Molecular Partners H1 2024 Earnings Call Transcript

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Provided by Quartr
August 27, 2024

There are 11 speakers on the call.

Operator

Good day, and welcome to the Molecular Partners First Half twenty twenty four Results Conference Call. All participants will be in listen only mode. After today's presentation, there will be an opportunity to ask questions. Please note, today's event is being recorded. I'd now like to turn the conference over to Seth Lewis, Senior Vice President, Investor Relations.

Operator

Please go ahead.

Speaker 1

Thanks, Rocco. Good morning and good afternoon, everyone. Welcome to the Molecular Partners First Half twenty twenty four results call. My name is Seth Lewis, Senior Vice President of Investor Relations, and I'm joined this morning by Patrick Amsoetz, CEO Philippe Lejean, Chief Medical Officer Donnie Steiner, Senior Vice President, Research and Technology and Robert Hendricks, Senior Vice President of Finance. Management will take a few minutes to make brief remarks, and then we will open up for question and answer period.

Speaker 1

If you have not had a chance to review the H1 press release, please feel free to do so on our website, www.molecularpartners.com. Also on the website is today's updated presentation, which management may refer to when speaking or answering your questions. As a reminder, today's call is being recorded. Today's discussion and presentation will contain certain forward looking statements based on the information available to Molecular Partners as of the date of this release, and actual results may differ materially from what's discussed today. With that, I'm happy to turn the call over to Patrick Emsetz, CEO to review the highlights and outlook for the company.

Speaker 1

Please go ahead.

Speaker 2

Thanks, Seth, for the nice introduction and a very warm welcome from my side to everyone on the call, investor, analysts and people interested in our update. As Seth alluded to, we have the slides on our homepage and what we will do is not go through every slide, but really jump to the highlights. We will say which slide number we are on and go rather fast that we have more time in the end to answer your question. With that, I will jump to Slide number 5, the corporate highlight of the first half of twenty twenty four. The first half was really active.

Speaker 2

We progressed a lot of programs and that will start with 533, where we have great progress. We have reached the top dose. And despite not reaching the optimal exposure or concentration due to half life and target mediated drug disposition, we see activity and Philippe will allude to that and we also see a way forward to those higher and more frequent. On the same with the immune cell engager front, I go to 6 to 1, where we have updated the molecule presented at EHA. And this is a c Kit targeting switch molecule, a very innovative way of killing HACTs and LSCs and best applied in for stem cell conditioning.

Speaker 2

On 3/17, that's where we have finalized the clinical trial for our tumor localized CD40 agonist. We have a nice safety profile and we can conclude biological proof of concept and are looking into combination settings going forward. And I do end with Kwasi, the most exciting part, which is the radiodarpins where with MPO-seven twelve, we have a first candidate that the DLL3 targeting, DARPIN optimized for low kidney uptake and high tumor accumulation and that is in a collaboration with Oronumab where we struck the strategic alliance earlier in the year to work together on targeting lead based radio isotopes via DARPAINT and we call that a strategic collaboration as we believe lead access, circumvents key limitations of other isotopes, including supply and Donnie can speak a bit more about that. On the operating side, we are in a strong financial position with SEK 159,000,000 in cash and that puts our runway into 20 27, which is a bit further than we had so far on our chart. Before handing over to Filip, I go to Slide, I think it's now number 6, where I have a really personal nice announcement to make.

Speaker 2

I'm very happy about it, which is that, Philippe Lejane has been promoted to full Chief Medic after serving a year in that role as acting Chief Medic. And he really deserved this role on the one hand by impressing impressive recruitment. I mean, our trials, the cohorts were full when they were opened and the execution was flawless. And for us in my new CEO of Biotech, we know how important that is. That's where you build all the credibility.

Speaker 2

That's where you build all the value. So big thanks to Filip and his team for that, just excellent execution. And that is only possible because Filip has a gift to engage investigators into our trials. So they think of our trials first. They understand the importance and he's really a strong networker there.

Speaker 2

And it doesn't really end on the investigator side. It includes the KOLs that he brings in to review our data, help us on the next steps and that's also how we came about how to move forward on 533 with the top global experts in the room. Given that he is not only an AML specialist, but he has a really broad understanding of tumors, he can apply that also to our earlier pipelines of DLL3, radiotherapy. So in that sense, he is in a perfect position to apply his knowledge, his skills and with his team bring forward the molecules in our pipeline. And there he profits also from his industry background with Novartis, GSK and Amgen.

