Human CCR8 blocking peptide (CDBP0728)

Synthetic Human CCR8 blocking peptide for BL

Product Overview
CCR8 (C-term) peptide (human)
Species Reactivity
0.2 mg/ml
50 μg
PBS with 0.1% BSA 0.02% sodium azide pH7.2
0.02% Sodium Azide
Upon receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes a member of the beta chemokine receptor family, which is predicted to be a seven transmembrane protein similar to G protein-coupled receptors. Chemokines and their receptors are important for the migration of various cell types into the inflammatory sites. This receptor protein preferentially expresses in the thymus. I-309, thymus activation-regulated cytokine (TARC) and macrophage inflammatory protein-1 beta (MIP-1 beta) have been identified as ligands of this receptor. Studies of this receptor and its ligands suggested its role in regulation of monocyte chemotaxis and thymic cell apoptosis. More specifically, this receptor may contribute to the proper positioning of activated T cells within the antigenic challenge sites and specialized areas of lymphoid tissues. This gene is located at the chemokine receptor gene cluster region.
C-C chemokine receptor activity; G-protein coupled receptor activity; chemokine receptor activity; coreceptor activity; receptor activity; signal transducer activity;
CCR8; chemokine (C-C motif) receptor 8; CMKBR8, CMKBRL2; C-C chemokine receptor type 8; CDw198; CKR L1; CY6; GPR CY6; TER1; CC chemokine receptor 8; chemokine receptor-like 1; chemokine (C-C) receptor 8; CC chemokine receptor CHEMR1; CC-chemokine receptor chemr1; chemokine (C-C) receptor-like 2; CCR-8; CKRL1; CMKBR8; GPRCY6; CMKBRL2; CC-CKR-8; MGC129966; MGC129973;


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Cytokines and chemoattractants in allergic inflammation


Authors: Romagnani, S

It is now generally accepted type 2 T helper (Th2) cytokines and some chemoattractants play an essential role in the pathogenesis of the allergic inflammation. The effects of Th2 cytokines, such as interleukin (IL)-4, IL-5, IL-9, and IL-13, account for virtually all the pathophysiological manifestations of allergy and asthma. Moreover, both Th2 cells and the effector cells usually present in the areas of allergic inflammation (basophils, mast cells, and eosinophils) express chemoattractant receptors, such as CCR3, CCR4, CCR8 and CRTH2. Therefore, interactions of eotaxin(s), eotaxin/CCL11, RANTES/CCL5, and MCP-1/CCL2, MCP-2/CCL8, MCP-3/CCL7, MCP-4/CCL13 with CCR3 are responsible for the recruitment of basophils, eosinophils and mast cells, whereas interactions of CCR4 with MDC/CCL22 or TARC/CCL17, CCR8 with I-309/CCL1, and CRTH2 with prostaglandin D-2 play a critical role in the allergen-induced recruitment of Th2 cells in the target tissues of allergic inflammation. The demonstration that Th2-polarized responses against allergens represent the triggering event for the development of allergic diseases, together with the recognition that some chemoattractants are responsible for the recruitment of both Th2 cells and other effector cells of allergic inflammation, can provide the conceptual basis for the development of new therapeutic strategies in allergic conditions. (C) 2002 Elsevier Science Ltd. All rights reserved.

Small molecule antagonists of CCR8 inhibit eosinophil and T cell migration


Authors: Karlsson, Anna K. C.; Walles, Katarina; Bladh, Hakan; Connolly, Stephen; Skrinjar, Marco; Rosendahl, Alexander

In this study, we demonstrate that in addition to T lymphocytes, human naive eosinophils and the differentiated eosinophil-like cell line, AML14.3D10 express CCR8 and respond to CCL1 through CCR8 engagement. The responsiveness of cells was dependent on maturation stage, since CCL1 induced pronounced chemotaxis only in differentiated CCR8 positive AML14.3D10 cells. Despite the low CCR8 surface expression, human naive eosinophils respond with a chemotaxis to high concentration CCL1. We further describe that Th2 clones in a maturation dependent fashion produce autocrine CCL1, which renders them unresponsive to further stimulation. An innovative method to enrich primary CCR8 reactive T cells was developed which demonstrates that primary peripheral CCR8 expressing T cells respond significantly to CCL1. We have developed novel small molecule CCR8 antagonists that are effective in inhibiting calcium mobilization and chemotaxis in differentiated AML cells as well as in human primary CCR8 positive T cells. Importantly, we demonstrate that the compounds can be divided into two subgroups: (i) compounds that are functional agonists for calcium mobilization and chemotaxis (ii) compounds that are pure antagonists. We demonstrate that agonism of these compounds does not correlate with their antagonistic potency. Taken together, we have identified a novel set of CCR8 compounds with antagonistic properties that inhibit CCL1 driven chemotaxis in both CCR8 expressing eosinophils as well as primary human T cells. (C) 2011 Elsevier Inc. All rights reserved.

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