EyePoint, Inc. Common Stock Citigroup’s Biopharma Back to School Summit 2026

Thanks for having us. Of course.

Sure. Thanks for the introduction and thanks for the invitation. At EyePoint, we are a company that specializes in drug delivery to the back of the eye. Our lead product is called DURAVYU. It is the vorolanib intravitreal insert. Vorolanib is a small molecule tyrosine kinase inhibitor, which has activity against all the VEGF receptors, PDGF, and JAK1, giving it an anti-inflammatory component. It is in our proprietary delivery system that allows it to have therapeutic levels in humans for at least six months with a single injection. As you mentioned, we are currently in two phase III programs, wet AMD and diabetic macular edema, or DME. We have four phase III trials ongoing, and the first trial, the LUGANO trial on wet AMD, read out several weeks ago.

The second trial, the LUCIA trial, started about 2 months after LUGANO, so we expect to read out about 2 months after the LUGANO readout. Then we have two fully enrolled DME trials, COMO and CAPRI, which fully enrolled approximately a month ago. Those will have readout in Q4 of 2027.

Sure. The trial enrolled 432 patients with wet age-related macular degeneration. Approximately 75% were treatment naive, and 25% were treatment experienced. They were randomized on day 1 to two groups. They either received 2.7 milligrams of DURAVYU every 6 months or EYLEA on-label control. Both arms were treated with monthly EYLEA at the start of the trial. Each then, all the patients were seen monthly, and every other month, the EYLEA arm received another EYLEA injection on schedule. Every 6 months, the DURAVYU arm received another DURAVYU on schedule. Both arms could qualify for a supplemental injection if they met specific criteria for disease activity. The trial execution was quite good thanks to Ramiro and his team. We had overall about a 6% dropout rate in both arms. None of the dropouts in the DURAVYU arm were due to the drug itself.

As you noted, the top line, which was non-inferiority change in visual acuity between day 1 and weeks 52 and 56 averaged. The top-line result for all patients was that we were not non-inferior. However, the most glaring unusual aspect of the trial was the behavior of the control group at what I'm referring to as the low-end division. In all previous studies of 2-milligram EYLEA on label in phase III, approximately 4%-5% of the EYLEA eyes lost 15 or more letters, either due to wet AMD activity or due to other things. Remember, these are elderly patients, and they can lose vision for things like cataract, glaucoma, retinal detachment, geographic atrophy. So the expectation is 4%-5%. It's varied between 3% to as high as 6%.

If you look at our phase II data, in phase II, 4.3% of the DURAVYU eyes lost 15 or more letters, and about 7%, actually, of the EYLEA eyes lost 15 or more letters. That gave us quite a bit of confidence going into phase III. But when we looked at the results, only 0.5% of the control eyes lost 15 or more letters. Just a very unusual result. Of course, that result really had nothing to do with our drug. Those eyes, obviously, they were control. They did not receive our drug. They received EYLEA on label. If you look at our inclusion and exclusion criteria, they really were not that much different than prior trials. Other than, I hate to say it, but bad luck.

It looks like a series of eyes that lost vision due to other things were randomized into our arm, and none of them got randomized into the EYLEA arm. Specifically, when we looked at, overall, the 15 letter losers in the LUGANO trial, it was about 4%, which is what one would expect. But it was virtually all of them except one was in our arm. Now, some of them were due to wet AMD that still had activity, but we had three retina specialists independently take a look at the eyes, and they all agreed that the primary loss of vision in nine of them was not wet AMD. In fact, those nine eyes, what we call this asymmetric cohort, they actually had good control of their wet AMD at the end of the trial. There was no wet AMD activity.

Based on the CST. Based on OCT, CST, color photographs, fluorescein angiography, all those tests we do to determine is there active wet AMD or not.

One of them lost vision due to retinal detachment. Retinal detachment was successfully repaired, but that patient had not had cataract surgery, and if you repair retinal detachment in an elderly patient using a vitrectomy technique, you get a cataract very rapidly, and that patient did get the cataract.

Easily obtained. Yeah. It had nothing to do with our drug.

And of course, when you look at the rate of retinal detachment, there was one in each arm, which is actually a little bit lower than one would expect.