Speaker 2

And as I just pointed out, it's also his personal dedication, passion, his team leadership and the way he works, not only with the KOLs, but also with us and with his team is inspiring every day. And it's a great pleasure to have you as full Chief Medic now, and it's also a great pleasure to give you the word to give us an update on the 533 molecule.

Speaker 3

Thanks, Patrick. I'm glad it's an audio and not video, otherwise you would be blushing. But I want to thank you for this. And again, it's an honor to be with this MP team and to help and lead and contribute to push our program to the clinic and having the fortune to be able to reach and work with the worldwide experts. So I will want to give you in a very quickly in a quick mode an update on the 533.

Speaker 3

And basically in my few minutes here, I will refer mainly to the slide number 14. We can spend more time later on to go through Q and A, come back to any slides where there will be questions, but basically I want to give you a summary and outlook of where we are. So on that slide 14, basically I would I have mainly four points of updates on the program. First of all, is that we are reporting here up to cohort 6. And as we speak, we are at cohort 7 now.

Speaker 3

But basically, we have seen an ongoing and very, very steady engagement from the PI teams and basically there is very good dynamics on this team on this trial recruitments from the very beginning up to now. What have we observed? We have observed first is that an acceptable safety profile, a manageable safety profile with mainly IR and TRS as would be expected on T cell engager. And we see them basically in the 1st cycle and rapid decrease in 2nd cycle onwards. We've seen indisputable activity, reduction in myeloblast on half of the patient population recruited and on 25%, more than 50% reduction in those.

Speaker 3

And that translates into ELN responses from with 1 responder per cohort from BR3, 4, 5 and 6. So, in this situation activity, yes, but in a way we need to have more than that to be completely satisfied and to qualify that we would unlock the potential of that compound. And when we observed in greater detail, in fact, we realized that we still have to improve the exposure of the product. We in fact, we need to increase that exposure and have it more durable in order to increase the response rate, the depth of response and the durability. And therefore, we are further amending the protocol for, again, a higher and more frequent dosing, especially in the 1st week to densify this exposure.

Speaker 3

And we will share later this year at the end and also especially in the next year 2025 results from those amended to Hema. So obviously, we will review those results very carefully to see whether we can truly gauge the future developments and move into the expansions in Phase 2 steps. So that's my update. And again, very glad to go into more detail in the Q and A part of the discussion of the session.

Speaker 2

Thanks, Philippe. And with that, I will then hand over to an update Omar on the radio side of Donnie Steiner, who is with his colleagues leading that effort.

Speaker 4

Thanks, Patrick. So happy to guide you through this update top line update on the radiodirping therapy It's the 1st candidate, as Patrick already introduced, MPO-seven twelve, the 1st program we're moving towards the clinics. So for those of you who are on the slide, I'm jumping now to Slide number 25. And as I said, top line update there and I'm super proud about the great progress the team has made to successfully move the RTT platform to profiles with an attractive biodistribution profile in terms of tumor to kidney to blood ratios. And we can dive into Q and A way more into the details if you're interested in your questions.

Speaker 4

So here the data on MPO-seven twelve, which has been selected as the lead candidate for targeted led-two twelve DLL3 program has been presented at SLR and it really showcased the strength of the platform that we have been establishing. And of course, the IND enabling activities are now ongoing with Oranumate and the initial clinical data is expected in 2025. So as I've been mentioning, super excited what the team has achieved here and even more excited about the opportunities that this all opens up. So of course, we are advancing 712 and the current pipeline together with Oranumet, which we see as a very strong and committed collaboration partner, but also with Novartis, where we have an ongoing collaboration since the start of our activities in the radioligand space, and we are evolving and expanding the platform for next differentiated RGT programs. And this is what I'm looking for most, and I'm going to tell you a bit more about this on the next slide.

