Conbercept
Based on 1 Customer Validation
Conbercept (KH902) is a recombinant fusion protein composed of VEGFR-1 (second domain) and VEGFR-2 (third and fourth domains) regions fused to human IgG1 Fc. Conbercept is a VEGF inhibitor (IC50 = 8.8 pM) and is a soluble receptor decoy that blocks all isoforms of VEGF-A (Kd = 0.5 pM), VEGF-B (Kd = 8 pM), VEGF-C, and PlGF (Kd = 5 pM). Conbercept has anti-inflammatory effects, can lower the levels of VEGF, TNF-α and IL-6, and reduce the infiltration of inflammatory cells. Conbercept decreases tumor growth in several oncology studies. Conbercept can be used for various eye diseases such as polypoidal choroidal vasculopathy (PCV), diabetic macular edema (DME) and pathologic myopia choroidal neovascularization (pmCNV).
For research use only. We do not sell to patients.
- Purity : 98.42%
- CAS No.: 1227158-72-6
- Molecular Weight:117.45 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All VEGFR Isoforms
More
Biological Activity
Description
IC50 & Target
[3]|
VEGFR1 |
VEGFR2 |
IL-6 |
In Vitro
Conbercept (0-586.9 pM, 4 d) shows an inhibition effect on VEGF-induced HUVEC proliferation with an EC50 value of 28 pM[3][5].
Conbercept inhibits VEGF-induced HUVEC migration and tube formation and suppressed the high glucose-induced migration and sprouting of human retinal endothelial cells[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Conbercept (10-50 mg/kg, i,v., single dose) significantly inhibits xylene-induced ear edema in mice[1].
Conbercept (0.64 mg, 40 μL, intravitreally injection, 4 times a week or 2 times every 2 weeks, for 2 weeks) has an inhibitory effect against VEGF over the course of 81 days in rabbit[3].
Conbercept (0.5 mg, intravitreally injection, single dose) is effective to prevent the formation of experimental choroidal neovascularization (CNV) and also to treat preexisted CNV without evidence of toxicity in monkey model[3][5].
Conbercept inhibits tumor growth in human hepatocellular carcinoma (HepG2), breast cancer (MCF-7), gastric carcinoma (A549), and colorectal cancer (LoVo) tumor xenograft models[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CIA model established in male Wistar rats (200 g, 4-6 weeks)[1]
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Dosage:10 mg/kg
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Administration:Intravenous injection (i.v.), once every other day for 2 weeks
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Result:Significantly reduced paw edema volume and significantly reduced ankle joint swelling in CIA rats.
Significantly reduced Arthritis Index (AI) scores.
Reduced serum VEGF levels, TNF-α, and IL-6 in rats.
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Animal Model:Xylene-induced ear edema model established in male Kunming mice (20-25 g)[1]
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Dosage:10, 25 and 50 mg/kg
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Administration:Intravenous injection (i.v.), single dose
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Result:Significantly inhibited ear edema in the medium and high dose groups.
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Animal Model:Experimental choroidal neovascularization (CNV) model established in rhesus monkeys[5]
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Dosage:0.64 mg, 40 μL
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Administration:Intravitreally injection, 4 times a week or 2 times every 2 weeks for 2 weeks
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Result:Significantly reduced the incidence of CNV and had a significant therapeutic effect on established CNV.
No significant difference in the effects between weekly and biweekly administration.
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
Application
ELISA, FACS, Functional assay
Verified Bioactivity
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Immobilized VEGF165 Protein, Human can bind Conbercept. The EC50 for this effect is 4.31 ng/mL.
Chemical Information
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CAS No. 1227158-72-6
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Appearance Liquid
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Molecular Weight 117.45 kDa
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Color Colorless to light yellow
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SMILES
[Conbercept]
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Synonyms
KH902
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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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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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 (263 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
[1]. Liu Y, Fu H, Zuo L. Anti-inflammatory activities of a new VEGF blocker, Conbercept. Immunopharmacol Immunotoxicol. 2021 Oct;43(5):594-598. [Content Brief]
[2]. Liu H, et al. Updates on the Management of Ocular Vasculopathies with VEGF Inhibitor Conbercept. Curr Eye Res. 2020 Dec;45(12):1467-1476. [Content Brief]
[3]. Lu X, Sun X. Profile of conbercept in the treatment of neovascular age-related macular degeneration. Drug Des Devel Ther. 2015 Apr 22;9:2311-20. [Content Brief]
[4]. de Oliveira Dias JR, et al. Fusion proteins for treatment of retinal diseases: aflibercept, ziv-aflibercept, and conbercept. Int J Retina Vitreous. 2016 Feb 1;2:3. [Content Brief]
[5]. Zhang M, et al. The pharmacology study of a new recombinant human VEGF receptor-fc fusion protein on experimental choroidal neovascularization. Pharm Res. 2009 Jan;26(1):204-10. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)