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Drug-Target Interaction

Drug

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PubChem ID:5142
Structure:
Synonyms:
1068-58-2
1068-58-2 (mono-hydrobromide)
14527-26-5
14527-26-5 (sulfate[1:1])
2-Methylisothiouronium chloride
2260-00-6
2260-00-6 (sulfate)
2986-19-8
4338-95-8
4338-95-8 (mono-hydriodide)
53114-57-1
53114-57-1 (mono-hydrochloride)
53212-69-4
72046-62-9
867-44-7
867-44-7 (sulfate[2:1])
AC1L1JP3
AC1Q1UA3
AKOS003291597
AR-1I1731
BB_SC-7197
C2H6N2S.H3O4P
Carbamimidothioic acid, methyl ester
CHEBI:346693
CHEMBL356703
EINECS 258-372-7
HSCI1_000214
Lopac-M-3127
Lopac0_000755
LS-50742
methyl carbamimidothioate
Methyl imidothiocarbamate
MolPort-001-641-058
NCGC00015664-01
NCGC00015664-02
NCGC00015664-03
NCGC00162238-01
S-Methyl isothiourea
S-Methyl-isothiourea
S-Methylisothiopseudouronium
S-methylisothiourea
S-Methylisothiourea hemisulfate
S-Methylisothiourea sulfate
S-Methylisothiouronium
S-Methylthiopseudouronium iodide
STK301762
ZINC04676170

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:

11164849
Intestinal ischemia induces late preconditioning against myocardial infarction: a role for inducible nitric oxide synthase.. Y Wang; H Xu; K Mizoguchi; M Oe; H Maeta (2001) Cardiovascular research display abstract
OBJECTIVE: We tested the hypothesis that occlusion of the superior mesenteric artery induces late preconditioning against myocardial infarction and examined the effects of pharmacological modifiers of inducible nitric oxide synthase activity on the late preconditioning in anesthetized rats. METHODS: Rats underwent an intestinal ischemia preconditioning protocol (30 min occlusion of the superior mesenteric artery) or were sham-operated. They were subjected to a sustained 30 min of coronary occlusion and 180 min of reperfusion 24 h later. RESULTS: In rats receiving no pharmacological intervention, the percentage of myocardial infarct within the area at risk and left ventricle was 72+/-4% and 31+/-2%, respectively, in sham-operated rats, and these were significantly reduced to 44+/-4% and 23+/-2% (P
11590326
Inhibition of inducible nitric oxide synthase reduces bacterial translocation in a rat model of acute pancreatitis.. I Simsek; M R Mas; M Yasar; M Ozyurt; U Saglamkaya; S Deveci; B Comert; A Basustaoglu; F Kocabalkan; M Refik (2001) Pancreas display abstract
INTRODUCTION: Translocation of bacteria from the gut into pancreatic necrosis is an important factor in the development of septic complications and mortality in acute pancreatitis. S-methylisothiourea (SMT) is an inducible nitric oxide synthase inhibitor that has been shown to decrease bacteria] translocation in sepsis and thermal injury. AIM: To investigate whether SMT could affect bacterial translocation in acute necrotizing pancreatitis. METHODOLOGY: Forty-five Sprague-Dawley rats were studied. Acute pancreatitis was induced in Group I and Group II by injection of taurocholate and trypsin into the common biliopancreatic duct. Group III underwent laparotomy with the manipulation (but not cannulation) of the pancreas and received saline injection. Group I rats received normal saline as a placebo, and Group II rats received SMT after surgery for 2 days. At 48 hours, blood was drawn for serum amylase determinations. Bacterial translocation to mesenteric lymph nodes and distant sites (pancreas, liver, and peritoneum) were examined. A point scoring system of histologic features was used to evaluate the severity of pancreatitis. RESULTS: Plasma amylase levels and pancreatic histologic score were significantly reduced in Group II rats given SMT compared with those in Group I rats given saline (p < 0.01, p < 0.05, respectively). All Group I rats had bacterial translocation to mesenteric lymph nodes compared with 7 of 12 rats in Group II (p < 0.05). There was no difference in bacterial translocation to distant organs between the two groups, although rates tended to be lower in Group II compared with Group I (p > 0.05). Bacterial counts in the pancreas were significantly reduced in Group II rats compared with those in Group I rats (p < 0.05). CONCLUSION: Treatment with SMT appears to have ameliorated the course of acute pancreatitis; however, mortality was not affected.
12810755
Downregulation of angiotensin subtype 1 receptor in rostral ventrolateral medulla during endotoxemia.. Julie Y H Chan; Ling-Lin Wang; Chen-Chun Ou; Samuel H H Chan (2003) Hypertension display abstract
We reported recently that an upregulation of the inducible nitric oxide synthase (iNOS) in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons are located, is a crucial determinant for the elicitation of cardiovascular depression during experimental endotoxemia. The current study evaluated the hypothesis that a downregulation of the molecular synthesis and functional expression of angiotensin subtype 1 receptor (AT1R) in the RVLM is consequential to this upregulated iNOS. In adult Sprague-Dawley rats maintained under propofol anesthesia, intravenous administration of Escherichia coli lipopolysaccharide (15 mg/kg) elicited a reduction, followed by an augmentation and a secondary decrease in sympathetic vasomotor outflow, together with progressive hypotension and bradycardia. There was also a progressive increase in iNOS mRNA and protein level in the ventrolateral medulla. This was followed by a significant downregulation of both mRNA and protein levels of AT1R in the ventrolateral medulla, alongside reduced efficacy of angiotensin II (50 pmol) to induce an increase in systemic arterial pressure, heart rate, or sympathetic vasomotor outflow on unilateral microinjection into the RVLM. Pretreatment with microinjection of a selective iNOS inhibitor, S-methylisothiourea (250 pmol) bilaterally into the RVLM significantly reversed the reduction in both synthesis and activity of AT1R. We conclude that a downregulation of molecular synthesis and functional expression of AT1R in the ventrolateral medulla is consequential to the overproduction of NO through upregulation of iNOS in the RVLM and may underlie the cardiovascular depression that takes place during experimental endotoxemia.