Okay. Ready to go. All right. So, Apellis, welcome. Great to see you. So, of course, we have Cedric Francois, CEO and also the co-founder and president of the company, and Tim Sullivan, CFO. So, welcome for those listening on the webcast and then in person. I'm Yigal Nochomovitz, biotech analyst at Citi. Been covering Apellis since the very beginning, a long time. So, it's great to be continuing to follow the story. So, Cedric, you want to just give us an update. You have a new indication with a drug which was approved in PNH, but now you have a new and very exciting indication. So, tell us about how that's going. You reported some early data, but there's a lot more to come. So, let's start there, and then we can talk about SYFOVRE a little later.
Yeah. Thank you, Yigal, and thank you for inviting us.
Sure.
It's great to be here again in the warmth in Miami. Pretty cold in Boston, from what I hear. So, yeah. So, Apellis is a company that is focused and highly specialized in the complement pathways. We've made it our trade to try to understand, to the best of our knowledge, how this ancient part of our immune system affects disease. And we really understand the role specifically of complement factor C3 very well and have a good idea about the many disease indications and therapeutic areas where controlling C3 with pegcetacoplan and other modalities in the future can make a big difference.
The easy way to think about the Complement pathway, which is highly complex, it's like the clotting cascade with about 30 enzymes interacting with each other, is like an hourglass, where you have several ways in which that cascade can get activated with a central point and then several effector pathways emerging from that. That central point is Complement factor C3. And that is the point in that cascade that we have specialized in really controlling the way that we do. We are a commercial stage company. We have two approved drugs on the market across four indications. So, there is, of course, EMPAVELI, which was our first approved drug in 2021 in paroxysmal nocturnal hemoglobinuria, and now recently with an approval in C3 glomerulopathy and immune complex membranoproliferative glomerulonephritis.
And then, of course, SYFOVRE, which was the first treatment for geographic atrophy, the leading cause of blindness in the elderly, which was approved in 2023. We are more or less cash neutral at this point of time and on a path to profitability with a lot of very exciting things coming up in 2026.
All right. So, that's a good start. So, tell us about C3G and IC-MPGN. I'm not going to say the whole thing. It's a lot. So, what is the opportunity? It's the first approval there. There's a lot of education and teaching and explaining to physicians that you have a new approach. So, tell us about that and what the uptake will look like as you get more experience.
Yeah. Thank you, Yigal. So, C3G and IC-MPGN are both kidney diseases, very similar in terms of how they present themselves, manifest themselves, probably also in the underlying pathology behind it. The difference between these two indications is that when you look on histopathology on biopsies in the kidney, in IC-MPGN, you will find kind of a co-localization of complement with antibodies, right? Other than that, these are very similar diseases. The prevalence in the United States is approximately 5,000 patients split between those two indications, and about 50% of these patients over the course of 10 years will progress to end-stage renal disease, meaning hemodialysis. When these patients get transplanted, they will typically relapse because the underlying cause behind this disease is genetic in nature.
There is an overactivation of complement that takes place in these patients that is rooted in genetics that leads to the deposition of complement elements, specifically complement factor C3, inside the kidney. We ran the so-called Valiant trial, which was our phase 3 clinical trial for C3G and IC-MPGN, where we took a very broad approach. We said, "We're going to look at this disease not just in the adults, but also in the pediatric population, not just in a pre-transplant setting, but also in a post-transplant setting, and not just C3G, but also IC-MPGN." And across the gamut, and that is reflected in our label, we showed similar and remarkable efficacy for EMPAVELI in controlling this disease. Control in this case means the trifecta of efficacy outcomes. On one hand, we show a dramatic reduction in proteinuria of approximately 68%.
