This is Zenio Smith Biotech Analyst here at B of A. Thanks for joining us. Our next presenting company is Dianthus Therapeutics. We have with us CEO, Marino, sorry about that, Marino Garcia. He is going to go through a few slides with you or with us for the next 15 minutes. I'll turn it over to you.
All right. Thank you. Thank you to Bank of America for this opportunity. I have a mic here. I'm good. Thank you to Bank of America for the opportunity to present today and update you on some of the great and exciting things going on at Dianthus. Before I start, obviously I'm going to be making some forward-looking statements. I ask you to refer to our Investor page and our SEC filings for more information on what's going on with Dianthus. It's a really exciting time because we are literally weeks from presenting our first top line data in any phase II of the neuromuscular franchise we're building with 103. We're rapidly advancing DNTH103, which is a highly potent active C1s inhibitor that selectively only inhibits the classical pathway.
The intention here is to develop a very potent complement inhibitor that can be delivered in a very patient-friendly, self-administered subcutaneous autoinjector like the autoinjector, the SHOMolly that Dupixent uses, and dosing it every two weeks, just like Dupixent, to treat severe autoimmune disorders. We have great first phase I data that supports that we'll be able to dose infrequently with our 60-day half-life that is highly potent. It has a differentiated safety profile, especially within the complement class, and has very strong in vitro potency versus another active C1s inhibitor from riliprubart from Sanofi, which I'll talk about in a moment. As I mentioned, we have a very near-term catalyst coming, our first phase II data in myasthenia gravis, where we're done with enrollment and we'll have top line data in September.
We have two other catalysts, another phase II study with MMN, which we'll read out in the second half of 2026. We are also in a phase III study in CIDP, a new exciting area where we will have interim responder analysis in the second half of 2026. We just put out our Q1 release. We have a very strong balance sheet with $332 million to take us, give us a runway up to the second half of 2027, which allows us to read these three catalysts out over the next year and a half and still have a healthy runway beyond that. DNTH103, like other complement inhibitors, is a pipeline and a product, and it has the potential to be a first-line, best-in-class biologic treatment across three different neuromuscular conditions.
We're building this really exciting neuromuscular franchise, this leading neuromuscular franchise by going after three allied diseases that give us very clear clinical development as well as commercial synergies. The three markets are myasthenia gravis, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy. These three alone in the U.S. account for about 150,000 patients. Each of these markets has significant unmet need and opportunity for something like DNTH103 to come in and really become a first-line preferred agent. Within generalized myasthenia gravis or AChR-positive patients, this is a multibillion dollar market that still continues to grow, where there's an opportunity for a safer, best-in-class complement inhibitor that can deliver a nice, robust, consistent symptom control like the C5s.
Within CIDP, we now have data from a competitor, riliprubart from Sanofi, an active C1s inhibitor that shows that active C1s inhibition may be the most effective way to treat CIDP. I'll talk a little bit about some of the data in a moment, but it could potentially be even better than the gold standard efficacy to the IVIG. We have an even better and more potent antibody that could really become the gold standard within CIDP. Finally, within MMN, this is a smaller market, but it's one like maybe myasthenia gravis was 10 years ago, maybe CIDP was five years ago. It's one where as more information comes out and more products are developed, there'll be a growing incidence. Right now, this is a market that is for complement inhibitors only. FcRns will not work. It's IgM driven.
We have in Pasiprobar, the C2 inhibitor from Argenx that has now provided proof of concept for classical pathway inhibition, delivering really impressive efficacy. We have these three conditions. We're developing DNTH103 to really be that first-line biologic choice across all three. Let's talk a little bit about MG. I'm often asked, what are we trying to achieve? This is the product profile. We are trying to do three things. We're trying to take the best parts of three approved labels, three best-in-class labels out there, and combine it into one offering for patients. First, efficacy. We are trying to deliver the C5-like efficacy, the Ultomiris, the Soliris, the Zilbrysq. They demonstrated somewhere between a 1.6-2.1 placebo-adjusted MG-ADL scores. That kind of efficacy, that robust continuous symptom control, is what we're aiming to deliver with 103.
The safety of the one C1s inhibitor that's approved on the market, that's Enjaymo, sutimlimab. It's a first-generation C1s inhibitor. It's not an active C1s inhibitor. It binds to all C1s, proform and active form. It's approved for cold agglutinin disease. If you look at their label, it is the cleanest, safest label of any complement inhibitor. It has no box warning, no REMS program for any safety issue. The precedent has been set. If you are a classical pathway inhibitor and you target C1s, you will avoid a box warning like the C5s. Finally, take the dosing and convenience of Dupixent with their sub-Q, their 2 ml autoinjector. It's a $14 billion franchise. Take that autoinjector, put it into the hands of patients, and dose every two weeks, just like Dupixent.
We think combining these three elements into one label, one offering, in MG, it's an obvious first choice for biologic for younger, healthier, more active patients who are diagnosed with myasthenia gravis. What gives us confidence that it will work in MG? We have from our phase I data very clear indication. At 300 mg, 2 ml shot every two weeks, we get significant inhibition of the classical pathway, significantly above the target, the IC₉₀, or 90% inhibition of the classical pathway as measured by the CH50 hemolytic assay. There is the science as well. We know that with AChR-positive patients in MG, this is a classical pathway-driven disease. It is very clear in the literature that it is the classical pathway within the complement system that is triggered for those patients.
