C 021 dihydrochloride
Chemical Name: 2-[1,4'-Bipiperidin]-1'-yl-N-cycloheptyl-6,7-dimethoxy-4-quinazolinamine dihydrochloride
Purity: ≥99%
Biological Activity
C 021 dihydrochloride is a potent CCR4 chemokine receptor antagonist (IC50 values are 0.14 and 0.039 μM for inhibition of chemotaxis in human and mouse respectively).Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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Potent and orally bioavailable CCR4 antagonists: synthesis and structure-activity relationship study of 2-aminoquinazolines.
Yokoyama et al.
Bioorg.Med.Chem., 2009;17:64
Product Datasheets
Citations for C 021 dihydrochloride
The citations listed below are publications that use Tocris products. Selected citations for C 021 dihydrochloride include:
7 Citations: Showing 1 - 7
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Recombinant CCL17-dependent CCR4 activation alleviates neuroinflammation and neuronal apoptosis through the PI3K/AKT/Foxo1 signaling pathway after ICH in mice.
Authors: Lei Et al.
J Neuroinflammation 2021;18:62
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Recombinant CCL17 Enhances Hematoma Resolution and Activation of CCR4/ERK/Nrf2/CD163 Signaling Pathway After Intracerebral Hemorrhage in Mice.
Authors: Lei Et al.
Neurotherapeutics 2020;17:1940-1953
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CCR4 expression on host T cells is a driver for alloreactive responses and lung rejection.
Authors: Palchevskiy Et al.
JCI Insight 2019;5
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CCL17/TARC and CCR4 expression in Merkel cell carcinoma.
Authors: Rasheed Et al.
Oncotarget 2018;9:31432
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Circadian Expression of Migratory Factors Establishes Lineage-Specific Signatures that Guide the Homing of Leukocyte Subsets to Tissues.
Authors: He Et al.
Immunity 2018;49:1175
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CCL2 Mediates Neuron-Macrophage Interactions to Drive Proregenerative Macrophage Activation Following Preconditioning Injury.
Authors: Kwon Et al.
J Neurosci 2015;35:15934
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Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline.
Authors: McMillin Et al.
J Neuroinflammation 2014;11:121
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