C-021 CCR antagonist

Cat.No.E0486

C-021 is a potent CCR4 antagonist with IC50 values are 0.14 μM and 39 nM for inhibition of chemotaxis in human and mouse respectively.
C-021 CCR antagonist Chemical Structure

Chemical Structure

Molecular Weight: 467.65

Quality Control

Batch: E048601 DMSO]150 mg/mL]false]Ethanol]23 mg/mL]false]Water]Insoluble]false Purity: 99.98%
99.98

Chemical Information, Storage & Stability

Molecular Weight 467.65 Formula

C27H41N5O2

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 864289-85-0 -- Storage of Stock Solutions

Solubility

In vitro
Batch:

DMSO : 150 mg/mL ( (320.75 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 23 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Mechanism of Action

Targets/IC50/Ki
CCR4 [1]
(in the [35S]GTPγS-binding and mouse chemotaxis assay)
39 nM
CCR4 [1]
(in the [35S]GTPγS-binding and human chemotaxis assay)
0.14 μM
In vivo

C021 is a potent CC chemokine receptor-4 (CCR4) antagonist, which significantly reduces microglia activation and phosphorylation of ERK1/2, also alleviates AOM-induced cytokine upregulation in azoxymethane (AOM)-treated mice.[2]

References

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