Innate Pharma SA (IPHA) November 10, 2026 Conference Transcript

All right. I think we're good staff. Good afternoon, everyone. Thank you. Good morning. We're here to turn up on a decent friend, CEO of Innate Pharma. Thanks for being here today. So maybe if you're doing some work from Indiana, you know, could you summarize what you're doing in your own purpose?

Absolutely. And first of all, thank you for the invitation to speak here today. So a little bit about Innate Pharma. So we're a company that today is very much focused on bringing to market a next wave of differentiated antibody drug conjugates. We have a historical background in antibody engineering, so we were a spin-out from the Marseille Immunology Institute. We've developed a range of products. So our lead ADC is IPH4502. This is a product against Nectin-4 that we're developing in solid tumors. We have a big data readout coming next week on the 18th of November. which we'll be presenting at the triple meeting. Our other assets that we're focused on today are actually licensed. So the first one is lacutamab, which is a CUR3-DL2-targeted antibody, which we're developing in cutaneous T-cell lymphoma. We have an accelerated approval pathway, a breakthrough therapy designation, and we're moving towards a BLA submission once we have a confirmatory study up and running. That's partnered with Sobe, who will take over the commercial assassination of the drug. And then the third asset that we're focusing on today is monoluzumab, which is our NKG2A targeted antibody, which is being developed in stage three non-resectable non-small cell lung cancer. This particular asset has basically completed a randomized phase two off the back of that in combination with AstraZeneca. It went into a large randomized phase three, the Pacific 9 study, and that study is projected to read out early next year and on the primary endpoint. So important milestones coming in the very near term.

Thank you for that, and we'll mostly dive on Lactamab and the UPC. So, first on Lactamab, so you're in CBCL, it's Alzheimer's Syndrome and the disease from the UPC.

Yeah, so as you stated, cutaneous T-cell lymphoma, the two most significant segments of CTCL are cesarean syndrome, which is the smaller one, and mycosis fungoides, which is the bigger. In terms of treatment needs, cesarean syndrome is all of the patients are stage four. There's a very high unmet medical need. The current standard of care today is mogumiluzumab. Post-mogumiluzumab, there are very few treatment options for patients. So, lacutumab basically is designed to work very effectively in cesarean syndrome, targeting And there's a large pool of patients who really need, basically, a next step. Mycosis fungoides is a little bit different. It's more of an indolent disease in the earlier stages. And the patients in the beginning are often treated with topical therapies in the earlier stages, stage 1A, stage 1B, sometimes stage 2A. And systemic therapies tend to be used later in the treatment of the disease as it progresses through the different stages. And this is where lacutumab can potentially have a very important role. Lacutamab, because it hits CUR3-DL2, which is expressed pretty much only on malignant T cells, which are causing the disease, when you treat with lacutamab... All you're really removing are the disease-causing cells. This means the drug is very well tolerated. We have patients who have been on the drug from the phase one over seven years, patients from the phase two for over five years, and that means this is a drug that can potentially be used earlier because of this pretty benign safety profile wherever systemic therapies are not used. And if you look at the survival of mycosis fungoides patients, there's a significant drop-off between stage 2a and stage 2b when you see the five-year survival drop from 78% to 47%. And systemic therapies have not traditionally been used to try and prevent that because of the toxicities associated with those therapies. And this is where, really, Lacutamab is uniquely positioned to be able to intervene at an earlier stage and potentially create a new market. So, very different in terms of cesarean derma.

Yeah, but you've already presented the beta, part of the phase 2 derma. Could you summarize what you've seen in the cesarean syndrome and how that makes the case?

Yes, I can, yeah. So if we look at the data, it's been presented at ASCO a couple of years ago and ASH. And what we were able to basically demonstrate was, in cesarean syndrome, a very high objective response rate in the context of this disease, with patients being pre-treated with mogumaluzumab, so it was 43% ORR. We see just over an 8-month PFS or 8.3-month PFS, and we see a very high clinical benefit rate of close to 90% in this patient population with a very high medical need. It's a little bit different in mycosis fungoides, so we see a 19% objective response rate, but also a very high disease control rate of close to 90%. Again, and a significant PFS, which is very important in the context of MF of around 10 months. So these were interesting data. FDA was particularly interested in the data, and they used this data from the TeleMAC2 study to give the BTD designation for cesarean syndrome. So, yeah, very important data.

