All right, welcome everyone to the 44th Annual J.P.Morgan Healthcare Conference. My name is Anupam Rama. I am one of the Senior Biotech Analysts here at J.P.Morgan. I'm joined by my squad: Joyce Zhou, Priyanka Grover, and Ratih Pinhey. Our next presenting company is Annexon and presenting on behalf of the company, we have CEO Doug Love. Doug.
Thank you, Anupam and J.P. Morgan. We're delighted to be here for our 10th J.P. Morgan presentation. A decade into the journey, we're more excited than ever to achieve our mission of delivering game-changing immunotherapy for patients suffering from devastating neuroinflammatory diseases. Grab a quick water, sorry. And so we're going to dive right in. Hopefully, I'll get my voice back. Oh, let's see. Great, there we go. I'll be making forward-looking statements and invite you to review our materials on file. All right, for those less familiar with Annexon, we're a Bay Area-based biotech company leveraging our unique immunotherapy platform to unlock the next era of new neuroinflammatory diseases to treat millions of patients suffering from these diseases.
We're led by two blockbuster registration stage programs with the opportunity to treat more than or to address more than $10 billion of market opportunities with these diseases and treat more than 10 million patients on an annualized basis. Our lead program is in dry AMD with geographic atrophy, a devastating disease, a leading cause of blindness, and our lead program, or drug candidate ANX007, has demonstrated outsized vision protection in this population. Our second drug candidate is ANX005 targeting Guillain-Barré syndrome, an acute neuromuscular disease, a really very significant disease. We've run the first programs in this therapy in this disease area in the last 40 years and demonstrated a robust win in our phase III program and now are pursuing global regulatory approvals.
Each of these programs are transformational and have the potential to completely reshape the treatment paradigm in their respective markets, as well as being market leaders in those areas as well, and so we're really excited to be advancing those as we move through 2026. 2026 is indeed a pivotal year for significant value creation for Annexon. Leveraging our clinically validated platform and our diverse portfolio of drug candidates, we have several key milestones over 2026 that we are seeking to achieve. First, with ANX007 and geographic atrophy, we will be releasing phase III data in the second half of this year, which we really are looking forward to. For ANX005 and GBS, we have filed for European approval last week, and we anticipate filing for approval of this drug with the FDA later this year.
And last, and certainly not least, is ANX1502, the first oral small molecule candidate targeting a host of autoimmune conditions targeting the C1 inhibitor. There we will have the first proof of concept data set in a Cold Agglutinin Disease population also later in 2026. Coupled with that, we're really well positioned to make the markets in each of these three therapeutic areas with funding into late 2027 or more than a year after our GA readout and the know-how to make these markets with effective targeted medical education, pre-commercial activities, and the like. So overall, we're really quite excited about the look ahead for 2026. Now, everything we do and our competitive advantage comes down to our scientific approach in our overall platform. Based on the discoveries of the late Dr.
Ben Barres, former chair of neurobiology at Stanford, Ben discovered the role of targeting C1q, the initiator of the classical pathway, which drives harmful inflammation in a host of neuroinflammatory diseases. Importantly, this approach is quite different from downstream first-generation approaches targeting C3 and C5, which provide some protection against harmful inflammation, but it's incomplete. As a result, we have seen differentiated efficacy and safety in all of the diseases that we have pursued in which they have also studied diseases like GBS, geographic atrophy, ALS, and more. And I'll show you some of that data. Based on this pipeline or this platform approach, we've built a robust pipeline that's diversified by drug candidates and types of diseases that we're pursuing. The common denominator for all of these diseases is C1 and the classical pathway, and we're targeted differently in different compartments of the body, brain, and eye.
With ANX005, we are targeting Guillain-Barré syndrome, which blocks C1q throughout the body as well as in the brain. ANX007 is a fragment of that, which selectively blocks C1q solely in the eye compartment. And of course, ANX1502, the first small molecule that I alluded to, blocks C1q in the body only in a host of autoimmune conditions. So we're really excited about where these are and where they're going. And importantly, the learnings from these lead programs have really informed what we're doing with our next wave programs.
We've got multiple next wave programs, all of which we've already studied in the clinic, and we look forward to updating next steps on them as we progress further into the year. One of the key interesting aspects of Annexon as we think about 2026 is this opportunity to cash in on our asymmetric value opportunity.
