Half Year 2022 Molecular Partners AG Earnings Call

Patrick Amstutz: If the partner product is given more often, and the Q3 weeks would allow you more extended, less frequent dosing, but then you can actually choose what you want to do. And I think partners will very much respect this extractive. Let's go to the next program, which is 533. Yeah, and so we're kind of recruiting, and we will update as we go. So let's go to the next program, which is 533. This is an evisity-driven selective killing instrument for blasts and leukemic stem cells. What's the problem?

Patrick Amstutz: The problem is AML remains a deadly disease. Leukimic stem cells are the driver, while labs are, call them the killer. We need to kill both, but we have to focus on the leukemic stem cells. They are really difficult because they're very less sensitive to chemo. They don't have good, strong surface markers.

Patrick Amstutz: And what we have now tried to do is the following. LSC, so in Kim Xemst, M-Plath, Saitu Express, CD33, 17, 112. ED70 is rather specific, so there we take a high affinity. Garpin, 33, and 123 are also unhealthy cells. So we go for lower affinity. That's what we call optimized affinity.

Patrick Amstutz: So we try to kill those cells and have either 70 and 33 and 123 and not the mono 33 and 123. And that would then open a therapeutic window that we can use MPO533 in AML for targets that usually have a very narrow or even closed window, and others have tritons. Free clinical results show that that works. We also could show the preferential killing of leukemic stem cells and blasts in ex-vivo patient samples.

Patrick Amstutz: And that's the strongest data you can get. That's what we say is high translatable value as we take samples from these patients and could show the differentiated killing. Earth and Human, we're very excited for that. So we're progressing toward that moment, and we will give you an update at Ash. I have a slide over.

Patrick Amstutz: How will the trial look? This is a bit more information. It's AML and high risk, and yes, patients. Inclusion criteria are listed here.

Patrick Amstutz: Also exclusion criteria, which is not to be underestimated. And you see, we'll try to include around 20 to 45 patients, primary and political, and tolerability, but the main secondary endpoints are also efficacy. We do believe that this molecule will show itself in phase one, and we will know if we have a drug candidate in hand or not, very different to 310 or 317 that needed to have much longer clinical trials until they did show BALS. Again, trial initiation plan for late 2022. And as I have pointed out before, slide number 10, the ash event.

Patrick Amstutz: So that's really the colleague curtain-raiser for the program. We want to bring together a key expert and also discuss with you how they see the program and where the value of it will be. A few words now on slide 11 on regular ligand therapy. So we all know radiation is a very good way to kill tumors. But we also know it is very limited in scope to tumors that are well localized.

Patrick Amstutz: And I think they can do up to five lesions, but then it's done. The delivery of radiation with small or large therapeutic modalities like antibodies or peptides can work, but it's risky. And we believe DARPIN could really bring a more general solution. It is small and has ultra-high affinity, and it can bring the radionuclide for high accumulation in the tumor. Very fast half-flight, so limited systemic exposure.

Patrick Amstutz: Good penetration through the size and high affinity will keep it at the tumor longer. What we're now working on is really kidney exposure, so limiting kidney exposure. That's work ongoing. We have demonstrated penetration at the affinity part.

Patrick Amstutz: We have validated this indirectly with the collaboration with Novartis, and the kind of ongoing is optimization for kidney exposure. And then when we're there and we're kind of moving forward, we will also work on the first candidates and announce those. Ideally, I hope I can be standing here and do that next year. Just two slides on the science, as we are excited about that. So I was before pointing out the antibodies and the peptides, so low molecular weight compounds are usually peptides or peptide derivatives.

Patrick Amstutz: Antibodies are good, but they are large. So they have less tumor penetration, and they also have higher exposure to normal tissue as they do circulate very long. And unfortunately, those antibody fragments up to single chains of these don't bring deep tumor penetration because they're too large.

Patrick Amstutz: You have to go below 20 kilodleton, and that's where darkens are. Now, peptides, low molecular weight compounds, they have many benefits, but usually they don't have the super high affinity, and they're also restricted to some targets. So that's kind of exactly the sweet spot where we think we can actually have all the benefits of the antibody combined with the benefits of the small. I'm just going to slide 13 so you understand how such a flow would look like, individual with the tumor, we infuse the drug.

