INCB 3284 dimesylateHCCR2 antagonist CAS# 887401-93-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 887401-93-6 | SDF | Download SDF |
PubChem ID | 11679268 | Appearance | Powder |
Formula | C28H39F3N4O10S2 | M.Wt | 712.76 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : ≥ 83.3 mg/mL (116.87 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | N-[2-[[(3R)-1-[4-hydroxy-4-(6-methoxypyridin-3-yl)cyclohexyl]pyrrolidin-3-yl]amino]-2-oxoethyl]-3-(trifluoromethyl)benzamide;methanesulfonic acid | ||
SMILES | COC1=NC=C(C=C1)C2(CCC(CC2)N3CCC(C3)NC(=O)CNC(=O)C4=CC(=CC=C4)C(F)(F)F)O.CS(=O)(=O)O.CS(=O)(=O)O | ||
Standard InChIKey | PNPNUHKICDECDH-SEBNIYPMSA-N | ||
Standard InChI | InChI=1S/C26H31F3N4O4.2CH4O3S/c1-37-23-6-5-19(14-30-23)25(36)10-7-21(8-11-25)33-12-9-20(16-33)32-22(34)15-31-24(35)17-3-2-4-18(13-17)26(27,28)29;2*1-5(2,3)4/h2-6,13-14,20-21,36H,7-12,15-16H2,1H3,(H,31,35)(H,32,34);2*1H3,(H,2,3,4)/t20-,21?,25?;;/m1../s1 | ||
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. |
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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. |
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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. |
Description | Potent, selective hCCR2 antagonist. Exhibits potent antagonism against monocyte chemoattractant molecule binding to hCCR2 and chemotaxis activity (IC50 values are 3.7 and 4.7 nM respectively). Also displays weak hERG activity; inhibits the hERG potassium current (IC50 = 84μM). Orally bioavailable. |
INCB 3284 dimesylate Dilution Calculator
INCB 3284 dimesylate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.403 mL | 7.015 mL | 14.03 mL | 28.0599 mL | 35.0749 mL |
5 mM | 0.2806 mL | 1.403 mL | 2.806 mL | 5.612 mL | 7.015 mL |
10 mM | 0.1403 mL | 0.7015 mL | 1.403 mL | 2.806 mL | 3.5075 mL |
50 mM | 0.0281 mL | 0.1403 mL | 0.2806 mL | 0.5612 mL | 0.7015 mL |
100 mM | 0.014 mL | 0.0701 mL | 0.1403 mL | 0.2806 mL | 0.3507 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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INCB 3284 is a potent, selective and orally bioavailable hCCR2 antagonist. INCB 3284 exhibits potenct antagonism against monocyte chemoattractant molecule binding to hCCR2 and chemotaxis activity (IC50 values are 3.7 and 4.7 nM respectively). INCB 3284 also displays weak hERG activity; inhibits the hERG potassium current (IC50 = 84μM).
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Klotho gene deficiency causes salt-sensitive hypertension via monocyte chemotactic protein-1/CC chemokine receptor 2-mediated inflammation.[Pubmed:24904083]
J Am Soc Nephrol. 2015 Jan;26(1):121-32.
Klotho (KL) is a newly discovered aging suppressor gene. In mice, the KL gene extends the lifespan when overexpressed and shortens the lifespan when disrupted. This study investigated if KL deficiency affects BP and salt sensitivity using KL mutant heterozygous (+/-) mice and wild-type (WT) mice (9 weeks of age, 16 mice per group). Notably, systolic BP in KL(+/-) mice began to increase at the age of 15 weeks, reached a peak level at the age of 17 weeks, and remained elevated thereafter, whereas systolic BP remained consistent in WT mice. High salt (HS) intake further increased BP in KL(+/-) mice but did not affect BP in WT mice. Blockade of CC chemokine receptor 2 (CCR2), involved in monocyte chemotaxis, by a specific CCR2 antagonist (INCB3284) abolished the HS-induced increase in BP in KL(+/-) mice. Furthermore, HS loading substantially increased the expression of monocyte chemotactic protein-1 and the infiltration of macrophages and T cells in kidneys in KL(+/-) mice, and treatment with INCB3284 abolished these effects. Treatment of KL(+/-) mice with INCB3284 also attenuated the increased renal expressions of serum glucocorticoid-regulated kinase 1, thiazide-sensitive NaCl cotransporter, and ATP synthase beta along with the renal structural damage and functional impairment induced by HS loading. In conclusion, KL deficiency caused salt-sensitive hypertension and renal damage by CCR2-mediated inflammation.
Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline.[Pubmed:25012628]
J Neuroinflammation. 2014 Jul 10;11:121.
BACKGROUND: Acute liver failure leads to systemic complications with one of the most dangerous being a decline in neurological function, termed hepatic encephalopathy. Neurological dysfunction is exacerbated by an increase of toxic metabolites in the brain that lead to neuroinflammation. Following various liver diseases, hepatic and circulating chemokines, such as chemokine ligand 2 (CCL2), are elevated, though their effects on the brain following acute liver injury and subsequent hepatic encephalopathy are unknown. CCL2 is known to activate microglia in other neuropathies, leading to a proinflammatory response. However, the effects of CCL2 on microglia activation and the pathogenesis of hepatic encephalopathy following acute liver injury remain to be determined. METHODS: Hepatic encephalopathy was induced in mice via injection of azoxymethane (AOM) in the presence or absence of INCB 3284 dimesylate (INCB), a chemokine receptor 2 inhibitor, or C 021 dihydrochloride (C021), a chemokine receptor 4 inhibitor. Mice were monitored for neurological decline and time to coma (loss of all reflexes) was recorded. Tissue was collected at coma and used for real-time PCR, immunoblots, ELISA, or immunostaining analyses to assess the activation of microglia and consequences on pro-inflammatory cytokine expression. RESULTS: Following AOM administration, microglia activation was significantly increased in AOM-treated mice compared to controls. Concentrations of CCL2 in the liver, serum, and cortex were significantly elevated in AOM-treated mice compared to controls. Systemic administration of INCB or C021 reduced liver damage as assessed by serum liver enzyme biochemistry. Administration of INCB or C021 significantly improved the neurological outcomes of AOM-treated mice, reduced microglia activation, reduced phosphorylation of ERK1/2, and alleviated AOM-induced cytokine upregulation. CONCLUSIONS: These findings suggest that CCL2 is elevated systemically following acute liver injury and that CCL2 is involved in both the microglia activation and neurological decline associated with hepatic encephalopathy. Methods used to modulate CCL2 levels and/or reduce CCR2/CCR4 activity may be potential therapeutic targets for the management of hepatic encephalopathy due to acute liver injury.