J 113863

Potent CCR1 chemokine receptor antagonist CAS# 353791-85-2

J 113863

Catalog No. BCC7422----Order now to get a substantial discount!

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Chemical structure

J 113863

3D structure

Chemical Properties of J 113863

Cas No. 353791-85-2 SDF Download SDF
PubChem ID 6918496 Appearance Powder
Formula C30H37Cl2IN2O2 M.Wt 655.44
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO and to 50 mM in ethanol
Chemical Name 2,7-dichloro-N-[1-[[(1E)-cycloocten-1-yl]methyl]-1-ethylpiperidin-1-ium-4-yl]-9H-xanthene-9-carboxamide;iodide
SMILES CC[N+]1(CCC(CC1)NC(=O)C2C3=C(C=CC(=C3)Cl)OC4=C2C=C(C=C4)Cl)CC5=CCCCCCC5.[I-]
Standard InChIKey FOAFBMYSXIGAOX-LQGGPMKRSA-N
Standard InChI InChI=1S/C30H36Cl2N2O2.HI/c1-2-34(20-21-8-6-4-3-5-7-9-21)16-14-24(15-17-34)33-30(35)29-25-18-22(31)10-12-27(25)36-28-13-11-23(32)19-26(28)29;/h8,10-13,18-19,24,29H,2-7,9,14-17,20H2,1H3;1H/b21-8+;
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of J 113863

DescriptionPotent chemokine receptor 1 (CCR1) antagonist (IC50 values are 0.9 and 5.8 nM for human and mouse CCR1 receptors respectively). Also displays high selectivity for human but not mouse CCR3 receptors (IC50 values are 0.58 and 460 nM respectively). Improves paw inflammation, joint damage and dramatically reduces cell infiltration into joints in collagen-induced arthritis in mice. Isomer of UCB 35625.

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Preparing Stock Solutions of J 113863

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.5257 mL 7.6285 mL 15.2569 mL 30.5139 mL 38.1423 mL
5 mM 0.3051 mL 1.5257 mL 3.0514 mL 6.1028 mL 7.6285 mL
10 mM 0.1526 mL 0.7628 mL 1.5257 mL 3.0514 mL 3.8142 mL
50 mM 0.0305 mL 0.1526 mL 0.3051 mL 0.6103 mL 0.7628 mL
100 mM 0.0153 mL 0.0763 mL 0.1526 mL 0.3051 mL 0.3814 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on J 113863

Modified Vaccinia virus Ankara but not vaccinia virus induces chemokine expression in cells of the monocyte/macrophage lineage.[Pubmed:25889495]

Virol J. 2015 Feb 12;12:21.

BACKGROUND: The orthopoxvirus strain Modified Vaccinia virus Ankara (MVA) rapidly induces innate immune responses. Previously, we demonstrated that CCL2 and CCR1 are important players in MVA induced recruitment of leukocytes to the lung. Alveolar macrophages are sentinel cells in the lung, which are likely amongst the first cells of the immune system to encounter and respond to virus during respiratory infection. Therefore we examined the potential of the murine alveolar macrophage MH-S cell line as a model to study chemokine expression during infection with MVA and vaccinia virus (VACV) strain Western Reserve (WR). FINDINGS: MVA but not VACV infected MH-S cells increased the expression of the CXCR2 acting chemokine CXCL2. MH-S cells constitutively produced CCL2 and CCR1 acting chemokines CCL3, CCL5 and CCL9. Consequently, supernatants of mock treated and virus infected MH-S cells induced chemotaxis of murine promyelocyte MPRO cells and human monocytic THP-1 cells at the same level. However, supernatants of MVA infected MH-S cells significantly increased chemotaxis of the CCR2 deficient human monocytic cell line U-937. Chemotaxis of all three cell types was inhibited by J 113863, a CCR1 antagonist. Additionally, we show that MVA but not VACV WR infection of THP-1 cells induces expression of C-C motif and C-X-C motif chemokines and generates a chemotactic activity for monocytes, which was J 113863 sensitive. CONCLUSIONS: These results extend our previous findings, demonstrating that MVA but not VACV WR induces chemokine production in alveolar macrophages and monocytes, which can induce recruitment of monocytes in a CCR1 dependent manner.

