ASRS 2023: Insights on Aviceda AVD-104 for the Treatment of Geographic Atrophy from Macular Degeneration


Tarek Hassan, MD, spoke with our team about a novel glyco-mimetic nanoparticle, Aviceda AVD-104, being developed for the treatment of geographic atrophy.

Tarek Hassan, MD, spoke with our team about a novel glyco-mimetic nanoparticle, Aviceda AVD-104, being developed for the treatment of geographic atrophy.

Video Transcript

Editor's note - This transcript has been edited for clarity.

Tarek Hassan, MD:

Hi, I'm Tarek Hassan. I'm a partner of Associated Retina Consultants in Royal Oak, Michigan. I'm here at the American Society of Retina Specialists meeting in Seattle.

Very excited to be here and present some of our early data using a new novel treatment paradigm, using glycobiology, glycoimmunology to try to treat geographic atrophy from dry AMD.

We are using a new compound that harnesses the body's own natural immune system to try to modulate the immune cells that directly are at the site of action of where the damage occurs in geographic atrophy. In our bodies, all of our cells are coated with things called sialic acids. They are sugars, and they're all over every cell. And those sugars are the immune model, immune identifiers to the actual immune cells. All different immune cells that have receptors that identify all of our cells in our body as either self or non-self; They're good or bad. So when these receptors on, for example, macrophages OR microglia, the immune cells that cause the damage and dry AMD, recognize damaged retina cells from the disease of macular degeneration, it turns on a whole process of inflammation, where the phenotype of macrophages that causes geographic atrophy turns on, and we figured out a way to present a drug to the eye that has sialic acids that mimic your own good sialic acids. So when the receptors come in, they meet our drug, and all the macrophages sort of stand down. They go from the activated state to the resolution state. And that happens for the phenotype of macrophages that causes dry AMD, and the phenotype of that causes wet AMD. The receptors, which are called siglecs, you'll hear that, you're going to hear that word more because it's the name of our clinical trial. Siglecs are simply the name of the receptors on all immune cells that recognize those sialic acids.

So our drug is a sialic acid mimetic. And by using it, we've been able to show in vitro and in vivo in multiple species of animals, great efficacy at reducing inflammatory cytokines, because we believe macular degeneration to be largely an inflammatory mediated disease, and also increase resolution cytokines. And we've been able to show significant efficacy, all the way up to now, hopefully, our human trials. So, we've introduced this siglec trial. It's phase 2/3 First, part 1 is enrolling now across the United States. It's a dose escalation study to determine our dose and biomarkers, and PK. We look to start enrolling our phase 2, or part 2 trial in the late part of this year, hopefully at the latest.

We have seen no safety signals whatsoever. There's no sign of inflammation in any animals that have been done in multiple species of multiple doses. We've seen no safety signals in the early clinical data that we've seen from the part 1 of the study, which was shown in a wonderful presentation by Carl Regillo, here at this meeting as well. So, we look forward to getting to talk to you more about siglecs, the receptors and silac acids in this new paradigm of glyco-immunology, using our own body's immune system, and the way it modulates inflammation, but we want to do it better with drugs that we can introduce into the eye.

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