Speaker 4

So if you move to Slide 26. So this is just an initial, I'd say, glimpse of preview of how we are thinking about leveraging the diapine properties to really build differentiated RDT and RDT portfolio and RDT candidate with a high level of differentiation. So if you look at the top panel of the slides, for me, this is just two examples. Then there is more and we got to tell you more about this in the month and future to come. These two examples of how we are thinking about targeting proteins, tumor targets, which are difficult to address with classical, I say, radioligand in the sense of low molecular weights or peptides.

Speaker 4

And one class depicted on the left hand side is like where you have a high amount of soluble antigen, which is interfering shed soluble antigen, which is interfering in your tumor uptake. And there we found an approach to target specifically the membrane bound form only that we're building on the selectivity and the binding properties of the therapy. And on the right hand side, you see another class of targets we are heavily investing to is like targets that have homologous high identity on healthy cells where you by using the selectivity of diapine can read tumor specifically target the diapine by only recognizing this specific form. And of course, on the other side, and that's at the lower part of the slide, we are building on the deep expertise we have built in making multi specific molecule here in the context of having a broader and more homogeneous tumor distribution to address heterogeneity, which we believe is especially in the context of short range alpha emitting particles, a key aspect to consider. And there and that's what we see on the left hand side, we are not thinking mainly about classical multi specifics as they are used in our IO project.

Speaker 4

It's really more building on the concept of having 2 paratodes in 1 single therapy domain, which we call it 2 in 1, which keeps the size of the molecule small by maintaining all the binding properties of the diapine. So this is something just a teaser in what to come in the next 12 months, looking very much forward to give you more details on that, starting to present on those approaches on conferences that is just like giving a bit of an outlook of what we are up for. And with this, I would like to hand over to Robert to give you an insight into our financial forecast.

Speaker 5

Thank you, Danny and prior speakers. Before we move to the summary and the Q and A, I will briefly guide you through the financial highlights and the key figures and the updated guidance for this year. My name is Robert Henriksen. I'm the SVP of Finance here at MP. The numbers I'll show are stated in CHF 1,000,000 and full detail of the financials is available on the website and on other means.

Speaker 5

If I move to Slide 28 with the highlights. I'd like to focus firstly on our cash position. We ended last year with around €187,000,000 and by the end of June, we are at €159,000,000 That's a cash burn of €28,000,000 in line with our expectations. If we take this to a full year 12 months running, the burn is €59,000,000 We had no additional cash coming in from collaborations in 2024. With that, moving on to the updated guidance for the full year.

Speaker 5

We are now guiding our operating expenses to end up in the €65,000,000 to €75,000,000 range. This is a reduction from the previous guidance, largely based on what we see in our actuals at the moment and the current expectations we have on the development of the cost and the workforce. We will not guide on revenue. And for clarity, this guidance is, as always, subject to the progress and changes of our pipeline. Thirdly, following also from the updated guidance is our runway.

Speaker 5

We are now feeling comfortable to say that we are funded into 'twenty seven, which is a small change from late 'twenty six, which we had guided on before. We do feel that this runway and the cash that we have at the moment do put us in a privileged position in the industry. It will allow us to reach the milestones as presented by my colleagues, in particular, the funds that we ring fenced for 533, as indicated by Philippe, as well as the further progression of the radio pipeline. We'll then turn over to the next slide. I'll briefly show a comparison with last year for 6 months running.

Speaker 5

Overall, the results you can see are in a pretty similar range. Revenue was slightly up as well as operating expenses, resulting in an almost equal operating results. Financial results was driven in the 1st 6 months by a positive exchange impact on our cash positions as well as an increase in the interest income on the same balances. The revenue that we show continues to be driven by the Novartis Radialigand contract collaboration. And a focus on operating expenses, R and D expenses are up a bit.

Speaker 5

G and A expenses came down a bit. On SG and A, we were able to see a reduction in our D and O insurance expense. When looking at R and D, in the 1st 6 months of 'twenty 4 in comparison to last year, we did invest more in drug product in the dose escalation trials for 533 as indicated by Philippe. We also were able to increase our investments in the overall platform and the radio space and a few reductions we saw on, for instance, 5,317 and some legacy programs. We are and do remain diligent and careful when looking at our expenses.

