The following transcript has been edited for clarity.
Hi, I’m Arshad M. Khanani, MD, MA, FASRS, from Sierra Eye Associates. At the ARVO 2026 meeting, I presented the first-time results from the phase 2 Alluvium study looking at the efficacy and safety of vamikibart (RO7200220; Hoffmann-La Roche) in patients with diabetic macular edema (DME). This is a very important study for the field, because this is the first time an anti–IL-6 treatment is being compared to anti-VEGF, and I don't think we're going to see a trial like that in the future. This is a trial that is validating the efficacy of anti–IL-6 in patients with DME.
As we know, IL-6 is a key driver of inflammation, and dysregulation of IL-6 may lead to recruitment of inflammatory cells and infiltration of surrounding tissues in blood-retinal barrier breakdown, leading to vascular leakage and macular edema. Therefore, targeting IL-6 may be beneficial for patients with inflammatory diseases, including DME, and we have already seen the positive results with treatment of vamikibart in patients with uveitic macular edema.
Looking at the Alluvium phase 2 trial, this is a trial where we studied 394 patients with center-involving DME, and they were randomized 1:1:1:1 to vamikibart 0.2 mg every 8 weeks, vamikibart 1 mg every 8 weeks, vamikibart 1 mg every 4 weeks, or intravitreal ranibizumab 0.5 mg (Lucentis; Genentech) every 4 weeks. The primary endpoint of this study is average change in best-corrected visual acuity (BCVA) at weeks 44 to 48 in 259 treatment-naïve patients that were enrolled in the study.
Looking at the baseline characteristics, these were well-balanced in terms of baseline BCVA and central subfield thickness (CST). For the primary endpoint, in treatment-naïve patients, we saw that vamikibart led to BCVA gains of approximately 6 letters from baseline across the 3 doses at the average of weeks 44 and 48. Looking at further efficacy results, 15% to 23% of treatment-naïve patients gained 3 lines of vision, so that’s 15 letters or more BCVA gains from baseline with vamikibart across all dosing arms until the primary endpoint.
Anatomy is important. Looking at CST in treatment-naïve patients, vamikibart led to improvement of 50 µm to 70 µm from baseline across the 3 dosing arms at the primary endpoint. In addition, looking at patients with resolution of DME, we saw 30% to 40% of treatment-naïve patients had CST less than 325 µm after treatment with vamikibart.
Safety is important for a new molecule. Looking at the safety of the vamikibart group and comparing it to ranibizumab, we did see a higher incidence of ocular adverse events, leading to treatment discontinuation in the vamikibart on treatment period. A higher incidence of intraocular inflammation was observed with higher (1 mg) dose of vamikibart. In addition, we saw that there was a low rate of cataract and elevated intraocular pressure across all treatment arms.
In conclusion, this is the first time we are evaluating vamikibart in patients with DME as a monotherapy to look at the efficacy of a treatment that can block IL-6. What we have seen here is that vamikibart monotherapy demonstrated improvements from baseline in both BCVA and anatomical outcomes across all doses in patients with DME. We did see higher rates of intraocular inflammation in the high-dose vamikibart group. But we also saw low incidence of elevated IOP and cataract across all treatment groups.
In my opinion, IL-6 inhibition with vamikibart provides a clinical effect distinct from VEGF blockade. These findings from the Alluvium study are super important for our field, and they provide a rationale for exploring a combination of anti–IL-6 and anti-VEGF to simultaneously target both inflammatory and angiogenic pathways in patients with DME.
Thank you for your attention. RP
