Signals for mineralization and inflammation are observed following treatment with fasinumab, a specific nerve growth factor inhibitor.
Poulabi Banerjee, Stephen J DiMartino, Haitao Gao et al.
✦ AI-curated · Sources linked
In 30 seconds
This post hoc analysis of Phase 2 and 3 clinical studies examined bone and mineralization markers, C-reactive protein (CRP), and MRI findings in 5772 patients with knee or hip osteoarthritis treated with fasinumab. Fasinumab was associated with dose-related increases in markers of bone formation and mineralization, as well as CRP. At 6 mg every 8 weeks, the Week 16 alkaline phosphatase increase was 10.36 U/L greater in patients with arthropathies than in those without (95% CI: 0.06-20.66 U/L). Changes were generally reversible and more pronounced with arthropathy.
Key findings
- Fasinumab treatment was followed by dose-related increases in alkaline phosphatase, BSAP, osteocalcin, and P1NP.
- At 6 mg every 8 weeks, the Week 16 alkaline phosphatase difference between patients with and without arthropathies was 10.36 U/L (95% CI: 0.06-20.66 U/L).
- At the same dose and time point, the CRP difference was 3.09 mg/L (95% CI: 0.07-6.12 mg/L); CRP returned to near baseline after the last treatment.
Why it matters
The findings identify biological signals accompanying fasinumab treatment that may help contextualize the joint-related adverse events reported with this therapy. The greater marker changes among patients with arthropathies and the return of CRP toward baseline after treatment provide relevant context for interpreting safety and biological effects, without establishing that these changes cause joint events.
What to keep in mind
This was a post hoc analysis of clinical studies, so the observed marker changes do not establish a causal link with joint-related adverse events.