product name MNS (MDBN)
Description: MNS is a tyrosine kinase inhibitor, inhibits Syk, Src, p97 with IC50 of 2.5 μM, 29.3 μM and 1.7 μM, respectively. MNS potently prevents GPIIb/IIIa activation and platelet aggregation without directly affecting other signaling pathways required for platelet activation. MNS is much more potent than genistein in inhibiting platelet aggregation and protein tyrosine phosphorylation.
References: Mol Pharmacol. 2006 Oct;70(4):1380-9; J Biol Chem. 2011 May 13;286(19):16546-54.
193.16
Formula
C9H7NO4
CAS No.
1485-00-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 39 mg/mL (201.9 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
2% DMSO+corn oil: 5mg/mL
Synonyms
other peoduct :
| In Vitro |
In vitro activity: MNS (3,4-methyl-enedioxy-β-nitrostyrene) completely inhibits 2 μM U46619-(a thromboxane A2 mimic), 5 μM ADP-, 100 μM arachidonic acid-(AA), 10 μg/ml collagen-, and 0.1 U/ml thrombin-induced platelet aggregation in a concentration-dependent manner with IC50 of 2.1 μM, 4.1 μM, 5.8 μM, 7.0 μM, and 12.7 μM, respectively. MNS inhibits platelet aggregation caused by either the calcium ionophore A23187 (1 μM) or the protein kinase C (PKC) activator PDBu (200 nM) with IC50 of 25.9 μM and 4.8 μM, respectively. MNS (20 μM) decreases dthrombin-induced P-selectin expression on platelets to levels comparable to those observed in PGE1-treated platelets. MNS (20 μM) markedly inhibits thrombin-but not PDBu-induced MARCKS phosphorylation in platelets. MNS (20 μM) markedly inhibits protein tyrosine phosphorylation at either 0.5 min or 3 min after thrombin or collagen stimulation in platelets. MNS stimulates UbG76V-GFP and ODD-Luc degradation with IC50 of 1.6 μM and 5.9 μM, respectively. MNS inhibits MG132-induced accumulation of the reporter with IC50 of 2.1 μM. MNS inhibits Gram-positive (Staphylococcus aureus and Enterococcus faecalis) and Gram-negative (Escherichia coli and Pseudomonas aeruginosa) bacteria with minimum inhibitory concentrations (MICs) of 128 mg/L. MNS is much more potent than genistein in inhibiting platelet aggregation and protein tyrosine phosphorylation. MNS (3,4-Methylenedioxy-β-nitrostyrene) is equally potent as inhibitors of platelet aggregation as 3,4-dimethoxy-β-nitrostyrene. MNS (20 μM) concentration-dependently prevents ATP release from platelets stimulated by thrombin or collagen. MNS (20 μM) inhibits thrombin-induced PAC-1 binding to human platelets. Kinase Assay: Cell Assay: |
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| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Mol Pharmacol. 2006 Oct;70(4):1380-9; J Biol Chem. 2011 May 13;286(19):16546-54. |
