Dupilumab  (Synonyms: REGN-668; SAR-231893)

Dupilumab (REGN-668) is a fully human mAb to IL-4 receptor α (IL-4Rα) that inhibits both IL-4 and IL-13 signaling, markedly improved moderate-to-severe atopic dermatitis^[1].

Human IgG4 kappa

Human IgG4 (S228P) kappa, Isotype Control

Human

Dupilumab suppressed mRNA expressions of genes related to activation of T cells, DCs, eosinophils, inflammatory pathways, and TH2-inducing chemokines in skin lesions. No significant reduction in IL-17A or IL-22 levels is detected, but large reductions in expression of IL-17–related genes, such as elafin (PI3), IL23p19/IL23A, and S100A8 and trends for suppression (CXCL1 and S100A7) are found with 300 mg of Dupilumab^[1].
Major suppressions of hyperplasia-related genes (eg, K16) and reductions in expression of S100A genes are evident with 300 mg of Dupilumab by using microarrays and qRT-PCR. The changes in other critical epidermal alterations in severe atopic dermatitis (AD) skin are also measured, including significant increases in claudin and lipid product levels with 300 mg of Dupilumab. A trend of dose-dependent increases in expression of differentiation genes (LOR and FLG) is observed after adjusting for suppression of epidermal hyperplasia, as demonstrated by K16 reductions with Dupilumab^[1].

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

147000.00

1190264-60-8

Liquid

Colorless to light yellow

[Dupilumab]

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

• 
  Human IgG4 kappa

• 
  Flow cytometry analysis of Raji cells labelling IL-4Rα with Dupilumab at 100nM (Red). Goat anti human IgG Fc(Alexa Fluor488) was used as the secondary antibody at 1/400 dilution. Isotype control - human IgG (Blue). Unlabeled control - Unlabelled cells (Gray).

• [1]. Hamilton JD, et al. Dupilumab improves the molecular signature in skin of patients with moderate-to-severe atopic dermatitis. J Allergy Clin Immunol. 2014 Dec;134(6):1293-1300.  [Content Brief]