IRLAB Therapeutics AB (publ) (IRLABA) Earnings Call Transcript & Summary

It's IRLAB Therapeutics and CEO, Gunnar Olsson. Welcome, Gunnar and please take it away.

Thank you very much, and good morning. It's a pleasure for me to give you an update from IRLAB. So the company, some key questions. What are we doing? Well, we strive to improve the life of people with Parkinson's disease by developing better and new medicines. And why are we doing this? Well, there is about 11 million people living with Parkinson's, and we see a very rapid increase doubling in the next 15 to 20 years. The disease is [indiscernible] and it comes with very serious complications and symptoms. And today, for many of the symptoms and complications, there are actually no treatments available. How are we doing this where we're utilizing the cutting-edge experience that has been developed over the years from the research group around Professor Arvid Carlsson, who received the Nobel Prize for all his work in Parkinson’'s disease. We have developed a unique discovery platform generating new candidate drugs, candidate drugs with high likelihood of success compared to industry standard. And this, of course, means reduced costs. Here is a picture of our pipeline. Our lead molecule, mesdopetam has now completed its Phase IIb activities in levodopa-induced dyskinesia. And we are now moving forward to go to the end of Phase II meeting with the FDA to define the Phase III program. Pirepemat, that is our compound where we are reducing the risk of falls. Today, we're running a study so that we are looking forward for top line results end of first half next year. 757, that is our compound in apathy, and this is, of course, for Parkinson's patients with abated, but also for other neurological diseases where apathy is a common symptom. Our 942 compound is to improve cognitive function. Of course, we see Parkinson's here again. But again, this is also for a broader population of patients with other neurological diseases, giving cognitive impairment. And the last but not least, 1117, our completely new treatment in Parkinson’'s. This will have the potential to displace levodopa in the future, and we anticipate this compound to be ready for Phase I in the next year. So some words now about the individual compounds. Mesdopetam, this is our treatment for levodopa dyskinesia with an addressable population of 1.5 million to 2 million patients. We should here understand that available therapies are not very well tolerated, meaning that there is a very huge undertreatment in this population with regard to these symptoms. The molecule works through a completely new innovative mechanism. We are inhibiting the D3 receptors in the brain. I mentioned that we just concluded our Phase IIb study. And here, you see the top line results. To the left, you see the results analyzed according to what we call FAS population, that is really the intention to treat. So based on the [indiscernible] group. To the right, you see the PS population, which is the per-protocol population. And since patients in the beginning of the trial could have one dose change, we have here analyzed the data according to the dose that the patients actually received during the treatment. As you can see, we have very clear dose response patterns, both for the clear anti-dyskinetic effect, but we can see through the effect on UDysRS and on “good ON”-time. Secondly, we also saw a clear anti-Parkinson's effect, and that is the effect you see on the off-time. And this was coupled with an excellent safety and tolerability profile, which actively was on par with placebo. When we have looked at the data and we have reflected upon what are the requirements for a U.S. registration, we have looked into the file of amantadine ER that is approved by the FDA. And of course, we've taken the information we've got from the interactions we've had with FDA in the past. And we can then see primary endpoint, key secondary endpoints, safety endpoints and optional endpoint as depicted on this slide. When we then look at the FAS population, which was the intention to treat population, we see that we actually reached the objective, both for the primary endpoint and for the safety endpoints meaning that if we can repeat the results from the Phase IIb study in a Phase III study, we actually have fulfilled the requirements. If we then look at the picture for the per protocol analysis, we actually can tick all the different boxes. And this is why we are now striving to get to an end of Phase II meeting, and we're doing this with experts in the United States in the form of [indiscernible]. Pirepemat, this is also a completely novel treatment mechanism and we are here aiming to improve balance to reduce the risk of force, one of the most common symptoms in Parkinson's. We have an ongoing Phase IIb study running in Europe. And when we look at all falls, we should remember that almost 1 in 2 patients will have recurrent falls and that brings us to an addressable population in the order of 2.5 million patients. The cost of fall injuries is extremely expensive, at least in the United States, as you see on the slide. And despite this very large unmet medical need, there is today no treatment available for the patients. The status of our program that is that we started the Phase IIb study last year. We have now all the centers activated in recruitment of patients and we foresee that we can give the top line results end of first half next year. Some words about our preclinical projects in development. The 757 for apathy and as I said, this is Parkinson's as well as other neurological diseases with apathy as a key symptom. We here see an addressable population in the order of 2 million to 7 million people. At the moment, there is no treatment available for apathy. Our program is now in late preclinical development, and we anticipate to have a Phase I ready project by year-end this year. The 942 compound, that is to improve cognitive function. And here, we are talking about, again, not just Parkinson's, but also other reasons for cognitive dysfunction, and that means that we have an addressable population of about 5.8 million. And as you are aware, we've seen in the first monoclonal antibodies for Alzheimer's, there's very little available in terms of effective treatment. We are now in the late ID-enabling studies. Maybe that we will have a Phase I ready project the first half next year. Last but not least, 1117. This is our very new, and we believe this would be the next-generation Parkinson's treatment for the hallmark symptoms: the rigidity, the tremor, the bradykinesia. We anticipate here on a conservative scale 4 billion people. It could very well be way above that. We're now running preclinical development, and we anticipate to have this Phase I ready by the end of next year. So to summarize, at IRLAB, we are working with pioneering biology based on all the work that has been done by the research team around Professor Arvid Carlsson and his team. And we've developed a platform, the ISP, to generate new innovative candidate drugs. Our strategy is focused on Parkinson's disease because of the very deep understanding and knowledge base we have in this space, but some of our compounds will, of course, also be effective in other neurological diseases. We have a validated business model. We have used our platform to identify new candidate drugs that we have taken past clinical proof of principle, and we have the experience of doing deals. We have a broad portfolio. And I would say we have a world-leading portfolio in the Parkinson's space, and all the compounds are coming out of our ISP platform and all of the compounds have a blockbuster potential. And we are a group of individuals in the organization positioned for success. And I think that this is the end of my presentation. So I think we should now move over to the Q&A session. Thank you.

