Ipafricept
Based on 4 publication(s) in Google Scholar
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.
For research use only. We do not sell to patients.
- Purity : 99.80%
- CAS No.: 1391727-24-4
- Molecular Weight:81.97 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Ipafricept
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Biological Activity
Description
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. Further protocols information, click here.
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Cell Line:Human embryonic stem cells
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Concentration:10 μg/mL
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Incubation Time:4 h
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Result:Markedly reduced the RL-QN15-induced increase in TCF7L1, TCF7L2 levels and stemness of hESCs, as well as CK19 protein levels in hESCs.
In Vivo
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].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Pancreatic cancer xenograft mouse models[2]
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Dosage:10 mg/kg weekly or 25 mg/kg every 2 weeks
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Administration:i.p., weekly or every 2 weeks for 42 days
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Result:Markedly increased the antitumor activity in combination with Gemcitabine (HY-17026) and Nab-paclitaxel (HY-P99974) in pancreatic cancer xenograft mouse models.
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Animal Model:Ovarian cancer xenograft mouse models[2]
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Dosage:45 mg/kg every 2 weeks
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Administration:i.p., every 2 weeks for 42 days
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Result:Resulted in greater tumor growth inhibition in combination with Nab-paclitaxel (HY-P99974) than Carboplatin (HY-17393) in ovarian cancer xenograft mouse models.
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Animal Model:Mouse full-thickness skin injury models[3]
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Dosage:10 mg/kg
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Administration:s.c., administered on day 0 and 3
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Result:Decreased the skin wound healing rate to less than 60% combined with RL-QN15 and inhibited RL-QN15-induced re-epithelialization in mouse full-thickness skin injury models.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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[FZD8 (frizzled class receptor 8, frizzled family receptor 8, Frizzled-8)]2-IGHG1 Fc (Fragment constant)
Application
ELISA, FACS, Functional assay
Chemical Information
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CAS No. 1391727-24-4
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Appearance Liquid
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Molecular Weight 81.97 kDa
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Color Colorless to light yellow
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SMILES
[Ipafricept]
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Synonyms
OMP-54F28; FZD8-Fc
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Shipping
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (4)
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Journal Impact Factor
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Most Recent
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Nat Biotechnol
Engineering bispecific exosome activators of T cells to target immune checkpoint inhibitor-resistant metastatic melanoma. [Abstract]2026 Jan 5. PMID: 41491256 -
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Protocols
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
Purity & Documentation
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Data Sheet (266 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Inhibitory Antibodies User Guide (603 KB)
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]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)