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Chemical Compound Review

BRNI     3-bromo-7-nitro-2H-indazole

Synonyms: Lopac-B-2050, Tocris-0735, CHEMBL479014, SureCN499421, SureCN499422, ...
 
 
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Disease relevance of INE

  • Pretreatment with 3-bromo-7-nitroindazole (7-NI) (25 mg/kg), a relatively specific inhibitor of neuronal NOS, significantly decreased contusion volume (1.27+/-0.17 mm3 [mean+/-SEM], p < 0.05) compared with that of control (2.52+/-0.35 mm3) [1].
 

High impact information on INE

  • Both DNA damage and cell death in the cerebral cortical neurons were abolished by treatment with 3-bromo-7-nitroindazole (30 mg/kg, intraperitoneal), which specifically inhibited nNOS [2].
  • This study investigated the effects of nitro-L-arginine-methyl ester (L-NAME) and 3-bromo-7-nitroindazole (7-NI) treatment on cNOS catalytic activity and sensorimotor behavioral outcome after TBI [3].
  • Specific inhibitors of neuronal NOS, 7-nitroindazole (7-NI; 20 mg/kg, i.v.) and 3-bromo-7-nitroindazole (3Br-7NI; 10 mg/kg, i.v.) were administered to assess the possible role of NO released from the trigeminal sensory fibres [4].
  • The vasorelaxant effect of PACAP could be significantly reduced by the inhibitor of neuronal N-type calcium channels omega-conotoxin GVIA (omega-CgTx), as well as by 3-bromo-7-nitroindazole (3Br-7-Ni), an inhibitor of the neuronal nitric oxide-synthase (nNOS) [5].
  • 3-bromo-7-nitroindazole, a neuronal nitric oxide synthase inhibitor, impairs maternal aggression and citrulline immunoreactivity in prairie voles [6].
 

Associations of INE with other chemical compounds

 

Gene context of INE

  • Tonic endogenous production of NO was observed as suggested by the increase in EPP amplitude by bath application of the NO scavenger hemoglobin and the neuronal NOS inhibitor 3-bromo-7-nitroindazole sodium salt [8].
 

Analytical, diagnostic and therapeutic context of INE

  • Intraperitoneal injections of the nNOS inhibitor, 3-bromo-7-nitroindazole (3-Br-7NI) (20 mg/kg), three time per day over 4 days resulted in significant impairment of the expression of maternal aggression in terms of the average time in aggressive encounters, the average number of attacks, and the average latency to first attack [6].

References

  1. Role of nitric oxide in traumatic brain injury in the rat. Wada, K., Chatzipanteli, K., Busto, R., Dietrich, W.D. J. Neurosurg. (1998) [Pubmed]
  2. In situ detection of AP sites and DNA strand breaks bearing 3'-phosphate termini in ischemic mouse brain. Huang, D., Shenoy, A., Cui, J., Huang, W., Liu, P.K. FASEB J. (2000) [Pubmed]
  3. Effects of L-NAME and 7-NI on NOS catalytic activity and behavioral outcome after traumatic brain injury in the rat. Wada, K., Chatzipanteli, K., Busto, R., Dietrich, W.D. J. Neurotrauma (1999) [Pubmed]
  4. Sensory nitrergic meningeal vasodilatation and non-nitrergic plasma extravasation in anaesthesized rats. Peitl, B., Németh, J., Szolcsányi, J., Szilvássy, Z., Pórszász, R. Eur. J. Pharmacol. (2004) [Pubmed]
  5. The vasorelaxant effect of pituitary adenylate cyclase activating polypeptide and vasoactive intestinal polypeptide in isolated rat basilar arteries is partially mediated by activation of nitrergic neurons. Seebeck, J., Löwe, M., Kruse, M.L., Schmidt, W.E., Mehdorn, H.M., Ziegler, A., Hempelmann, R.G. Regul. Pept. (2002) [Pubmed]
  6. 3-bromo-7-nitroindazole, a neuronal nitric oxide synthase inhibitor, impairs maternal aggression and citrulline immunoreactivity in prairie voles. Gammie, S.C., Olaghere-da Silva, U.B., Nelson, R.J. Brain Res. (2000) [Pubmed]
  7. The role of nitric oxide in the pathophysiology of thromboembolic stroke in the rat. Stagliano, N.E., Dietrich, W.D., Prado, R., Green, E.J., Busto, R. Brain Res. (1997) [Pubmed]
  8. Differential frequency-dependent regulation of transmitter release by endogenous nitric oxide at the amphibian neuromuscular synapse. Thomas, S., Robitaille, R. J. Neurosci. (2001) [Pubmed]
 
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