KalVista Pharmaceuticals, Inc. (KALV) Earnings Call Transcript & Summary

Good afternoon. I'm Serge Belanger, one of the health care analysts at Needham. I want to welcome you to the 21st Annual Needham Healthcare Conference. We're happy to have for our next session KalVista Pharmaceuticals, one of the pure-play HAE story. They are seeking to address both the acute and prophylactic segment of the HAE space, both with oral products as well as new mechanisms of action. So today with us, we have Andy Crockett, the CEO; Ben Palleiko, CFO; and Chris Yea, the Chief Development Officer of the company. So I'll hand it over to Andy to give us a brief overview of the company, then we'll proceed to Q&A. And for those listening online, there is an option to submit questions via the portal. I'll be checking that as we move to the Q&A portion of the presentation. So Andy, please take it away.

Thanks, Serge, for having us. Happy to be here today. Just as an overview, we are focused on discovery and development of small molecule protease inhibitors. As Serge said, we're -- our disease area focus is primarily HAE although we also have interest in diabetic macular edema as well. Our lead programs are in HAE are KVD900, which is a small molecule plasma kallikrein inhibitor for the treatment of on-demand attacks of HAE. That program recently started a Phase III clinical study following a very successful Phase II clinical study that we ran out last year. And KVD824, a distinct molecule also, a small molecule plasma kallikrein inhibitor for the treatment of prophylactic -- prophylactic treatment of HAE. And that program is now in a Phase II clinical study. The strategy of the company is to be able to provide kind of a full suite of oral therapies for HAE patients. And so these 2 plasma kallikrein inhibitors in the on-demand and prophylactic space, respectively, are the company's first entree into HAE. [ Love ] to commercialize those molecules as well in addition to getting them approved to the various regulators and commercialize those in the major -- certainly in the U.S. and Europe ourselves. In addition to our work with plasma kallikrein inhibitors, we're also discovering and bringing forward to development oral Factor XIIa inhibitors. We believe we're the first company in the world to do that. Also, interested in pursuing indications in HAE with our Factor XIIa program as well as potential additional indications as we make for kind of down the road. But that's a high-level summary of where we are. The molecules, Serge, we discuss here have all been discovered at KalVista. We have our own research and development groups here, and we'll be looking to bring those forward as quickly as we can in clinical development. I'm happy to chat through any questions you might have.

Great. Maybe let's start with like a deep dive on the HAE market. I think with the new products and -- there's been some changes between the acute and prophylactic segment. But maybe we can just talk about the overall number of patients in both The U.S. and outside The U.S. diagnosed and treated, just so we get an idea of what kind of markets you're looking you can address?

Benjamin?

Sure. So the HAE market, HAE is obviously a very rare disease. It's about -- the estimates vary, but most people circling on around 150,000, some a little higher, some a little lower. So that suggests you've got something in the order of 7,000 to 8,000 patients in The U.S. In Europe, similar. There's really never been any [ ethical ] ratio or any other distinctions identified in terms of incidence rates. So generally worldwide, we believe that to be true. And so again, those 2 markets add up to about 15,000 or 16,000 patients in the rest of the world so it's usually more overall.

[ And I was going to say ], out of those 8,000 patients, were the vast majority of them treated -- or diagnosed and treated? Or there's still some out there that remain undiagnosed?

The U.S. in general is very highly diagnosed. I generally believe that most patients in The U.S. have been identified. Europe is somewhat less than that. Again, it probably becomes a little more geography dependent. But outside of those geographies, you've got large parts of the world where there's very low diagnosis rates. But in Japan is one example as a country where, in theory, there's a couple of thousand patients just based on the population. But to date, the identification rates and treatment have been very low. The other thing that goes against that is, to some degree is, there are -- even though it's familial and obviously, it is monogenic -- there are about 25% of patients who are believed to be new. I mean spontaneous mutations that come up. So you do have a fair number of patients that come up on a de novo basis. But again, especially in The U.S., they -- the treatment for those folks has dramatically improved over the last 10 years or so. A while ago, you heard these horrific stores of patients who went 10, 20 years, sometimes longer, trying to get diagnosis and going through these terrible procedures and in some cases, these just terrible surgeries as doctors tried to understand what happened. You hear that less frequently now, again, in The U.S., but ex U.S. is very common. I mean a 10-year journey for a patient to get to a HAE diagnosis if they don't have -- come from a family with a known history is not an uncommon thing.

