Alumis Inc. Common Stock Wells Fargo 21st Annual Healthcare Conference
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All right, everyone, I think we will get started here with our next session. My name is Derek Archila. I am one of senior biotech analysts here at Wells. With me, we have Alumis, and from the company, we have Martin Babler, President and CEO, as well as Jörn Drappa, Chief Scientific Officer. Gentlemen, thank you so much for joining us.
Thank you for having us.
Thank you. Excellent. We just had some data for your lead product, envudicitinib, phase II in lupus.
Maybe first just recap what we learned, and then we can dig into a little bit more of the specifics.
Yeah. This was a phase IIb dose-ranging trial of envudicitinib, three different doses versus placebo in patients with moderate to severely active lupus. Was a one-year trial with a primary endpoint being BICLA at week 48. The trial did not meet the primary and its key secondary endpoints in the overall population. It became quickly apparent that in the population that has the type 1 interferon signature, there was a strong response and consistent response across multiple different endpoints. That includes the BICLA, the SRI-4, the CLASI, joint counts, as well as remission. But in the type 1 interferon signature negative population, there was really no benefit at all. In fact, some of the active group appeared to be doing even worse, which is primarily due to an extremely high placebo response in that subpopulation.
Since this interferon signature negative group constituted an unexpectedly high proportion of the overall trial participants, that sufficiently diluted the overall outcome to become negative. In the past, we've typically seen approximately 80/20 distribution between signature positive and signature negative ones in trials in this population. In our trial, it was approximately 60 to 40, so this was a large enough population to render the all-comers outcome negative.
Got you. I guess, what do you think explains that lower than expected interferon high patient in the population? As you said, generally we see that 80/20 split. What do you think went wrong? Was it more a geographic thing or race and ethnicity? What kind of mix did we end up getting here?
Yeah. We're still digging through this data. We only got the top line data a week ago, and the biostats team is buried in a mountain of work. We're trying to dig through by site, by region, by country level, where all these type 1 signature negative patients came from. My preliminary sense is that a lot of them actually came from the U.S. Fewer of them came from Latin America and especially Asia. In Asia, typically, patients have a higher proportion of the signature than in other regions, and that, in our hands, was also reflected in a much larger clinical response in Asian patients than in, for example, the U.S.
In the United States, we were in a situation where there's a lot of competition for patients with moderate to severely active lupus, and especially at the time when we began to enroll in North America, because other countries joined later on, we had initial very slow enrollment and had to compete with a lot of other companies that had late-stage trials going on. I think that probably led to the fact that we had a somewhat milder phenotype than we had expected, and that was then also reflected in the lower proportion of the signature negative patients.
Got you. Beyond just your data that you generated here, I guess, how predictive do you think the interferon gene signature is for envudicitinib's response, across maybe other trials? Maybe just give us the totality of the evidence that points that way.
I think it's been a very consistent observation by now with drugs that target the type one interferon pathway. We've seen that first in the anifrolumab program that I was involved in many years ago, where basically the type one interferon negative subgroup did not contribute almost any response. The delta was close to zero, and all the delta came basically from the type one interferon positive subgroup, and that was primarily due to an elevated placebo response rates in the negative subgroup. It's again been seen with the deucravacitinib program, where the responders mostly came from the positive subgroup, and there was very little of any delta in the negative subgroups for most of the dose arms. Now we have seen it again consistently, no benefit whatsoever.
Across three different programs now, we have seen the same thing over and over again, and I think we can now safely conclude that there is just no benefit for these patients for this type of therapeutic approach.
Got you. Although a failed trial, it does add to the learning of trying to almost homogenize this patient population to a degree where you can have and run a successful trial. Is that fair? We're just narrowing the population to some degree?
Yeah, I think so. Obviously you want to target treatments to patients who have a good chance of responding to them and not to those who have very little evidence to support that they would derive any benefit from it. Going forward, I think the rational way to proceed to next steps is to hone in on those patients that have a chance of responding, and that is the type 1 interferon signature positive ones. And we have a lot of work ongoing to see whether in addition to the interferon signature, we can come up with other markers that are associated with response.
We've basically obtained RNA samples at multiple time points from every single patient in the LUMUS trial, and over the next several weeks and months, we will analyze all this data to see whether, in addition to the type 1 interferon signature, there's other things that we can potentially use to narrow down the population and hone in on those that have the best chance of responding.
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