C1Q complex

It's now von Oprument.

It's a C1q complement inhibitor.

What's so unique about this trial?

So that's a great question, Scott.

Really over two years, we don't see much difference in visual acuity in their phase three studies, no difference in fact.

This is going to work differently.

And I think it's important for retina specialists to understand how this C1q inhibitor works.

Basically, what this does is that it activates a membrane attack complex at the photoreceptor level.

We are spun out of Stanford University, where discoveries were made there by the late Dr. Ben Barres, who was chair of neurobiology.

He discovered the role of a particular pathway in our immune system called the classical pathway, which is driven by or activated by a component called C1q.

So it activates this, this aspect of our immune system that drives this harmful inflammation.

So that is the founding in which-- and that was the technology in which Anexen was founded.

Our first disease that we chose to study in the clinic was indeed Guillain-Barré syndrome.

And our drug is Tanruperbart, as you alluded to.

What Tanruperbart does is it recognizes and immediately stops this inflammatory cascade by blocking C1q, the initiator of the classical pathway inflammation that is driving the damage and, you know, aspect of, of Guillain-Barré syndrome.

So it's a, it's an m- full lymph monoclonal antibody.

C4 is down, cryoglobulinemia.

Mutations in C1q can cause familial SLE in some families.

I have made a YouTube clip on it.

It shows up in the NBME.

You have to know that.

C1q mutations can cause SLE in some patients.

Most of the time, autoimmune diseases, SLE, RA, IBD, et cetera, they're polygenic, multifactorial, okay? The vast majority of autoimmune diseases.

So let's just whip through the others.