We then also show a stabilization on eGFR, which already after six months was statistically significant, and then we show that after six months of treatment, and this, I think, is particularly important, is that on histopathology, already in 70% of patients, there is no more trace of C3 deposition. What that means is that these kidneys on histopathology now actually look quasi-normal, right, unless you have underlying fibrosis. At 52 weeks, that data was further confirmed and present recently at ASN. Also, these data, coincidentally, this week came out in the New England Journal of Medicine, so very exciting kind of affirmation of the outcomes that we have and something we're very pleased to be able to present to the nephrology community.
You have a lot there that's different and potentially very differentiated versus the other option, which is, there's an oral drug. How do you see yourself in terms of the differentiation and the competitive dynamic? You have a broader label, and you can treat both, as you said. You can treat the pre- and post-transplant and all the range of ages.
Yeah. So, there is a competing product, which is an orally available product, where there was quite a substantial differentiation in terms of what the efficacy looked like. But I think importantly as well, as you mentioned, kind of the breadth of the number of the phenotypes that we looked at, right? So, the competing product was studied solely in C3G patients and solely in adults, so not in pediatric, not in IC-MPGN, and not in a post-transplant setting. I think noteworthy as well is that we were able to file with six-month data instead of the full 12-month data, kind of further kind of establishing that differentiation.
So, tell us more about what it's going to take to get a larger piece of that 5,000 prevalent pool that you mentioned in the United States? I mean, you're off to a good start. I think you've said, Tim said, around 225 start forms by the end of the year. So, that's essentially 5% of the market.
Correct.
In five months. So, how are you going to prosecute that and get into a larger share of that 5,000 over time?
Yeah. I'm happy to answer that. I think the main driver is education. This is a community, and we kind of divide this community, the nephrologists, into three categories. There's the transplant nephrologists, there's pediatric, and then there's adult. And they all kind of work in different ways with slightly different mindsets. But the pediatric nephrologists, specifically, for example, they prefer our route of administration, right? They see the efficacy profile. They tend to be quick-acting because these are young kids. They want to give them the best opportunity to save their kidney for the longest period of time. And the transplant nephrologists, while similar, they have a much more complicated patient they're dealing with. These are patients that have, in some cases, multiple medications, immunotherapeutics, and things they want to be a little more cautious about.
So, they are also quite interested, and the way they think is sort of in a group that adopts over time. So, typically, you'll have a couple of big centers leading the way, and then subsequently, other centers will follow over time. And then there's the adult nephrologists, and they admittedly act a little more slowly. They're used to medications that don't do a whole lot more. So, for them, this is kind of a lightning bolt. They're not really used to it. This is a disease-modifying therapeutic, and some of them take a little bit of a wait-and-see approach or maybe need to become educated. And a key to that is what Cedric just mentioned, which is the New England Journal of Medicine article.
In our discussions with a lot of these adult nephrologists, they want to see a peer-reviewed publication of the data, and that's what's going to get them kind of thinking more deeply about treating their patients. So, early on, what we've seen is a pretty significant adoption in the pediatric population, a number of patients in the adult population, and then also the transplant centers are based on the data that we have in the Noble study as well as the transplanted patients in the Valiant study. There's a great deal of interest there as well. And just anecdotally, just for what it's worth, we had one physician who had three pediatric patients in our study, and one of those patients was on the placebo group, clearly, and then eventually, after the six-month evaluation period, went on drug.
And that patient was a young woman who's now no longer pediatric, and she did so well that not only did she, but also the physician and two nurses got the logo of our drug tattooed on their arm. That's how much of a difference it made in their lives. So, when I was talking to that doctor, there were two other doctors who hadn't really adopted or thought about putting a patient on the drug, heard that there was a clear sense of FOMO. And so, word of mouth is starting to spread about the drug, and I think they tend to, like many communities, work in packs. So, a lot of things are kind of working in favor of getting the word out there on what this drug can do for patients, and part of that's just education and time.
Do they distinguish between the C3G and the IC-MPGN at the clinical level? I mean, because you mentioned it's this biopsy finding with the staining of the C3. How much do they really distinguish there when it comes to when the rubber meets the road in terms of treatment? I mean, you have both labels, obviously, but I'm just curious just how the physicians think about it.
