CCR2 selective antagonists are pharmaceutical compounds designed to specifically block the activity of the CCR2 receptor. As mentioned earlier, CCR2 is a chemokine receptor found on the surface of certain immune cells, including macrophages. Chemokine receptors like CCR2 play crucial roles in guiding immune cells to sites of inflammation or infection in the body.
When a CCR2 selective antagonist binds to the CCR2 receptor, it prevents the binding of chemokines that normally signal for the migration of immune cells, such as monocytes and macrophages, to the site of inflammation. This blockade effectively inhibits the recruitment and activation of these immune cells, particularly macrophages, in response to inflammatory stimuli. Creative Biolabs offers tissue-specific macrophage blockade services based on CCR2 selective antagonists to help you accelerate your specific research on macrophages.
Fig.1 Schematic diagram of CCL2 signaling.1
CCR2 selective antagonists can modulate macrophage responses by inhibiting their recruitment and activation, thereby impacting the overall inflammatory environment. Creative Biolabs is committed to providing customers with one-stop macrophage blocking services, from the establishment of relevant animal models, cell culture and differentiation, in vitro and in vivo functional validation, to the molecular structure of antagonists, to create a comprehensive solution for you. We offer you the following services:
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Small Molecule Antagonists | Small Molecule Antagonists | Peptide Antagonists | Allosteric Modulators | Biased Ligands |
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These are low molecular weight compounds that bind to the CCR2 receptor and block its activity. Small molecule antagonists can be developed through high-throughput screening of compound libraries or rational drug design approaches. | Monoclonal antibodies are proteins designed to bind specifically to the CCR2 receptor and inhibit its function. These antibodies can be generated using hybridoma technology or through recombinant DNA technology. Monoclonal antibodies offer high specificity and potency but may have limitations in terms of tissue penetration and duration of action. | Peptide antagonists are short chains of amino acids designed to mimic the binding site of the natural ligands of the CCR2 receptor. These peptides competitively inhibit the binding of chemokines to CCR2, thereby blocking receptor activation. Peptide antagonists can be designed using computational modeling techniques or identified through peptide library screening. | Allosteric modulators are molecules that bind to sites on the CCR2 receptor distinct from the ligand-binding site and modulate receptor activity indirectly. Allosteric modulators can enhance or inhibit the effects of endogenous chemokines on CCR2 signaling, offering potential advantages such as improved selectivity and reduced side effects. | Biased Ligands: Biased ligands are compounds that selectively activate or inhibit specific signaling pathways downstream of the CCR2 receptor. By targeting specific intracellular signaling cascades, biased ligands can modulate CCR2-mediated effects in a more selective manner compared to traditional orthosteric antagonists. |
Efferocytosis and metabolic reprogramming of macrophages play a crucial role in myocardial infarction (MI) repair. This study reveals a novel role of macrophage-specific TREM2 in myocardial infarction, linking excretion during cardiac repair to immunometabolism.
CCR2 chemokine receptor antagonists block the recruitment of circulating monocytes. | |
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![]() Fig.2 CCR2 chemokine receptor antagonists block the recruitment of circulating monocytes.2 |
This study blocked the recruitment of circulating monocytes with CCR2 chemokine receptor antagonists, but this did not affect the number of resident macrophages. In the control group, CCR2 inhibitors resulted in a decrease in EF and an increase in infarct size, but did not affect cardiac function after myocardial infarction in Mac-TREM2KO mice. |
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