to the monthly and every other month, as you know, in a submission, you include all of the data. We believe based on the data that we have, that we have a drug that is efficacious both for a monthly and for every other month. The pooled sham data is just kind of a beautiful pre-specified analysis that kind of further confirms our belief in the activity of the drug, but everything will be included there. As it relates to the doctor's feedback, we have been talking to some KOLs and will of course be talking to many more. That has been overwhelmingly positive so far. I think that physicians, the ones that we spoke to, looked at the totality of the data, looked at the unmet need that exists in this field. I think that the every other month dosing and especially the favorable safety profile that we have, makes them very excited about finally having an option available for these patients. That is as far as doctors are concerned. Your third question, you were breaking up a little bit on the exudation. What was your question there, Alethia? Just the protocol differences in phase III versus phase II, do you think that's what essentially helped the rate become lower? Yeah. We reported these as physician-reported exudations in the phase II and in the phase III. The principal reason why there is a difference in terms of exudations is we believe really related to the fact that the patients that enrolled in the study in phase III had a prevalence of fellow eye wet AMD that is much more representative of the overall population being at approximately 20%. In the phase II clinical trial, as you may recall, that was 38% of patients. These subjects have a threefold higher chance of developing exudations. That undoubtedly contributed to the imbalance between the phase II and what we saw in the phase III, along with the better control, of course, of how this is read out and done. Great. Thanks so much. You're welcome. Thank you. Our next question will come from Ellie Merle with UBS. Please go ahead. Hi, guys. Thanks for taking my question. Just going back to the analysis that you have on slide 11 around the lesion growth in the untreated fellow eye. Can you talk a little bit maybe about the implications of the differences between what was seen there between DERBY and OAKS, and I guess maybe any conclusions we can make about what this suggests about kind of the underlying patient population, if at all? Then just in terms of the exudations, just can you comment maybe on average when time-wise in the study the exudations were seen and maybe the, also the average length of anti-VEGF usage if patients were able to discontinue anti-VEGF usage? Then last question, sorry, logistical one. Sorry if I missed it, but just what percent of the patients on the studies overall had the extrafoveal lesions versus foveal? Thanks. Okay. Thank you so much, Ellie. First of all, there was lots of questions in one thing. The untreated fellow eye. I want to reiterate what this means. If you have patients with bilateral GA, it is well known from natural history that those patients, when you analyze them on a pooled basis, have two eyes that progress at similar rates. Right? Now if you look at the fellow eye, you can actually have a determination of what the underlying growth pattern is in these patients. In the sham control, for example, in FILLY, as well as in OAKS and DERBY, we see very similar rates between the shams and the untreated fellow eye. You could say, "Oh, that's a great control. Why don't you use that in your studies for your primary endpoint reader? Well, we don't do that, us or anybody else, because there's something called a fellow eye effect. With many drugs, when you treat one eye, the fellow eye can benefit from that. Imagine in this study, it's not inconceivable that the fellow eye could have slowed down because of the treatment in the study eye. Right? Nonetheless, in spite of that possibility, even if you factor that out, we see this very interesting pattern of an effect. When you then look at the baseline progression in the fellow eyes of these patients in isolation, and you look at the sham compared to the active arms, we see this pattern where, for reasons we don't understand and cannot explain, that the sham patients seem to have been slower progressers by nature than the patients that were actually enrolled in the active arms. That especially stood out in the monthly arm in DERBY. As it relates to your second question, I tried to write it down so I could follow it, but when did the exudations take place? We don't have a pattern there where there is a time period where it happens more than in others. That's very similar to what we saw in FILLY as well. The time of VEGF treatment. When patients went on anti-VEGF treatment, which again was the majority of these patients with exudations, we put them on per protocol treatment with either Eylea or Lucentis, per posology, so per label. There's no kind of moment in time where physicians during the study could discontinue that. In the GALE study, which is the three-year extension study for DERBY and OAKS, we will actually stop treating patients with anti-VEGF, and we will find out if they need continued treatment with anti-VEGF. That's something to look forward to, but that we don't have data on yet. As it relates to the percentage of patients that have extrafoveal lesions. Again, as I mentioned, the majority of patients, reported as high as 85% of patients, start off geographic atrophy in the periphery