With two lead blockbuster late-stage programs, we have the opportunity to create really unique value not only for patients, but for shareholders, particularly in comparison to the first-generation drug candidates who have set a strong foundation or precedent for value creation at the phase III and registration stage. That's exactly the stage we're at. You see where our value is in relation to these opportunities. And so this is not a bad time to think about joining us on this journey. Last but not least, in our windup, we're led by a very seasoned crew of biotech leaders. Collectively, we have more than 100 years of biotech experience ranging from corporate through research, development, of course, commercial, a lot of experience bringing first-in-kind drug therapies, blockbuster therapies in a range of diseases.
We always talk about internally, the game actually doesn't start until you run into adversity and figure out how to navigate through that. We've been able to do that over the last 10 years, and we're now at an inflection point for which we're really quite excited. So with that windup, let me take you through some of the programs for which it is generating this excitement, the first being ANX007 for the treatment of geographic atrophy and with the potential to be the first vision-sparing therapy in this space. You all may be familiar with geographic atrophy, but suffice to say, the unmet need remains, and it's really quite significant.
And that's because there are multiple approved therapies, but none of which have been approved to preserve vision in this very large patient population, 8 million patients worldwide, a million and a half to 2 million patients in the U.S. alone. And one of the really unique characteristics of geographic atrophy is it is indeed a disease of aging. So it strikes patients at a really vulnerable time. The average age of the patients entering into our study is 79 years old. And as you can see in the picture here on the right, they're losing their central vision. So at that point in their life, they're in effect losing their independence. They lose the ability to make out faces, to read, to make their breakfast in the morning.
And so it's a really significant disease for which we are sharply focused on and ensuring that we can at least preserve their vision and allow them to operate independently. One of the questions we get regularly is, how are we able to demonstrate vision preservation when the early generational programs targeting C1, C3, and C5 were unable to do so? The short answer is by blocking complement right where it starts on disease tissue, we're able to preserve against the loss of photoreceptor neurons that are responsible for visual acuity. geographic atrophy is a disease of neurodegeneration. You very rarely hear that said, but indeed, that is what it is. When you lose your photoreceptor neurons, you lose your ability to see. C1q localizes on photoreceptor cells and synapses shown here in the blue and red on the far left.
This is a picture, a histopathology of a geographic atrophy patient's eye. You can see here on the left in blue and red, the photoreceptor neurons are in red or in blue. The photoreceptor synapses are in red. That connects the neurons and allows you to see. Really, really critical. On the far left, those are fully intact, and so that's a healthy aspect of the retina. As you move closer to the right, however, you can see that the photoreceptors in blue and in red become dysregulated and actually become sparse and begin to go away. It's only at the far right when you actually begin to see loss of RPE cells or lesion growth.
The two programs that have been approved prior to us are studying against the loss of RPE cells, which are in green at the bottom there on the far right.
The challenge with that is by the time you are targeting RPE cells, you have already lost your photoreceptors and your photoreceptor synapses, so you have already lost your vision. Protecting against the loss of RPE cells is a good thing to do, but it will not preserve your vision. And we see that not only in our data, but we see that in the approved drugs data where you're looking at three, four years' worth of data where they're protecting photoreceptors or RPEs in the neighborhood of 20%-30%, but they have no vision preservation. And so it's a completely different mechanism targeting complement upstream versus downstream. And that's the key takeaway for what we're doing. And I can show you that with actual data.
Looking in the central retina of the patients in our phase II, we're able to measure protection against loss of photoreceptor cells in the eye. Here we're showing a whopping protection of between roughly 50% and 60% of your photoreceptors in the central retina of the eye that is responsible for visual acuity. This data has never been shown before by any other therapy or approach in the geographic atrophy space. And it's just simple math. If you protect the neurons that are responsible for vision, you will protect vision. And that's exactly what we did. Looking at the functional endpoints in our study, first on the left, looking at best-corrected visual acuity, 15-letter loss, this represents 50% of your vision loss over a one-year period of time.
By law, you are required to turn in your driver's license. So indeed, you have lost your vision.
What we demonstrated with ANX007 treatment every other month in the blue and every month in the red was a dose-dependent significant protection against vision loss. Patients who were not treated with ANX007 in the sham arm, 21% of them lost 50% of their vision in one year versus roughly 10% in every other month and roughly 6% in the every month arm. We are moving forward. We have moved forward the every month arm into our phase III study. Looking at a companion assessment of vision loss with LLVA or low luminance visual acuity, this is an assessment of vision loss in low light conditions. Rarely do we have perfect light, so it's important to show that your drug can protect against the loss of vision in all conditions.