Okay. And the number of treated and non-treated patients, is it still kind of 70% to 30%?

Yes, that's generally accepted. Again, the rates fall off precipitously as you get outside the U.S. and major European countries. But yes, anyway that's, that's [indiscernible].

And patients that choose to go untreated typically, is it mostly because they have kind of a milder disease or they have found a way to cope with it that they feel they don't need a treatment?

It's a little bit of both. And again, some of these are the folks who really haven't chosen it. They just haven't been diagnosed yet coming back to de novo population.

Okay. So let's move to the -- there's numerous prophylactic treatments as well as options on the -- for acute -- for the treatment of acute attacks. Maybe just talk about how the overall therapeutic market has changed over the last couple of years?

The primary change in the market in the last year or so has been the launch of ORLADEYO, which is a BioCryst drug. This was approved in late 2020, I guess, and launched in early 2021. So that's been the most significant one. Before that, the most recent launch of a drug was TAKHZYRO, which is a prophylaxis injectable that was approved and launched in 2018, I guess, '19. And before that, it'd been several years since you had another therapy to come along. So the market nowadays has got 3 major competitors in the prophylaxis space. [indiscernible]. Then you've got TAKHZYRO and HAEGARDA, which is CSL Behring drug that's been marketed for a while. Those are probably the primary ones in that world. And then on the acute space, Firazyr, generic of Icatibant is far and away the market leader there. It's probably got pushing 80% market share. And then you've got a number of smaller players. CSL has its lesser drug, [indiscernible] has [indiscernible] which is a lesser drug, so you've got a few other options in the acute space.

Okay. And the therapeutic market is -- well, yes, widely known to be about a $2 billion market, split to be 60% towards prophylactic and 40% towards the acute segment. Most of the growth has been on the prophylactic side. Just what are your thoughts on the current segment -- acute segment and its growth projections?

The reason that, that acute sales have actually come down substantially has less to do with growth in the prophylaxis space and more with the fact that Icatibant went generic 3 years ago. And so generic pricing, of course, is dramatically lower than the branded price. Generic Icatibant is probably about 25% of the price of branded Firazyr. And so the sales have really come down overall. Even though if you look at the scripts, the scripts haven't really moved in 3 years. I mean acute scripts are essentially -- have essentially been flat for 3 years. And so again, a lot of this sort of significant shift people talk about does relate at least to some extent to the fact that the pricing has come down so much in the space with the [ adding of ] generics. We -- our view was that from a patient preference and I'm focusing on The U.S. here, our view was that from a patient preference standpoint in The U.S. and [indiscernible] moving this a little bit, although the data has really not been seen yet. By and large, it's fairly stable at this kind of 60-40 split between prophylaxis and on-demand. Again, there are large numbers of patients who choose to treat their disease on-demand almost unrelated to their -- to the frequency or severity of their attacks. Patients like the fact that they feel like they have more control like if they treat attacks when they come on. Patients with lesser formed disease may view it as a favorable dosing profile compared to giving yourself a couple of injections of TAKHZYRO a month or a couple of week of HAEGARDA. Patients actually may view themselves as having to take fewer injections if they use an on-demand therapy. The average HAE patient has about 2 attacks a month. And so if you're treating 2 attacks a month with Icatibant or you're taking 2 injections a month of TAKHZYRO or 8 of HAEGARDA, that's a trade-off patients who actually are going to think about. That overwhelmed the question of whether or not how [indiscernible] in some cases, the severity of those disease questions. So the point is we don't see any wholesale shift away from it. We think it's a very complicated dynamic with patients that involves, obviously, the physical manifestation of the disease, but also a lot of the mental health impacts and other factors you see that come into play here. And those are relatively stable, which is why the shares are relatively stable.

