Ipafricept (OMP-54F28) is a recombinant fusion protein consisting of the extracellular portion of the human frizzled-8 receptor fused to a fragment of human IgG1 Fc, and a Wnt inhibitor that blocks Wnt signaling.Ipafricept is a decoy receptor for Wnt ligands and has anticancer activity, and may be useful in the study of solid tumors.

Ipafricept inhibited the proliferative and migratory effects of the peptide RL-QN15 on human embryonic stem cells (hESCs) after treatment with 10 μg/mL for 4 hours. When Ipafricept was treated with 10 μg/mL for 0-48 hours, it reversed the RL-QN15-induced activation of the Wnt/β-catenin signaling pathway, which in turn reversed the effects of RL-QN15 on the proliferation, migration and stemness of hESCs. [1]

Ipafricept administered intraperitoneally at a dose of 10 mg/kg per week or 25 mg/kg every 2 weeks for 42 days in combination with Gemcitabine (50 mg/kg per week or 5 mg/kg per week) and Nab-paclitaxel (10 mg/kg per week) significantly enhanced tumor growth inhibition.
In a mouse model of ovarian cancer xenografts, Ipafricept administered intraperitoneally at a dose of 45 mg/kg every 2 weeks for 42 days, in combination with Nab-paclitaxel (7.5 mg/kg/week), demonstrated enhanced anti-tumor activity over Carboplatin (30 mg/kg/week).
In a mouse model of total skin injury, Ipafricept administered subcutaneously at a dose of 10 mg/kg on days 0 and 3 was able to compete with RL-QN15 for binding and reduce the interaction of RL-QN15 with FZD8, thereby counteracting its activation of the Wnt/β-catenin signaling pathway. [1][2]