And that's what this shows here on the right, where 20% of the patients who weren't treated lost vision versus 7.5% in those patients in the every other month arm and 10%. So a really profound effect. This is just a snapshot of our data. We actually protected vision on every measurement of visual acuity in the study. So we're really, really encouraged by the outlook for that. Importantly, by protecting vision with ANX007 on an every month basis, we reduced the risk of losing vision by 73% at month 12. That's a really significant number. So when a patient comes in to see a physician, the physician's talking point is very simple. If you take this drug, you reduce the risk of losing your vision over 12 months by roughly 75%. And that's really important.
It's also important to note that that protection against vision starts right around month six. And as you can see on this slide, it increases over time such that by month 12, the impact is greater. The longer you treat, the greater your impact will be in preserving against the loss of vision. And perhaps the most important slide, and certainly the most important slide from a regulatory perspective, is what ANX007 did in preserving vision on treatment versus off treatment, which really evidences its disease-modifying mechanism of action. The on-treatment portion is in the left, the unshaded area. And you can see, similar to the other slide, the prior slide, that starting right around six months, you begin to see protection with the treatment in the blue and the red through month 12 when we stopped the drug.
We then followed these patients for six months after stopping treatment. And what you see is the patients begin to lose their vision again after we stopped treating them. What's really important, however, is that we reset the baseline for the disease in these patients. Although they began to lose vision at a rate similar to sham in the off-treatment arm, they never caught up to sham. So we reset their baseline, which is important from a disease-modifying perspective. That's not chance. That's biology. And so we're really encouraged by that. We've taken these learnings to develop a really well-informed and well-powered phase III study.
It's virtually identical to the phase II study with some important kind of enhancements, one of which is we enrich for patients who are most likely to lose vision over a 12- to 15-month period of time, but they are not so far gone that you can't protect them against the loss of that vision. So we have a lot of information on how to do that, and we enriched this study for that, which increases our overall PTS. This is a large study, 659 patients, exceedingly well-run. One of the things to note is that as we went out and explained our data and our mechanism of action to physicians across the globe, studies run in the U.S. and Europe, the study was enrolled roughly two months ahead of schedule and over-enrolled by 30 patients.
That's a really good sign. Well-run studies tend to produce better outcomes.
The primary analysis is at 15 months. Recall that the phase II primary analysis was at 12 months, and the protection was getting bigger over time. At 15 months, it will get even bigger, and as I said before, primary endpoint is best-corrected visual acuity, 15-letter loss, what I showed you previously in the phase II study for which we had statistical significance. We have global regulatory alignment on this single protocol approval, so this is the study for approval. We've got PRIME designation in the E.U., fast track in the U.S., and so we're really encouraged at bringing forward the potentially first vision-sparing therapy for the treatment of GA. This study will read out, as I said, in the second half of 2026.
Last slide, as it relates to geographic atrophy, relates to the market opportunity. This is a mega blockbuster opportunity. The opportunity in this space is somewhere between $7-$10 billion on an annualized basis. What you're currently seeing in the space is the two approved drugs that protect against lesion growth or surrogate biomarker for vision, currently doing about a combined $1.5 billion a year in sales. Our view is by offering a drug that preserves vision, which is keenly most important to patients and the physicians, we have an opportunity to capture this entire market. And we're actively preparing for it. One of the things I didn't touch on is I showed you where we do on efficacy from a vision preservation perspective. I'll just quickly state that we also have a very differentiated advantage from a safety perspective.
Our drug is a very small fragment, 50 KD, low viscosity, and importantly, non-peylated. So we have not seen many of the safety events that have been observed in other clinical studies with GA, with other downstream complement approaches. And last but not least, because our mechanism is only blocking the classical pathway and allowing the lectin and alternative pathways to remain intact to perform their immune function, we have not seen conversion to wet AMD. You will recall that the approved drugs have conversion to wet AMD in the neighborhood of 10%-15%. Our conversion to wet AMD was virtually no different between sham and the treatment arm. So we like the overall benefit-risk from the profile of this drug, very differentiated from the drugs that are currently approved on mechanism, on efficacy, and also as it relates to safety.
