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Drug-Target Interaction

Drug

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PubChem ID:11045
Structure:
Synonyms:
2,4,6-Dinitrobenzenesulfonate
2,4,6-Trinitrobenzene Sulfonate
2,4,6-Trinitrobenzene sulfonic acid treated BSA
2,4,6-Trinitrobenzene sulfonic acid treated bovine serum albumin
2,4,6-Trinitrobenzene sulfonic acid treated BSA
2,4,6-trinitrobenzene sulphonate
2,4,6-Trinitrobenzene-1-sulfonic acid
2,4,6-TRINITROBENZENESULFONIC ACID
2,4,6-Trinitrobenzenesulfonic acid solution
2,4,6-Trinitrobenzenesulphonic acid
2508-19-2
2508-19-2 (Parent)
5400-70-4
5400-70-4 (hydrochloride salt)
85600-65-3
92822_FLUKA
92823_FLUKA
92823_SIGMA
AC1L1WHZ
AG-E-75789
AIDS-189652
AIDS189652
Ammonium, (3,5-dinitro-2-sulfophenyl)hydroxyoxo-
Benzenesulfonic acid, 2,4,6-trinitro-
CHEBI:53063
CID11045
CPD-12153
D014302
EINECS 219-717-7
EINECS 226-441-0
LS-31193
MolPort-002-727-543
NSC 127994
NSC127994
P1447
P2297_SIGMA
Picryl sulfonic acid
Picrylsulfonic Acid
Picrylsulfonic acid solution
Sodium trinitrobenzenesulphonate
STK683795
Sulfonate, Trinitrobenzene
TNBS
Trinitrobenzene Sulfonate
Trinitrobenzenesulfonic acid
Trinitrobenzenesulfonic acid [UN0386] [Explosive 1.1D]
Trinitrobenzenesulfonic acid [UN0386] [Explosive 1.1D]
Trinitrobenzenesulfonic Acid, Sodium Salt
UN0386
ZERO/004001

Target

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Uniprot ID:Q62710_RAT
Synonyms:
Nitric oxide synthase
EC-Numbers:-
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

9384236
Time-dependent actions of nitric oxide synthase inhibition on colonic inflammation induced by trinitrobenzene sulphonic acid in rats.. J Kiss; D Lamarque; J C Delchier; B J Whittle (1997) European journal of pharmacology display abstract
The time-dependent actions following pretreatment or delayed administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on colonic inflammation and inducible NO synthase activity following the intrarectal administration of trinitrobenzene sulphonic acid (TNBS) were evaluated in the rat. Intracolonic instillation of TNBS (30 mg in 0.25 ml of 50% ethanol) led to macroscopic injury, an increase of mucosal myeloperoxidase activity and the expression of the Ca2+-independent inducible NO synthase over 8 days. The inflammatory response following TNBS reached maximum levels between 12 and 72 h and then it declined until 14 days. Oral administration of L-NAME (25 mg/kg per 24 h in the drinking water) 2 days before TNBS augmented macroscopic damage and increased colonic inducible NO synthase activity 6, 12, 24 and 72 h after TNBS administration. In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. These findings indicate that the timing of administration of non-selective NO synthase inhibitors such as L-NAME, in models of colitis is critical to the eventual outcome. Thus, pretreatment with L-NAME, which will inhibit constitutive NO synthase, exacerbates the subsequent damage following challenge. In contrast, delayed administration of L-NAME at the time of inducible NO synthase expression, has a beneficial action on the colonic injury and inflammation.