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Drug-Target Interaction

Drug

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PubChem ID:28718
Structure:
Synonyms:
17737-65-4
2-(2'-Methyl-3'-chloro)anilinonicotinic acid
2-(2-Methyl-3-chloroanilino)nicotinic acid
2-(3-Chloro-2-methyl-phenylamino)-nicotinic acid
2-(3-Chloro-2-methylanilino)nicotinic acid
2-(3-Chloro-2-methylanilino)nicotinic acid;
2-(3-chloro-2-methylanilino)pyridine-3-carboxylic acid
2-(3-Chloro-o-toluidino)nicotinic acid
3-Pyridinecarboxylic acid, 2-((3-chloro-2-methylphenyl)amino)-
3-Pyridinecarboxylic acid, 2-[(3-chloro-2-methylphenyl)amino]-
3-Pyridinecarboxylic acid, {2-[(3-chloro-2-methylphenyl)amino]-}
5-22-13-00597 (Beilstein Handbook Reference)
AC-1607
AC1L1FWY
AIDS-129188
AIDS129188
AKOS003188453
ASN 04881975
BRN 0483212
C13H11ClN2O2
CBA 93626
CBA-93626
Chlonixin
Clonix
Clonixic acid
CLONIXIN
Clonixin (USAN/INN)
Clonixin [USAN:INN]
Clonixine
Clonixine [INN-French]
Clonixino
Clonixino [INN-Spanish]
Clonixinum
Clonixinum [INN-Latin]
D03555
Deltar
EINECS 241-730-1
HMS2231D05
I14-0464
LS-96542
MLS001240214
MolPort-000-051-786
NCGC00160384-01
nic acid, 2-(3-chloro-o-toluidino)-
Nicotinic acid, 2-(3-chloro-o-toluidino)-
NSC 335505
NSC335505
SBB067003
Sch 10304
Sch-10304
SMR000768694
UNII-V7DXN0M42R

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:

11292364
In vivo and in vitro effects of lysine clonixinate on nitric oxide synthase in LPS-treated and untreated rat lung preparations.. A M Franchi; G Di Girolamo; M Farina; A R de los Santos; M L MartÝ; M A Gimeno (2001) Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society display abstract
Recent studies have shown that some nonsteroidal antiinflammatory drugs (NSAIDS) inhibited the inducible NO synthase (iNOS) without direct effect on the catalytic activity of this enzyme. This study was conducted to investigate the in vitro and in vivo effects of lysine clonixinate (LC) and indomethacin (INDO) on NOS activity in rat lung preparation. LC is a drug with antiinflammatory, antipyretic, and analgesic action. In the in vitro experiments, rats were injected with saline or lipopolysaccharide (LPS) and killed 6 h after treatment. Lung preparations were incubated with LC at 2.3 x 10(-5) M or 3.8 x 10(-5) M. The minimum concentration did not modify NOS activity in control or LPS-treated rats but the maximum dose inhibited increased NO production induced by LPS. Furthermore, INDO at 10(-6) M had no effect on enzymatic activity in control or LPS-treated rats. In the in vivo experiments, 40 mg/kg of LC were injected ip. Such a dose did not affect basal production of NO. When LC and LPS were injected simultaneously 6 h before sacrifice, a significant decrease in LPS-induced NOS activity was observed. INDO 10 mg/kg injected in control animals had no effect on NOS activity and did not block LPS induced stimulation of NO production when injected simultaneously. Finally, when LC (40 mg/kg) was injected 3 h after LPS, the enzymatic activity remained unchanged. Expression of iNOS was detected by Western blotting in rats treated with LPS plus 4, 10, 20, and 40 mg/kg of LC. The lowest dose was the only one showing no effect on LPS-induced increase of iNOS. In short, LC is a NSAID with inhibitory action on the expression of LPS-induced NOS, effect that was not seen with INDO in our experimental conditions.