Pharmacological blockade of CCR1 ameliorates murine arthritis and alters cytokine networks in vivo.[Pubmed:17016504]

Br J Pharmacol. 2006 Nov;149(6):666-75.

BACKGROUND AND PURPOSE: The chemokine receptor CCR1 is a potential target for the treatment of rheumatoid arthritis. To explore the impact of CCR1 blockade in experimental arthritis and the underlying mechanisms, we used J-113863, a non-peptide antagonist of the mouse receptor. EXPERIMENTAL APPROACH: Compound J-113863 was tested in collagen-induced arthritis (CIA) and three models of acute inflammation; Staphylococcus enterotoxin B (SEB)-induced interleukin-2 (IL-2), delayed-type hypersensitivity (DTH) response, and lipopolysaccharide (LPS)-induced tumour necrosis factoralpha (TNFalpha) production. In the LPS model, CCR1 knockout, adrenalectomised, or IL-10-depleted mice were also used. Production of TNFalpha by mouse macrophages and human synovial membrane samples in vitro were also studied. KEY RESULTS: Treatment of arthritic mice with J-113863 improved paw inflammation and joint damage, and dramatically decreased cell infiltration into joints. The compound did not inhibit IL-2 or DTH, but reduced plasma TNFalpha levels in LPS-treated mice. Surprisingly, CCR1 knockout mice produced more TNFalpha than controls in response to LPS, and J-113863 decreased TNFalpha also in CCR1 null mice, indicating that its effect was unrelated to CCR1. Adrenalectomy or neutralisation of IL-10 did not prevent inhibition of TNFalpha production by J-113863. The compound did not inhibit mouse TNFalpha in vitro, but did induce a trend towards increased TNFalpha release in cells from synovial membranes of rheumatoid arthritis patients. CONCLUSIONS AND IMPLICATIONS: CCR1 blockade improves the development of CIA, probably via inhibition of inflammatory cell recruitment. However, results from both CCR1-deficient mice and human synovial membranes suggest that, in some experimental settings, blocking CCR1 could enhance TNF production.

Design, synthesis, and discovery of a novel CCR1 antagonist.[Pubmed:11311066]

J Med Chem. 2001 Apr 26;44(9):1429-35.

The CC chemokines may play an important role in the pathogenesis of chronic inflammatory diseases including rheumatoid arthritis, and their effects are thought to be mediated through CCR1 receptors. Several nonpeptide CCR1 receptor antagonists that showed high affinity for human CCR1 receptors have been identified; however, their effectiveness in animal models of inflammatory diseases has been scarcely demonstrated, probably due to species selectivity of the antagonists. To elucidate the pathophysiological role of CCR1 receptors in murine models of disease, we looked for a potent antagonist for both murine and human CCR1 receptors. Screening of our chemical collection for inhibition of (125)I-MIP-1alpha binding to human CCR1 receptors transfected in CHO cells led to the identification of xanthene-9-carboxamide 1a as the lead compound. Derivatization of 1a by quaternarizing the piperidine nitrogen with various alkyl groups and by installing substituents into the xanthene moiety dramatically improved the inhibitory activity against both human and murine CCR1 receptors. As a result, 2q-1 showing IC(50) values of 0.9 and 5.8 nM for human and murine CCR1 receptors, respectively, was discovered. This compound is the first murine CCR1 receptor antagonist and may be a useful tool for clarifying the role of CCR1 receptors in murine models of disease.

Description

J-113863 is a potent and selective CCR1 (CD18) antagonist with IC50 values of 0.9 nM and 5.8 nM for human and mouse CCR1 receptors, respectively. J-113863 is also a potent antagonist of the human CCR3 (IC50 of 0.58 nM) , but a weak antagonist of the mouse CCR3 (IC50 of 460 nM). J-113863 is inactive against CCR2, CCR4 and CCR5, as well as the LTB4 or TNF-α receptors. Anti-inflammatory effect.

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