I'm Mike Perone, Baird's Healthcare Specialist, and I'm pleased to be joined by Dianthus CEO, Marino Garcia, and my colleague, Baird's Senior Biotech Analyst, Joel Beatty, who will be moderating the discussion. As a reminder, Baird's Biotech Discovery Series is an opportunity for investors to hear directly from interesting and innovative biotech companies and at a fireside chat format. A few quick logistics: if you would like to submit a question, you can do so via the webcast portal at the bottom, or you can email Joel at jbeatty@rwbaird.com. Finally, before we begin, I'm required to remind attendees to please refer to the event calendar, published research, or Baird's website for important disclosures regarding the companies discussed during this event. I'll now hand it over to Joel to kick off the discussion.
Thanks, Mike, and thank you, Marino, for joining us today for the discussion on Dianthus. Maybe to begin, could you provide a little bit of overview of what's new with Dianthus, and then we'll jump into some Q&A?
Sure, thank you, Joel, and thank you to Baird for the opportunity to update everybody on some of the exciting things going on at Dianthus. Dianthus, we at Dianthus Therapeutics are focused on rapidly advancing DNTH103, which is our highly potent, differentiated classical pathway inhibitor that selectively targets only the activated form of the C1s protein within the classical pathway and not the proform of C1s. The idea here is to be able to effectively treat classical pathway-driven diseases like those that I'll be talking about in a few moments, but leaving the lectin and alternative pathways intact so that they could continue to do what they're supposed to do, which is fight against the risk of infections, serious infections from encapsulated bacteria, things like meningitis.
The whole intention with DNTH103 is to be conveniently delivered via a simple, one-click, self-administered autoinjector, much like Dupixent's autoinjector, and dosed only every two weeks. Let me move to the next slide. Just a reminder, though, I should have mentioned this, we'll be making some forward-looking statements, so please refer to our website and to our SAC filings for further information. We're developing DNTH103 as a pipeline within a molecule. As you can see here, we're on the verge of three very exciting catalysts, starting with our myasthenia gravis phase II results this September. Just yesterday, we announced that we're done with recruitment around our MG trial, our phase II trial, and that we will be releasing top-line results in September of this year. That is the first of three very exciting catalysts.
Our next two catalysts after that are MMN, a phase II trial, which we'll read out by the second half of next year, 2026, as well as our phase III pivotal trial in CIDP, which will have an interim responder analysis announcement also in the second half of 2026. We're feeling really, really confident that the data we'll see in September will be positive in myasthenia gravis. Part of what gives us that confidence is, as you can see on this slide, is partly based on our phase I data, where we saw that we have a very potent antibody that has a nice long, healthy half-life of about 60 days.
As you can see on this chart, when we model all the PD/PK data that we collected from our phase I trial, we can see that the steady state of dosing DNTH103 after a loading dose, so dosing DNTH103 at our target dose of 300 mg in a 2 ml shot every two weeks, that the PK levels are significantly above the IC90, which is our target for very potent inhibition of the classical pathway, meaning that we get significantly above what we think we need to be in order to get efficacy in conditions like myasthenia gravis. Because of this data, you know, we feel like MG is going to be positive data. We also have precedent with MMN and CIDP, where we've already seen really impressive efficacy results from other classical pathway inhibitors from our competitors, which we can get into later.
I think in terms of this myasthenia gravis data will be a pivotal moment for us in terms of de-risking the molecule in the three conditions, the neuromuscular conditions that we're going after. Just one more slide just to set the stage here for our conversation. I find this slide very useful to just kind of explain what are we trying to achieve, like what is our ambition, our eventual goal in terms of DNTH103. The idea here is to get combined three best-in-class labels, the best parts of three different best-in-class labels, and combine it into one offering for patients with myasthenia gravis.
First of all, in terms of efficacy, achieving anywhere close to the level of efficacy that we see from C5 inhibitors such as Ultomiris, Soliris, Zilbrysq, in other words, somewhere around a 1.6-2.1 point difference on the MG-ADL versus placebo, that would be a win. That's a nice, very strong, robust, continuous symptom control. In terms of safety, we're trying to achieve the same label as the other C1s inhibitor that's approved, although it's not selective for active C1s. It binds to all forms of C1s that's in Enjaymo, but it is the only classical pathway inhibitor approved, and it's also the only complement inhibitor that doesn't have any box warning for any safety issues. Very clean label, no box warning, no REMS program. That precedent's been set for C1s inhibitors, and that's what we're aiming to also achieve with our label.
