≥99% for sensitive chromatographic and analytical workflows requiring minimal baseline interference.
Store at 2-8°C,Protected from light,Desiccated Ships Wet ice Check lot-specific COA for exact specifications.
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Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
RWJ-56110 dihydrochloride is a potent, selective, peptide-mimetic inhibitor of PAR-1 activation and internalization (binding IC 50 =0.44 uM) and shows no effect on PAR-2, PAR-3, or PAR-4. RWJ-56110 dihydrochloride inhibits the aggregation of human platelets induced by both SFLLRN-NH2 ( IC 50 =0.16 μM) and thrombin ( IC 50 =0.34 μM), quite selective relative to U46619 . RWJ-56110 dihydrochloride blocks angiogenesis and blocks the formation of new vessels in vivo. RWJ-56110 dihydrochloride induces cell apoptosis
In Vitro
Proteinase-activated receptors (PARs) are a family of G protein-coupled receptors activated by the proteolytic cleavage of their N-terminal extracellular domain, exposing a new amino terminal sequence that functions as a tethered ligand to activate the receptors. RWJ56110 inhibits the aggregation of human platelets induced by both SFLLRN-NH2 (IC 50 =0.16 μM) and thrombin (IC 50 =0.34 μM) while being quite selective relative to collagen and the thromboxane mimetic U46619 . RWJ-56110 dihydrochloride is fully inhibits thrombin-induced RASMC proliferation with an IC 50 value of 3.5 μM. RWJ-56110 dihydrochloride shows blockade of thrombin’s action with RASMC calcium mobilization (IC 50 =0.12 μM), as well as with HMVEC (IC 50 =0.13 μM) and HASMC calcium mobilization (IC 50 =0.17 μM). RWJ56110 (0.1-10 μM; 24-96 hours) inhibits endothelial cell growth dose-dependently, with half-maximal inhibitory concentration of RWJ56110 is approximately 10 μM. RWJ56110 (0.1-10 μM; 6 hours) inhibits DNA synthesis of endothelial cells in a thymidine incorporation assays. Endothelial cells are in fast-growing state (50-60% confluence), RWJ56110 inhibits cell DNA synthesis in a dose-dependent manner, but when cells that are in the quiescent state (100% confluent), the inhibitory effect of PAR-1 antagonists is much less pronounced. RWJ56110 (0.1-10 μM; pretreatment for 15 min) inhibits thrombin-induced Erk1/2 activation in a concentration-dependent manner. However, when endothelial cells are stimulated by FBS (final concentration 4%), it reduces partially the activated levels of Erk1/2. RWJ56110 (30 μM; 24 hours) has an inhibitory effect on endothelial cell cycle progression. It reduces the percentage of cells in the S phase, while alterations in the percentages of G1 and G2/M cells are less pronounced. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: Endothelial cells Concentration: 0 μM; 3 μM; 1 μM; 3 μM; 10 μM Incubation Time: Pretreatment for 15 min Result: Resulted in MAPK activation in Endothelial cells. Cell Cycle AnalysisCell Line: Endothelial cells Concentration: 0 μM; 3 μM; 1 μM; 3 μM; 10 μM Incubation Time: Pretreatment for 15 min Result: Reduced cell number in S phase.
Form:Solid
IC50& Target:IC50: 0.44 uM (PAR-1) IC50: 0.16 μM (the aggregation of human platelets induced by SFLLRN-NH2) IC50: 0.34 μM (the aggregation of human platelets induced by thrombin)
| Canonical Smiles | O=C(N[C@H](C(NCC1=CC=CC=C1)=O)CCN)[C@@H](NC(NC2=CC3=C(C=C2)C(CN4CCCC4)=CN3CC5=C(Cl)C=CC=C5Cl)=O)CC6=CC=C(F)C(F)=C6.[H]Cl.[H]Cl |
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| Molecular Weight | 863.65 |
Comprehensive hazard, handling, storage, and regulatory compliance document.
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View spec sheet →| Solubility | DMSO : 200 mg/mL (231.58 mM; Need ultrasonic) |
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