For research use only. Not for therapeutic Use.
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].
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].
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].
| Catalog Number | I042679 |
| CAS Number | 862111-32-8 |
| Purity | ≥95% |
| Reference | [1]. Klettner A, et al. Effects of aflibercept on primary RPE cells: toxicity, wound healing, uptake and phagocytosis. Br J Ophthalmol. 2014 Oct;98(10):1448-52. [2]. Kim ID, et al. Aflibercept, a VEGF (Vascular Endothelial Growth Factor)-Trap, Reduces Vascular Permeability and Stroke-Induced Brain Swelling in Obese Mice. Stroke. 2021 Aug;52(8):2637-2648. [3]. Dong ZC, et al. The vascular endothelial growth factor trap aflibercept induces vascular dysfunction and hypertension via attenuation of eNOS/NO signaling in mice. Acta Pharmacol Sin. 2021 Sep;42(9):1437-1448. |