Finally, the convenience of a $14 billion blockbuster like Dupixent, with its very simple autoinjector, the SHL Molly autoinjector, one click, five to seven seconds. That is the same autoinjector we are looking to develop DNTH103 in. Again, with one click, every two-week dosing, much like Dupixent after a loading dose. Essentially, we believe if we can achieve this label, the efficacy of C5s, the safety of Enjaymo, the convenience of Dupixent, there is just nothing that compares to it in terms of a first-line biologic offering for MG patients. That is what we are trying to develop at Dianthus.
Great. Thanks, Marino. A lot of points to dive into, more of those. Maybe the first area I'd like to go is talk a little bit more about the dosing and the convenience. Later in the call, we'll circle back to the other two components on a disease-related basis. If we think about dosing, you're looking for a 300 mg dose every two weeks compared with Riliprubart, which is 600 mg every week. What gives you confidence that you can achieve the differentiated dosing?
I would just go back again to first the previous slide here. Hopefully, you can see this. First off, we know 300 mg every two weeks gets significantly above the IC90, which even Sanofi with Riliprubart has talked about being, you know, the bar for really strong, potent efficacy. So we know dosing 300 mg, 2 ml every two weeks gets us a good amount above the IC90 target of 87 micrograms per mL. We're hovering around 120, so it's a good 40% buffer right there. We haven't seen CH50 IC90s from Riliprubart, but what we have, and you can see this in our corporate deck, is we conducted six different in vitro experiments comparing ourselves in terms of potency versus Riliprubart. And right across the board, you see we're anywhere from, you know, four to eight to even, you know, more times more potent than Riliprubart.
We believe the reason they're dosing much higher, 600 mg, 4 ml every week, so more frequent, higher doses, is just not as potent as DNTH103 is in terms of binding to activated C1s. The efficacy we've seen with Riliprubart in CIDP was game-changing, I think, for us, for patients. We're confident we'll achieve at least similar efficacy, if not better, because of our more potent antibody.
Great. What helps give confidence that being above IC90 is enough as opposed to maybe needing a little bit higher, possibly?
Interestingly, to answer that question, we are testing a higher dose, what we call our high dose. We doubled, so our MG trial, MMN trial, as well as our CIDP trial have placebo in the blinded portions, but as 300, which is our target dose, but we also are testing 600. And 600 mg every two weeks gets significantly above the IC95 for us. IC95 for us is about 149 micrograms per ml, so just below where 300 mg gets to every two weeks. With 600, because of our linear PK, you know, we're getting well above 200 micrograms per ml, which is significantly above the 149 target for IC95. We are testing the theory. What happens if you get even higher levels of inhibition above IC95 with a classical pathway inhibitor in these conditions?
Frankly, Joel, it's not our expectation that we're going to see a difference between 300 and 600. We're testing that just to make sure that we don't leave any efficacy on the table, that we have two shots on goal, and to reassure investors, of course, as well. I really believe 300 maxes out efficacy, and that 600 won't provide any additional benefit. Part of what gives me that confidence, gives us that confidence, is that there's really only one dose-ranging trial that's been done in MG with a complement inhibitor, and that's Zilbrysq in their phase II. They tested a low and high dose. The low dose achieved about 88% inhibition, so just below IC90, and the higher dose achieved 97% inhibition, so above IC95.
Frankly, at the end of that 12-week trial, they did not really see any real difference between the two doses. That study seems to suggest that as long as you are getting close to the IC90, you should be maxing out on efficacy. You know, I really think DNTH103 at 300 mg every two weeks will achieve the maximum efficacy you can get out of a classical pathway inhibitor in MG, and that 600 will be equivalent. Just to make sure we do not leave anything on the table, we are testing that higher dose.
Great. Maybe one more question while we're on the slide here is, could you help us think through what happens in the early days of the studies? On the slide, you're showing IV loading dose. Is that how you're running the clinical trials in phase II? I forget, or if not, how soon does it take to ramp up above IC90?