Not as very, very different, to be honest. Look, there are plenty of examples of patients with sequential biopsies where, on one biopsy, you will see those antibodies and classify it as IC-MPGN, and on a subsequent one, you don't see the antibodies and it's C3G, right? So, there's definitely overlap between the two. I think what's important here is that the presence of antibodies implicates the classical pathway of complement activation, right? Which, if you go further upstream and you have, for example, factor B inhibition, you theoretically do not control the classical pathway, right? So, I think just in terms of providing that comprehensive view of control over the complement pathway, that is the most important aspect of having included IC-MPGN in this population.
Okay. And then as far as just the PNH quickly, I mean, can you just comment? It's stable. Do you see potential for growth there, or do you feel that that's sort of reached the level where it's going to be for the time being?
Yeah. So, PNH is interesting, right? I mean, there's actually a lot of clinical trials going on in PNH and a lot of developmental work, but the data that we now have from the real world in patients with PNH with EMPAVELI is truly remarkable. I would say that what's been most gratifying is to kind of hear and see how good patients feel when they are on treatment with EMPAVELI in PNH, which is harder to track, right? It's not like a hemoglobin level. It's more like a subjective element. But when oral alternatives came on the market in PNH, we expected a large exodus from EMPAVELI. That did not happen. And as a matter of fact, of those patients that tried the oral solution, now already in a cumulative way, 15% have come back to EMPAVELI.
So, I think, again, it's very neat to kind of see the evolution of the drug in PNH. Between our partners, Sobi and ourselves, in PNH primarily, but in the other disease indications as well, we have north of 3,000 patient years of accumulated dosing safety available to us. I think what's noteworthy there as well, and then never something that we would have expected, is that after 3,000 patient years, you would have expected probably to see between 10 and 15 cases of meningococcal infection. Now, we have not seen a single case of encapsulated meningococcal infection over the course of these 3,000 patient years. So, it's a drug that, on the safety side, has turned out to be remarkably safe as well. So, something that we will continue to monitor.
And then beyond PNH and C3G, IC-MPGN, the others that you're looking at are interesting: FSGS, which is another important market, and delayed graft function. So, how do you think about those? Are those kind of like moonshots, or do you have good reasons to think that those are going to be successful trials as well?
Yeah. We, of course, believe that it has a probability of success. Our belief in that is rooted in the mechanism behind the disease. It is also rooted in the fact that, say, the most important element is probably that overactivation of complement at the level of C3 is associated in this disease state in FSGS with a more rapid decline in eGFR, markedly. So, that association exists, and we're very excited about seeing what we can do for these patients. FSGS is similar to C3G and IC-MPGN, maybe a little bit more aggressive even in terms of the progression. There are 13,000 patients with FSGS compared to 5,000 with C3G and IC-MPGN, and we look forward to hopefully a positive readout in that trial. Delayed graft function, so my background is in transplantation, actually, so near and dear to my heart.
The role of complement in delayed graft function and in ischemia reperfusion injury is decades old. I mean, it's always been suspected as being very important. It'll be really, really interesting and fun to see if we can do something to improve the quality of these kidneys when they get transplanted and to avoid that decline that you sometimes see. That's what delayed graft function is. You do the transplant, and within a week, you're going to see an elevation in creatinine, and you have to monitor it and make sure that the kidneys do well. That is associated with a more rapid progression to failure of those kidneys in the long run. Being able to see if we can do something about that will be very exciting.
What are the timelines for those studies?
These trials have just opened now, and we will provide more updates next year as it relates to completion and readout.
Okay. But those are phase 3 trials, yes?
That is correct. Both of those are phase three trials.
And the DGF, who's eligible for that? Is that anyone that any reason to have a kidney transplant, or does it have to be because of chronic kidney disease, or what are the criteria for who could get into that trial?
