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Drug-Target Interaction

Drug

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PubChem ID:4553
Structure:
Synonyms:
123653-11-2
AC1L1IF7
AC1Q20LP
AR-1K3665
Bio2_000472
Bio2_000952
BRD-K53364951-001-02-6
BSPBio_001264
C080955
C13H18N2O5S
CCRIS 8523
CHEBI:101699
CHEMBL7162
HMS1362P05
HMS1792P05
HMS1990P05
I14-10018
IDI1_002227
IN1319
KBio2_000604
KBio2_003172
KBio2_005740
KBio3_001067
KBio3_001068
KBioGR_000604
KBioSS_000604
LS-90104
Methanesulfonamide, N-(2-(cyclohexyloxy)-4-nitrophenyl)-
N-(2-Cyclohexyloxy-4-nitrophenyl)methanesulfonamide
N-[2-(Cyclohexyloxy)-4-nitrophenyl]methanesulfonamide
N194_SIGMA
NCGC00024892-01
NCGC00024892-02
NCGC00024892-03
nchembio.147-comp10
NS 398
NS-398
NS398
NS4
Tocris-0942
ZINC03791739

Target

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Uniprot ID:PGH2_MOUSE
Synonyms:
COX-2
Cyclooxygenase-2
Glucocorticoid-regulated inflammatory cyclooxygenase
Gripghs
Macrophage activation-associated marker protein P71/73
PES-2
PGH synthase 2
PGHS-2
PHS II
Prostaglandin G/H synthase 2
Prostaglandin H2 synthase 2
Prostaglandin-endoperoxide synthase 2
TIS10 protein
EC-Numbers:1.14.99.1
Organism:Mouse
Mus musculus
PDB IDs:1CVU 1CX2 1DCX 1DD0 1DDX 1PXX 3PGH 4COX 5COX 6COX
Structure:
6COX

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----
----
--22-
--50-
--810-

References:

11399653
Effect of COX-2 inhibitor NS-398 on expression of PGE2 receptor subtypes in M-1 mouse CCD cells.. R Nasrallah; O Laneuville; S Ferguson; R L Hébert (2001) American journal of physiology. Renal physiology display abstract
Our present study has investigated the effect of cyclooxygenase-2 (COX-2) inhibition on prostaglandin E2 (PGE2) receptor expression in M-1 cortical collecting duct cells and measured their response to PGE2. Using a semiquantitative titration analysis method, we show that following the addition of the COX-2-specific inhibitor NS-398, E-prostanoid receptor subtype (EP3 and EP4) mRNA expression was found to increase threefold each vs. the vehicle-treated control. We also observed that EP1 but not EP2 is expressed in M-1 cells and EP2 levels are not induced by NS-398. To determine the status of the PGE2 response on exposure to NS-398, we measured cAMP levels in cells after stimulation with varying concentrations of PGE2, then pretreated the cells with 10 microM NS-398 before PGE2 exposure and found a significant rise in the stimulatory effect of PGE2 on cAMP production. Finally, Western blot analysis of the levels of the EP4 receptor protein in control vs. NS-398-treated cells revealed an induction in protein levels in these cells, correlating with the induction in EP4 mRNA. We conclude that NS-398 upregulates the expression of EP3 and EP4 mRNA in M-1 cells. Also, EP4 protein levels are increased, resulting in an increased stimulation of cAMP production by PGE2.
11788337
Cyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury.. Martin G Schwacha; Chun-Shiang Chung; Alfred Ayala; Kirby I Bland; Irshad H Chaudry (2002) American journal of physiology. Cell physiology display abstract
Macrophage (Mphi) prostaglandin (PG)E(2) production has been implicated in immunosuppression and increased susceptibility to sepsis after thermal injury. Deficient interleukin (IL)-12 production has also been implicated in these postburn complications. The present study examined the relationship between Mphi cyclooxygenase (COX)-2 activity and IL-12 production after thermal injury. C57BL/6 female mice were subjected to a 25% total body surface area full-thickness burn. Mphi were isolated 7 days later, or the mice were subjected to sepsis by cecal ligation and puncture (CLP). IL-12 production by Mphi from injured mice was suppressed by >50%, whereas COX-2 expression and PGE(2) production were increased twofold. The COX-2 inhibitor NS-398 suppressed PGE(2) production and normalized IL-12 production in the injury group, whereas it had no effect on IL-10 production. Injured mice subjected to CLP had lower IL-12 plasma levels compared with sham-treated mice subjected to CLP. NS-398 treatment prevented the suppression in plasma IL-12 levels in the injury group. Thus elevated Mphi COX-2 activity, independent of IL-10, suppresses Mphi IL-12 production after thermal injury and may play an important role in the observed immunosuppression under such conditions.