And so that was the basis for Telemax 3, which is the P3 that you talked. So you said it's going to be a bit different because in single-single, you'll find it for access to the Google. In MS, it will be the registration trial. So maybe on this time, how does it work on the P3?

Yeah, so basically what we have is the TELEMAC3 is a randomized study. It's controlled. So we have two statistically powered cohorts in the study. One for cesare, which is basically confirmatory of the accelerated approval, which we're expecting to get. And in that particular arm, all of the patients are post-mogamiluzumab. It's a head-to-head study of lacutumab versus romidepsin, an HDAC inhibitor, basically to confirm the accelerated approval. Then from a mycosis fungoides perspective, we have another statistically powered cohort of patients where we go head-to-head of lacutumab versus mogamiluzumab. And the endpoint of both of these cohorts is a PFS bi-blinded independent review. Key secondaries in CESI is overall survival, which is important in the context of the severity of the disease because all of the patients are stage four. And then if we look at MF, it's PFS as the primary, but then health-related quality of life assessments as the key secondary endpoints. Endpoints. And this was something important, which I didn't mention in terms of the results from the phase two. What we were able to demonstrate both in sensory syndrome and mycosis fungoides was. Excellent improvement in quality of life for patients. These patients, particularly the MF patients, have problems sleeping, they have severe itch, and what we saw in the phase two was that the quality of life goes from poor to good within a very short period of time when you administer the lacutamab treatment. So really improving patients' well-being and quality of life.

In terms of where you put the treatment from a physician perspective, so in a sense, it's post-modalizumab, the susceptibility is quite clear, although there could be a case of moving it earlier into the line of treatment. I think, Ellen, there's more heterogeneous treatment. There's not a line of modalizumab that is clearly established. What's your aim about this? Is it made for a system of therapy for other patients?

Yeah, so the design of the study basically is around proving superiority over mogumaluzumab. So the idea here is that basically you would be the first systemic therapy that the physicians would look to in mycosis fungoides and to establish lacutumab as the standard of care in MF. And I think particularly what we want to be able to do is to position the drug in those earlier stage patients that I mentioned this transition between stage 2A and 2B and the drop-off in survival. If we can position lacutumab to be used in stage 1B or stage 2A patients to prevent that progression of survival, that will have a huge impact for patients. But it will also open up this potential new market where mainly topical therapies are used today. And this is actually where the MF patients are diagnosed. So this is the opportunity to intervene early when the patients are diagnosed and hopefully change the treatment course for those MF patients. Also for cesare, I mean, we will come post mogumeluzumab. Our expectation, based on the discussions we've had with U.S. physicians, is that lacutumab will be included in the NCCN guidelines for cesaree, and it will be in a very open context. So physicians will be able to use the product at any stage and potentially use it earlier. So we may see a situation where physicians choose to use lakutumab, even ahead of moguluzumab, based on the better tolerability profile of the product. So I think that's important. Maybe another important consideration is that we've also been told that lakutumab will also go into the NCCN guidelines at the accelerated approval for cesaree-4-MF. So despite not having an approval in mycosis fungoides, physicians may choose off-label to actually use lacutumab in mycosis fungoides based on the accelerated approval in Caesaree syndrome. It's always good for physicians, and I think if you're thinking from a promotion perspective, there's a very large overlap between the physicians treating cesarean syndrome and mycosis fungoides. It's pretty much the same customer. In the U.S., we know that the majority of patients are treated in 50 centers. So basically any work that you're doing in terms of promoting incesary syndrome is actually doing the pre-approval promotion for mycosis fungoides.

It's obviously one of the...

Yeah, so the deal was very important for Lacutamab. Basically, the deal with the 75 million up front and the 14 million in potential short-term milestones associated with the accelerated approval in Cesare syndrome, it's allowed us to initiate the TELEMAC3 study and basically take that forward. In terms of responsibilities moving forward, we will continue to run the Phase III confirmatory study. That's very important that we have that in our control. The reason for that is that we have the expertise in CTCL. We've run the TeleMAC2 study. That was a 160-patient study in nearly 50 centers. So we have a lot of knowledge of where and how CTCL is treated. So we are ideally placed to be able to drive forward the TELEMAC3 study. Then we will also be in control of submission of the BLA for the accelerated approval. We have a good relationship with FDA under the BTD designation. We've had multiple backwards and forward interactions with FDA and, as I said, have a really good working relationship with FDA. So, again, based on our knowledge of the data and the studies that have been done so far, we're, again, in the best place to be able to pull together the BLA submission package to file that and to bring the product through to the accelerated approval. And really, that's the point then when SOBI will take over the commercialization. As I think you're all aware, SOBI has a world-class expertise in rare orphan diseases, and in particular in oncology hematology. So really, they're the perfect partner to take forward the cesaree syndrome indication, which is a rare orphan disease, and then the mycosis fungoides indication when the registration comes through. So we have already started the pre-commercialization work and are working diligently to be ready to be able to market the product at the accelerated approval. So we expect to have the first patient initiation in the Telemax 3 study in Q1 next year, BLA submission in the second half of next year, and then the approval early 2028. So we're in the countdown and in that pre-commercialization period now from a SOBI perspective.

