RS 102895 hydrochloride
Chemical Name: 1'-[2-[4-(Trifluoromethyl)phenyl]ethyl]-spiro[4H-3,1-benzoxazine-4,4'-piperidin]-2(1H)-one hydrochloride
Purity: ≥99%
Biological Activity
RS 102895 hydrochloride is a CCR2-selective chemokine receptor antagonist (IC50 values are 0.36 and 17.8 μM for inhibition of human recombinant CCR2b and CCR1 receptors respectively). Blocks MCP-1-stimulated calcium influx and chemotaxis with IC50 values of 32 nM and 1.7 μM respectively. Also inhibits α1A, α1D and 5-HT1A receptors.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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Synthesis and antihypertensive activity of 4'-substituted spiro[4H-3,1-benzoxazine-4,4'piperidin]-2(1H)-ones.
Clark et al.
J.Med.Chem., 1983;26:657 -
Identification of the binding site for a novel class of CCR2b chemokine receptor antagonists.
Mirzadegan et al.
J.Biol.Chem., 2000;275:25562
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Citations for RS 102895 hydrochloride
The citations listed below are publications that use Tocris products. Selected citations for RS 102895 hydrochloride include:
5 Citations: Showing 1 - 5
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Blocking the CCL2-CCR2 Axis Using CCL2-Neutralizing Antibody Is an Effective Therapy for Hepatocellular Cancer in a Mouse Model.
Authors: Teng Et al.
Mol Cancer Ther 2017;16:312
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The Chemokine CCL2 Mediates the Seizure-enhancing Effects of Systemic Inflammation.
Authors: Cerri Et al.
J Neurosci 2016;36:3777
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Tumor-derived CXCL8 signaling augments stroma-derived CCL2-promoted proliferation and CXCL12-mediated invasion of PTEN-deficient prostate cancer cells.
Authors: Maxwell Et al.
Oncotarget 2014;5:4895
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CCR2(+) monocytes infiltrate atrophic lesions in age-related macular disease and mediate photoreceptor degeneration in experimental subretinal inflammation in Cx3cr1 deficient mice.
Authors: Sennlaub Et al.
EMBO Mol Med 2013;5:1775
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Monocyte chemoattractant protein-1 affects migration of hippocampal neural progenitors following status epilepticus in rats.
Authors: Hung Et al.
J Neuroinflammation 2013;10:11
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