InflaRx N.V. Common Stock H.C. Wainwright 28th Annual Global Investment Conference

Thank you. Thanks for having us.

Excuse me. Absolutely. First of all, Matt, thanks so much for inviting us.

Really a pleasure to be here. We have done a recent financing earlier this year in May to do a therapeutic shift, if you will, but not really just something completely new to us, something that we anyways had on the map, the broader renal space and particularly a space called ANCA vasculitis. It is a rare disease that is driven by anti-neutrophil cytoplasmic antibodies that can cause a vasculitis that is life-threatening. That was a bit prompted by the fact that, A, we have a very good new asset, a receptor, C5a receptor blocker that we believe has best-in-class potential.

It was also driven by the fact that, the only competitor out there, which is Amgen's TAVNEOS, was reporting, A, very good sales, and B, got a bit in an argument with some regulators around trial conduct, and also has been pulled now in Europe and in U.K., but not yet by the FDA in the U.S. So all of a sudden, there was this interesting, probably EUR 1.4-plus billion market opportunity. This is data that other analysts have brought up that seemed to be creating a big opportunity. I want to remind you, we have also an antibody to the ligand C5a, so we're a complement company that really focuses on the terminal complement pathway.

This ligand has an approval in a vascular-type disease, which is COVID, in the end-stage COVID situation that creates a lung failure, ARDS, in Europe, and it has an emergency use authorization for a similar, but not the same indication in the U.S. So we know the pathway, we know the role in vasculitis, we know the role in vascular dimension. We've previously developed with our vilobelimab antibody in ANCA vasculitis. A lot of investors were not convinced is it a real market, and if there's an oral, how much of a gain you would have. But we completed these studies, and our drug is licensed in China with a seller in there called BDB-001. They actually ran a successful phase II trial, showing that you completely throw out corticosteroids on day 1, which was numerically the best treatment groups.

Now they're in phase III with a BVAS non-inferiority study that the FDA did not allow or did not agree to back then with ChemoCentryx. So we know the field very well. We have drugs that could address it, particularly izicopan. We're going to be speaking about that drug a bit.

Yep. I want to take that up front, but this is really the space we're operating in.

The drug has gotten some interesting data, early data in a skin disease called hidradenitis suppurativa and in CSU, chronic spontaneous urticaria. So the pathway seems to be very meaningful, and we're really excited to push this out further in the I and I space.

Yeah. So, I was one of the research team that uncovered the signaling of the receptor, so we're really excited about having a drug that could address it. You're right, it's been a challenging field in the past, but not so much because the target wasn't known. I think it's one of the best-researched I and I space targets out there when it comes to preclinical research, and there's no like bless you. There's no kind of a signal that suggests that blocking the receptor could have a toxicity, right? In fact, it has been shown organ protective even in the liver. So, why is it a bit challenging? Because in the '90s, there were cyclic peptides. They were kind of toxic molecules, but very good blockers. With an antibody, this is a tough target because it constantly recycles.

It can be almost in every tissue of the human body upregulated during inflammation, so tough to catch it with an antibody and fully control it. But chemicals, ideal if they work, and there probably have been many efforts, but ChemoCentryx, kudos to them. They really found that allosteric binding site in the lipid layer of the receptor. So in one of the transmembranes, so to speak. But as it indicates lipid layer, so this has to be a very lipophilic molecule. In vitro, this is a perfect blocker. And our drug has pretty much the identical IC50 in various in vitro assays. But in vivo, the problem, the challenge seemed to be that the PK, so the uptake from the gut into the system in animals and then later in humans was difficult. It has, I think, a 13-week accumulation to reach steady state.

It starts at a pretty low plasma level that may not be enough to fully cover the signal from the beginning. So there was this opportunity to create a drug that actually addresses these shortcomings. Back then, the toxicity wasn't really known much. That is more of a recent signal that became larger and larger in recent years, so one or two years or so. But that being said, the real challenge for us, the initial challenge was can we work on the findings of ChemoCentryx, really, to find a way to generate a drug that addresses this, has a better plasma presence? And as you may have seen, a couple of years ago, we put out this interesting phase I data. We had a tenfold area under the curve increase, threefold higher peak, completely different uptake, really good plasma presence.