No, no. The reason we're doing a loading dose, absolutely. That's because these are just 12, 13-week trials. It would take a while, right, if you just dose one shot every two weeks for steady state to be achieved when you have a 60-day half-life. We're doing a loading dose upfront and get patients quickly above it, and then we start dosing every two weeks, starting at day seven. If you look at the Dupixent label, they have a loading dose, right? They have, I think it's two subcu shots upfront, and then they start dosing, I believe it's at day seven every two weeks. That's kind of the idea, that you do a quick loading dose, get people above a certain target, up PK level, and then start dosing every two weeks right after that.
Great. All right. Let's jump into myasthenia gravis, where you know, as you mentioned, you just completed phase II enrollment. I believe we're expecting data in September. Maybe to begin, could you walk us through the mechanism? I think we know inhibiting the complement cascade later can be very effective in myasthenia gravis, but how much do we know about whether C1 inhibition can be enough?
The idea behind targeting C1 was to try and find a safe target within the classical pathway only, that shuts down the classical pathway and shuts down the cascade that eventually leads to, you know, triggering C5 and the formation of MAC. The idea here is, especially in MG with ACHR-positive patients, what we know, you know, it's certain antibodies that are triggering the classical pathway of the complement system for those patients that's leading to the damage being done by the membrane attack complex. You know, myasthenia gravis, at least with ACHR-positive patients, it's always, you know, very commonly, let's say, referred to as a classical pathway-driven disease, whether it's in the literature and so on. It's one of the better understood rare diseases, actually.
We picked it as our first indication because it was where the science was clearest that if you just shut down the classical pathway, leave the lectin and alternative pathway intact to be able to fight against the risk of infections, those pathways are not triggered by ACHR-positive patients, MG patients, that you could essentially get at least similar efficacy to C5s, but in a safer manner. By triggering and going after only the activated form of C1s, which is much less prevalent than the proform C1s, which we leave intact and still floating around, then you could deliver that in a very low-volume shot you could put into an autoinjector. You know, that's kind of ironic, actually, Joel, because a couple of years ago, MG was the least risky indication, so we made it our first indication.
Since then, now we've seen data from empasiprubart by Argenx, riliprubart by Sanofi in MMN and CIDP, respectively, where they've shown classical pathway inhibition showing really impressive efficacy in those two conditions. That's data and science that didn't exist before those two companies, you know, revealed their phase II results. Now it's actually MG where there's no data for a classical pathway inhibitor only. It's going to be very interesting, but if, you know, that data in CIDP and MMN, where it was more uncertain, has only made us even more confident that it should work in MG, where the science is clearest.
That makes sense. Looking ahead to September, what would be good data?
Good data, I'll go back to this slide. If we can show similar efficacy to C5s, no serious infections from encapsulated bacteria related to drug, and that 300 mg every two weeks works and can deliver that, that's a win. There's just nothing, whether on the market or in development for MG, that comes close to having these benefits combined into one package for patients. This would be a big win.
Got it. I was going to ask for, you know, a specific improvement on the primary endpoint, but I see it's on the slide here, a 1.6-2.1 point improvement, which I believe is from the labels of the few agents that are already approved.
Yeah, if I can just correct one thing, Joel, our primary endpoint in our phase II is it's a safety study. So it's not really an efficacy study. MG-ADL, QMG, et cetera, are all secondary endpoints. It is the largest phase II trial done in MG. It's a third larger in size, approximately a third larger than the Zilbrysq study was. We're confident we should be able to see a robust efficacy endpoint. I mean, if you look at, for example, Ultomiris, which, you know, sells a couple of billion dollars, last quarter, I think AstraZeneca just announced, you know, grew by 22% over first quarter 2024, still being used first line as a first-line biologic in the myasthenia gravis space. That's where a lot of their growth, or most of their growth, is coming from still.
You look at their label, they had a 1.6 difference versus MG-ADL, sorry, versus placebo on the MG-ADL. That is really considered the efficacy gold standard. It's, you know, very robust efficacy, very, for patients where it works, obviously, very robust and continuous symptom control. Anywhere north of 1.6 is a win. It essentially says we have similar efficacy to Ultomiris, but in a much safer, much more convenient package for patients.
When you say anything north of 1.6 is a win, is that in reference to the phase II trial or like the phase III label?