Patrick Amstutz: These are not one-for-one, not half-life extended, so no HSA darpin. The drug sluts through the whole body, goes everywhere, also into the tumor, and deep into the tumor. We stopped the infusion. The drug excretes very fast through the kidney.

Patrick Amstutz: This is the first kidney pass. So literally within an hour or so, the body has no darpin or radioactivity, and we actually, with the high affinity, stay in the kidney. tumor for a long time, and the radiation can do its job.

Patrick Amstutz: We're very excited about this. Obviously, we can't do that alone, so we're also speaking with companies that have radio ligands, and that work is also ongoing by our collaboration and aligned team. With that, I will kind of stop here, and I'm happy to hand over to Andreas to give you a bit more flavor on the financials where we stand. Andreas, the floor is yours.

Andreas: Thank you, Patrick. I hope you hear me well on this mobile connection. With that, I'm very happy to give you some background on the financials, which look very, very good for the first half year, as well as that we have a very strong balance. So on the balance sheet, we have 285 million in cash, as Patrick was saying, which gives us a very substantial long runway to execute our strategy. In the first half of 22, we booked 184.5 million in revenue, and the big bulk of that is coming, or it was coming from Novartis, primarily due to the 150 million milestone payment for the development of Enzovi Bedop.

Andreas: With that, we generated high operating cash mainly from this collaboration and a total of 151 million in age 122, resulting in operating profit of 146.3 million and a net profit of 148.6 million. And as we repeatedly said, you're funded into 26, and we also updated the full year expense guidance. It was 75 to 85 million range.

Andreas: We have reduced it now to 70 to 80 million. I would say the point of that is certainly a reasonable assumption to take for full-year expenses. And last but not least, we also issued 3.5 million treasury shares. Actually, that was yesterday.

Andreas: And this is the result of our shell filing, a free one, which we did on July 22, which is very customary for U.S. listed companies to do that within one year of the listing. Then I move to slide number 16. Keep figures. Again, a bit of the same, but this time compared with the first half of 21. Revenues, again, much, much higher than last year, as you can see. And a bit more background on the details.

Andreas: Out of the 184,000, 168 came from Novartis, and interest from the other collaborations. Total operating expenses were 38.3 million; that's about a million less than the first half of 21. The 38.3 were invested in personnel of about 20.5 million, external R&D 9.5, and other expenses of 8.3. The operating result, again, was 148, versus an operating loss of 34.8 last year. The net financial result is 2.3, and we made a profit there mainly driven by the non-realized currency gains on the US dollar position, resulting into a net result of 148.6, as I said before, versus a loss last year. One thing to add, we have not been paying taxes because we have losses carried forward in the balance sheet. Last year we had $212 million in tax losses carried forward.

Andreas: Of course, we could use a big bulk of that now, and so that we didn't have to pay taxes, and we still have some tax losses carried forward left. Yeah, net cash from operations 151 versus net cash out of 52.5 last year. The first six months, cash balance 285, which is 110 million more than a year ago. And FTEs, yeah, grew a bit, but not much, from 158.3 to 164 FTEs on our payroll. Now I move to slide number 17, the balance sheet. It's very simple, but very remarkable.

Andreas: We have a test-free, obviously driven by the cash balance, 285, and then some other assets on the asset side and, on the right hand side, equity, very strong, 266 million and some liabilities of 33 million, but 14.4 of these 30.3 are not true liabilities. It's the 14.4 are so-called deferred revenues from the Nipper collaboration for radio ligand therapy. The 14.4 million, maybe that's more for the analysts to note, I expect, of them to be recognized in the second half of this year, 5 million in 23 and 3 million in 24. Obviously, this is subject to progress and can always change, but just to give you a bit of guidance so that you can do your maths properly.

Andreas: With that, I move to the guidance, 22. Again, just in summary, I expect total expenses of 70 to 80 million for the full year, of which around 9 million are non-cash effective costs, and yeah, the 285 million gives us a runway into 26, and all this excludes any potential receipts from current or potential future partnerships. And obviously, everything is subject to progress and changes in the pipeline, as well as, as we all know, the financial market can sometimes make a difference.