Okay. Thank you very much Gunnar for a great presentation. So first off, when it comes to the Phase IIb results with mesdopetam, you mentioned here that the results differed between the full analysis set and per-protocol analysis, and this is maybe a bit complex. Could you elaborate a bit on that? And yes, why results were that?

I wouldn't say that they're different. The patterns are very similar. Where there is a difference that is with regard to [indiscernible] for the “good ON. Here, I think that very much of that is due to more variability in the intentional treated population based on the ability for the patient and physicians to make one dose adjustment during the course of the study.

And given that there were a different number of patients in the protocol analysis and the full analysis set, would you say that the characteristics, the background information on the patients are similar in the 2 groups or could per-protocol analysis patients differ in some way that could be useful when you design a Phase III trial?

We have not seen any major differences between the 2 populations. So I would say that they are some. I think that all the clinical studies were done with mesdopetam, has now taught us very much about selection of endpoints, how to get patients being included. I should also say that the Phase III [indiscernible] Phase I studies, maybe to look at things like, is there a difference in PK, that is body handling of the compound depending on where you have your genetic background or whether you have other ongoing treatments. So drug-drug interactions and such things. That has really given very reassuring picture. We don't have any variability depending on genetic makeup. We don't have variability due to drug-drug interactions. What we know so far, building that in the Phase III program, we can have a very broad population of patients with levodopa-induced dyskinesia.

And you mentioned that you are planning for an end of Phase II meeting. What do you hope to achieve with this meeting? What would be the optimal outcome?

The aim for an end of Phase II meeting is of course, to present ideas for a Phase III program and then get a common view between the authority and the company that with the design of the Phase III, if this title comes out positive, you will receive the approval and the label that you are intending. So we are definitely hoping that we will leave the meeting with a full understanding on how we should design the Phase III program.

And you mentioned this a bit also in the presentation, but you have a precedent with amantadine being approved. But in this Phase IIb trial, you mainly showed an effect on UDysRS, right? So, yes, would you still need to show an effect in both good on-time and UDysRS in the Phase III trial? Or what...