You're asking me about the data we're expecting to see in September. If we see a 1.6 or greater difference on the MG-ADL versus placebo, that's a win. That tells us we have C5-like efficacy, but with the other, the safety and the convenience advantages.
Yeah, that makes complete sense. And then on the powering, if you happen to be, say, 1.6, would that be enough to be stat-sig, or is the trial, you know, or the, you know, are you saying like the magnitude is great, but the powering of the study isn't large enough to be stat-sig with that?
It is the largest phase II trial. It is a third larger than Zilbrysq's trial was. Assuming, you know, the efficacy and the placebo rates are, you know, as we expect, then yeah, it should be stat-sig. It is a secondary endpoint. It is not a primary endpoint. The study was not designed for that. It was designed for safety. Of course, we are looking at efficacy endpoints, and I know investors are very interested in seeing that as well. We will be very clear and transparent with that in September.
Great. So assuming that, you know, the phase II goes as hoped for here, what would be remaining for the clinical development, like, you know, kind of what type of phase III program would need to be run?
Essentially the same as our phase II, potentially only one active dose, one arm, obviously. It's just going to be larger. It's still going to be about a 13-week. Again, we're going by precedent of what's been done before and what's been approved by the FDA. It would be another 13-week study, placebo versus active. We'll pick the dose based on the phase II results and just larger numbers where we move efficacy to be primary endpoints.
Great. With this profile that you've laid out here on the slide, ultimately, where would that put you in the kind of like lines of treatment or a treatment choice for myasthenia gravis patients?
I think this would put us as a first-line biologic. I mean, this profile really is ideal for that younger, more active patient. It's ideal for pushing biologics even earlier in treatment because it's not disruptive to people's lifestyle. It would, you know, based on the early market research we have, and we'll present that in the not too distant future when we're complete, I mean, the vast majority of physicians, when you offer them this kind of profile, they tell you like, yeah, this would be the ideal situation for me to be able to treat more patients earlier in their disease course with a biologic. I just remind you, again, I just mentioned this earlier, I mean, the C5s are still being used first line quite a bit. There's much more switching going on from FcRn to C5s than you see from C5s to FcRn.
The growth with Ultomiris and that whole franchise, the C5 franchise from AstraZeneca, is pretty impressive and continues despite the added competition from other C5s as well as the FcRn class. For us, it's very much being a first-line therapy with whatever might be the best FcRn out there. Our goal is to be a best-in-class complement inhibitor and compete against whatever the best FcRn will be when we get to market. Those, you know, that's it. It's essentially those two mechanisms of action with whatever the best thing in each class is, competing for first-line use in a very large, very, you know, multiple blockbuster market like myasthenia gravis. That puts us in a really good position.
Got it. Makes sense. I guess maybe on that, continuing that last point, how large is a market opportunity here? I think Dianthus has been doing some work on that.
Yeah, I mean, we just hired our Chief Commercial Officer, John King, who used to be the Chief Commercial Officer at Horizon Therapeutics, and he's doing some great early work in trying to, you know, better understand the potential for, but it's clearly a multi-billion dollar blockbuster potential. That's not just with MG, right? It's then these allied sort of neuromuscular conditions where it's the same target where we have the synergies from a not just a development standpoint, but from a commercial standpoint, like CIDP and MMN. I mean, in CIDP, you potentially, if you look at the Riliprubart data versus placebo from their phase II, sorry, if you look at their open label phase II trial, you know, that's a very impressive efficacy signal there.
is so impressive that it seems to suggest that it could be even better than the gold standard in IVIG, sorry, in CIDP, which is IVIG. Riliprubart and Sanofi are so confident that they're doing a head-to-head trial versus IVIG. Now you're seeing empasiprubart with their complement inhibitor also doing trials versus IVIG, again, feeling very confident in CIDP and MMN that it could be more efficacious. You know, it's not just about the MG market, of course. When you put all these three indications together, you could see classical pathway inhibition specifically targeting active C1s could be a game changer in all these three conditions that are all allied and could have a nice benefit, you know, halo benefit for each other in the minds of physicians and patients. I mean, there's just, we're very excited about the potential for DNTH103.
Great. Yeah. So let's jump into those other indications. Maybe the CIDP, but we'll go to next. You know, as you've talked about, there have been some development of other agents in that space, like Riliprubart. Could you tell us more about the data as it currently stands in the validation for C1 inhibitors and CIDP?
