Sprifermin
Human recombinant FGF18
From Wikipedia, the free encyclopedia
Sprifermin (INN; development code AS-902330[1]) is a recombinant human fibroblast growth factor 18 (rhFGF18) analog,[2] originally developed by Merck, and now being further developed by TrialSpark’s subsidiary, High Line Bio (now Formation Bio), for the treatment of osteoarthritis.[3] FGF18 and sprifermin act via the Fibroblast Growth Factor Receptor (FGFR) family, with preferential activity via FGFR3c.[4]
| Clinical data | |
|---|---|
| Other names | AS-902330; rhFGF18; L-Methionyl(human fibroblast growth factor 18 (FGF-18, zFGF5)-(1-169)-peptide) |
| Identifiers | |
| CAS Number | |
| UNII | |
| Chemical and physical data | |
| Formula | C876H1396N258O256S6 |
| Molar mass | 19830.71 g·mol−1 |
| 3D model (JSmol) | |
| |
Osteoarthritis
In 2020, Merck reported 5-year follow-up data from the Phase 2 clinical trial for knee osteoarthritis (OA). The placebo controlled, multi-center study demonstrated that sprifermin was able to promote statistically significant improvement in cartilage thickness relative to control in a dose-dependent manner, meeting the primary endpoint of the study.[5] The findings suggested the ability of FGF18 to arrest progression to joint replacement, with 0% of patients in the high dose group progressing to Total Knee Replacement (TKR) surgery over the 5 year study period; in contrast, nearly 1 in 10 patients of the high risk subgroup progressed to TKR when treated with the placebo.[6] These findings suggest significant potential of FGF18 as a disease modifying drug for the treatment of OA (DMOAD) and warrant further clinical evaluation.
Sprifermin was well tolerated with no severe adverse events associated with the treatment.[5] Long-term follow up showed that continual injections (up to 12 per year of bilateral treatment) may need to be sustained over a period of multiple years to prevent recurrence of cartilage loss.[5] Improvement in WOMAC, a secondary endpoint, was met for the Subgroup at Risk.[5] Subsequent analysis further demonstrated that a clinically meaningful reduction in the rate of symptomatic progression (WOMAC) was demonstrated in the full trial population and Subgroup at Risk by the high treatment dose.[7]