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7-NINA

CAS# 161467-34-1

7-NINA

Catalog No. BCC5674----Order now to get a substantial discount!

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Chemical structure

7-NINA

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Chemical Properties of 7-NINA

Cas No. 161467-34-1 SDF Download SDF
PubChem ID 23661758 Appearance Powder
Formula C7H4N3O2Na M.Wt 185.12
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 2 mM in water and to 50 mM in DMSO
Chemical Name sodium;7-nitroindazol-2-ide
SMILES C1=CC2=C[N-]N=C2C(=C1)[N+](=O)[O-].[Na+]
Standard InChIKey DJMLKKIIBMJGIQ-UHFFFAOYSA-N
Standard InChI InChI=1S/C7H4N3O2.Na/c11-10(12)6-3-1-2-5-4-8-9-7(5)6;/h1-4H;/q-1;+1
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 7-NINA

DescriptionSodium salt of the non-selective NOS inhibitor 7-nitroindazole.

7-NINA Dilution Calculator

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7-NINA Molarity Calculator

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Preparing Stock Solutions of 7-NINA

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.4019 mL 27.0095 mL 54.019 mL 108.038 mL 135.0475 mL
5 mM 1.0804 mL 5.4019 mL 10.8038 mL 21.6076 mL 27.0095 mL
10 mM 0.5402 mL 2.701 mL 5.4019 mL 10.8038 mL 13.5048 mL
50 mM 0.108 mL 0.5402 mL 1.0804 mL 2.1608 mL 2.701 mL
100 mM 0.054 mL 0.2701 mL 0.5402 mL 1.0804 mL 1.3505 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 7-NINA

The neuronal NOS inhibitor L-MIN, but not 7-NINA, reduces neurotoxic effects of chronic intrastriatal administration of quinolinic acid.[Pubmed:9439850]

Brain Res. 1997 Nov 14;775(1-2):229-32.

Rat striata were exposed to 15 mM quinolinic acid (QUIN), or QUIN plus the nitric oxide synthase inhibitors S-methyl-L-thiocitrulline dihydrochloride (L-MIN) or 7-nitroindazole monosodium salt (7-NINA) for 21 days. Co-administration of 100 microM or 1 mM L-MIN with QUIN significantly reduced lesion volume compared to QUIN alone. Co-administration of 1 microM or 10 microM L-MIN with QUIN had no significant effect. There was no significant effect of 7-NINA co-administered with QUIN compared to QUIN alone. L-MIN reduction of lesion volume supports the contention that neuronal nitric oxide synthase is a mediator of excitotoxic injury.

Neuroprotective effects of 7-nitroindazole in the gerbil model of global cerebral ischaemia.[Pubmed:8884206]

Eur J Pharmacol. 1996 Aug 29;310(2-3):115-22.

To evaluate the role played by nitric oxide in global cerebral ischaemia we examined the effects of 7-nitroindazole and a sodium salt of 7-nitroindazole (inhibitors of neuronal nitric oxide (NO) synthase) and NG-nitro-L-arginine methyl ester (a more general inhibitor of NO synthase) in the gerbil model of cerebral ischaemia. Four experiments were carried out. In the first experiment, animals were either sham-operated, subjected to 5 min bilateral carotid occlusion (BCAO) or administered 7-nitroindazole or NG-nitro-L-arginine methyl ester immediately after occlusion followed by three further doses at 3, 6 and 24 h post-occlusion. In the second experiment, we examined the effects of a sodium salt of 7-nitroindazole, which is more soluble than 7-nitroindazole, using the same protocol. In the third experiment, the effects of the sodium salt of 7-nitroindazole administered at 10 mg/kg at 0, 3, 6, 24, 27, 30, 33, 52, 55, 72, 75 and 78 h post-occlusion or at 0.05 mg/h for 72 h via mini-pumps were evaluated. In separate experiments, we examined the effects of three reference compounds dizocilpine (MK-801), 2, 3-dihydroxy-6-nitro-7-sulphamoyl-benz(F)-quinoxaline (NBQX) and eliprodil using the same model. Extensive neuronal death was observed in the CA1 layer of the hippocampus in 5 min bilateral carotid occluded animals 5 days after surgery. Both 7-nitroindazole and NG-nitro-L-arginine methyl ester provided significant neuroprotection (P < 0.01) against this neuronal death. The sodium salt of 7-nitroindazole showed no protection when administered up to 12 times post-occlusion, but did provide significant (P < 0.01) neuroprotection when administered via mini-pump. The neuroprotection was similar to that provided by MK-801 and eliprodil, but not as good as that observed with NBQX. These results indicate that nitric oxide plays a role in ischaemic cell death and that selective neuronal nitric oxide synthase inhibitors can protect against ischaemic brain damage.

Increased striatal dopamine efflux in vivo following inhibition of cerebral nitric oxide synthase by the novel monosodium salt of 7-nitro indazole.[Pubmed:7533610]

Br J Pharmacol. 1995 Jan;114(2):257-8.

The role of nitric oxide (NO) in striatal dopamine release has been controversial. Most NO synthase inhibitors affect more than one isoform of the enzyme and exert vasoconstrictor effects which may also affect striatal dopamine function. We now report on the effect of a soluble monosodium salt of the selective brain NO synthase inhibitor 7-nitro indazole (7-NINA). Using 7-NINA the first study of selective inhibition of the brain isoform of NO synthase on dopamine efflux in rat striatum was undertaken by use of in vivo microdialysis. Perfusion with 7-NINA (1 mM) increased striatal dopamine efflux. The effect of 7-NINA was partially antagonized (67%) by co-perfusion with L-arginine (1 mM), the precursor of NO formation in vivo. This suggests that 7-NINA induces a competitive inhibition of NO synthase activity. These data show that endogenous NO has an inhibitory effect on striatal dopamine efflux in vivo.

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