Okay. And from a payer reimbursement perspective, I know you don't have a commercial product out in the market right now, but from your interactions and research, has there been any changes there, especially as there's more and more treatment options. You now have a generic on -- the generic Icatibant product. Do you expect the landscape to change, especially given that most products have been able to price with an orphan premium level. Just curious how you're thinking about that going forward.

We've done some other pricing studies, and we haven't gotten any sensitivity from payers whatsoever, took pricing in the range of branded therapies. I just [indiscernible] space. So -- and branded there's $12,000, $13,000 a dose. Some of -- there's a couple of therapies that are higher. There's a couple of therapies that are in their ballpark. Our early work compares with indication of sensitivity to all. We obviously tested a range and we actually got no sensitivity even at higher prices. And again, the argument to come in with is we're providing better patients with better control of their disease, they have better outcomes, they've better quality of life, right. All those measures sort of work for us. So there's really been no specific payer pushback, and that comes in the rate -- I should point out, we did that in the presence of generics. And so even there, generics obviously go in generic tier. It's kind of a fundamentally different thing. But we don't anticipate any problems with having scripts written for KVD900 as a branded product of having to deal with the generics as part of that. So the pricing is really not an issue. Payers are certainly starting to become a little more attentive to the orphan space generally and obviously, HAE specifically. But -- and so we do -- we are starting to have some early interactions with those folks. We will think carefully about how the pricing structures work and how we actually interact with them to sort of help them provide them the outcome measures and the real-world evidence that they need to support pricing decisions. But we have no great concerns about that, and we're always confident we'll get there and get to a reasonable price that works for everybody.

Okay. So let's move to the KVD900 program. I think everybody is kind of familiar with the mechanism of action here, plasma kallikrein inhibition is well established for HAE. But an oral acute treatment is a very different change to the paradigm that has previously been used for in the acute segment. So maybe just talk about that what an oral product would offer in the acute segment. And what would be the ideal product profile?

Yes, I mean, I think when you think about an HAE patient and kind of the journey they've been through over the past decade or so as these treatments have evolved, we're -- as we just highlighted with a number of treatments, they're in a much better place now than they certainly used to be. But the reality is, is even patients that are well managed on prophylaxis have experienced quite often breakthrough attacks. So patients, whether they primarily manage their disease with acute or on-demand therapy or whether those therapies are a rescue therapy or breakthrough therapy, right, for their prophylactic, everybody is advised to have on-demand therapy with them, right? The challenges of injectable, whether that be IV or subcutaneous on that therapy shouldn't be underplayed, right? So these are therapies that you have to have a kind of a moment's notice, which means you have to carry them with you. They have storage condition issues, right? The portability of those treatments are challenging, right? What those also lead to -- those type of challenges have led to patients either not treating all their attacks or delaying their treatment, okay? And that functional delay leads to core outcomes for patients, whether that is a completely untreated attack or whether symptoms get much more severe than they need to because of this delay in treatment. The concept behind oral on-demand therapy is that you kind of remove those barriers to treatment. And you encourage patients to treat at the earliest sign of attack, which is what the current guidelines in HAE are asking patients to do, right, because we know that the earlier you treat, the better your outcomes will be. And we think that -- and this is the way the KVD900 was designed, was to be something that was obviously imminently portable, easy to take with you and works very quickly. I think that's the other key aspect is the drug had to get on board very quickly and be effective very quickly. And perhaps that's one of the things that maybe is most surprising about KVD900 when we talk to people about the drug is how quickly even as an oral therapy that it works. We know that we get to effective concentration in minutes. So our PK/PD data will tell you that and then our clinical data reinforced that. And that's critical, right? So that it tells patients that, yes, the ease of taking this drug, right, combined with how quickly it works, should remove those barriers to treatment that they currently face with injectable therapy. So the ideal therapy in the on-demand space is something that you can take very quickly, has no barriers, you can carry it with you. And that's what KVD900. We hope KVD900 will be in the fullness of time once it's approved.

Okay. And I think it was over a year ago now, you reported positive results to be proof-of-concept Phase II data. Maybe just highlight the efficacy that you saw there and how it compares to current available treatments.