Yeah. It is any cause for kidney transplantation, but it has to be a deceased kidney donor. So, typically, with a living kidney donor, yeah, you don't see delayed graft function as much as you see, obviously, with deceased donors.
Okay. What are some of the other good comps for a rare disease launch similar to C3G, or what would you point to as being a helpful indicator as to how your launch could perform?
Yeah. So, I think, look, I mean, obviously, with what we have seen in the kidneys so far, most of the work has been in IgAN. Some work also in lupus nephritis. So, there's not really a good comparator for C3G and IC-MPGN. I would say that the important metric is the one that you mentioned earlier, right? I mean, having ended the first full quarter with close to 5% penetration into the epidemiology tells you that, A, you're having a very good launch, a very good launch, and B, that you are probably on track towards that epidemiology of 5,000 patients. Because I think one of the questions that we often get is, I mean, how do you know that there are 5,000 patients out there? Well, if we exit the year with 225 patients after our first full quarter, that is certainly indicative of.
It would be good to be at 100% share, but you're probably not at 100% share.
That we will probably not have 100% share. But I think it's noteworthy here that we'll share more about that in the next quarter, that the launch is going very well also compared to, I think, if you want to take one other launch, of course, it's the other drug that is available for C3G, IC-MPGN. So, we'll be able to show some comparative metrics on that end as well.
And your analogy with the hourglass at the beginning, I mean, does this mean that people that have C5 inhibitors wouldn't have much success in C3G? It wouldn't be a strategy that would be likely to be successful, or?
Yeah. So, it's interesting that you mentioned that because I still remember several years ago when a good friend of mine in Holland, who's a pediatric nephrologist, called me about EMPAVELI and said, like, look, we actually get reimbursed in the Netherlands for the use of Soliris, Ultomiris, so the standard C5 inhibitor, off-label in the treatment of C3G and IC-MPGN. And it does have an impact on proteinuria. That's why it got reimbursed. But when you take a biopsy from these kidneys, you see that massive C3 deposition that is unaffected by controlling C5 and going downstream from C3. That is, I think, the key thing here, is that the driver of the disease is not impacted unless you really go for the root.
Yeah. And for what it's worth, the published magnitude of that proteinuria benefit is closer to what Fabhalta gives. It's more like 25-ish%, 30%.
Well, I remember when you said when you got the 68% result, that was very, very strong. I think that exceeded your expectations of what you might achieve. By the way, the other question I get, which I think is kind of not really a debate anymore, but just, obviously, Fabhalta's oral, yours is not, but given the severity of the disease and the prognosis, that seems to be a non-issue. My sense is that that's sort of like a non-issue. Is that true?
Yeah. Well, I think, look, I always think it's good to have options available. I think it's worth mentioning that the pediatric population typically is more rapidly progressing or believes to be more rapidly progressing than the adult population. And if you have a mild form of the disease, maybe an oral option is good for you. But I would say that your statement that efficacy stands first and foremost, obviously, when you know that hemodialysis has a life expectancy of only a couple of years, I mean, it's not something that you want to ever get into. So, I think the setup is very good in that regard.
Okay. All right. Well, let's shift to GA briefly. So, tell us about the sort of state of the union of SYFOVRE. There's been ups, there's been downs. Now it's stabilized. What is your view of the path forward? How much more growth can you believe you can extract out of the product? Yeah, just kind of walk us through what your latest thinking is there.
Yeah. So, 2025 for the retina practices was a very difficult year. Across the many types of treatments, that includes wet AMD treatments, GA treatments, etc., there was a lack of foundation money to help to about 20% of patients that need assistance in order to afford the copay that is needed for these treatments. And that caused a lot of disruption in the flow of these retina practices. And I think that is, that's unfortunately a little bit the story of 2025, is that in these retina practices, where many of these specialists will do 60-100 or more injections per day, right? If your front office has to figure out who can afford the copay, who cannot, if they cannot, what do you resort to, right? That was very difficult for the retina specialists to deal with.