We stop the complement cascade very early on by inhibiting active C1s and stop the complement cascade from eventually leading to form the membrane attack complex. The other benefit of stopping this process early on and inhibiting only the classical pathway, as I mentioned earlier, is we're leaving the lectin and alternative pathways intact. Those are the pathways that are triggered by the presence of encapsulated bacteria. Those are the pathways you need to fight against the deadly infection risk of meningitis if it detects an encapsulated bacteria in you. That precedent, as I mentioned, has been set by Enjaymo. You'll avoid the box warning if you're a classical pathway inhibitor and don't touch lectin or alternative pathway. There's nothing on the market for MG like this today, and there's nothing in development like this for MG in anybody's pipeline.
It is the combination of that potency in shutting down the classical pathway and the ability to selectively only inhibit the classical pathway that can give us that benefit of the efficacy with the additional safety compared to other complement inhibitors. That is in myasthenia gravis. The other market that a lot of investors are quite excited about in CIDP. Frankly, last year in January of 2024, we raised $230 million through a PIPE, and that was not catalyzed by any internal catalyst from our side. That was based on this data on this slide, which is the phase II Riliprubart data in CIDP. This is the first time a complement inhibitor has been shown to work in CIDP. It is the first time an active C1s inhibitor has been shown to work in any neuromuscular condition.
What Sanofi with riliprubart was able to show, their second-generation active C1s inhibitor, is that in patients who are treated with IVIG and were doing fine, so they're SOC treated patients, the first chart, the group A. These are patients that are on IVIG, CIDP patients who are on IVIG and doing well. Despite the fact that they're all already doing well, when switched to active C1s inhibition, over 50% of them improved. That's pretty significant. That means that somehow active C1s inhibition was able to extract even more efficacy than IVIG was in these patients. The second group they looked at is patients who are refractory to IVIG. This is a group that FcRns will never allow into their trials because it won't work. FcRns, I think most people understand, is not as effective as IVIG. If IVIG didn't work, FcRns won't work.
Riliprubart allowed patients who are refractory to IVIG into the trial, switched them to active C1s inhibition, and again, 50% of patients improved. That is really good news for patients who are trying IVIG and it will not help them. Of course, with those who were naive to IVIG, they saw very robust efficacy. This data is really, really impressive. It has given Sanofi the kind of confidence to go ahead and do a head-to-head study versus IVIG. They are in a phase III study, and they will read out results from that head-to-head study likely in the beginning of 2026. That could be a very, very powerful catalyst for us. Why? Because the next question, of course, is then how does DNTH103 compare to Riliprubart? The key thing to note here is that Riliprubart is dosed 600 mg, 4 ml every week.
That is, if you were to put it into an autoinjector or 2-ml autoinjector, that's two autoinjectors every week or eight autoinjectors every month. What we did is we conducted six different head-to-head in vitro experiments to compare our potency versus Riliprubart to very convincingly show that DNTH103 is orders of magnitude more potent than Riliprubart. We did two affinity assays, SPR, Kinexa. You can see anywhere from 4x-8x more potent. We have single-digit picomolar affinity. An enzymatic assay, and then we did three functional assays. I'll tell you that the middle one, the CH50 hemolytic assay, that's the one we think that has more translational value and really is the best one to look at. You can pick any of these and you can see that 103 really outperforms in an in vitro setting versus Riliprubart.
That CH50 hemolytic assay pretty much says that we are 7x more potent. What does that mean? It means that we need to achieve PK levels that are 7x lower than Reliprubart in order to shut down the classical pathway. We can give a lot less drug, less often, and still get efficacy. The question in CIDP really is, because we are so much more potent and they are dosing 4x more drug than us and more frequently, do we have equal efficacy or do we have potentially even better efficacy than Reliprubart in CIDP? That question remains to be answered, but it is very clear that we do have a more potent and more patient-friendly version of active C1s inhibition than Reliprubart. Finally, MMN, as I mentioned earlier, this is a smaller market, but it is one that is growing and will grow.
It is one where FcRns do not compete. There are only two classical pathway inhibitors being studied here, us and Pasiprobar, the C2 inhibitor from Argenx. That is it. Yes, it is a smaller pie, but where 103 can get a much larger share. This is a market where FcRns will just not work. It is IgM driven and it is classical pathway driven. Both Pasiprobar, their C2 inhibitor, blocks classical pathway and lectin pathway. Obviously, they are getting their efficacy, and they say this themselves, through the inhibition of the classical pathway. As I mentioned, we know we have a powerful classical pathway inhibitor, so we both should work. The difference is that they block lectin. As I mentioned earlier, if you block the lectin pathway, you are going to have a higher risk of infections. You are going to get a box warning.
There's no way the FDA is going to allow a product that blocks the lectin pathway not to have a box warning around the risk of infections like meningitis. We preserve the lectin pathway. We preserve the alternative pathway so that it can continue to fight against the risk of infections. Finally, it is an IV that's given every week or every two weeks. Again, we are looking at a 300 mg, 2 ml subcutaneous shot that patients get self-administered through an autoinjector every two weeks. We are clearly a much more convenient option for patients. That's it. There's nothing else being studied in MMN. This is a market that we're also very excited about for 103. With the short amount of time I have, let me go straight to the MG program. We are looking at a three-arm study. We are over-recruited.
We finished recruitment. We have 65 patients instead of 60, as we had targeted. We're looking at placebo, 300 mg every two weeks. We're also testing a higher dose, 600 mg every two weeks, just to have two shots on goal, just to answer the question, what if you get above IC₉₅? Does that provide any additional benefit? We don't believe we're going to see a dose response. We don't believe we're going to see a difference between 300 and 600. We believe 300 is going to show that that's maximum efficacy because it's very, very potent. We will have the data for this trial in just a matter of weeks in September. That will be the first of three catalysts as we go into 2026 for our next two catalysts with MMN and interim responder analysis from our phase III and CIDP, both in the second half of 2026. Thank you very much.