Chris?

Yes, I can talk to that. So the primary outcome of that Phase II was the time to use of conventional attack medication. So patients have access to their usual acute medication at all times during the study. So after taking the investigational drug, they could, if there are symptoms, demand it use their conventional attack medication or rescue medication, if you will. KVD900 significantly extended that time to use of rescue medication versus placebo, but if you took up within 12-hour period, and then that efficacy is maintained up to 24 hours. I think really importantly, though, KVD900 also met the vast majority of secondary endpoints and majority of the exploratory endpoints. And in the secondary endpoints, we have more, if you will, patient reported outcome. So the patient reporting how their attack was progressing or otherwise. One of those was something we called a Patient Global Impression of Change. This is where we ask the patient at regular intervals, how do your symptoms rate now compared to when you first took your investigational medication? And that was a 7-point scale from much worse up to much better. This was actually an outcome that was used essentially the identical outcome for the approval of RUCONEST, which was a study that was run 7 or 8 years ago. Really importantly, that showed a really good treatment effect of KVD900 versus placebo. And that will be the primary outcome in our Phase III study, and we've agreed that primary endpoint with the FDA. But I think the nice thing was all of the other endpoints, which use separate instruments. So how do you rate your symptoms at this time from none to severe and also using visual analog scale, all repeated that really strong efficacy signal of KVD900 versus placebo.

Okay. And then I think as Andy said in his opening comments, the Phase III trial, it's called CONFIDeNT, recently got underway. Maybe let's just talk about the design of it and how similar it is to the Phase II trial and maybe some of the difference besides the endpoint -- the primary endpoint that you just mentioned?

Yes. So it is very similar to the Phase II study. So the Phase II study was 600-milligram dose of KVD900 versus placebo. And in that study, patients treated 2 attacks, one with KVD900, one with placebo in a randomized blinded sequence. Let's say, some treated with 900 first, some treated with placebo first. The Phase III study is a very similar crossover study design. One difference is we're looking at a second dose level of KVD900. So we're looking at 600 milligrams as per the Phase II. We're also looking at dose level 300 milligrams and then placebo. So we are blinded 3-way crossover. So patients will treat 3 attacks in that study. But it's essentially the same study design as the Phase II. We'll be looking to recruit a very similar patient population, although in this study, we will be also recruiting some adolescents to help support a broader label for treatment down to 12 years of age. We'll also be treating patients who are already on prophylaxis therapy. So I think Ben's talking about patients treating on prophylaxis do get breakthrough attacks. Those attacks need to be treated. So we will be treating those attacks in the Phase III study as well. We'll also be including laryngeal attacks, which weren't eligible in the Phase II study, because of course, we did not prove an efficacy at that time, and they can be life-threatening. So we'll be including those attacks. But I think it's fair to say, generally, the study design and study outcomes that we expect to see will be similar between the Phase III and Phase II. [ So I mean to say ] that the change in the endpoint is just -- it's a promotion of an endpoint. There was a secondary endpoint and a priority secondary endpoint in the Phase II will be promoted to the primary outcome or the primary endpoint I should say, actually.

Did you find this new primary endpoint is more reflective of what the FDA is looking for? It's even as important to the patients and physicians who treat these patients?

Absolutely, yes. The primary endpoint for the Phase II, the physicians have very much a new treatment paradigm, this early intervention. So whilst patients who have already been told, you should treat all of your attacks, and you should treat them as early as possible. None of the clinical trials have actually been run under that paradigm. The older clinical trials where the attack had to actually escalate to moderate to severe -- moderate severity at least before it's treated. So it's more of a resolution. However, patients were told, treat your attacks as soon as possible. So we were trying to do that and replicate that those treatment guidelines in our Phase II. Because of that, of course, there was very little data out there to help guide us other than one previous study in which BioCryst had shown this positive impact on the use of rescue medication. So when you use that primarily there's a pragmatic approach is something that we could power place to reach. To your point, you're absolutely right. This outcome of how do you rate your symptoms now compared to when you first took your attack medication. Actually, it's really meaningful to patients. And because of that, it's meaningful to the FDA. So obviously, we took our Phase II data to FDA. We took also the feedback from patients and from doctors regarding that endpoint. And I have to say, when you speak to a patient, the patients we spoke to, it's very interesting. What they were most concerned about when they take their medication is they want to feel their medication starting to work and they want to fill that as quickly as possible. Once they feel that, and they've dealt with their attack and they can get on with their day, if you will, rather than perhaps a longer monitoring of severity. That was -- whilst, of course, they want the severity to reduce and they want the attack to resolve. It was this very early indication that the medication is starting to work. It was probably the thing that was most important to patients.