Andreas: With that, I hand back to Patrick, and I'm sure you might have one or the other questions. Thanks, Andrea. And before we actually go to questions and summary, I would just have two or three slides on Abikipar, which is a long-standing program. It was our first to go to the clinics. It was with Allergan.

Patrick Amstutz: It was a Yavi transition, and we have regained Ryan. Let me just quickly recap where we are with that. So, it's slide 20 now.

Patrick Amstutz: This part is a long-awaited antibetchus in white A&D, obviously with potential in DME and RVO. It's a huge market. And there is a new player out there, a new winner called Forescimop or the Obismo, and that's a fixed eight week treatment and treatment extends to 16 weeks. The treatment extends looks great in clinical trials, but in real world settings, patients lose vision. So we actually think that our 12-week dosing, I'm now in the history of a Bicipar, actually could even be at least a good competitor to Ferry C-Mop. So 12-week dosing six, nobody has shown that so far.

Patrick Amstutz: You all know that the problem was, or is, inflammation, and that led to a complete response letter as the risk reward was not given, especially as Novartis and Bayou had also inflammation problems, and that did change the tone at the agency. So we got a complete response letter, which ended in Visi Bar being returned last year to molecular partners. Now, we believe that we have identified and can remove the inflammation-causing agent that was actually worked on by an ex-allergan team and also some support by Advi and our guys. And then our team went to the FDA to find out what it would take to redirect the drug. This is a single safety trial versus ILEA.

Patrick Amstutz: It's a 40-week readout with around 550 patients. And we are not going to run that trial, but with that, we have something in hand that we can at least offer to partners. Just slide 21 to recap the data because it is amazing data, and it also once again shows that darkens are highly effective. What you see here is central rectinal thickness. That's the call it a biomarker that cannot lie. Sometimes visual acuity is a bit difficult because you can get a bit lucky with that, but the central rectinal thickness is a hard fact.

Patrick Amstutz: And you see, with 10 injections of bickipar, you actually end up more or less exactly at the same spot after two years as 25 injections of Lusent. So the fixed token regime works. I don't want to take away the 15% inflammation.

Patrick Amstutz: Definitely not good, but we do believe that we can solve that. And again, we're not going to move that forward ourselves, but we're speaking to the interests of parties, and there's also interest from investors to fund that trial as it is a single trial towards approval. So those are the avenues we're looking into. For the experts in business and finance, there are very high question marks here about whether this deal can happen or not.

Patrick Amstutz: We just wanted to raise it to your attention that we are having such discussions, as we felt people kind of had totally disregarded that opportunity. Good. With that, I want to come to the outlook. Enzo, you and I were touched.

Patrick Amstutz: EOA is open to mint net. We're sort of waiting for next fall and winter. Let's see. Let's hope we don't need it, but if we do it, there. The full phase three is still under discussion. That's a difficult situation for everyone.

Patrick Amstutz: Nobody knows how to run such trials at the moment, but we're working on it, or we have a next generation one, should a pandemic rise from the current, 310, we got back at the tumor local T-cell activator. We as molecular partners will conclude phase one and then shelf it to see if there are applications, if others validate 401 as a good target, which has not happened so far. So that's one that we keep, but we don't invest in going forward and see how 401B develops as a target.

Patrick Amstutz: 317 CD40, We talked about initial results first, the second half of this year, and then more to come early next year, and definitely is slated for partnering. 533, that's where we want to find the signal ourselves, highly excited, get the trial up this year, and collect data next year.

Patrick Amstutz: The basic part, we just touched on, and then radio licking, but also other things we're doing in these really exciting times. We're building value in our pipeline, and we really look forward, especially to next year, when we can unveil a few of our programs that are then likely going to reach candidate stage, and we'll be ready to be discussed with it. you. Most importantly, cash into 26.

Patrick Amstutz: I don't think many biotechs at this point in time can say that. We are well funded. We are less hit by the biotech crisis.

Patrick Amstutz: We're in a great situation. Proven technology, a super motivated team. We know we can do it, and we have the means to do it. So, really, a good moment for us and definitely a moment where we see a lot of value ahead. With that, I really want to thank the team that was with me on this call, but actually the entire molecular partners team. They are super energetic.

