Anti-Human CD64 (FCGR1) [Clone 10.1] — Alexa Fluor® 647

Rheumatoid synovial fluid cells and fibronectin purified human monocytes.

This Alexa Fluor® 647 conjugate is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.
Alexa Fluor® is a trademark of Life Technologies Corporation.

Liquid

This Alexa Fluor® 647 conjugate is stable when stored at 2-8°C. Do not freeze.

Research Use Only

2-8°C Wet Ice

Red Laser (633 nm) Alexa Fluor® 647 has a maximum emission of 668 nm when it is excited at 633nm / 635nm.

Clone 10.1 recognizes the alpha subunit of human FCGR1.

FCGR1 antibody, 10.1, recognizes high-affinity immunoglobulin gamma Fc receptor I (FCGR1), also known as CD64. FCGR1 is a 72 kDa type I transmembrane glycoprotein expressed on monocytes, macrophages, and dendritic cells (DCs). FCGR1 can also be induced on neutrophils with IFNγ and G-CSF¹. FCGR1 binds with high affinity to monomeric IgG1 and IgG3, and to a lesser extent, IgG4², resulting in phosphorylation of the intracellular FCGR1 ITAM motif and subsequent recruitment of Syk. FCGR1 contributes to inflammation via several mechanisms, including promoting antibody-dependent cell-mediated cytotoxicity (ADCC), clearance of immune complexes, cytokine production, and antigen presentation^1,3. CD64-based targeted therapies eliminate M1 pro-inflammatory macrophages and show clinical potential for the treatment of macrophage-mediated chronic inflammatory diseases, such as chronic cutaneous inflammation and rheumatoid arthritis⁴. In addition, CD64 promotes antitumor responses and mediates cytotoxic killing of tumor cells by macrophages⁵.

FCGR1 is expressed on monocytes, macrophages, dendritic cells (DCs), and activated granulocytes.

IgG receptor

1. Hulett MD & Hogarth PM. (1998) Mol Immunol. 35(14-15):989-96
2. M. Daëron., et al. (2009) Blood. 113: 3716–3725
3. Alter G., et al. (2011) Epub. 415(2):160-7
4. Barth S., et al. (2017) Biomedicines. 5(3):56
5. Keler T., et al. (1998) Clin Cancer Res. 4(9):2237-43