And in terms of the successful outcome, obviously, for the FDA beating out placebo is a main goal. But I guess for more marketing aspect, do you need -- since this is a time-related primary endpoint, do you need to be better or on par to the existing treatments like Icatibant?

So it's tough to make those comparisons. So it's one of the comparisons that you can make is that we can [indiscernible] [ I referred to earlier, ] where they use essentially the same endpoint as we used. So bearing in mind the study, design differences and the severity of attacks at the time of administration to take that as a caveat. RUCONEST actually met that same endpoint as our primary endpoint in the Phase III at 1.5 hours. And in the Phase II, KVD900 delivered that endpoint in 1.6 hours. So what that says is -- and remember, RUCONEST is intravenous infusion. So it's about as quickly as you can deliver a drug materially. So if you take them at the same time, KVD900 works as quickly as an intravenous drug. Remember, of course, as Andy alluded to, patients delayed using their injectables. And we know that for Icatibant as well in some real-life data with Icatibant that says generally, it's kind of 1.5 to 2 hours before patients use their Icatibant injection. So not only if you take them at the same time, it works as quickly. However, our expectation, of course, is that KVD900 will be dosed significantly quicker. In the Phase II study, we know the mean time to administration after the patients reported onset of the attacks, 30 minutes. And bearing in mind, in that 30 minutes, they also had to contact their doctor to confirm the eligibility of the attack. So we think in a real-life setting, KVD900 will be administered much earlier. And so as we do know, for Icatibant and all the other products, the earlier you intervene, the better the treatment outcomes. So I think there's a good body of evidence that we work very quickly. The PK/PD supports that. The clinical efficacy data I think we just got back supports that. And of course, will go on to show that patients actually administer their KVD900 much quicker than they do their current therapies.

And you're running the patient population a little bit in the Phase III with adolescents as well as laryngeal attacks. Just curious if you -- is the drug expected to have a different PK/PD profile in younger patients and were these laryngeal attacks harder to treat than other kinds of attacks -- of HAE attacks?

As far as the PK/PD, our expectation in adolescents is it will be the same. So we've done some -- obviously, we've done our population PK modeling. There's nothing in that modeling to suggest that adolescents will show any different PK/PD profile to adults. There will be a limited number of adolescents in the study as well. As far as the laryngeal attacks go, there are very -- I mean patients don't thankfully experience that many laryngeal attacks. So I think it will be a small number in the study. There's no evidence from any of the other treatments. Kalbitor works just as well on laryngeal attacks. Lanadelumab in prophylactic setting, certainly, you don't get more laryngeal breakthroughs than you do in other types of attacks. So -- and [indiscernible] mechanistic rationale to think that plasma kallikrein inhibition won't be just as effective on laryngeal attacks as it did on any other type location.

Okay. And like as Andy said earlier this -- the CONFIDeNT trial, just recently got underway. I don't know if there's any feedback yet on what -- how enrollment is going. As COVID restrictions lessen here, are you seeing better enrollment than what you saw when -- in the Phase II trial?

Yes, we've got -- we've got the things publicly to say about enrollment. Safe to say, certainly, the enthusiasm from the site, it's very high for KVD900. I think you mentioned earlier that KVD900 is a real paradigm shift in the on-demand treatment area. And we know that generally patients' demand for oral therapy is extremely high in its indication. And this being the first opportunity that patients have to treat their attacks on demand with an oral therapy really is -- I think it's exciting to them. And it's also exciting to the investigators to better provide that opportunity to their patients. So the general feedback we get is very positive for this trial. And to date, recruitment is going as we would anticipate. And as you say, we're just starting the study. So yes, we're excited in CONFIDeNT that this is a study which really should pull patients in very effectively.