Turning quickly to ANX005 and Guillain-Barré syndrome, a program that we are really, really proud of. This program represents our mission-based approach to make our drugs available to patients suffering from neuroinflammatory diseases around the world. Guillain-Barré syndrome is a gnarly disease. For those of you who are not familiar, as I said before, it is the number one cause of acute neuromuscular paralysis, and it is a sudden, indiscriminate, life-altering disease. The way it works is you get some type of preceding infection. It could be food poisoning. It could be the flu. It could be a vaccination. For whatever your immune system turns on, drives inflammation to clear that infection out of your body, which is its appropriate role. Sometime later, two to four weeks thereafter, your immune system drives inflammation, this time attacking your peripheral nerves.
Two or three days after that, you are oftentimes bedbound with the inability to walk without assistance. Two or three days after that, many, many patients, one in four, are on a ventilator in the ICU. You are otherwise completely normal when you are struck with this disease. Fortunately, it is a rare disease, but it is not a small rare disease. It impacts 150,000 people worldwide, 8,000 in the US, 15,000 in Europe, and there are no approved therapies. IVIG is used off-label. It has not been studied in randomized studies.
It has a modest effect on this disease, but even with IVIG, 30% of patients are still going to the ICU, 75% are requiring ventilation in the ICU, and 20% cannot walk after one year. And so there is a real need to tackle this disease. It is a very expensive disease. Patients are hospitalized. Patients are in ICU. Patients are ventilated.
They ultimately will go to skilled nursing facility, physical therapy, etc. It costs the healthcare system in America more than $7 billion a year to treat 8,000 patients. These are million-dollar patients. And so we're encouraged at getting after this and providing a real solution with a targeted immunotherapy that's fast-acting and it's complete. And I'll show you some information on that. Importantly, from a market opportunity, although it's a rare disease, it's a unique disease in that it's actually a blockbuster opportunity. And the reason for that is 23,000 patients a year get this disease. 90-plus %, actually it's 95% of patients get treated currently with IVIG or plasmapheresis.
So you have a ready-made market. Everyone gets treated because of the devastating nature of the disease. You're trying to stop it as quickly as possible. And it's a very concentrated commercial market here in the U.S.
Our top 50 healthcare systems see more than 50% of the patients on an annual basis. And so that allows you to target your resources, your sales force, your MSLs, your medical education, etc., towards that. And then I'll just say ANX005 is very uniquely situated to capture this market. It's a single infusion that shuts down this entire inflammatory pathway. 90% of the patients that we treated improved by week one. The safety data looks like placebo, which is really, really important. And we offer a potential savings to the U.S. healthcare system based on other measures, which I'll show you momentarily. Looking at our study, one of the key measurements in the study are these inflammatory biomarkers that are responsible for driving the disease.
There's 25 of them. In our study, ANX005 reduced all of the biomarkers within the first week of treatment. Really, really important.
Whereas when you look at IVIG and placebo on the right side in this panel here, they had no effect on these biomarkers. What that tells you is that the current treatments actually are not immediately arresting the disease, which is leading to the large disability that occurs with this disease. By knocking down these biomarkers rapidly, what we showed is that by week one, we were able to have a significant impact in returning your muscle strength. This is a 10-point improvement on MRC sum score, which is a whopping score versus placebo, and by doing so, by week 26 or month six, we gave patients a two and a half times greater likelihood to returning to a normal state, completely unheard of in the history of this disease, and we're really excited about that.
Most important to patients and healthcare providers, it's this slide here and some of the data. With our treatment in our phase III study, we were able to return patients to walking 31 days sooner than placebo. We got them off a ventilator 28 days earlier. We got them out of the ICU seven days earlier. So we were able to return patients back to their activities of daily living much sooner than had they not been treated with ANX005, which is really, really important from a patient's independence perspective and also from a value perspective. There are hard dollars associated with being in the hospital and with being on a ventilator in the ICU, and we're saving all of those dollars. So we're really, really encouraged.
One of the things I didn't mention is that our phase II program is the only, or our phase III program is the only placebo-controlled program that's been run in this space in 40 years. And so we're encouraged that we were able to go ahead and do this. We are now running an open-label FORWARD study. We're calling the FORWARD study in the U.S. and EU. All patients are getting treated, and we're encouraged by the early results and what we're seeing in that study. This is just an example patient that I have here. This patient came into the study with moderate to severe disease, meaning that he was bedbound and hospitalized. We were able to treat this patient within four days of signs and symptoms. By day eight, the patient walked out of the hospital with a cane.
