A missense variant in GLP1R carried by roughly 40% of European-ancestry patients adds 1.7 pounds of weight loss — and hands payers a stratification lever they did not have in March.
Reuters and Nature covered the biology on April 10; the insurance-coverage implication has not yet been written up.
X reads the 23andMe paper as the moment pharmacogenomics stops being a research poster and starts being a prior-authorization checkbox.
The Nature paper arrived April 8 under the byline of Su and 17 co-authors at the 23andMe Research Institute, a genome-wide association study of 27,885 people who had taken GLP-1 receptor agonists. [1] The index variant, rs10305420, is a missense substitution in the signal peptide region of the GLP1R gene, the receptor that semaglutide and tirzepatide target. Carriers of one copy lost an additional 0.76 kilograms — roughly 1.7 pounds — over a median eight months; carriers of two copies lost about 3.3 pounds more than non-carriers. [2] Variants in both GLP1R and GIPR were linked to nausea and vomiting, with the GIPR side-effect signal specific to Eli Lilly's tirzepatide, which is sold as Mounjaro and Zepbound.
The paper's Monday coverage treated the 28,000-person cohort as biology. Tuesday is when the biology arrives at insurance. The paper reports that roughly 40% of European and Middle Eastern ancestry carries the responder variant — a concentration high enough that payers now have a genetic stratification lever they did not have in March. Reuters noted that 23andMe members saw self-reported weight loss vary between 6% and 20% of starting body weight. [3]
The question the paper is asking Tuesday: if a payer can identify which 40% of patients will lose the extra pound-and-a-half, does that responder population become the covered population? Lilly and Novo Nordisk have not commented. CMS has not commented. The report sits on a desk at 23andMe's Total Health platform, available to members. The underwriting conversation has not started.
-- NORA WHITFIELD, Chicago