Yeah. Riliprubart in November of 2023 at ANEM Congress that was being held in Phoenix revealed their interim, their first data in CIDP with their active C1s inhibitor, Riliprubart. That was a bit of a game changer. For CIDP, it is the first time a complement inhibitor has been shown to work. In CIDP for classical pathway inhibition or active C1s inhibition, it is the first time it has been shown to work in any neuromuscular condition specifically. If you look at their data in their poster, and we have some of that data in our corporate presentation, you know, in patients who are refractory to IVIG, in patients who are stable on IVIG, in other words, doing well, switched immediately to active C1s inhibition or to Riliprubart, you know, you had over 50% of patients responding to and getting better than they were doing on IVIG.
That data is what quite honestly led to our pipe in January of last year for $230 million. There were no internal catalysts that triggered that financing. It was data that was presented by Sanofi with Riliprubart. What I think got most investors excited was not just that efficacy data, is that then when you look at how we compare to Riliprubart, and that's also in our data, as I mentioned earlier, we're a much more potent, lower dose, less frequent active C1s inhibitor. The exciting potential here is for us to be equal in efficacy, but a much more convenient dosing administration profile, or potentially maybe even more efficacious. We'll have to see when we look at the data from our CIDP trial. Interestingly, Sanofi has two phase III going on right now. One is versus placebo in refractory patients.
The other is that head-to-head versus IVIG and placebo study in patients who are stable on IVIG. Those two should read out by the first half of 2026 because they indicated that they would file for an indication CIDP by the end of 2026. Between our MG data in September and our own two other catalysts, which you can see on the slide here in the second half of 2026, there is going to be significant new data coming out from Sanofi that could potentially be very interesting catalysts for us as well. That should be in the first half of 2026. That is in CIDP.
Yeah, that makes sense that that will be an important catalyst for, you know, understanding the potential in CIDP. In the second half of 2026, as you show on the slide, there's an interim responder analysis from this phase III trial. Could you talk us through how that's designed and what we learned from that analysis?
Sure. Our CIDP trial is very similar to the Argenx single trial that got them the indication for all adults with CIDP, with a couple of important differences, but essentially similar in that we have a part A, which is patients being dosed 300 mg every two weeks in open label. Part B, where only patients that respond to DNTH103 in part A are then randomized to 600 mg, 300 mg, or placebo in a blinded randomized fashion. This interim responder analysis is once we see the first 40 patients in part A in the open label piece, it is for us to then announce to the street if we are seeing the efficacy we expected and will we continue on with the trial. Very similar to what Argenx did with their single phase III trial.
Got it. If the profile plays out as you hope for, could you help us think through how would the competitive landscape look? How would DNTH103 fit in that?
In CIDP?
Yes.
Very similar to MG, just less crowded. By the time we get to market, there would be Vyvgart, ITRULA, I believe, with their indication being used in CIDP, and then Riliprubart out there educating the market, the CIDP market on the benefits of active C1s inhibition or classical pathway inhibition. We would come obviously with a much more convenient, potentially even more efficacious version of active C1s inhibition or with DNTH103. What's interesting, what's different from the MG market in CIDP is that it's pretty clear IVIG right now is considered the gold standard therapy. It's also pretty clear, and we're hearing that and seeing that in the market play out, that FcRNs or Vyvgart are not as efficacious as IVIG. FcRNs are essentially a better tolerated, more patient-friendly version of IVIG, but they're not seen as efficacious.
There are a lot of case reports of patients who are on IVIG being switched to FcRNs or Vyvgart and not doing as well. There is a switching study that Argenx is conducting to try to help, you know, physicians in the market figure out what, you know, who are their ideal patients and how to switch them. It's pretty clear that IVIG is seen as superior in efficacy to FcRN. If the Riliprubart data demonstrates—it's a non-inferiority head-to-head study—but if it demonstrates non-inferiority to IVIG, essentially it will say that active C1s inhibition is at least as good as IVIG. That would be a huge win. That is a situation that might be different, where classical pathway inhibition could be seen as at least equal to IVIG and superior to FcRN in CIDP.