I'm just going to call on the online timeline, so we have to explain what's going on to some of us to do that. What do we expect to do?

Yeah, so... The plan is, as I said, first quarter, we have the first patient initiation. That will allow us to establish a recruitment trajectory pretty quickly into the study, which will allow us to file the BLA submission and then the BLA approval early next year. But then in terms of the timelines, we're expecting roughly 15 to 18 months recruitment period for MF. MF will be quicker. Cesare will take a little bit longer, and then we roughly need 12 months follow-up after the last patient initiation. And then, so basically, you're looking in the 29 timeframe to have data, full approval. In MF sometime 2030, cesare syndrome a little bit later because it takes a little longer to recruit the patients because if you look at the incidence prevalence of the two diseases, in the U.S., for instance, we have about 300 patient incidence per year with about 1,000 patient prevalence pool, whereas MF, we're looking at about 3,000 patient incidence and 12,000 patients prevalence. So you can go quicker in MF than you can in cesare.

Okay, perfect. So maybe we can use your iTunes first-party, if I can do something exciting, coming in just a little bit. The winner next thing for you will be evaluating the target on the market.

Yeah, that's a really good question, and we spend a lot of time designing IPH4502 as a second generation Nectin-4ADC to overcome the limitations of the first generation. So what does that mean specifically? Well, first of all, the epitope that we hit with the antibody is non-overlapping with PADCEF, with EV. What does that mean? It means that we have activity from a preclinical perspective, not only in the high-nectin-4-expressing tumors, but also the low-moderate-expressing tumors and those with heterogeneous expression of nectarine-4. That means that it could potentially open up opportunities to go into different tumor types, where you have lower levels of expression of Nectin-4. Also, from an internalization perspective, the antibody has demonstrated better internalization. So that's important from a payload perspective and tumor cell killing. And if you combine that with the binding affinities, then we think we're differentiated on that particular part. The next level of differentiation is around the payload. And we have basically switched out the payload versus PADCEF. So instead of a tubulin inhibitor with an MMAE payload, we have a TOPA1. In this case, we chose exotecan. And that gives us the ability to overcome the resistance in patients to the phalene PADCEF. They have a regulation of MDR1. Exotecan is not subject to that resistance mechanism, so we're able to go potentially post-PADCEF and generate activity, and this is something that we've been able to demonstrate pre-clinically, but also more recently we've disclosed that we have seen responses post-PADCEF in our phase one dose finding study. And then the final level of differentiation is around our linker. We have a proprietary linker. We very tightly bind the payload, and that means we have low levels of three circulating exotecan, which helps to improve the tolerability of the product. And again, something that we've communicated from our dose-finding study is that we've seen very low levels of hematological toxicity, which would be the expected off-target tox associated with an exotecan payload.

Next question about the data you presented at CIMA, so you'll have 76 patients, 11 patients, very, very broad, I'd say, but what would they say about the correction between those?

Yeah, so we basically have completed the enrollment in the dose-finding study. We completed in July this year. We have 76 patients, as you mentioned. What I would emphasize is this is a basket study tumor approach, so there are over 10 different tumor types in the study across a range of different doses. So what are we going to be able to see from this data? Well, clearly we'll be able to profile the safety in a very effective way, and that will be one key thing that will be presented at the ENA meeting next week. The second will be around the PK, and this is important from a three circulating payload perspective, which is associated with potential So we'll be able to very nicely profile the PK. And then the final piece is we will be able to see signs of activity in a very heavily pretreated patient population. What we will have to do is to look at the totality of the data, because you can imagine with 10 different tumor types across a range of pharmacologically active doses, with maybe a handful of patients in each of those different subgroups, it will be very difficult to draw general conclusions on individual doses or individual tumor types, probably even more complicated. So from a totality of data perspective, we will be able to see the level of clinical activity and how that changes by dose.

