Alemtuzumab  (Synonyms: Campath-IH)

Alemtuzumab (Campath-IH) is a humanized monoclonal antibody against CD52. Alemtuzumab does not cross-react with murine CD52. Alemtuzumab selectively targets the CD52 antigen to induce profound lymphocyte depletion, followed by recovery of T and B cells with regulatory phenotypes. Alemtuzumab is capable of complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity (ADCC), as well as induction of apoptosis. Alemtuzumab has the potential for B-cell chronic lymphocytic leukaemia research^[1][2].

Human IgG1 kappa

Human IgG1 kappa, Isotype Control

Human

CD52

Alemtuzumab (Campath-IH; 0.5-5 mg/kg; ip) with a single dose results in the dose-dependent depletion of B and T lymphocytes in the peripheral blood and lymphoid organs^[2].

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

1043  [NCBI]

P31358

ELISA, FACS, Functional assay

Unconjugated

The product can be reconstituted/diluted with sterile PBS or saline.

146.06 kDa

216503-57-0

Liquid

Colorless to light yellow

[Alemtuzumab]

Shipping with dry ice.

Please refer to the lot-specific COA for specific buffer information.

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

• 
  Human IgG1 kappa

• 
  Flow cytometry analysis of PBMC cells labelling CD52 with Alemtuzumab at 20 nM (Red). Goat anti human IgG Fc (Alexa Fluor488) was used as the secondary antibody at 1/1000 dilution. Isotype control - human IgG (Blue). Unlabeled control - Unlabelled cells (Gray).
• 
  Immobilized CD52 Protein, Human (His, HY-P72123) can bind Alemtuzumab. The EC₅₀ for this effect is 1.1 ng/mL.

• [1]. Kashani N, et al. Immune Regulatory Cell Bias Following Alemtuzumab Treatment in Relapsing-Remitting Multiple Sclerosis. Front Immunol. 2021;12:706278. Published 2021 Oct 28.  [Content Brief]

  [2]. Yanping Hu, et al. Investigation of the mechanism of action of alemtuzumab in a human CD52 transgenic mouse model. Immunology. 2009 Oct;128(2):260-70.  [Content Brief]