If, of course, they're able to show superiority, that's, I mean, that's going to completely turn that market on its head. You know, active C1s inhibition will be seen as the gold standard, you know, above IVIG. We are very eager to see the data from Sanofi in the first half of next year.
Great. Moving to the third indication, MMN, maybe first, you know, what's the status of understanding how C1s works in the setting?
MMN is a smaller of the three, but it's also one where FCRNs won't play. It's a complement-only market. Right now, the only competitor we have in that market is Empasiprubart, the C2 inhibitor from Argenx. They demonstrated previously, they're now in phase III with Empasiprubart and MMN, but they previously demonstrated with phase II very impressive, you know, relapse prevention data in MMN. They very clearly state that that is purely driven from the inhibition of the classical pathway. The downside of a C2 inhibitor, there are two major downsides with the C2 inhibitor or Empasiprubart from Argenx. One is that it also blocks the lectin pathway. The lectin pathway is the pathway that's triggered by the presence of encapsulated bacteria.
In our opinion, you're going to have a higher risk of infections by blocking the lectin pathway, which provides no real benefit for MMN patients. It very likely would end up with a box warning in a REMS program. The efficacy, they've stated very clearly in published that it's all about the classical pathway. We have now proof of concept for classical pathway inhibition providing really effective control for MMN patients. The other downside, it's an IV every week or every two weeks. Obviously, we're aiming, as I mentioned, for an autoinjector, self-administered every two weeks. In terms of, you know, if we can deliver similar efficacy, but obviously, again, with a safer profile and a more convenient profile, that's it. That's our competition. FcRns won't work in MMN.
It is a smaller market, but it's one where we could have a much larger piece of the pie.
What's the trial design here in MMN?
The trial design is on our corporate deck as well. It's very similar to the phase II that Argenx conducted. Just it's slightly larger, just a couple of minor differences, but it's essentially the same as what they've done. We're basically replicating what's worked for others. Our phase III with CIDP, same as ADHERE trial from Argenx, and our phase II, very similar to the study that Argenx conducted with Empasiprubart. We're also testing, I should mention, 300 and 600. Again, making sure we don't leave any efficacy on the table and see and test the theory of whether we really need to get above IC95. The MG data is going to be very, very informative there.
I think if we don't see a difference there, there's going to be a big question as to whether it really would provide any benefit in any of the other neuromuscular conditions as well.
Makes sense. After phase II for MMN, what would be remaining for development in that setting?
Phase III very similar to essentially, I mean, you could pretty much assume it would be similar to what Argenx is doing, which is versus placebo and IVIG. We assume that that's what they agreed to with the FDA, obviously. We are also assuming we would be held to the same standard.
Got it. That makes sense. All right. Maybe to close out the call, go switch back to some higher level questions that get from investors beyond just these indication-specific ones. You know, now that phase II results are coming for GMG in September, I think one of the questions are, you know, what would results in that setting mean for, you know, the other two success in the other two trials? I think, you know, if it's successful, that's easy to see that. I think it also is, you know, all the more successful, meaningful and positive for the other two settings. The more tricky question is like, you know, what if it's negative or, you know, the magnitude of the benefit misses expectations? Could you help me think through?
Is there a rationale to, you know, why, you know, still believe in the other two settings even if GMG fails?
It's an excellent question, Joel, actually. Two to three years ago, it would be like, you know, that's a tough question. But now, I mean, CIDP, you look at the Riliprubart data, it's really impressive. We're going to see their efficacy data very soon in phase III. And it's very clear we have a better, more potent, more convenient option. If they continue to show that impressive like data for, you know, anything similar to what they had in their phase II in CIDP, there's no reason we wouldn't work. MMN, same thing. I mean, there was never any proof of concept for, you know, complement inhibition in MMN until Empasiprubart. And we know we have a very potent classical pathway inhibitor. They will tell you themselves that the efficacy in MMN is coming from the inhibition of the classical pathway, not the lectin.
The lectin does not provide any benefit. There would very clearly be a rationale to continue in those indications. It is actually MG where there is no proof of concept, interestingly, even though, again, as I mentioned, that is where the science is clearest. If somehow DNTH103 does not work, we are either going to learn something very significant about MG in terms of its science, or there was something that went wrong in the execution of the trial. I am very confident in the team. The team has been executing incredibly well. I really, and I do not think there is anything new in the science that we are going to discover. Really, I mean, again, you know, I am just thinking forward. The only thing I really am very curious to see is, is there a difference between 300 and 600?
