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ActiveMax® Recombinant Mouse VEGF120  pdf  pdf  pdf

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VE0-M4211-1mg (250ug x 4)
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ActiveMax® Recombinant Mouse VEGF120 (ActiveMax® Mouse VEGF120) Ala 27 - Arg 146 (Accession # AAB22254.1 ) was produced in human 293 cells (HEK293) at ACROBiosystems.

Molecular Characterization

VEGF120 (Ala 27-Arg 146)AAB22254.1

ActiveMax® Mouse VEGF120 contains no "tag", and has a calculated MW of 17.2 kDa. The predicted N-terminus is Ala 27. The reducing (R) protein migrates as 18-22 kDa in SDS-PAGE due to glycosylation.


Less than 1.0 EU per μg by the LAL method.


>95% as determined by SDS-PAGE.


Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally Mannitol or Trehalose are added as protectants before lyophilization.

Contact us for customized product form or formulation.


See Certificate of Analysis for reconstitution instructions and specific concentrations.


Avoid repeated freeze-thaw cycles.

No activity loss was observed after storage at:
In lyophilized state for 1 year (4°C); After reconstitution under sterile conditions for 3 months (-70°C).



ActiveMax® Recombinant Mouse VEGF120

ActiveMax® Mouse VEGF120 on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.


Immobilized ActiveMax® Mouse VEGF120 (Cat# VE0-M4211) at 2 μg/mL (100 μl/well) can bind Human VEGF R1, His Tag (Cat# VE1-H5220) with a linear range of 3-50 ng/mL.



Vascular endothelial growth factor A (VEGFA) is also known as Vascular permeability factor (VPF). VEGFA belongs to the PDGF/VEGF growth factor family. VEGFA is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Alternatively spliced transcript variants, encoding either freely secreted or cell-associated isoforms, have been characterized. VEGFA is produced by a group of three major isoforms as a result of alternative splicing and if any three isoforms are produced (VEGFA120, VEGFA164, and VEGFA188) then this will not result in vessel defects and death of the full VEGFA knockout in mice.

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