Speaker 5

We feel that we are cost effective. We're on a tight ship that remains on course for us to deliver on the promises. In combination, I think that these numbers continue to show the strong financial base entering into the second half that will allow us to keep investing in the pipeline. Thank you for your attention. Any questions, happy to take them in the

Speaker 2

Q and A. And now I hand back to Patrick. Thanks, Robert. Thanks, Donnie. Thanks, Filip.

Speaker 2

Thanks, Seth. And before turning to questions, let me quickly summarize. I'm on Slide 34, which is the outlook on the upcoming milestones. 533, we heard we're testing both higher and more frequent dosing to come to a conclusion on the potential of this molecule where we will update in 2025. Switchedarpin, we are in animal trials.

Speaker 2

We'll summarize the data present and then define next development steps for that molecule. 317, the Phase 1 is completed. We are in discussions with investigators to do investigator initiated trials for that. We don't plan to invest heavily ourselves, but we would like to understand more on 317, what combination trials could help and there is a good means to test that. And last but not least, obviously the radio franchise where going into clinics next year.

Speaker 2

I'm also very excited as Downey pointed out, the differentiated DARPIM programs where we will update our portfolio and give you deeper insight how we are thinking about those programs and how clinical value can then build in the future. And obviously we're not doing that alone. We're working with Novartis and especially also with Oronomid where we are excited to be working with the leader in the lead based isotope field. As Robert said, we're running at high chip. So the cash runway is now into 2027.

Speaker 2

And I think with really the effectiveness of our research and development engine, it puts us on course to find many important programs, many updates to come and a really exciting year ahead of us. Before moving on to Q and A, I would like to take the opportunity to first of all, thank the people here with me in the room, my speakers, but also all other co workers at Molecular Partners. We are partners, we're co workers, we're a team and what we present to today is really the hard work of the whole company coming together and executing and debating and thinking and positioning our DARPAIN work. I would also like to extend the thanks to our partners Novartis and Oronomed, but also our academic partners that we have And obviously also our investigators and KOLs who are using our molecules or applying the molecules in the clinic. And there my last thanks goes to all the patients in our trials and their families because without them, this is not really possible.

Speaker 2

That links me back to the key purpose of our company. We're all here today to make drugs that matter. And with that, I would close the presentation and open for your questions. Thanks.

Operator

Thank And today's first question comes from Dana Graybosch with Leerink Partners. Please go ahead.

Speaker 6

Hi, guys. Thanks for the update and the question. I have one back on MPO-five thirty three. I left your thoughts on how you're thinking about escalating now the higher doses and the trade off between efficacy and tox. And I wonder, as you get to these higher doses, do you expect to bind and single antigen expressing tumor cells or normal cells?

Speaker 6

And what specific talks are you looking for that might indicate that you're actually at such a high dose that, you no longer have the advantageous therapeutic window of needing to buying multiple antigens? So basically, what are you looking for in the clinical signal to balance that tox and efficacy as you go higher? Thank you.

Speaker 2

I can lead in as maybe more of the generalist view and then I'll hand over to Filip for more expert view. I think, first of all, why are we going to higher doses? And it was an observation also by our KOLs when we looked at the data is that we have the dose option where we have an induction at a very low dose and then we go up and that was to manage the safety. And so we started low dose and then over the 1st 20 days, we had injections with always higher doses. And they realized that with maybe a bit faster PK than expected and maybe also more target mediated drug deposition than expected, we were not getting the exposure that we were hoping for and we were rather under dosing.

Speaker 2

So the dose intensification now is that we will give more higher doses, but maybe not even higher top doses, but just go faster to the full dose and then dose more frequent. The side effects that we have seen so far are IRRs and CRS, which is really the T cell activation. So far, I don't think we have seen target dependent toxicities and Felix can talk about that. Now if the patients will tolerate this intensification, that's what we have to explore. There is and maybe there will even be a lower dose, but more frequent dose that will actually end up being the most efficacious dose in the beginning.

Speaker 2

We also know that once the disease is under control, we cannot dose every 2, 3 days. That's not possible and also not practical. So then we'll go back to the weekly dosing scheme at that point in time. So that's why we're talking about the dose intensification in the early weeks and then back to weekly. Hopefully that's been enough once the disease is under control.

Speaker 2

We also don't expect the target mediated drug deposition anymore. So Filip, maybe you can explain a bit more. And there's also some slides in our deck that where we show that especially the low patients with low disease burden profited more because obviously they also had maybe a bit less of those problems and there was just enough drop to keep the disease under control. Philippe? So thanks to add a couple of compliments to what Patrick just said.