So, yeah, as you say, it will be a handful of patients that are chemotized, but you'll have to take the drug somewhere, obviously, you know. First, do you have any internal benchmark of efficacy to get further, or would you go, you know, then prospectus, to get further, whether it's congressionally, you have some responses, but it would also make sense to go for the certification. So the question is, what is your symptom for taking the drug into the next steps?

There are basically a number of aspects to that. So clearly there are some benchmarks out there. EV302, the PADCEF study, in the patients who failed the therapy, they went on, a good proportion went on to receive platinum-based chemotherapy. And that really provides, I would say, an evidence base for what chemotherapy can deliver post-PADCEF, and it's around a 20% objective response rate. So clearly that's the lower end of the benchmark that you need to be able to achieve moving forward. You need to be able to beat that. If we look at some of the data sets that are out there that have come from potential competitive products, you're looking in the 30%, low 30s that you would need to be able to get to. So we need to be confident from our data set that we can deliver at least that level of efficacy to be able to move into the next steps, which would be dose optimization and taking the product forward to those next steps. And you'll be able to see this data at the INAH presentation next week.

And we'll have the next steps.

And we also plan to illustrate the next steps. We have an investor event, which we will do post the data presentation at the INA meeting in Barcelona. We will do this event in London at the Jefferies Conference off the back of it. We will basically have a standalone investor event where we'll have a KOL who will be discussing the data and the context and where this can go next.

And there is a good benchmark in terms of what you want to achieve, but there's also other metrics for advancing. Most of them are at the same stage. As you used the phase 1 with phase 1-2, what would you need to demonstrate against those impacted communities of the state?

So I think there are a number of potential angles here that would basically allow us to go forward. I think what we need to be able to demonstrate, first of all, is that we have a reasonable level of activity, or we have a way to get to a reasonable level of activity. That's critical. If we look at the other Nectin-4 ADCs that basically are being developed, particularly with a Topo 1 payload, most of them seem to have fallen by the wayside recently. So we saw at ASCO that Lilly had two assets that they presented. One was discontinued, the product with the Exetecam payload. The product with the Camto 98 payload seems to at least be on hold. It doesn't seem to be making the next steps, and that's maybe because of the metabolism issue they have with Camto 98, which is linked to CYP2D6 metabolism, where there's genetic variation, and they saw extreme toxicity in the low metabolizers. So that doesn't look to be moving forward at this point in time. The Merck product seems to have been discontinued, as we found out last week when it was dropped from their portfolio. So the only exotecan-based ADC that's left is the Henguru product, which is being developed in head and neck cancer. It's predominantly with Chinese data today, so I think it's a different benchmark. We've benchmarked internally versus that from a preclinical perspective and shown superiority over the Henguru compound. So I think we feel quite confident that we have a good path forward where we will have differentiation. It's probably a mixture of the tumor types we choose to take forward and really seizing, I think, the obvious opportunities as we move forward.

When will do you have time to bring the process to call for the class? How far are you going to be around the world?

Yeah, it's a very good question. So, I think what we're doing is basically very much keeping our options open here. We're funded to be able to make the next steps in terms of moving into the dose optimization phase for IPH 4502. I think what we need to do is look at the data and look at what makes the biggest business sense for our stakeholders. Is that developing across multiple tumor types based on the data and having a very extensive program, in which case maybe we need a partner and maybe we need a partner reasonably quickly? Or is it that we focus on driving maybe a urophileal cancer indication post-pacitive, which is maybe a simpler and easier route to take initially, and certainly something that we could do ourselves. But I think the key thing here is that we evaluate the options and we'll make the decision that's really best for the product, for our shareholders, and for the patients.

And you're going to be generating some more data about that. Absolutely. So, we have 20 seconds left. So, we can summarize the information, I'd say, 12, 18 months.

Yeah, key milestones. So, first of all, we have the data readout for IPH 4502 next week, at ENA. We then have lacutamab, first patient initiation, Q1 next year. Then, the submission of the BLA for accelerated approval, second half of next year. Then, accelerated approval, First half of 2028, and then from a monoluzumab perspective, we have the key readout of the PAC-9 phase 3 in the first half of next year.

Very good. Thank you very much. Thank you. Thank you.