EyePoint (EYPT) 3rd Annual Guggenheim Healthcare Innovation Conference summary

Wet AMD phase III results

• LUGANO (July) and LUCIA (October) missed the primary endpoint: non-inferiority in visual-acuity change averaged at weeks 52 and 56 vs. on-label 2 mg EYLEA.

• Across ~450 DURAVYU-treated patients, including re-injection, safety remained favorable; pooled floaters were under 10% but ~2.5x more frequent than in the control arm.

• Pooled OCT data showed a 10-micron difference at week 56; both trials showed vision improvement and an average of two fewer injections after loading vs. control.

• Results were broadly similar in treatment-naive and previously treated patients; previously treated patients did somewhat better, but neither subgroup established statistical non-inferiority.

DME evidence and clinical plans

• VERONA showed DURAVYU eyes were ~4 letters better and 40–50 microns drier at week 4; over 70% of DURAVYU eyes were rescue-free, gained >10 letters and had a 120-micron fluid reduction.

• At VERONA's end, about half of DURAVYU eyes no longer had DME, while all EYLEA eyes retained some DME; vessel leakage was significantly lower with DURAVYU in a dose-dependent manner.

• COMO and CAPRI are fully enrolled with ~550 patients total and a 75% treatment-naive, 25% previously treated mix; FDA-set non-inferiority margin is -4.5 letters.

• Both DME trials use the average visual-acuity endpoint at weeks 52 and 56; DSMC meets every six months and is expected to review DME safety again in December 2026.

• FDA expects two DME trials; both readouts are targeted for very early Q4 2027.

DME rationale and market

• Management views DME as involving inflammatory pathways beyond VEGF; vorolanib inhibits JAK1, which may block downstream IL-6 effects implicated in DME.

• Estimated DME market is ~$5B globally and ~$3B in the U.S.; management cited treatment burden, with 11 expected first-year injections vs. three received on average and ~40% off treatment by one year.

• Management sees potential for combination treatment through complementary extracellular ligand-blocking and intracellular TKI mechanisms, while anti-VEGF remains the mainstay.