Speaker 2

First of

Speaker 3

all, again, we have seen good tolerability, manageable toxicity up to now and mainly CRS with very little pattern beyond that CRS IRR. So and we've been carefully looking for example at cytopenia or neutropenia, which could be expected which we have seen on some other programs. So we want to identify, as Patrick said, why? Because we see a higher sync for targeted disease drug disposition than we had anticipated. And so we want to and also because it's safe so far, we think we can go quicker high.

Speaker 3

So we have to put that in place. We don't know yet what will be the exact impact on the half life, but we may still have significant sync. And that's why we do not anticipate so far too much drug accumulation. Therefore, we do not think that we wish we would get much more on target toxicity. And but we will be especially monitoring the cytopenia.

Speaker 3

So that's the one we will be looking at mostly for the moment. Can I

Speaker 6

ask a follow-up then? So as you have modeled out the PK and the drug mediated clearance, do you model a specific dose? What sort of dose level do you expect to sort of maximize your activity then in the exposure based on your preclinical model?

Speaker 3

Basically, we are ready and part of all the amendment which we are currently putting in allows for a few higher dose escalation. So not a dozen, but a few higher dose escalation. And again, counting a lot on the densification even more than the higher than the dose increase. So that's basically we want to modify the exposure. We are not very far from where we would be hoping to be in terms of Cmax, but we need to work on the C trough and longer exposure or at least identifying all those peaks, which we already see, but want to really harmonize, if I may say.

Speaker 2

Philippe, is it fair to say from the modeling we saw that with just the max increase, we will not reach what we need. That's why we need to intensify with more dose.

Speaker 3

Yes. We see again, on one hand, we are reassured and the experts with us are reassured that we see there is an impact on the tumors. There is an impact on the glass. We really hit them. But we think it's not long lasting enough, it's disappearing too quickly and we need to modify that trend.

Speaker 3

So to gain that increase in effects and especially the duration of effect. Thanks.

Operator

Thank you. And our next question today comes from Richard Vosser at JPMorgan. Please go ahead.

Speaker 7

Hi, thanks for taking my question. And maybe another one on 533. Just back on that, I suppose, the dose intensifying after a period of time. If you then go to back to weekly dosing, are you going to have enough drug on board to maintain the response? How should we think about that will be the first question?

Speaker 3

Very good question. You should join us for our protocol discussion. But what we hope is that we are going to debulk, if I may say, or reduce the tumor magnitude to tumor burden because we see again we see that we have more responses in the lower tumor burden than in the higher. So we want to and we hope that when we are there, then we may need less because there could be some less of a sync. So that's one aspect.

Speaker 3

We are still discussing, in fact, in terms of we also want to avoid by design having chronic exposure because we are also conscious of that concept of T cell exhaustion. So we wouldn't want to be continuous all the time. Then the question is how little is enough. And so we are in fact discussing in OTTIBU one day of re exposure in that maintenance phase or more than one day, but we know that it will not be continuous and it will be a short time. So we are just finalizing that discussion as we speak, but very, very close to finalize and submit.

Speaker 2

Excellent.

Speaker 7

I've got a separate question not related. So I'll get back in the queue and ask it in a second if it's still there. Thanks.

Speaker 2

Thanks, Richard. Thank you.

Operator

And our next question comes from Sebastian Van Der Schuet with Kempen. Please go ahead.

Speaker 8

Hi, team. Thank you for taking my questions. Regarding the radiodarpin, can you remind us on when the clinical trial is supposed to start? And can you also give some insight into what the clinical trial design will be? How you are thinking about the different steps?

Speaker 8

And when we can see first data for the DARPAIN conjugated to the lab payload? Thank you.

Speaker 2

Yes. So I can give you a rough outline. So we have defined the candidate. We are now starting off production. It's going to be GMP production.

Speaker 2

Then we will be working with Oronomib for the net payload. So we are expecting clinical entry next year, second half. So first half is not possible. And then we have guided that we are expecting to have first data. And the data will not be efficacy or safety, it will be images where we can follow the molecule.