with extrafoveal lesions, and then afterwards, ultimately, typically towards the end of the disease, the fovea becomes involved. It's kind of well known that the fovea, again, for reasons we don't really fully understand, is more protected against the growth of GA than the periphery of the macula. Sorry, just in the studies themselves, in DERBY and OAKS, what percent, I guess, were extrafoveal versus foveal? Sorry. No, sorry. In the study, approximately 60% of the patients that were enrolled were patients with foveal lesions, and the remaining 40% were patients with extrafoveal. Got it. Thank you so much. Sorry for so many questions. You're welcome. Thank you. Our next question will come from Matthew Luchini with BMO. Please go ahead. Hi. Good afternoon, and thanks for taking the questions. Two from me, I think. First, just given the stronger effect in patients with extrafoveal lesions, can you comment on at least if there was directional benefit in foveal patients? I apologize if I missed that. Secondly, going back to the physician feedback that you have heard. Previous to today, you've emphasized a lot this idea of a 20% difference as being the minimum clinically relevant threshold as outlined by your KOL feedback as being an important cutoff. I'm just trying to get a little bit of a gauge on what you're hearing, 17% is obviously close to 20%, but just a little bit more on the actual results here, if you've had a chance to discuss them. Thanks. No, thank you so much, Matt. I think as far as it relates to the directional difference that it makes in foveal, the answer to that is yes, and we'll share more data on that at meetings to come. As it relates to the clinical benefit, this is absolutely a number that circulated and was important. It's important to contextualize that 20% number. You have to remember that that is the type of benefit that physicians thought of in the context of a product that was believed to be needed on a monthly basis, and that was believed to be potentially associated with these exudative events. Right? The increased safety profile that we have seen, the favorable safety profile, we believe lowers the thresholds for the efficacy need as well. In combination with that, again, the extrafoveal, where you are at 26% and 23% for monthly and every other month, respectively, which no one would argue is well within the clinical meaningful threshold. We have circulated that with Key Opinion Leaders, and again, as I mentioned earlier, the feedback there has been very positive. Great. Thank you. Thank you. Thank you. Our next question will come from Chris Howerton with Jefferies. Please go ahead. Hi. Excellent. Thanks for taking the questions and congratulations on the results to you, Cedric, and the team. I think most of the pertinent questions have been asked at this point. I guess two from me. One would be just following up on the fellow eye analysis. Obviously, I hear you that you're saying that they both ought to progress at basically the same rate. I'm curious if there's a meaningful difference in the baseline lesion size between the study and fellow eye. Do you think that that could account for a meaningful difference in terms of the growth rates between the two? The second question is just a standard Wall Street question, check the box. Could you give us a current status of your cash balance and expected runway? Thank you. Yeah, thank you so much, Chris. Again, the fellow eye, we think, is a really important kind of confirmatory analysis of efficacy. It's one that we used in FILLY, as you may recall, and it is one that we are applying to these studies as well, to really give us confidence in the data as we see it. The difference in lesion size, patients with large lesions progress more than patients with small lesions. That is something that is, of course, well known. This is also why in the FILLY study, we did the square root analysis, which we did not do in the phase III clinical trial until the overall lesion sizes. Whether that played a role or not, currently does not seem to be the case, but we're going to do more work on that, and more will follow. As it relates to the cash question, I'm going to hand it over to Tim to answer that for you. Yeah. Thanks, Chris. We ended the second quarter with, excuse me, approximately $600 million in cash, that gives us approximately year in runway. Obviously at some point, we'll have to finance again. We figured we'd wait for the data and see how that goes and then take our time in figuring out what that plan is. Okay, very good. Thanks for taking the questions. Thank you, Chris. Thank you. Our next question will come from Joseph Stringer with Needham & Company. Please go ahead. Hi, everyone. Thanks for taking our question. Most of our questions have been answered already, but just to circle back on potential EMA discussions with EMA. In terms of, as Cedric previously mentioned, just need to see a trend on the functional endpoints, reading speed, and microperimetry. Just curious if any of these scenarios in terms of 1 trial meeting the primary endpoint or another 1 missing the primary endpoint came up in your discussions. I guess were there any qualifiers in terms of, or prerequisites for 1 or both or the pooled hitting primary endpoint in addition to the trending on the secondary endpoints? Thank you. Yeah. Thank you, Joey. Neither with the FDA or with EMA did we discuss in advance that particular eventuality. That's, at least in our experience, not how these discussions