Patrick Amstutz: They know what they are doing. I'm repeating myself, but it's so important in a biotech crisis to have such a team that is not thinking twice but executing, with the cash and with the cash that we have. I also want to thank all of our collaborators. We're not doing this alone. We're working with clinicians. We're working with partners, with suppliers, and all of them are really helping us to move forward. And especially, we want to thank the physicians and the patients in our trial because that's really why we get up in the morning.

Patrick Amstutz: We are a totally patient-centric patient focus company, and that's linking myself back to my intro. When we see that we can bring value, we know we have to write about it. With that, I thank you for your attention, and I am open to questions.

Operator: We will now begin the question and answer session. To ask a question, you may press star more than one on your touchtone phone. If you are using a speakerphone, please pick up your handset before pressing the keys.

Operator: To withdraw your question, please press star, then two. At this time, we'll pause momentarily to assemble our roster. Our first question comes from Georgi Yardinov from Cowan and Company. Please go ahead. Hey guys, congratulations.

Georgi Yardinov: and all the progress, and thanks for taking questions. So maybe starting with 317, what should investors expect or, I guess, focus on from the data disclosure later this year? And maybe can you just walk us through how you expect to use the

Georgi Yardinov: This initial data for a go or no-go decision for further development.

Georgi Yardinov: And then just on 533, as we're thinking about the phase one trial, do we have any data on

Georgi Yardinov: The percentage of AML blasts that express at least two of these markers. And do we know whether this ratio is also seen in heavily pre-treated patients and in specific patients?

Georgi Yardinov: of observation you're targeting into Please One trial. And maybe if you can talk about whether or not

Georgi Yardinov: You can talk about whether or not you expect to see monothera activity, and then we have just one follow-on question.

Patrick Amstutz: Sure, hey, thanks, Georgie. All good questions.

Patrick Amstutz: So I'll start with 317, and it is not so easy to kind of, kind of, what data we will share that is sort of interesting or valuable for, let's call it, analysts and investors, as what we want to do is partner. So most of the data we will not actually share with the public, but in partnering discussions. And what we are aiming to do is show that the drug is active and show that it does not have the side effects that other non-tumor targeted activities of CD40 have. So many companies are working on CD40. People believe that there is value in that pathway, but they can't unlock it.

Patrick Amstutz: So the first thing, and that's why we were really excited today to show that one milligram is that you actually can go into a region where you hope you'll actually have. Then the PD markers, that's paired biopsies, that's a bit more up in the air because, yes, you can really show how that works, but I think safety is key. And with the paired biopsies, that's what we need to convince partners to enter into the discussions and, in the end, partner with us to look for combination trials. So the data we will share with the public is maybe much more limited than what we share with potential partners. And those partnering discussions are starting up.

Patrick Amstutz: And the good thing is that the industry likes and believes in the target. So we can sort of ask those companies, large ones, mid-sized pharmas that are on that pathway, and the interest is definitely given to look at the data and then let's see when the data holds also partners. Now, 533 is the phase one trial, and you were kind of asking what the percentage of co-expression is. And I think the percentage is very high, so we're talking above 90% for sure about co-expression.

Patrick Amstutz: And also the pre-treatment. And here we have an interesting situation, as one of the successful drugs there is Venetoprase, and Vanessa Glocks actually drives CD-70 outbreaks.

Patrick Amstutz: So we believe the right pre-treatment can actually help us to have more effect with our CD70 targeting domain that is in there. And so we actually do expect that most patients, in principle, will be able to benefit. It won't be 100% for sure, but we definitely believe that the number of patients that have the phenotype to profit is above 50%, at least. And so we are kind of looking into this, and we will. get the data. And to your last point, we do expect that we should be a single-agion activity. You actually need single-age activities.

Patrick Amstutz: This disease is so deadly that if we don't have even fast single-hation activity, it won't help. So we need to see this early. And the drug is designed to do that. But I think the risk, call it risk, is maybe less on the targeting side and more on the T-cell side. The question is, how many active T-cells do the patients have? And that's why you will see some of our exclusion criteria; those patients that have no T cells can also not profit. So we have to make sure that they actually have a good immune system that can be activated.

