Anti-Advanced Glycation End Products (AGE), Methylglyoxal (MG) [3D11] Antibody

This IgG monoclonal antibody was generated against methylglyoxal (MG)-modified ovalbumin, and is reactive against human, mouse and rat MG.


  • Reacts with human, mouse and rat MG
  • Suitable for Western Blot, ELISA and Immunohistochemistry applications

Recombinant versions available at our sister company, Absolute Antibody:

Methylglyoxal (MG) also referred to as pyruvaldehyde or 2-oxopropanal is formed as a side product of several metabolic pathways. Importantly, it has shown to be involved in the formation of advanced glycation end products otherwise known as AGEs. AGEs are formed both outside and inside the body. AGEs are substances that can be a factor in the development or worsening of many degenerative diseases including Diabetes and Alzheimer's disease.

From the laboratory of Helen Vlassara, MD, Icahn School of Medicine at Mount Sinai

The Investigator's Annexe Part of The Investigator's Annexe program.

Catalog Number Product Size AVAILABILITY Price Qty
Anti-Advanced Glycation End Products (AGE), Methylglyoxal (MG) [3D11] Antibody
50ug In stock
Regular Price:$320.00

Product Type: Antibody
Name: Anti-Advanced Glycation End products (AGE), Methylglyoxal (MG) - AGE-MG [3D11] Antibody
Molecular Weight: 45.4 kDa
Isotype: IgG2a, Lambda
Clonality: Monoclonal
Clone Name: 3D11
Reactivity: Human, Mouse, Rat
Immunogen: MG-modified ovalbumin
Species Immunized: Mouse
Purification Method: Protein G Affinity Chromatography
Buffer: 0.1M Sodium Phosphate, pH 7.4, 0.15M NaCl, 0.05% (w/v) Sodium Azide
Tested Applications: WB (1:800-2000), IHC (1:10-20), ELISA (1:1000)
Storage: -20C
Shipped: Cold packs


Binding inhibition curve of anti-MG derivative (MG3D11)

Affinity of mouse monoclonal antibody (MG3D11) was determined by a competitive ELISA. Competitive inhibition of antibody binding by modified and unmodified proteins (left) or lipid lipoprotein preparations (right)

Adapted from: Cai W., et. al Mol Med 8: 337-346, 2002.

From the laboratory of Helen Vlassara, MD, Icahn School of Medicine at Mount Sinai
  1. Cai W., Gao G.D., Zhu L., Peppa M., Vlassara H. Oxidative stress-inducing carbonyl compounds from commn foods: novel mediators of cellular dysfunction. Mol Med 8: 337-346, 2002.
  2. Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R, Dardaine V, Peppa M, Rayfield EJ. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. roc Natl Acad Sci U S A. 2002 Nov 26;99(24):15596-601.
  3. Cai W, Ramdas M, Zhu L, Striker GE, Vlassara H. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Proc Natl Acad Sci USA 109: 15888-15893, 2012.

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