And within that context, a prioritization towards how do you take care of patients with wet AMD is a natural place to go, right? On wet AMD, if you could not afford the copay on drugs like Vabysmo or Eylea HD, right, a lot of retina doctors had to resort either to samples or, if that was not possible, resort to generic Avastin, which happened in a lot of cases. Now, generic Avastin is something that has to be given monthly instead of every two to three months. So, you can already see how kind of there's a whole place of resettlement. And I think GA treatments this year took a little bit. A lot of practices said, "I'm going to take a little bit of a break on that until all this gets figured out." And now we're starting to slowly see that pick up again.
I think what is very exciting, actually, in geographic atrophy is that the data continues to accumulate from the real world, as well as the long-term data that we now have available from the Gale study, as well as the functional data that we've been able to generate, which tells us that SYFOVRE is a very good drug for patients with geographic atrophy. The opportunity that lies in front of us is, I think, on one hand, kind of re-exploring with the retina community what does it mean to have geographic atrophy, because the functional decline in that disease is very underappreciated and misunderstood. We can help with that. We now have the tools available to image function in the back of the eye.
And I think the story of 2026 in the retina will be that when you look at function in patients with macular degeneration, whether it's wet or dry, right, the decline that happens in the periphery, which before we couldn't really image, is meaningful and severe. And how do we address that, whether it's with SYFOVRE with a class or with new therapies that come onto the market? And we look forward to being a part of that.
As far as the competitive dynamics with Izervay, is it kind of stabilized now, or what's the latest snapshot there? I mean, the share was sort of shifting around. I mean, at one point, you had the vast majority, and then it got closer to 50-50. What does that look now?
Yeah. We've continuously been, since the start, the market leader and stabilized just north of 60% in terms of market share. On new injections, in the course of 2024, we kind of dipped in a meaningful way, but then had a recovery in the beginning of this year and have been at around 55%. That is on new patients going on treatments with the share staying north of 60%. So, that is how we're entering into 2026. I think we have substantially more data available to us, I mean, multiples, right, in terms of.
Your study, is it still you did five years? Yeah?
Yeah. So, we just had the no, it's five years. That is the end, right? But it was very exciting, right? I mean, we had a press release on it in the beginning of October. We will present that data at the Macula Society in February. But the bottom line is that over the course of five years, you can save about a year and a half worth of vision loss, right? Very meaningful in terms of what it can do for these patients. What we're going to do now next is to see how can we, in a quantifiable way, make that information, in other words, show the benefit of the drug to the patients and to the physicians as they are on treatment.
So, you'll have some quantitative tell us more about that in terms of how that's going to work, because that's sort of a newer thing.
Yeah. So, I think, look, this is kind of what I was referring to about the next year. I mean, forget about what it means for the drug, which is, of course, a very important consideration for us, but what it means in terms of physicians understanding the decline of function in these patients. So, both in geographic atrophy as well as in wet AMD, the main standard for visual function has been and continues to be best corrected visual acuity, which is a bit of a poor name because it identifies your ability to look through a very small straw and read the letters on the Snellen chart, which is from the 19th century, right? Now, you can have 20/20 vision because you have that straw available to you, but everything else can be lacking.
Imagine walking through these corridors and living looking through a tiny, tiny straw while having 20/20 vision.
That's a point that you've made to me before about how you can actually read the small letters better than the big letters.
That is correct, yeah. So, but it is the standard. It's what everybody's used to, right? But what that means, and to give you an example, again, forget about the drug. If you take patients with geographic atrophy that progress 50% faster than patients, another group of patients, you will not see a difference in best corrected visual acuity between these patients over years of follow-up. That is what a meaningful, how "irrelevant" or dissociated from the disease progression that particular endpoint is. Now, the solution to that is you want to be able to see what goes on in the periphery, right? And we now have a technology available to us, and you'll hear much more about that in the next year, that allows us to image that function, that light sensitivity across the whole retina.