Patrick Amstutz: I'll repeat myself, we expect data next year. I cannot say when, it depends on which dose actually shows activity. I do have to say that we will start with a very low dose, as we have no cross-reactivity to monkeys, so there's no formal monkey talk, so we have to start at a lower dose. But we definitely see fast dose escalation. I would invite you all to Ash. That's where the experts can answer all those questions, much more intelligently than I.

Patrick Amstutz: And so I think that's a good repetition of the Ash event. Thanks, Patrick. Thank you so much. Georgi, it's Seth as well.

Seth D. Lewis: Just to follow up on Patrick's point, you were asking about the amount of patients who would have expression of these markers. And he's right, it is a very high number, but you have to remember the mechanism of action for 533 is indiscriminately driven to activate the CD3 T-cell engager in the presence of either two or three of the expressed markers. So that high number would be any combination of those.

Seth D. Lewis: of those three markers resulting in that high number of expressed patients, just to make sure that was clarified.

Georgi Yardinov: Great, thank you. And then just finally, the Radio Ligens assay is also a very interesting application of the DARPIN technology. Maybe just briefly, are there any initial educations you feel like you could be differentiated in?

Georgi Yardinov: And when would we be expecting the next milestone in terms of payment from your collaborators? Yeah, indications, you're looking at really hard-to-treat tumors that are, let's call it, highly metastatic, so where any kind of other, let's say, approaches will not be ideal. So you have to go into that segment where you kind of, where the highest value lies.

Patrick Amstutz: Um, that big milestone next year would be that we kind of come up with, or come up with, targets; then we disclose which targets we're working on and maybe present the development candidates. And then this can be rather rapidly progressed toward the clinic, because this is a monodarkin, and it just needs to be linked. So this is a rather simple pause forward.

Patrick Amstutz: The milestones with Novartis, I can't comment on because that's kind of undisclosed when they come. I can't say that the collaboration is going really well, where we're kind of making very good progress, but on the milestones and timing of that, I cannot. Thank you, guys. Thank you so much.

Patrick Amstutz: Maybe I'll just add that, I mean, if the radio ligand space works, we're not, in principle, restricted to radio ligands as warheads. For us, it's a great showcase to optimize the tumor to call a kidney ratio. And then we can also replace a radio ligand with another drug conjure. So this is also a bit of proof of principle for short, fast in, fast out, hits hard approaches, starting with radio ligands, because there you see everything.

Patrick Amstutz: You can follow it. You can do the science. And if that works, you can also then have a spillover effect into the drug conjugate space, so DARPIN drug conjugates. And we're not engaging yet there, but keep that in mind when if this works. There's more to come.

Operator: The next question comes from Richard Vosser from J.P. Morgan. Please go ahead.

Richard Vosser: Sorry, excuse me, hi, thanks for taking my questions. So just two, please. Just on in Soverbeb, you mentioned the path forward and Novartis looking at a face three trial. How long do you think it will take for them to maybe work through that and get that started? Just some idea of timelines, if possible, would be useful. And then on Abisipar, maybe you could elaborate a little bit on the causes of information and the processes to remove that information given that many processes have been tried in the past and if you have any data to show that I don't know preclinically or whatever with that the information has gone into the new material, thanks, sure. No, no.

Patrick Amstutz: Sure, no, no. So I'll take the difficult question first, which is Enzovip. So the problem with Enzovip at the moment is that the endpoints that we had in phase two, which were hospitalization and death, have changed. So you can't use it at this point in time.

Patrick Amstutz: You might use the same endpoints, but the number of patients you would have to include is very high. So that's not a straight path forward. Then again, we have variations of different viruses. And so it is really, how would you prepare to be ready for the next variant to come so that you then have an agreed endpoint, and you can run that trial fast. And I really find it difficult, and I know that Newarkis is engaging in that discussion, and I also know from other companies who are in that space. It's a very challenging space to run trials. I actually get calls from others just kind of asking similar questions. How is it for you?

Patrick Amstutz: I think we're all experiencing that this is a bit on-chartered territory, at least for these so-called early intervention drugs. This depends again on the variant of concern. If one comes back, it has higher hospitalizations; I think then it's much easier.

Patrick Amstutz: Then the drug is also more needed. If we are more towards a seasonal flu with less hospitalization, I think, then that's definitely more difficult to design that trial. Timing, when we will know, I cannot comment on that. That's really something for Novartis. But again, the EUA is open.