Speaker 2

That is the beauty of this setup where we can create an image after dosing and seeing where the drug is. And I think from the image we can do some predictions. I mean, is it less in the kidney, more in the kidney, more in the tumor, but the safety and efficacy will obviously follow later. Now I'll be happy to hand over to the experts and Philippe on the clinical side. And I think the good thing is the image is actually available rather short after dosing.

Speaker 2

So you don't have to wait for 3 months for the pictures. You actually can get them rather fast. That's why clinical entry and initial data are rather close together. Vivek?

Speaker 3

Thanks a lot for that. So again, we're going to very quickly or quickly after patients are included, they will be imaged for biodistribution and dosimetry. And then on the heels of that, obviously those escalation starts. So I just also want to make sure this we're envisioning a single trial which has we'll have those 2 steps. But again, the images come first and then therapeutic comes in.

Speaker 3

So that's and obviously, we would want to go what we are planning to do for the moment is to include patients with small cell lung cancer mainly. And depending on the signal that we get, we'll expand in potentially the prostate neuroendocrine. But I think it's a bit difficult to integrate both subpopulation at the very start.

Speaker 8

Got it. Very clear. Thank you.

Operator

Thank you. Our next question comes from Mike Mitalkovich with TD Cowen. Please go ahead.

Speaker 9

Thanks for the question. I have another follow-up on 533 and this is maybe a slightly different version of a question that was already asked. But do you all have a C MAX or an exposure level in mind at which you would expect activity or at least more activity than you've seen and are aiming for that level? Or are you approaching this more empirically in trying to raise the dose and the dose frequency, and the dose regimen and just waiting to see what you see? So that's the first question.

Speaker 9

And then I have to admit that the language around this program is a little bit ominous in the slides. If we learn in about a year that you have discontinued this program, what do you think would be the most likely reason? Would it be because your hypothesis has not panned out? Or would it be that you have so many other compelling opportunities that resource allocation has to come first and you'll pursue those other opportunities? And I realize that's not the fairest hypothetical, but I'm just curious where your minds are

Speaker 3

at the moment.

Speaker 2

Thank you. Maybe Philippe can take the first and I'll take the next one. Congratulations on your promotion, Philippe. Please go ahead.

Speaker 3

Thanks for this. Very good question again on the Cmax and our model. Obviously, we model and we think that we are not very far in terms of Cmax from where we were where we wanted to be and we see activity. So it's more about we see too much too quickly disappearance of the drug. That's why we need to change our dosing pattern, our scheme of administration to really, let's say, have a more, again, dense approach during that first phase.

Speaker 3

So we are not very far and we still think we can go a bit higher and we'd like to tease that out. Again, we can do this because it has been safe up to now or safe enough. But it will be much it will be more about looking at the shape of that exposure curve more than the Cmax. And again, we'll have a heavy focus on the trough because we need to have more time with higher than mean expected exposure during that time. And

Speaker 2

maybe just kind of obviously, I'm not a medic, but a bit more delay man view and please apologize if it is too crude, but this disease progresses very fast. If you cannot control the patient in the first days even, you are behind the disease. And if you look at the data that we also did show, I think on Slide 12, you see we have some impact and then just the disease takes off. And so it's very important that we not only and I think it's more the trough that we actually give the dose and we give it also faster just to get the drug more chance to actually act before it's too late. And I would and you were asking about the empiricism of it.

Speaker 2

I personally was surprised that we saw, let's say, no dose response in the sense of we had patients in almost all those cohorts that responded, but we don't see it dose response on in that sense, we see activity in patients that have low disease burden. And maybe that's also why we just need to tease that out and see if we can expand that activity to more patients by what we call intensifying the dose. And we will have a post red ASH where you then can see what those we have now. And it is definitely less than we would like. And I think that was the modeling, call it a bit surprised that we saw less drug in circulation and that's what we are correcting for based on also some responses we save in despite the low exposure.

Speaker 2

I'll now take the other part of the question, which is sort of what to expect. And it was a good discussion with our investigators and there is just a high medical need and everyone in the room, the KOLs on the trial, but also those not on the trials that we should really test it. As we have activity, there is a need there and the higher dosing is just what just jumps into the eye when you saw the data that we have. So I think there is almost an ethical imperative for us to test this. At the same time, outcome, we will see what it is.