And that allows you to see in GA and in wet AMD how these patients decline. Now, why does that matter? Imagine if you're a patient with GA and you go see your retina physician, and you're there with your daughter or your son, and the physician takes an OCT, then takes an OCT from a year ago, and is going to look at these two OCTs and, in many cases, unfortunately, just visually look at them and say, like, "I don't see a lot of change between these two images." And your BCVA is stable. And the retina physician will tell you, "hey, you know what, overall, it looks like your disease is stable." And you're like, "but wait, I see a lot worse.
Because in the meantime, unbeknownst to the physician and not measurable until recently, in the periphery, your photoreceptor cells are dying, your vision is declining, and you do indeed see worse, but it's not seen. The retina physician doesn't know about it, and your family members think that it's in your head, right? That is something that we need to change, and we have the tools and the capabilities to do that, so the science is there. 2026 will be the year in which the academic community will dive into this, and that will start in February at Angiogenesis, and then we have the engineering job in front of us of being able to make that technology available to the retina doctors in an easy fashion within their practices.
So, they'd be able to track the progression before the patient is on SYFOVRE. And then once they start, they could also manage and track the slowing progression. Is that the basic goal?
That is the ultimate goal, right? I mean, think about it this way. With that functional mapping, you can take a picture, and you can pixelate that picture to kind of represent what the patient actually sees, and because it's based on SD-OCT, it's not a new technology. You can go back and use historical data to say, this is what that picture looked like five years ago, three years ago. This is what it looks like today. In the future, we'll be able to say, this is where it's headed unless you do something, and this is what you could expect if you go on treatment. All of that is now available to us, and it will make a huge difference, and something else, it's more, again, all in the context of making these patients feel seen.
We have an augmented reality headset that, when you take an OCT of a patient, you will be able to recreate for a family member what your dad or mom actually has to live with. Not just today. With a click of a button, you could go back in time and relive what it was three years ago and how it has changed. So, all of that is like right in front of us. And I will tell you that, again, forget about Apellis, forget about SYFOVRE. The Holy Grail in the retina is to be able to image function in the back of the eye. And we are very close to having that available.
Now, I have to ask, is this sort of related to large language models and AI technology that's allowing you to do this sort of sophisticated connecting of the dots with the imaging, or is it more basic technology that's already been worked out?
No, no. This has everything to do with machine learning and AI.
We haven't seen much. This is just you’re giving us a bit of a preview here. We haven't seen any presentation yet of this.
That is correct. So, well, we have been with advisors and with key opinion leaders and with potential partners, we have been talking about these things. But I think, again, in terms of, like, let's table SYFOVRE for a minute now. I think it's very important, obviously, for SYFOVRE, but on a broader level, to kind of redefine how the retina community understands these diseases, I think it's going to make a big difference.
When could such technology become available? I mean, is this something that would become software that would be in the retina practices within the next year or two, or what kind of time frame are you referencing here?
Yeah. So, again, kind of the analysis on real-world data, et cetera, that will come very, very soon, and the appreciation of what it means for patients and the impact, et cetera. In terms of having a practical tool available within a retina practice and making that widely available, that is something that will take time. Not as long as drug development, but still, it takes time.
But is that part of a business objective for Apellis, or that's something that's just with the academic community to support better treatment, better management of GA and potentially other retinal diseases?
So, it is our technology. We generated it with the data available from Oaks and Derby, specifically the microperimetry data that allowed us to train these algorithms. But it's something that we share and something that we believe will very much serve the greater purpose of treating this disease.
Okay. Can we just do a quick five seconds on just financial health? I think Cedric mentioned just being sort of cash flow neutral now. What's your perspective on the P&L over the next four to six quarters?
