OR-486Catechol O-methyltransferase inhibitor CAS# 7659-29-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 7659-29-2 | SDF | Download SDF |
PubChem ID | 1810907 | Appearance | Powder |
Formula | C6H4N2O6 | M.Wt | 200.11 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in ethanol and to 100 mM in DMSO | ||
Chemical Name | 3,5-dinitrobenzene-1,2-diolate | ||
SMILES | C1=C(C=C(C(=C1[N+](=O)[O-])[O-])[O-])[N+](=O)[O-] | ||
Standard InChIKey | VDCDWNDTNSWDFJ-UHFFFAOYSA-L | ||
Standard InChI | InChI=1S/C6H4N2O6/c9-5-2-3(7(11)12)1-4(6(5)10)8(13)14/h1-2,9-10H/p-2 | ||
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 and selective inhibitor of catechol-O-methyl-transferase. |
OR-486 Dilution Calculator
OR-486 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.9973 mL | 24.9863 mL | 49.9725 mL | 99.945 mL | 124.9313 mL |
5 mM | 0.9995 mL | 4.9973 mL | 9.9945 mL | 19.989 mL | 24.9863 mL |
10 mM | 0.4997 mL | 2.4986 mL | 4.9973 mL | 9.9945 mL | 12.4931 mL |
50 mM | 0.0999 mL | 0.4997 mL | 0.9995 mL | 1.9989 mL | 2.4986 mL |
100 mM | 0.05 mL | 0.2499 mL | 0.4997 mL | 0.9995 mL | 1.2493 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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Hispidulin alleviated methamphetamine-induced hyperlocomotion by acting at alpha6 subunit-containing GABAA receptors in the cerebellum.[Pubmed:27385415]
Psychopharmacology (Berl). 2016 Sep;233(17):3187-99.
RATIONALE: Hispidulin is a flavonoid we isolated from Clerodendrum inerme, an herb that effectively remitted a case of intractable motor tic disorders. Hispidulin was shown to be a positive allosteric modulator (PAM) of GABAA receptors, including the alpha6 subunit-containing subtype (alpha6GABAAR) that is predominantly expressed in cerebellar granule cells and insensitive to diazepam. OBJECTIVES: We explored the action mechanism(s) of hispidulin using hyperdopaminergic mouse models induced by methamphetamine and apomorphine, based on the hyperdopaminergic nature of tic disorders. RESULTS: Hispidulin significantly inhibited methamphetamine-induced hyperlocomotion (MIH) at i.p. doses without affecting apomorphine-induced hyperlocomotion and stereotypy behaviors or having significant benzodiazepine-like effects (BZLE), including sedation, anxiety, and motor impairment. When given by intracerebellar (i.c.b.) microinjection, hispidulin also alleviated MIH and this effect was prevented by i.c.b. coadministration of furosemide, an alpha6GABAAR antagonist, and mimicked by i.c.b. Ro 15-4513, an alpha6GABAAR PAM. Conversely, i.c.b. diazepam did not affect MIH while it reduced MIH at i.p. doses having significant BZLE. In a screening assay for 92 neurotransmitter receptors/degradation enzymes/transporters, hispidulin displayed significant (>50 % inhibition of radiolabeled ligand binding at 10 muM) binding affinity only at the benzodiazepine binding site of GABAARs (IC50 0.73 approximately 1.78 muM) and catecholamine-o-methyl-transferase (COMT) (IC50 1.32 muM). OR-486, a more potent COMT inhibitor than hispidulin, did not affect MIH. CONCLUSIONS: It is suggested that hispidulin alleviates MIH via acting as a PAM of cerebellar alpha6GABAARs, but not through COMT inhibition or affecting dopamine receptor responsiveness. Thus, selective alpha6GABAAR PAMs may have the potential to be a novel treatment for hyperdopaminergic disorders.
Inhibitors of catechol-O-methyltransferase sensitize mice to pain.[Pubmed:20726980]
Br J Pharmacol. 2010 Dec;161(7):1553-65.
BACKGROUND AND PURPOSE: Catechol-O-methyltransferase (COMT) inhibitors are used in Parkinson's disease in which pain is an important symptom. COMT polymorphisms modulate pain and opioid analgesia in humans. In rats, COMT inhibitors have been shown to be pro-nociceptive in acute pain models, but also to attenuate allodynia and hyperalgesia in a model of diabetic neuropathy. Here, we have assessed the effects of acute and repeated administrations of COMT inhibitors on mechanical, thermal and carrageenan-induced nociception in male mice. EXPERIMENTAL APPROACH: We used single and repeated administration of a peripherally restricted, short-acting (nitecapone) and also a centrally acting (3,5-dinitrocatechol, OR-486) COMT inhibitor. We also tested CGP 28014, an indirect inhibitor of COMT enzyme. Effects of OR-486 on thermal nociception were also studied in COMT deficient mice. Effects on spinal pathways were assessed in rats given intrathecal nitecapone. KEY RESULTS: After single administration, both nitecapone and OR-486 reduced mechanical nociceptive thresholds and thermal nociceptive latencies (hot plate test) at 2 and 3 h, regardless of their brain penetration. These effects were still present after chronic treatment with COMT inhibitors for 5 days. Intraplantar injection of carrageenan reduced nociceptive latencies and both COMT inhibitors potentiated this reduction without modifying inflammation. CGP 28014 shortened paw flick latencies. OR-486 did not modify hot plate times in Comt gene deficient mice. Intrathecal nitecapone modified neither thermal nor mechanical nociception. CONCLUSIONS AND IMPLICATIONS: Pro-nociceptive effects of COMT inhibitors were confirmed. The pro-nociceptive effects were primarily mediated via mechanisms acting outside the brain and spinal cord. COMT protein was required for these actions.