BioMarin Pharmaceutical (BioMarin) announced on May 20, 2026, that the Phase 3 CANOPY-HCH-3 trial of vosoritide (Voxzogo) in children with hypochondroplasia met its primary endpoint, demonstrating a statistically significant improvement in annualized growth velocity (AGV) of 2.33 cm/yr over placebo at week 52 (p<0.0001). The findings represent the first positive pivotal trial result in hypochondroplasia, a rare skeletal dysplasia for which no therapies are currently approved by FDA or the European Medicines Agency (EMA). A supplemental new drug application (sNDA) submission to FDA is planned for the third quarter of 2026.1
Key facts
- Drug: vosoritide (Voxzogo; BioMarin Pharmaceutical)
- Class: C-type natriuretic peptide analogue
- Indication studied: hypochondroplasia (ages 3–17)
- Trial: CANOPY-HCH-3; phase 3; study 111-303
- Primary endpoint met: AGV +2.33 cm/yr vs placebo
- Secondary endpoints: standing height, height Z-score, arm span (all significant)
- Safety: consistent with achondroplasia profile; no new signals
- Regulatory status: sNDA submission planned Q3 2026 (FDA)
- Current approval: achondroplasia (US, EU, Japan, Australia)
- Geography: global (multicenter)
"As someone who treats children with hypochondroplasia, I find these positive results tremendously encouraging,” said Andrew Dauber, MD, lead study investigator and Chief of Endocrinology at Children's National Hospital in Washington, DC, in a company press release.1 “Seeing these improvements in growth is a milestone we have hoped for after so many years without treatment options."
What did the CANOPY-HCH-3 trial design and primary efficacy results show?
CANOPY-HCH-3 (Study 111-303) is a global, randomized, double-blind, placebo-controlled phase 3 study enrolling 80 children aged 3 to 17 years with hypochondroplasia in a 1:1 treatment allocation. The primary endpoint was changed from baseline in AGV at 52 weeks. Vosoritide produced a least-squares mean difference of +2.33 cm/yr versus placebo (p<0.0001), accompanied by statistically significant improvements in standing height (p<0.0001) and height Z-score (p<0.0001). A prespecified secondary endpoint, arm span, also showed statistically significant improvement (p=0.004), a finding considered clinically relevant given its association with reach, daily activities, and functional independence. Participants will continue into a long-term extension study. Full data are expected to be presented at an upcoming medical meeting.1
What is hypochondroplasia, and why has the condition historically lacked approved treatments?
Hypochondroplasia is a rare autosomal dominant skeletal dysplasia caused predominantly by gain-of-function variants in the fibroblast growth factor receptor 3 gene (FGFR3), most commonly the p.Asn540Lys substitution, though the genotype–phenotype relationship is variable.2 The condition is characterized by disproportionate short stature, rhizomelic limb shortening, and potential complications including spinal stenosis, otolaryngologic involvement, and neurodevelopmental concerns.2