go, right? Again, the totality of the data makes us very confident with the FDA in the U.S. as well as with EMA. It's important to point out here, and I'm kind of rehashing the obvious here, but that when we look at the growth of GA in the eyes, we look at the continuous loss of photoreceptor cells. That ultimately will translate into a functional difference, right? It's just a matter of how long does it take to see that, considering the variability that exists in these endpoints, and how do you pick it up? It can be hard to measure. We fully expect at the two-year time point that these functional endpoints will start following what we see on an anatomical basis as well. Great. Thanks for taking our question. You're welcome. Thank you. Our next question will come from Yigal Nochomovitz with Citi. Please go ahead. Yeah. Hi. Thank you very much for taking the question, Cedric. Not sure if this was asked since I jumped on late. For the phase III trials for DERBY and OAKS, did you measure vision? If so, could you comment at all on whether you saw differences in BCVA among the three arms of each study? Thanks. Thank you so much, Yigal. Our visual acuity measurements will follow at later conferences. They were of course tracked, but as you know, in geographic atrophy, visual acuity is mainly something that we track out of concern for safety. Visual acuity, as a quick reminder, is foveal acuity. Really is the piece in the middle that you need to read a reading chart, and that in GA is actually protected until the very end when you lose that. The reason why GA is a disease that significantly impacts function without necessarily impacting visual acuity is because imagine reading a chart through a little tube, but then having to walk around on the street with that, of course, is a very different story. Visual acuity will follow, but in the context of the efficacy evaluation was not something that was important for now, but will come in the months to come. Okay, got it. I just want to make sure, going back to slide 11, the untreated fellow eye underlying lesion growth. I just want to make sure I'm understanding this correctly. You're saying that in the monthly arm for both DERBY and OAKS, in the untreated fellow eye, actually saw a faster increase in GA lesion growth as compared with the sham or the every other month, which would seem a little counterintuitive, maybe. Yeah, no, you're absolutely correct. The untreated fellow eye in the active arms of both studies were progressing more quickly than the untreated fellow eyes in the shams of both studies. Yeah. Okay. Was that result a surprise for you? To me, it seems a little bit maybe counterintuitive. It was a surprise to us, absolutely. Yeah. Okay. Got it. Okay. Thank you so much, Cedric. You're welcome. Thank you. Our next question will come from Laura Chico with Wedbush. Please go ahead. Good afternoon. Thanks very much for taking the question. Just a couple clarifications since it's a longer call here. First, I just wanted to clarify, in terms of the extrafoveal analysis, did patients in DERBY actually demonstrate a similar benefit as they did in OAKS? This is specific to the extrafoveal patients. Yes. This is an effect that we saw across both studies. Got it. Okay. In terms of the discontinuation rates, I'm just wondering if you could kind of circle back on that. I don't think I actually heard you compare, perhaps, discontinuation rates in the studies relative to your prior expectations. What were discontinuation rates across DERBY and OAKS? Did they differ substantially? Yeah. We will talk about that more in the months to come, about the discontinuations and the missing images. Suffice it to say that this is not something that we believe meaningfully contributed to what we saw in these studies. Okay. Just lastly, you mentioned you're speaking with the regulators coming up here following the data release here. I'm just kind of wondering what outcomes might actually come about from the meetings, and would you imagine that you could get clarity on submitting pooled data at this point? Thanks very much. Thank you. Again, the pooled data is just one piece of the puzzle here, right? Remember, in OAKS, we have highly statistical significance, both for every other month as well as for monthly. We have that in FILLY as well. Then you have the pooled analysis, of course. When we do a submission to the FDA or to EMA, it is the completeness of the data package that will be evaluated and that we believe is very strong. Thanks. You're welcome. Ladies and gentlemen, thank you for participating in today's question and answer session. I would now like to turn the call back over to Mr. Cedric Francois for any closing remarks. Thank you so much, and thank you everyone for joining our call this afternoon. Our phase III DERBY and OAKS results are an important step forward in hopefully bringing pegcetacoplan to the millions of patients living with GA. From the beginning, we have been convinced that controlling C3 provides unique therapeutic benefits, as it is the only target in the complement cascade that can control all of the damaging downstream effects of complement activation. This has been demonstrated in our commercial product in PNH and now in the first positive phase III in GA, further underscoring the potential of targeting C3 to develop transformative treatments across a broad range of debilitating diseases driven by complement. Thank you. Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.