Patrick Amstutz: I think that's what we sort of, this is an insurance policy, should a really bad strain come up, and that's the way we see it for now. And then again, let's see how this drug can be developed once we know more about the variants that come. This will also depend a bit on the vaccines. You could think that now we will have Omicron vaccines. The Omicron vaccines will then give protection more to Omicron, but maybe we'll then see research of the original variants again, and maybe that's then the time for Enzo. But that's just me speculating here, and I'll leave it with that.

Patrick Amstutz: For Abikipar, and I think that's a great question. So I can tell you what we found. So first of all, we have invested a lot in purity, and purity is really the first thing we had to get right. And it took several iterations until we think now, and we can also have experiments to show that we are at a very, very good purity that should not cause inflammation. And then we have the conundrum that we have this high purity, but still inflammation. And that was the Maple trial.

Patrick Amstutz: And we were a bit surprised that we had the 9% in. And this is good and bad, it's actually a contaminant you introduced into the syringe, which is silicon oil. Silicon oil is used to lubricate syringes, and with the darapin that is peculated, you can cause, call it, cell physical particles that can drive inflammation. Basically, take non-silicinoids syringes; you can take that away, and we actually have shown that with very impressive animal data in Rabin.

Patrick Amstutz: And rabbits have a more sensitive vibe than humans, and there we really bring the inflammation down to quasi-zero. So we're very fortunate to have found what it was. It was not called DARPIN or not there, but it is not in the DARPIN substance. It is in the syringe. So all the material we have, we can actually use. So while it is, let's say, not ideal that you find it out slowly, at least it is something we can easily do.

Patrick Amstutz: Very clear. Thank you. The next question comes from Dana Graybosch from SVB Securities. Please go ahead. Hi, there are a couple more in Inzovip. I wonder if you can clarify whether you've looked in vitro at Enzovap's activity with

Daina Michelle Graybosch: The next question comes from Dana Graybosch from SVB Securities. Please go ahead. Hi, a couple more.

Daina Michelle Graybosch: So I think I'll start where we're not active, just to remind everyone we're super transparent there. The one mutation where Entoveb will not be active is the 486 mutation. We always do that as the Achilles heel.

Patrick Amstutz: You find that in the variance four and five. But the V82 does not carry that mutation, so we see activity there, and we actually have shown that. So that's sort of the good news. And if now the boosters come with the more

Patrick Amstutz: Omicron variants, I think that's definitely not a bad thing for us. So, in principle, we believe the drug should be active or has a good chance to be active in future variants. Let's keep going with that. We never know what happens.

Patrick Amstutz: So let's see how it pans out. I think the other one is really a deeper discussion, and I don't think anybody knows how this will be developed, also as Novartis. There are different angles.

Patrick Amstutz: I was on the phone also with Lutz, the head of global health, because this is about global health, and it is, or might be, a real global health issue. So there are different ways to look at this. Now, Novartis, at this point in time, will not comment on that. I think we have to understand that, we have to respect that, and that is what it is.

Patrick Amstutz: They have done a great job in bringing it forward. I can tell you they have also done a great job in manufacturing. So the manufacturing is flawless, and that's also a good validation for the whole platform. Just at a conference and just the ability to manufacture large amounts of tri-specific, by specifics, or whatever, that's actually a differentiating feature that our platform has that sometimes goes undervalued. So I just thought of that. But on timing and on design, I think that I really need to leave in the LARC scan. But thanks, Dena, great questions, but unfortunately not for me to answer.

Operator: The next question comes from Joe Walton in the credits. Please go ahead.

Joe Walton: Thank you, just a few financial questions really. Firstly, just to understand your freedom to operate in Radio Ligans outside of Novartis. So all the work that you're doing at the moment is effectively within that collaboration, but you talk about your proprietary work and freedom to operate. When would you expect everything to be with those artists for the next couple of years, or when would you expect to be able to do something on your own?

Joe Walton: My second question is just a tiny one on Ensovibet and the Swiss authorities who put money up there. Is there a chance that the Swiss will see any progress outside of the US? I know we're incredibly focused on what the FDA wants to do.