Speaker 2

The good thing and I'll turn almost your question around is we have options. We don't have to progress this one if the radio franchise works well. It means not that we would stop it for no reason, but it puts a clear bar that we can put out there and say, if we don't reach 20 or even 30 plus response rate, if we don't have the duration of 3, 6, maybe 9 months, that's just not going to be good enough. It's not going to be a clinical response. I mean, that's what we're looking for.

Speaker 2

And I think the cost base more or less the same as we always have. I mean, that's what would allow you to move forward into Phase 2registrational trial. And we can just be very clean about that. I don't think it will just go away. So we will definitely update on the data.

Speaker 2

We want to update on the data and our reasoning why we would stop it or not. So, but I do think that the idea that we have options obviously is a good one. And the more competition there is for the cash we have, it's a good sign for the company. Very helpful. Thank you.

Speaker 2

Thanks, Mike.

Operator

Thank you. And our next question is a follow-up from Richard Vosser at JPMorgan. Please go ahead.

Speaker 7

Hi, thanks for taking my question. It was back on the Radiodarpin side of things. Just maybe an update on the Novartis partnership as much as you can give. Just where we are with that one? How that's progressing relative to 712?

Speaker 7

And when we might see something from that side of the collaboration?

Speaker 2

Maybe Donnie can give a short update and maybe just frame that obviously in our pipeline, our compounds are like we have 5 and they're all 5 high priority and in Novartis' pipeline, they're close to 30 compounds and that explains maybe a bit less speed, but maybe over to Donnie to explain how we are progressing our on

Speaker 4

the on the slide, it's 2 specific targets we are collaborating on with Novartis. As Patrick said, we are part of a bigger endeavor that Novartis takes in the whole race and agent space, which makes a lot of sense for them to keep the leadership in a space, which they've been entering as one of or as the first one in the field. So we're progressing there with the candidates. We're analyzing the candidates. And as many of you know or might know that are well knowledgeable in the field is like it's a lot about testing, but bringing forward molecules, testing them in vivo models, they're going through the iterations.

Speaker 4

And there it's just like what observation we are making with Oranomaid and that's sort of the other side of the whole equation. With Oranomate on board, we found a partner that is extremely agile and following our approach to test as quick as possible as many as possible candidates in the relevant models, often in vivo models. Unfortunately, there is not a lot of preclinical in vitro models that help you to predict the outcome in the in vivo model. So that's how we are progressing and that's why I think also we that allowed us that agility and way to maneuver that whole preclinical pipeline allowed us to nominate the first candidate before ADOMID and I'm very much looking forward to also nominate further candidates in that collaboration.

Speaker 2

And maybe just I will add because there is a bit of a conceptual difference between how Novartis looks at radio and we and it goes back to the isotopes that we have. And we work with lead, which has a very short half life and the decay in the blood is likely going to be much more safe than if you have lutetium or even actinium and the jury there is out. But Novartis also is looking for a slightly different profile than what we are looking for because we have different isotopes. So not all learnings and not all technology that we are developing for our pipeline is 1 to 1 addressing the Novartis need. So it's also there a slight difference.

Speaker 2

So not every learning from Oronomib collaboration from what we do applies directly to Novartis. And that is their history on beta and now maybe more actinium versus lead. Excellent. Thank you. Thanks.

Operator

Thank you. And our next question is a follow-up from Dana Graybosch at Leerink Partners. Please go ahead.

Speaker 6

Thank you, guys. The discussion on MPO-five thirty three has been very helpful. So I have one more follow-up there. And when I look at Page 11 in your presentation in the talks, I do see some of the talks you said you'd be looking out for. So it looks to me like 2 Grade 3 febrile neutropenia as well as some Grade 3 lymphopenia.

Speaker 6

And I wonder if you could talk through those top vicitis in those patients and why that shouldn't be concerning in terms of the therapeutic window and the talks that is most on target?

Speaker 2

Yes. I'll just like in general, that's why I think just to try and what Filip was saying, we're not only trying to do the Cmax, but the C trough by more frequent dosing. But Filip, maybe you'll give insight. Yes. So

Speaker 3

good review. And obviously, we are following those. What we do, we also have obviously a dose escalation committee. What I want to say is that we are following those very carefully and not just us, okay? So I'm comfortable talking here with our dose escalation committee and our safety review committee.

