Lumasiran, an RNAi Therapeutic for Primary Hyperoxaluria Type 1

Sander F. Garrelfs(Université Claude Bernard Lyon 1), Yaacov Frishberg(Université Claude Bernard Lyon 1), Sally A. Hulton(Université Claude Bernard Lyon 1), Michael J. Koren(Université Claude Bernard Lyon 1), William O’Riordan(Université Claude Bernard Lyon 1), Pierre Cochat(Université Claude Bernard Lyon 1), Georges Deschênes(Université Claude Bernard Lyon 1), Hadas Shasha‐Lavsky(Université Claude Bernard Lyon 1), Jeffrey M. Saland(Université Claude Bernard Lyon 1), William G. van’t Hoff(Université Claude Bernard Lyon 1), Daniel G. Fuster(Université Claude Bernard Lyon 1), Daniella Magen(Université Claude Bernard Lyon 1), Shabbir H. Moochhala(Université Claude Bernard Lyon 1), Gesa Schalk(Université Claude Bernard Lyon 1), Eva Šimková(Université Claude Bernard Lyon 1), Jaap W. Groothoff(Université Claude Bernard Lyon 1), David J. Sas(Université Claude Bernard Lyon 1), Kristin Meliambro(Université Claude Bernard Lyon 1), Jiandong Lu(Université Claude Bernard Lyon 1), Marianne T. Sweetser(Université Claude Bernard Lyon 1), Pushkal Garg(Université Claude Bernard Lyon 1), Akshay Vaishnaw(Université Claude Bernard Lyon 1), John M. Gansner(Université Claude Bernard Lyon 1), Tracy L. McGregor(Université Claude Bernard Lyon 1), John C. Lieske(Université Claude Bernard Lyon 1)
New England Journal of Medicine
March 31, 2021
Cited by 492Open Access
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Abstract

BACKGROUND: Primary hyperoxaluria type 1 (PH1) is a rare genetic disease caused by hepatic overproduction of oxalate that leads to kidney stones, nephrocalcinosis, kidney failure, and systemic oxalosis. Lumasiran, an investigational RNA interference (RNAi) therapeutic agent, reduces hepatic oxalate production by targeting glycolate oxidase. METHODS: In this double-blind, phase 3 trial, we randomly assigned (in a 2:1 ratio) patients with PH1 who were 6 years of age or older to receive subcutaneous lumasiran or placebo for 6 months (with doses given at baseline and at months 1, 2, 3, and 6). The primary end point was the percent change in 24-hour urinary oxalate excretion from baseline to month 6 (mean percent change across months 3 through 6). Secondary end points included the percent change in the plasma oxalate level from baseline to month 6 (mean percent change across months 3 through 6) and the percentage of patients with 24-hour urinary oxalate excretion no higher than 1.5 times the upper limit of the normal range at month 6. RESULTS: A total of 39 patients underwent randomization; 26 were assigned to the lumasiran group and 13 to the placebo group. The least-squares mean difference in the change in 24-hour urinary oxalate excretion (lumasiran minus placebo) was -53.5 percentage points (P<0.001), with a reduction in the lumasiran group of 65.4% and an effect seen as early as month 1. The between-group differences for all hierarchically tested secondary end points were significant. The difference in the percent change in the plasma oxalate level (lumasiran minus placebo) was -39.5 percentage points (P<0.001). In the lumasiran group, 84% of patients had 24-hour urinary oxalate excretion no higher than 1.5 times the upper limit of the normal range at month 6, as compared with 0% in the placebo group (P<0.001). Mild, transient injection-site reactions were reported in 38% of lumasiran-treated patients. CONCLUSIONS: Lumasiran reduced urinary oxalate excretion, the cause of progressive kidney failure in PH1. The majority of patients who received lumasiran had normal or near-normal levels after 6 months of treatment. (Funded by Alnylam Pharmaceuticals; ILLUMINATE-A ClinicalTrials.gov number, NCT03681184.).


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