Really a stunning outcome, but very consistent with what we saw in our phase III study. And by day 29, the patient was walking independently. And so we're continuing to run this study. It's really important that physicians get experience with our drug in the U.S. and Europe. And we'll also be providing this data as part of our BLA submission package to the FDA in 2026. So with that, I'm going to come to a close. This is a really important year, as I said, 2026 for Annexon. It's a transformational year to create outsized value for patients and our shareholders. We're sharply focused in really changing the treatment paradigm and geographic atrophy with our phase III data later this year and getting ANX005 approved in GBS worldwide for the 150,000 patients afflicted by that.
And then last but not least, our mid-stage program, ANX1502, we will have proof of concept data in that as the first oral inhibitor for a host of neuroinflammatory autoimmune conditions that are currently being treated with IVs and subqs. So an opportunity to really shape the market in that space as well. With that, thank you for your attention, and we're open to any questions, yeah.
Thanks, Doug. I'll ask the first couple of questions, but we'll also open it up to the audience to get their questions in. Just raise your hand and I can call on you. On just ARCHER II, can you remind us what the powering of the study is and kind of what would be a win scenario? You're obviously moving with the monthly, which had a 73%, I think. Yeah, 73% reduction of risk. Yeah, really good question.
The phase III is powered, as a standard phase III would be powered to a high power, so greater than 90% power with regard to that. A win is any statistical win on best corrected visual acuity. No drug has ever demonstrated that before other than our drug in the phase II study. That's protecting 50% of your vision. Any significant win on that measurement is considered clinically meaningful. But if I could push, what are you assuming in the sham arm of what kind of decline you would see there and then what kind of benefit on top of that would be clinically meaningful? Yeah, in the sham arm, what we saw in our study is that when you confirmed at 15 months, patients lost about 15%, high teens, 17-18% in the sham arm.
You saw our treatment effect in the phase, and I'll just kind of go back to that while I'm kind of talking you through that. In our treatment arm, we saw a protection every month group of roughly 6%. We did a conservative powering estimate, meaning we reduced what we anticipated the sham arm would be in our phase III study, and we also reduced the treatment effect on what we would see on the treatment arm from ANX007. So we were conservative on both ends of the barbell to ensure that we're exceedingly well powered for this phase III win. Your competitor actually talked yesterday or maybe a couple of days ago about having a prefilled syringe really opening up the market. Do you guys have plans for a prefilled syringe? Absolutely. Yeah. And really uniquely situated to do so.
As I said before, ANX007 is a drug that is a very small Fab fragment, 50 KD, and perhaps more important, it's really low volume, 25 microliters, which is about a quarter of the microliter levels of our competitors. They're about 100. What that makes it is uniquely situated for a prefilled syringe. So we're doing that as well as extended release formulations for the commercial presentation. We'll launch with every month, but ultimately be looking to dose this drug once a quarter or so. And how are you thinking about the OUS opportunity for the drug? It's been difficult for competitors. Yeah, really, really important for us. Again, because we are studying vision, visual preservation, best-corrected visual acuity, we have full alignment with the regulators in the EU for approval of this drug with a win on this study here.
And so there's three plus million patients in the EU who get GA every year, and it's a meaningful commercial opportunity. We've got prime designation with the FDA, with the Europeans, which is in effect breakthrough designation in Europe, which we're encouraged by. They've also assigned a specific product development coordinator to our program. This is a pilot program that's being run out of Europe for 17 select programs of high interest for the European regulators. So we really have an opportunity to have up close and personal interactions with the regulators in Europe on this program. We've had multiple interactions. So we're really encouraged with the outlook for the approval of this drug in Europe as well as in the U.S. Questions from the audience? Yeah, over there. Yeah. Will there be any timeline for the GBS?
Because we decided to talk with the U.S. government, and I don't know what kind of data we still need to have a conversation with the FDA.
Yeah, really good question, so as I said before, we filed for regulatory approval with the E.U. last week. That package consisted of substantial evidence as well as a generalizability assessment. That'll be the same package that will go into the FDA, but we will supplement that package with additional U.S. and European data from this open-label FORWARD study. This is why this study is so important. We have real-time data that we're able to provide the regulators here in the U.S. in conjunction with that submission, and so once we get an appreciable number of patients in this study, and it's enrolling pretty well as we sit here today, we will then go see the FDA and submit our package. Thank you.