It would be really, really surprising if this didn't work, at least as well as the C5s.
Great. The rationale makes sense. It's always exciting to see well-designed trials reading out where, you know, the science supports it and, you know, hopefully it works. At a minimum, you're going to learn a whole lot from the study.
Exactly. We're very excited. It is, it's going to be a very interesting sort of 12 months from the data from the point when we see MG data. Nice combination of external and internal catalysts. It is really going to be not even a finish line. It is going to be a starting line for us for our very exciting following 12 months.
If you get successful results in September, do you start thinking about other potential indications to expand into?
We're not waiting. We're actually doing a lot of that work right now. I will say, you know, I, the team, have a very high bar for any new indications. The reason we picked these three indications is because we felt the science was there and the probability of success was there and needed to be above a certain level, but also where the commercial opportunity is very clear. Any new indications that we were to add, you know, we would want to make sure that we, you know, hit those two bars, get above those two sort of parameters, if you like. It needs to be where the science is pretty clear and where the commercial opportunity is significant.
The team's doing all the work right now to see if we can identify anything that, you know, hits on those two, you know, bars, gets above those two bars. Oh, sorry, Joel, if you're talking, I can't hear you for some reason. Can you hear me?
I do hear you. Do you hear me? Okay. Sounds like it's back. A question again on safety occasionally. I'll ask it here. It's just what do you need to show to get the, you know, to have no black spots warning on the label? Is there anything you kind of need to proactively show in your clinical trials or it's just a matter of following precedent from Enjaymo?
It's a little bit of that. We need to, we're going to follow the precedent. One way we do that is we conducted an in vitro experiment, which you can see in the appendix of our corporate deck, where we show very clearly that, you know, patient serum where DNTH103 is added and you add the Neisseria bacteria, that the serum can still go ahead and kill all that bacteria versus C5 where 100% of the bacteria survive. We have that experiment in the appendix of our corporate deck. Of course, we just need to have clean data. I mean, we need to make sure that in our clinical program, if there are any infections from encapsulated bacteria, that it's very clearly defined. If there are none that are related to drug, then that's essentially what Enjaymo saw and what Riliprubart is seeing so far.
Great. What's the cash runway?
We just reported over $330 million. We have cash up until the second half of 2027. The good news, again, is that provides us with enough cash to read out these three internal catalysts, right? The phase II data from MG, the top line data from MMN, and the interim responder analysis from CIDP. Yeah.
Great. Anything I didn't ask about before we go?
I don't think so. Again, I just want to say thank you for the opportunity. I know it's a bit of an interesting day out there today, but I do appreciate the opportunity to update everybody. We're just really excited. We're done with the MG trial. We over-enrolled. Yeah, we're just getting ready for that. Like I said, September will be the start of a really exciting time for the company.
You know, I wasn't going to bring it up because it's so fresh in the news of today being an interesting day. Any thoughts on how it impacts Dianthus or maybe too soon to think it through or really just a matter of execution for you guys?
I'm going to resist. No, I'm not going to comment. Look, I think my job as CEO and our team's job as part of Dianthus is just to focus on what we can control and that's executing around DNTH103. And it's really amazing when you think about it. I mean, it was less than just about three years ago, actually, we came out of stealth mode with our Series A $100 million announcement and we were still preclinical program and just a handful of employees. And to think that we are now here three years later in a phase III trial, two phase II trials, you know, with 300, I need to update this slide, but we just announced, oh, sorry, you know what? We haven't announced that yet. I'm sorry about that. $357 million as of the end of last year.
I mean, that's pretty, it's pretty impressive what the team's done. It's all about just continued excellent execution, rapid execution. That's what we're going to stay focused on.
Awesome. Thanks a lot for joining us, Marino.
All right. Thank you.
Yeah, great. Thanks again, Marino and Joel, for monitoring or helping out here. For the investors on the line, if you'd like to connect with Dianthus, please let us know. Specifically, thanks, Marino, for such a crazy day in the market. Biotech's never boring, but we know that good data cures all ill. Best of luck. Thank you so much.
Thank you. Really appreciate it.