1. Protein Tyrosine Kinase/RTK
  2. VEGFR
  3. Aflibercept

Aflibercept  (Synonyms: VEGF Trap; VEGF-TRAPR1R2; VEGF-trapR1)

Cat. No.: HY-108801 Purity: ≥97.0%
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Aflibercept (VEGF Trap) is a soluble decoy VEGFR constructed by fusing the Ig domains of VEGFR1 and VEGFR2 with the Fc region of human IgG1. Aflibercept inhibits VEGF signaling by reducing VEGF-regulated processes. Aflibercept can be used for thr research of age-related macular degeneration (AMD) and cardiovascular disease.

For research use only. We do not sell to patients.

Aflibercept Chemical Structure

Aflibercept Chemical Structure

CAS No. : 862111-32-8

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500 μg USD 530 In-stock
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5 mg USD 1950 In-stock
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Description

Aflibercept (VEGF Trap) is a soluble decoy VEGFR constructed by fusing the Ig domains of VEGFR1 and VEGFR2 with the Fc region of human IgG1. Aflibercept inhibits VEGF signaling by reducing VEGF-regulated processes. Aflibercept can be used for thr research of age-related macular degeneration (AMD) and cardiovascular disease[1][2][3].

In Vitro

Aflibercept (500 μg/mL; 24 h and 7 d) shows no toxicity on RPE cells, neither in MTT-assay nor in trypan blue exclusion assay[1].
Aflibercept (500 μg/mL; 24 h) shows a statistically significant effect on wound healing compared with control in the confluent RPE cell layer with three wounds[1].
Aflibercept (500 μg/mL; 7 d) displays a significantly diminished phagocytosis of opsonised latex beads compared to untreated control[1].
Aflibercept (1 and 10 μg/mL; 10 h) inhibits VEGF signaling by reducing VEGF-regulated processes, such as permeability and angiogenesis[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Aflibercept (10 mg/kg; 3 h post-middle cerebral artery occlusion (MCAO)) reduces stroke-induced VEGF-A and VEGFR2 expression, and brain edema, and BBB disruption and improves poststroke survival in obese mice[2].
Aflibercept (18.2 mg/kg and 36.4 mg/kg; i.v. once) affects BP, ROS and eNOS production in mice[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male C57BL/6 mice[3]
Dosage: 18.2 mg/kg and 36.4 mg/kg
Administration: Intravenous injection; 18.2 mg/kg and 36.4 mg/kg once
Result: Rapidly and dose-dependently elevated BP in mice and markedly impaired endothelial-dependent relaxation (EDR) and resulted in NADPH oxidases 1 (NOX1)- and NADPH oxidases 4 (NOX4)-mediated generation of ROS, decreased the activation of protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) concurrently with a reduction in nitric oxide (NO) production and elevation of ET-1 levels in mouse aortas.
Clinical Trial
CAS No.
Appearance

Liquid

Color

Colorless to light yellow

SMILES

[Aflibercept]

Storage

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

Purity & Documentation

Purity: ≥97.0%

References
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Aflibercept Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Aflibercept
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