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MedChemExpressModel Ipafricept - 1391727-24-4

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Ipafricept (OMP-54F28; FZD8-Fc) is a first class recombinant fusion protein with the extracellular part of the human frizzled-8 receptor fused to a human IgG1 Fc fragment that binds Wnt ligands, which blocks Wnt signaling. Ipafricept reduces tumor growth and results in a decrease in both liver and lung metastases combined with Gemcitabine (HY-17026) in pancreatic cancer mouse models. Ipafricept shows solid tumor inhibition activity with well tolerance, such as desmoid tumor, germ cell cancer, ovarian cancer[1][2][3].
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Ipafricept

MCE China:Ipafricept

Brand:MedChemExpress (MCE)

Cat. No.HY-P99667

CAS:1391727-24-4

Synonyms:OMP-54F28; FZD8-Fc

Purity:99.80%

Storage:Please store the product under the recommended conditions in the Certificate of Analysis.

Shipping:Shipping with dry ice.

Description:Ipafricept (OMP-54F28; FZD8-Fc) is a first class recombinant fusion protein with the extracellular part of the human frizzled-8 receptor fused to a human IgG1 Fc fragment that binds Wnt ligands, which blocks Wnt signaling. Ipafricept reduces tumor growth and results in a decrease in both liver and lung metastases combined with Gemcitabine (HY-17026) in pancreatic cancer mouse models. Ipafricept shows solid tumor inhibition activity with well tolerance, such as desmoid tumor, germ cell cancer, ovarian cancer.

In Vitro:Ipafricept (10 μg/mL, 4 h) inhibits the pro-proliferative and and migration effects of peptide RL-QN15 on human embryonic stem cells (hESCs) [3]. Ipafricept (10 μg/mL, 0-48 h) reverses the RL-QN15-induced activation of the Wnt/β-catenin signaling pathway, leading to the reversal of the effects of RL-QN15 on the proliferation, migration and stemness of hESCs[3].

In Vivo:Ipafricept (10 mg/kg weekly or 25 mg/kg every 2 weeks, i.p., for 42 days) promotes tumor growth inhibition when combined with weekly Gemcitabine (HY-17026) (50 mg/kg or 5 mg/kg weekly) and Nab-paclitaxel (HY-P99974) (10 mg/kg weekly) in pancreatic cancer xenograft mouse models[2]. Ipafricept (45 mg/kg every 2 weeks, i.p., for 42 days) results in greater antitumor activity of WNT blockade and tumor growth inhibition in combination with Nab-paclitaxel (HY-P99974) (7.5 mg/kg every week) than Carboplatin (HY-17393) (30 mg/kg every week) in ovarian cancer xenograft mouse models[2]. Ipafricept (10 mg/kg, s.c., administered on day 0 and 3) competes with RL-QN15 for binding, reducing the interaction of RL-QN15 with FZD8, thereby counteracting its activation of the Wnt/β-catenin signaling pathway in mouse full-thickness skin injury models[3].

IC50 & Target:Wnt ligand[1] In Vitro Ipafricept (10 μg/mL, 4 h) inhibits the pro-proliferative and and migration effects of peptide RL-QN15 on human embryonic stem cells (hESCs) [3]. Ipafricept (10 μg/mL, 0-48 h) reverses the RL-QN15-induced activation of the Wnt/β-catenin signaling pathway, leading to the reversal of the effects of RL-QN15 on the proliferation, migration and stemness of hESCs[3]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Ipafricept Related Antibodies Western Blot Analysis[3] Cell Line: Human embryonic stem cells

Species:Human

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References:

[1]. Jimeno A, et al. A First-in-Human Phase I Study of the Anticancer Stem Cell Agent Ipafricept (OMP-54F28), a Decoy Receptor for Wnt Ligands, in Patients with Advanced Solid Tumors. Clin Cancer Res. 2017 Dec 15;23(24):7490-7497.  [Content Brief]

[2]. Fischer MM, et al. WNT antagonists exhibit unique combinatorial antitumor activity with taxanes by potentiating mitotic cell death. Sci Adv. 2017 Jun 21;3(6):e1700090.  [Content Brief]

[3]. Li Y, et al. Peptide RL-QN15 regulates epidermal stem cell function to accelerate wound healing via the FZD8/β-catenin axis[J]. Authorea Preprints, 2024.

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