And remind me again, have you given timelines on when a potential readout would be? Or it's too early at this point to talk about that?

Sorry, yes, we've guided second half of next year for results.

Okay. Great. And then I'm going to ask you to look in your crystal ball here. But like I said earlier, this would be a significant change to the treatment paradigm of acute HAE treatment. Do you expect an oral product would garner market share from the current injectables or bring back some of the prophylactic treated patients to treat individual attacks with an acute oral treatment?

Serge, our expectation is, again, based on the data we've seen to date, that this should meet all patient desires. It's designed to be a very patient-friendly, right, easily portable, easy to take, easy to deal in all directions, a therapy that can be taken at the first signs of a pending attack. And so we think it's going to have a very high degree of receptivity in the patient population. This has been in our respect, designed and executed to date to meet the needs we've heard from patients in the marketplace. So absolutely, we fully expect this to capture a very large share of the existing on-demand marketplace. We think it becomes an obvious place to go for patients in the breakthrough space. So we think there's a fair number of patients who maybe don't nowadays treat as many attacks, and we think that -- so treatment rates should actually go up because patients now, I mean, again, [indiscernible] number of attacks really aren't treated or treated too late. And this can solve all those problems. So we think increased usage can resolve from this. And then certainly, to your point, we -- based upon what we've seen and what we've heard so far, I think we're beginning to believe that we have the opportunity to take some of these patients who maybe have transferred of their prophylaxis because they want oral therapy now all the data is available to them or just because, again, from an attack basis, they see better -- sort of essentially less injections by using prophylaxis as opposed to on demand. We think a lot of those patients would actually be very seriously interested in KVD900 and may in fact be interested in moving back to an on-demand from that. So we think the opportunity, to your point, is not -- it's certainly the market share gain. It's very high. But in terms of just the market growth opportunity that comes primarily to us as a result of that, and we think it's dramatically underestimated [obviously ].

And then KVD824, the prophylactic HAE program. I think the path -- the development paths in the prophylactic area is a little more established and well-known given the recent approvals of other products. But maybe just talk about the goals you're looking to achieve with KVD824 as a product profile?

Yes. So I mean, I would guarantee very similar to what we want to achieve with KVD900, which is providing oral therapy to patients and not asking them to sacrifice in efficacy, right, so that's kind of the whole idea behind the development. Our research with patients, our interaction with patients that said, patients want really 2 things out of their HAE therapies. One of them, obviously, they need their therapies to be effective. With these really effective therapies in the market, patients, we don't see them over a long-term basis going backwards in efficacy. These therapies have really improved their lives and efficacy is paramount. And then also the other clear desire from patients is oral therapy. And so with KVD824, what we're looking to do is provide patients with that in prophylaxis, that same kind of level of efficacy they come to expect, but with oral therapy. And again, it's very similar to what we're trying to achieve with KVD900, but in the prophylactic space.

Okay. So complete trial is underway. Well, it got underway last year. So I know you don't give enrollment updates. But what is the potential timeline for readout with this trial.

We expect data sometime around the middle of next year, Serge.

Yes. And assuming this is positive, the next step would be a single pivotal Phase III trial similar to what we've seen with ORLADEYO?

Yes, other precedents being set to take ORLADEYO [indiscernible], yes.

Okay. All right. And then lastly, your Factor XIIa program. I think that's one. It's a new mechanism of action, definitely less known than plasma kallikrein inhibition. So maybe just give us an overview of where it fits on the cascade that leads to HAE attacks and where a Factor XIIa inhibitor product could -- what kind of role it can play in the treatment paradigm.