Go ahead. Just following on from that, would you then plan to launch in Europe before an FDA approval? It's a really good question. That's a TBD. The hope is the European review process is a bit longer than the FDA's process. Typically, it's 12 to 15 months. The thought is, depending upon when we submit for approval here in the U.S., approval will be close in time with the Europeans, in which case we would certainly prioritize launching in the U.S. first to establish pricing and other things before going to Europe. Understood. Thanks.
Just one question. That's a really good question. What's going to be the size and scope of the FORWARD study? And has FDA talked about how much data and follow-up you need from FORWARD study to file again? Yeah. So the FORWARD study is currently up to 30 patients.
We don't believe you need 30 patients to actually add as a supplement to our overall submission package. We have not had a specific discussion with the FDA on the number of patients, and so we intend to just go in and let the data speak for itself. One of the things that's very unique about ANX005 and GBS is the data is highly consistent. As I showed you before, 90% of the patients roughly got better at week one. We anticipate that's what we will see in the Ford study. We also know the PKPD profile of our drug, having dosed our drug not only in GBS now here in the West, but also in diseases like Huntington's disease and ALS, so the PKPD profile from a bridging study is already well elucidated.
So we anticipate it's just a handful of patients that we would need to support our overall package. But we'll have that discussion with the FDA once we have the data in hand, the full data set. Questions from the audience? Go ahead. Yeah, I just watched very closely about your data about GA. And for the inflammation rate, I think it's much higher than Regeneron Eylea in wet AMD. So is there any improvement maybe about the injection procedure or maybe we have a longer half-life? I'm not sure. Could you maybe repeat that?
You said what was it? Yeah, yeah, yeah, yeah, according to your data, and I noticed that the inflammation rate. The what rate? Inflammation rate.
Inflammation.
Yeah, is higher than something like in like a wet AMD. Yeah. Well, these are very different diseases. So the thing with wet AMD is a very fast-acting disease.
You actually, your endpoint there is actually vision enhancement, whereas in geographic atrophy, the way that the inflammatory disease process plays out is very different. And so what you're looking to do is just preserve the loss of vision. It would take years, if ever, for you to return vision. In fact, I think it's unlikely because with inflammation playing out over the course of a slow-acting disease, you're losing your photoreceptor neurons. They're dying, and they don't regenerate. When you lose neurons, they don't come back. So it's really not a good corollary to compare wet AMD to dry AMD. They're completely different diseases.
Maybe we could touch a little bit on ANX1502. I noticed that you're going to have some POC data this year.
Just walk us through where you are in terms of what you're trying to accomplish in the proof of concept study relative to what you learned last year about the compound. Yeah, yeah, really good question. So this is an audacious program.
Let me just start there. No one has tried to bring forward a small molecule program for autoimmune conditions, particularly neuromuscular autoimmune conditions. But given our research and our learnings with our antibodies and our understanding of the pathway where we have more than 40 de novo assays, we've made drug candidates against every node of the classical pathway. We've ventured into the small molecule space, and we've taken learnings every step of the way. As you alluded to, Anupam, last year, what we learned is that our drug initially in its film-coated presentation caused a bit of emesis in patients.
And so we switched over into an enteric-coated formulation, which solved that topic, but it created a new topic in and around a food effect. And so what we've learned is that patients really need to be fasted around two hours or so before or after taking the medicine. And then it appears that the drug has exceeded our target drug levels. So we are now running the proof of concept study where the patients are fully fasted. This is BID dosing. They're fasted in the morning and in the afternoon. And we then want to see what their drug levels are. The key measurements for this are super objective.
So this is done in Cold Agglutinin Disease, and we're looking at hemolysis, namely looking at bilirubin and looking to bring down patients' bilirubin levels to levels of normal, as well as complement activation, which goes up exceedingly high in a disease like Cold Agglutinin Disease. So with really a well-controlled drug that does not have the food effect that we've seen here to date and the impact on bilirubin and complement levels, we'll be excited about moving this program forward. It may require some additional formulation work because I think we can probably solve this food effect with doing that. But first, we want to make sure we understand this drug's target drug levels. If it achieves the target drug levels, we consider that a home run. We'll then go solve the formulation topic and keep going forward with this.
Any final questions from the audience? Okay.
Thank you, Doug. All right. Thank you all.