Yeah, sure. So, I think just to clarify, we are nearing on a cash OpEx basis. So, if you take net revenue, net product revenue, and then net expenses that are cash expenses, so adding back depreciation, amortization, that sort of thing, and any one-timers, we've been skating close to that for a few quarters now. So, if that gives you a sense of where we are from a financial health point of view, I think that's a pretty strong measure. We had a little over $450 million in cash. We just did that deal with Sobi where we monetized the ex-US royalty for EMPAVELI. And we feel very good about where we are from a financial health perspective. And we certainly feel we have what we need to become profitable based on our commercial products and our expense profile.
And there's another program too, I just remembered. Isn't there the siRNA combo that you're doing? Where does that one stand?
This is.
Have a double knockdown of C3.
Correct. So, that is a registrational phase two clinical trial that's currently rolling. What we do there is we have a subcutaneous, what will ultimately be an autoinjector that you combine with the intravitreal injection of SYFOVRE. And it knocks down the systemic levels of C3 by approximately 90%. And we believe we can do that safely, and we have a lot of data behind that. And we know that that translates into about a 90% lower level of C3 in the vitreous as well as in the aqueous humor. That then provides a stoichiometric advantage to SYFOVRE that we believe will further allow us to have an outsized impact on the retinal pigment epithelial cells and further slow down the disease progression beyond what SYFOVRE does on its own. So, the benefit that we there are two benefits that we're trying to get out of this study.
Number one is to be able to dose every three months instead of every two months. Number two, to go beyond what we can currently do in terms of slowdown with SYFOVRE.
That siRNA technique, where's that technology coming from? Who did you partner with? What would be the phasing of the dosing for that versus the every three months SYFOVRE?
Yeah, so that was built in-house, and we are testing this as an every three months in combination with SYFOVRE.
Oh, so they're on the same calendar.
Correct.
Okay.
The idea being that a patient would be able to go into a physician's office for their regular. Imagine if you're a retina doctor, you have patients who are on every two months SYFOVRE. Should the drug be approved, you could then bring in that patient every three months and give them a subcutaneous injection before you give them an intravitreal.
Okay. And I know you've said this before, but has anything changed with the foundations and getting that rebooted, or is it just the base case now is we shouldn't assume that that funding source is going to change in the future?
Yeah, that's correct. We can't really predict what's going to happen with the patient copay assistance foundations. What we can say is that it's been a massive impact for patients, right? So, patients just not only in the wet AMD space, but also particularly in the GA space where there's no alternative generic or something else that they can where they can afford that out-of-pocket cost. It's been a dramatic impact. And so, it's affected a number of GA patients. And it's also affected practices that have been where there's increased friction in the concept of having that discussion with a GA patient or bringing patients in and considering treating them.
We saw, as we mentioned in our earnings call, we saw a massive uptick in free goods over the first three quarters of this year, amounting to close to $40 million in sort of in free goods product that would have otherwise, we think, likely been commercial product. And that's just a reflection of what this impact is, right? That's a pretty big impact on those are existing, primarily existing patients, maybe some new. But you think about other patients who are new patients, and they're just not having the conversation with the doctor because the doctor has a lot of other things to do, and it becomes a friction problem for them. So, it's a deep concern to us and to patients.
I know you did the DTC campaign with Henry Winkler. I've seen the ads. They're good. Like the snail. But are you doing more of that, or do you need to do more of that to offset what you just referenced? What's your level of investment on that front?
We're turning a lot of our energy towards the physicians. That's not a DTC campaign. What we found is that the patients are already ready to be treated in many cases. And the interest level in being treated is fairly high. There is some friction among the doctors, right? And that's where we're focusing a little more of our energy right now. We'll, of course, reconsider more DTC effort at some point, but at least at the moment and heading into 2026, our focus is on physician education and those sorts of priorities.
All right. Okay. Well, very good. Looking forward to a strong 2026.
Thank you.
Thank you very much.
Thanks, Yigal.
Thank you.
All right.