Joe Walton: If there were to be some sort of resurgence in Europe, could there be a small amount of income that you could get from, perhaps, Switzerland this year? And my final question is really about finance. So you are spending 70 to 80 million a year, and that's, you know, and there's a bit that's non-cash within that. And you say you've got funding until 2026. But that doesn't really allow for much of a step up in your spending, and you're at the very, very early stages with a lot of your products, and I would imagine that you wanted to actually do more of the work yourself.

Joe Walton: So can you just tell us a little bit more about your ambition as to where you would want to do more work yourself, which will keep more reward for yourself but will be expensive versus your willingness to partner?

Patrick Amstutz: It's really great questions. Let me first focus on the freedom to operate, as you call it. So what we have licensed to Novartis yet is the exclusivity for radio ligand therapies and monoactivity on two individual tumor associated antigens. So two column targets are with Novartis, and Molecular partners have the full right to do anything on all other targets in radio ligand therapy. So there's absolutely no.

Patrick Amstutz: exclusivity going on with Novartis. So we can start high programs tomorrow if we want. So we actually have, call it pre-programs. So we have research activities on targets, obviously ongoing as we do. And so that's important. So we're not linked to Novartis. But we collaborate with Novartis on two targets. It also makes maybe sense because what type of radio ligands might be indication specific or might be targeting specific. So to be two exclusives in the beginning to one ligand is maybe not the right way to go.

Patrick Amstutz: Then take your question on, and Toby Beck, outside the U.S., that's a very interesting one, and I actually haven't thought it through, but if we have, let's say, a wave of a variant in a specific country, how will that pan out? I don't know, but it's definitely something I will bring up to Novartis. So take a local wave in India or wherever and end the work. I think there is a moral obligation to make that drug available to that country.

Patrick Amstutz: So I'll bring that up, and let's see, and maybe you'll ask them too, because it's important. I mean, and I haven't thought it through, because you're right, the approval, the EUA, is in the U.S., and many countries will follow the U.S. But what changes if you have a local search?

Patrick Amstutz: I don't know, but it's a great question. Your last question about kind of how far does the money bring us? And I love it because I can actually explain how capital-effective we are. And our strategy, keep in mind, we're now looking for programs at 533, like also radio Liggins. After a few patients, we will know in principle if this drug works. We don't have to run phase one safety trials and combination trials. And manufacturing is not that expensive.

Patrick Amstutz: So with a rather limited amount, and that is in those 70 to 80 million per year, we can bring compounds to the clinics. We can manufacture, we can run those trials.

Patrick Amstutz: And then when we have the signal, you're absolutely right. If AML, if we have a drop that we think we need to move forward with, then our cash will not be sufficient. Then we would have to raise new cash, but that's after that signal. So this is a worst-case scenario, if you want, that we will not have a signal too late. If that happens, we hit early; the share price can react, and then we would also have to raise capital either through a partnership or through a capital raise that we will have to find out about. It also depends on which one of the compounds hits and how it looks.

Patrick Amstutz: But so we feel we can run into 26. We have several chances of clinical readouts that can bring us kind of where we need. And then, obviously, we can reshape the strategy and then the capital needs. If we're going to phase two and three, for sure, that will not

Patrick Amstutz: Thank you. I'm being a little thick here, just one more clinical question. Please.

Joe Walton: I just didn't understand your comment about how we wouldn't see much data on 317 because most of it would be based on discussions with partners. Isn't it to your advantage to make everything as obvious as possible in order to bring the partners in? Or are you already having good discussions with partners, which is why you won't need to show it to us, the independent investors?

Patrick Amstutz: Yeah, I think you see those companies who know CD40; we are in contact with them anyway. So yes, we might show data, but if you go for a public publication, or let's say we wait through AETR or whatever to publish, like we can't wait. We have to share that with those partners as we get the data. And it will also likely, hopefully at least, be a competitive process, and it actually seems to be that way, so people are asking because this is a target people are following. So that was my comment. We will also show you all the data, but we will definitely give a preferential look to those parties who are interested in a transaction.

Patrick Amstutz: And you're still expecting to show us some data late this year.

