Inflammasome inhibition with K8 in geographic atrophy: A Q&A

Geographic atrophy (GA), the advanced form of dry age-related macular degeneration, is a multifactorial disease in which multiple stressors drive retinal pigment epithelium (RPE) and photoreceptor cell death. Kamuvudine-8 (K8; Inflammasome Therapeutics) is an investigational dual inflammasome inhibitor delivered as a bioerodible sustained-release intravitreal implant dosed every 3 months. In a multicenter US phase 2 trial (NCT06164587), 30 participants with bilateral GA received a K8 implant in the worse-seeing eye at baseline and month 3, with the untreated fellow eye serving as the control, and 3 doses were evaluated (0.3 mg, 0.7 mg and 1.05 mg).¹ The 6-month results, first reported at the American Society of Retina Specialists 2026 Annual Meeting in Montréal, were presented at The Empire Forum: Retina Pipeline and Markets, held November 5, 2026, in New York, New York.

Modern Retina spoke with Jayakrishna Ambati, MD, president of Inflammasome Therapeutics, director of the Center for Advanced Vision Science and DuPont Guerry III Professor of Ophthalmology at the University of Virginia in Charlottesville, about the phase 2 results he presented at the meeting. In the following Q&A, Ambati discusses why single-pathway approaches have fallen short in GA, how K8 targets inflammasome activation, the trial's structural and functional findings, the design of K8's dosing and delivery and the potential of the platform beyond GA.

This Q&A was taken from a video interview. To watch the video interview, visit Empire Forum 2026: Ambati on K8 phase 2 results in geographic atrophy.

Modern Retina (MR): Why have single-pathway approaches fallen short in geographic atrophy, and how does inflammasome inhibition with K8 differ?

Jayakrishna Ambati, MD: Geographic atrophy, like many other chronic diseases, is really a multifactorial condition in which there are multiple factors, like toxins and stressors, that cause RPE cells and photoreceptors to die. So approaches that have targeted a single pathway, for example, complement, have been generally unsuccessful or barely successful. And so what we have done is identify a final common pathway that addresses not just complement activation but also a whole host of other factors upstream of RPE and photoreceptor cell death. It's very fortuitous, really, that inflammasome activation is the final common pathway for multiple GA stressors. And we have a molecule in K8 that blocks these multiple factors that culminate in this final common death pathway.

MR: How did K8 perform overall in the phase 2 geographic atrophy trial?

Ambati: Our phase 2 delivered exceptional results. K8 is now the first drug to achieve both structural efficacy of greater than 50% reduction in disease progression as well as a 4-letter best-corrected visual acuity improvement, all within 6 months. So we're very encouraged about the future potential for K8 and really disrupting the landscape of GA as we treat it today.

MR: How did K8 perform in the phase 2 geographic atrophy trial, both structurally and functionally?

Ambati: Our phase 2 study showed some very important things. First of all, we showed that our lead dose of 0.7 mg reduced disease progression by more than 50%, 54%, to be exact. And actually, when we broke it down into a piecewise model, in the first 3 months, there was a 43% reduction, and in the second 3 months, there was a 70% reduction, which is astounding and unheard of in the field today. So we see acceleration of effect once the drug actually has time to work. The second thing that we showed is, in terms of function, we saw [a] 4-letter visual acuity benefit in the non-subfoveal lesions, where there’s still visual acuity that can be preserved or improved.

MR: How were the dosing and delivery characteristics of K8 designed with patients and physicians in mind?

Ambati: These are characteristics we have built in, engineered to allow patient and physician convenience. We believe [in] the quarterly administration as opposed to a monthly administration. We believe that having a non–cold chain–requiring product will greatly expand physician reach to patients, particularly in satellite offices, and reduce capital burden. Having a preloaded injector, which is what K8 is, also further enhances patient convenience. In addition, the overall volume of our injection is just 1 microliter or less compared with the 100-microliter injections of the 2 approved products. And that's why we saw no intraocular pressure issues. So what we think this is going to do is expand the treatment population as well as treatment persistence. Therefore, we strongly believe that K8 could transform what is now a $1 billion annual market into a $10 billion annual market in GA.

MR: What other diseases could the inflammasome platform address beyond geographic atrophy?

Ambati: Inflammasomes, interestingly, are involved in many different diseases. Diabetic macular edema is one in particular. We have shown that a parallel molecule called K9 has tremendous neuroprotective and neuro-restorative effects. In models of multiple sclerosis, we completely reversed vision loss and paralysis, which was highlighted by both the National Institutes of Health director and the Department of Health and Human Services in recent posts. So we have strong hopes for this platform approach of K8 and K9 in treating not just geographic atrophy but many neurodegenerative diseases as well.

Reference
1. Inflammasome Therapeutics reports positive six-month phase 2 results for K8 in geographic atrophy. News release. Inflammasome Therapeutics. July 17, 2026. Accessed November 11, 2026. https://www.businesswire.com/news/home/20260717057639/en