Speaker 3

So basically, those are mainly or those are mainly disease related and they are non lasting. So and it's always difficult to adjudicate in the context of such a trial. But for the moment, we have not seen, we have disclosed at length and have not they are in a way, it's hard to completely say that they are not related because they happen near temporally during the trial. However, with adjudication, they are not worrying from the study safety committee standpoint. So we will keep obviously looking at this and we want to see whether is that transforming into a pattern or not.

Speaker 3

But so far, we do not think it is.

Speaker 6

Very helpful.

Speaker 3

But again, just maybe one last thought on this. As Patrick has mentioned, we need to the best proof of that will be to show that because the drug is active very quickly in those patients, basically, we see a reduction or non occurrence of those. It's very difficult to keep that promise in the context of a relapsed refractory patients. But that's what we want to aim at. And that's why we say we should take more risk to finally see in terms of safety as we think we can identify that exposure during the 1st week.

Speaker 2

Thanks, Philippe. Thanks, Dana.

Operator

Thank you. And our next question today comes from George Zimmerman with Octavian. Please go ahead.

Speaker 10

Yes. Thank you. Thank you to the Molecular Partners team for the presentation and answering all the questions. So we've talked quite a bit about MP-five thirty three and the radiodarpine area and platform. I feel we have not talked too much about the switch program.

Speaker 10

So maybe just a little update as well on the progress with your switch platform. And you specifically mentioned additional preclinical data announced in H2 this year still. So what can we expect there? Can you give us a little bit of flavor also in particular to the translatability of those data?

Speaker 2

Great question. And so maybe I'll quickly allude to the switch platform that is an eitheror DARPAIN. So we can create in an immune cell engager an off DARPAIN that is switched on while we target while an on target. And in this case, it's a C KIT, switched on C KIT, where we then bind or open block CD47 and engage NK macrophage to kill. So this molecule is at the moment we are running non primate trials and we expect translatability to be rather high from the data we have in the signal versus the human.

Speaker 2

The data we'll collect and that will also inform obviously a clinical trial and there we are looking into different routes and one could be more into call it AML, the other more into more global stem cell conditioning. AML is very high barbed because you need very complete killing. A stem cell conditioning is a high medical need in the field for all the gene therapy companies, but a bit less on our radar as that is really more than again in some in a setting of a partnership as the key value is in stem cell transplant. So we are taking the data and we will then also analyze and see what the best clinical route is based on that data. And so I think your question is spot on.

Speaker 2

That again will link to what is the best clinical position and how to investigate that versus maybe the other pipeline assets. So I think that we didn't speak about it that strongly is because we have to focus on radio. Radio is really where it's happening, where it's groundbreaking. While stem cell transplant given the high medical needs, it's maybe a bit less, call it, strategic for molecular partners. That's the way to think about it.

Speaker 2

At this point in time, we believe it's high value because of high translatability and the medical needs. We will definitely see how if and how we then would move forward seeing the rest of the pipeline developing. I hope that helps you more on the strategic side, how we think about this.

Speaker 10

Yes, certainly very helpful. Thanks.

Operator

Thank you. And this concludes our question and answer session. I'd like to turn the conference back over to Patrick Hamstach for closing remarks.

Speaker 2

So big thanks to everyone and especially all the great questions we had. And I think it has turned out a good way to do it. I think we'll keep on doing a rather extensive slide deck, shorter presentation and opening for the Q and A as you guys are following our work. You have the questions and we love to take the time to listen to you. See how we can answer those questions and remain in a very open and good dialogue.

Speaker 2

With that, I thank you all for that. All the others who were listening, thanks to our investors for the trust and support you give us to the team again. And we look forward to meet you at investor conferences as they come or reach out to us if you want the meeting. We have a lot to tell. We will be sharpening the story a lot about the radios to therapy, be out there and really look forward to interact with all of you.

Speaker 2

Thanks for that. Take care and stay safe.

Operator

Thank you. This concludes today's conference call. We thank you all for attending today's presentation. You may now disconnect your lines and have a wonderful day.

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Earnings Conference Call
Molecular Partners H1 2024
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