Patrick Amstutz: I mean, some data will definitely be, for this year, mostly safety data. Yes, we definitely can give you an update. We're now in a dose cohort of one milligram per kilogram, and you can go to other CD40s, and you will see that not many have reached one milligram per kilogram. So we're already at a dose. That's why the disclosure today is, I would say, meaningful in that sense.

Patrick Amstutz: We will escalate to higher doses. We will keep you posted. We will go to more frequent injections, and then they'll call it, maybe, another biomarker. Data showing that the immune cells locally react is something more for the beginning of next year. We will definitely keep you guys updated, but there is a preference, obviously, also to show the part. But Joe, this is Seth, directly to your point. Yes, we've submitted to Scientific Congress for the second half of this year, based on the accumulation of data that we're already gathering now. And yes, the plan is.

Seth D. Lewis: And yes, the plan is to have person human data displayed publicly at scientific Congress this year.

Patrick Amstutz: Thank you very much. That's right. You can do it.

Operator: You can go out, what is it, 60, what is it? I will tell you when we get accepted. Good.

Operator: Again, if you have a question, please press star than one. Our next question comes from Zoe Cara Manoli from RBC Capital Markets. Please go ahead.

Zoe Cara Manoli: Hi, thank you for taking my questions. Two questions, please. The first one: from the presentation today, it sounds like you're putting more resources and focus on radio ligand therapy. I'm just wondering, does this mean that the next candidate that will be added to your pipeline will be a radio ligand rather than another multidarpin? That's the first question. And then the second question about MP-3-10.

Zoe Cara Manoli: I'm wondering if you can give us some more color on your decision not to pursue further development. And I imagine that this means, then, that you're not looking to partner this asset anymore. Good.

Patrick Amstutz: I'm glad you asked. So we took the radiolican because it's also very different from the multi-darpin approach. So we also have exciting multi-darpin approaches that are not behind radiolican therapy, and actually in oncology and in birology there.

Patrick Amstutz: So if it is, we will find out. But we're making good progress on radiolipan therapy, and it is a bit of an antithesis to the multi-multi-darpin. So that's one reason we wanted to also highlight this this time.

Patrick Amstutz: But it makes good progress, but I'm not saying the others are not. And it might well be that we choose another one that next candidate and not this one. So, or even two in parallel can happen. So, so, so. But thanks for asking.

Patrick Amstutz: So we're not trying at this point in time; it's still signal seeking its research. Nothing has to say that dice have not been rolled on which program is the next one. 310, I think that's one that, again, came back.

Patrick Amstutz: It likely, I mean, it was a strategic decision, but possibly also driven by this overlaying toxicity of IRRs of these cell engagers and this molecule makes sense. Again, the repartnering, that could be one option. It's just that 4-1b at this point in time, I wouldn't say it's as hot as CD4T. And I think there are a few trials, especially the Roche trial. They also have the SAP 401B that is ongoing.

Patrick Amstutz: And our feeling is that at this point in time, it's better to invest time in 317, call it a better target for the moment. There is more impact. And 4-1B is rather underwhelming in this combination for now. We did not have a lot of activity so far. Doesn't mean the drug doesn't work, but it needs the combos.

Patrick Amstutz: But it's also not that partners are kind of knocking on our door. If that was the case, we would definitely partner too. But I think we just need a bit more data out there that would validate the target. So let's put it like that.

Patrick Amstutz: We have it. We have it. It's called that on the show.

Patrick Amstutz: we'll finish the work. And if OMB, especially with FAP, has a revival, we will have it. And if not, I think we have other places where we get a better return on investments.

Operator: There are no more questions in the queue. This concludes our question and answer session. I'd like to turn the conference back over to Patrick Amstutz for any closing remarks.

Patrick Amstutz: Hey, thanks for all those great questions. It's great to have you guys out there asking those and bringing the story across to investors. So thanks to all my analysts here. It's a pleasure to work with all of you. Thanks to my team, all out there, getting everything ready and prepared, and definitely looking forward to a very exciting end to this year, but especially to 23. And a lot of the earlier research science will also be made more public. And also, I can also

Patrick Amstutz: say that I will bring my team more often to such calls. So, as of next year, I think a bit larger group will do the communication efforts. Looking forward to that, and also very much looking forward to working with all of you in the future. Thanks. Take care.