Yes. Good question. So Factor XIIa actually sits at the top of the cascade that ultimately leads to these HAE attacks. And so for a long time, I think everybody in this space has thought this would be a very interesting place to intervene. Actually CSL has antibody, garadacimab, which is a Factor XIIa antibody. It's now in Phase III. That's some fantastic Phase II clinical results. Just validating, I think what scientifically we believed all along this is an appropriate place to intervene. We've actually been working on this target for a number of years now. And from a small molecule, oral drug, [ handing ] perspective, from medicinal chemistry perspective, it's been a really challenging target. One of those reasons is because no one's ever done it before. And so it becomes a challenge because there's nowhere to start, you're doing all that yourself. But the great thing for us now is then also now becomes a huge competitive advantage for us because we've done the work. We now have selective oral potent molecules for multiple series moving toward the clinic and we're looking to file an IND next year. We're distant, I think, it remains to be seen, right, we think that what we want to do, as I've said now multiple times is, be kind of one provider of really effective oral therapies in HAE, be that on-demand prophylaxis or the plasma kallikrein inhibitor, Factor XIIa inhibitor, right. The new ones some differences is how Factor XIIa may or may not dependent on plasma kallikrein is yet to be seen, right. It certainly sits at the top of the cascade. It certainly gives us opportunities if you course dose twice daily. Perhaps that gives us an opportunity to get to a once-daily really effective therapy we'll see. But from an R&D company like ourselves, though, what we want to do is bring forward more therapies to try to fill patients -- what the patients really need in the space. And Factor XIIa also, we don't have much time to talk about it today, but it also gives the opportunity to move beyond HAE and to some other potential indications that as a company, we're looking at more closely and we'll provide more information as we move in that direction.

And I think you're planning an IND for next year for this program?

Yes, we are.

Do we know at this point if it's going to be an oral treatment and whether you're targeting acute or prophylactic?

Oral treatment for sure. And yes, right now, I think our focus would be prophylaxis. But we'll see how the molecules pan out.

Okay. And is there any reason to believe that since this is a new mechanism of action that you wouldn't be able to follow the same path that KVD824 is taking right now as a prophylactic treatment in development?

I don't think so. Again, I mentioned this garadacimab is following a very similar type of paradigm that we've seen with the other approved therapies in prophylaxis. So no, no reason to think that would be different.

Okay. And you've mentioned a couple of times today that there could be a potential role for Factor XIIa inhibitor outside of HAE. Is that something you plan on evaluating as a company? Or if you will remain an HAE focused player?

Well, we certainly -- HAE is an important focus of the company, right? But as we have opportunities beyond HAE, we'll explore them. And as I mentioned, as we move those things forward, as we get more information, we'll share that. And -- but certainly, we're interested in where else this might take us.

Okay. I think we only have a few minutes left. So maybe I'll ask Ben to give us kind of a financial overview of cash balances and operational runway?

Yes, sure. We report on an April 30 fiscal year. So the last quarter, we reported publicly was -- ended January 31. At that point, we had $195 million on the balance sheet. We've guided that carries us into at least early 2024. So we're very comfortable with our financial position.

Okay. And in terms -- obviously, in The U.S., I think you can take on the development of both 900 and 824. Outside U.S., is that something you're willing to do on your own or you're starting to look at potential partnering opportunities?

We have always said that our plan is to commercialize this in both The U.S. and major European countries. It's the perfect disease for a biotech company to market in. I mean it's addressable with a few -- basically a few dozen sales reps in each geography. The cost is eminently doable. So this is by no means an extreme goal for a company of our size, given the marketplace and given how the patients roll out and how the doctors work. We've also always said that we're more likely than not to partner in most of the rest of the world. We do want to -- routine basis, get expression [indiscernible]. Those have obviously picked up a little more as we move into Phase III. We intend to be thoughtful in what we do. We are considering a variety of different structures [indiscernible] as we move forward and we make some decisions on that. We'll talk to people about it. But for all the reasons we talked about earlier, this is a very attractive therapy worldwide and the interest to date reflects that.

Great. Well, I think we've reached the end of our time. So we'll have to wrap it up. I want to thank you for spending some time with us today. I know it's late in the U.K. So I'm sure you're happy that the day is almost over. But thanks for the overview, and we look forward to seeing some data next year.

Thanks, Serge.

[indiscernible] talking to you, Serge.

Thank you.