Regeneron, Sanofi post good PhIII asthma data for Dupixent — but it’s losing its halo
Just days after AstraZeneca and Amgen managed to catch analysts sleeping with a promising new asthma drug called tezepelumab, Regeneron and Sanofi are coming in with new data for Dupixent (dupilumab) which they are betting will pave the way to a new approval next year.
But several analysts are saying Monday morning that the new data are a step down from the exciting mid-stage results these two major league partners put up. And they’re wondering whether Dupixent — a one-time darling — can live up to some old expectations.
The data for uncontrolled asthma looked easily good enough for an OK as Regeneron and Sanofi lined up for their next BLA with Dupixent.
At 52 weeks, in the 300 mg dose group, dupilumab reduced severe asthma attacks by 46 percent in the overall population, 60 percent in patients with 150 eosinophilic cells/microliter or greater, and 67 percent in patients with 300 eosinophilic cells/microliter or greater (p less than 0.001 for all groups). At 12 weeks, in the 300 mg dupilumab dose group, mean improvement in lung function over placebo as assessed by forced expiratory volume over one second (FEV1) with dupilumab was 130 mL (9 percent) in the overall population, 210 mL (11 percent) in patients with 150 eosinophilic cells/microliter or greater, and 240 mL (18 percent) in patients with 300 eosinophilic cells/microliter or greater (p less than 0.001 for all groups).
Biren Amin at Jefferies looked it over and summarized it this way:
This data is comparable to the IL-5 Nucala on exacerbations reduction but superior on FEV1 improvement. Based on today’s data, we believe dupi will be competitive but not the clear choice in asthma.
Said Regeneron chief scientist George Yancapolous:
Dupilumab has now demonstrated positive late-stage results in two serious allergic diseases — asthma and atopic dermatitis — with robust efficacy and an extensive safety database. These results continue to support our hypothesis that the IL4/IL13 pathway is a critical driver of allergic disease, and we remain committed to further investigating the IL-4/IL-13 pathway in other allergic diseases.