Disease relevance of C11797

• The hyperphagia induced by tifluadom was antagonized by naloxone, suggesting that the effect was mediated by an action at opiate receptors [1].
• In adrenal demedullated rats, tifluadom induced initial arrest of heart was not affected but the subsequent bradycardia was blocked [2].

Psychiatry related information on C11797

• Administration of the kappa-opiates tifluadom (2.5 mg/kg i.p.) or ketazocine (5 mg/kg i.p.) caused a marked initial decrease in locomotor activity lasting about 15-20 min, followed by an increase in locomotor activity at about 40 min after drug administration [3].

High impact information on C11797

• The influence of oral (p.o.) administration of kappa-(U-50488, tifluadom) and mu- (morphine, DAGO) opioid substances on gastric emptying of liquids and solids in a standard canned dog food meal was evaluated using a double-radiolabeled technique in dogs fitted with gastric cannulas [4].
• Cholecystokinin-A receptor ligands based on the kappa-opioid agonist tifluadom [5].
• The kappa opioid agonists U50,488, bremazocine, ethylketazocine and tifluadom and the opioid antagonist naltrexone were examined alone and in combination with morphine in a squirrel monkey shock titration procedure, before and during chronic morphine administration [6].
• During tests of substitution, the selective kappa-opioid agonists bremazocine, U50, 488 and tifluadom substituted for the bremazocine stimulus, whereas the less selective kappa-opioid agonists ethylketocyclazocine, levallorphan, proxorphan and nalorphine substituted for the fentanyl stimulus [7].
• In order to determine the functional significance of the increased density of brain kappa opioid receptors in SHR rats, the effect of the kappa receptor agonists, tifluadom, U-50,488H and bremazocine, on two known actions associated with kappa receptors, namely analgesia and diuresis, were determined in SHR and normotensive rats [8].

Chemical compound and disease context of C11797

• Effects of the opioid benzodiazepine tifluadom and its optical isomers on spontaneous locomotor activity of mice [9].
• Diazepam enhanced drug-induced hyperactivity, while tifluadom had no effect or reduced locomotor activity [10].

Biological context of C11797

• Tifluadom-induced diuresis in rats. Evidence for an opioid receptor-mediated central action [11].
• Tifluadom inhibited the binding of [3H]MeTRH with an IC50 value of 1.88 microM [12].
• Levorphanol, tifluadom, bremazocine and MR 2034 produced dose-related decreases in minute volume, tidal volume and respiratory frequency [13].
• The effects of the kappa agonists bremazocine, ethylketazocine, tifluadom and U-50,488 were examined in rhesus monkeys with four experimental procedures: urinary output was measured in normally hydrated monkeys; muscle relaxation and stupor were observed; and the time it took monkeys to withdraw their tails from warm water was evaluated [14].
• Finally, using another kappa agonist, tifluadom, we showed that the effect on food intake is stereospecific [15].

Anatomical context of C11797

• Morphine, bremazocine and tifluadom did not significantly alter the activity of the vas deferens enzyme [16].
• Morphine had antagonist properties on the dorsal root potential, as did the kappa agonists ethylketocyclazocine and bremazocine, but not U50488 and tifluadom [17].
• In the isolated guinea pig gallbladder, tifluadom antagonized CCK-8 induced contractions with an estimated pA2 of 6 [18].
• The effects of tifluadom and ketazocine on behaviour, dopamine turnover in the basal ganglia and local cerebral glucose utilization of rats [3].
• It is concluded that kappa-opiate drugs inhibit the binding of [3H]MeTRH to brain membranes in a stereoselective manner with tifluadom being the most potent drug [19].

Associations of C11797 with other chemical compounds

• The effects of the mu-selective opioid, levorphanol (0.03-1.0 mg/kg), and the kappa-selective opioids, U-50,488 (0.03-1.0 mg/kg), tifluadom (0.01-0.3 mg/kg), bremazocine (0.0003-0.01 mg/kg) and MR 2034 (0.001-0.03 mg/kg), on ventilation and on schedule-controlled behavior were studied in rhesus monkeys [13].
• Since tifluadom is suggested to be a kappa-opioid agonist, the effect of other kappa-opiate ligands were also tested for their ability to affect TRH receptors [12].
• The effects of three kappa opioid agonists namely, bremazocine, tifluadom and U-50,488H were studied on blood pressure and heart rate in urethane-anesthetized normal and bilateral adrenal demedullated rats [2].
• Differential, postnatal ontogeny of opiate and benzodiazepine receptor subtypes in rat cerebral cortex: binding characteristics of tifluadom and brotizolam [20].
• This effect was reproduced by oral administration of tifluadom (0.01 to 0.1 mg kg-1) and by N-desmethyltrimebutine (0.1 to 1 mg kg-1) [21].

Gene context of C11797

• The influence of tifluadom on cholecystokinin-induced antinociception [22].
• Scatchard analysis indicated the inhibition of CCK binding by tifluadom was competitive in nature [18].
• An ethological analysis of the effects of tifluadom on social encounters in male albino mice [23].
• In this study we found that the ob/ob mouse was mildly resistant to the ability of three kappa agonists, viz, butorphanol, tifluadom, and ketocyclazocine to induce food intake [24].

Analytical, diagnostic and therapeutic context of C11797

• Tifluadom dose-dependently induced diuresis in rats after subcutaneous injection and oral application [11].
• Finally, in a third set of experiments, carried out with non-familiarized mice, a 15 min immobilization stress, which was ineffective when administered alone, enhanced the effects of tifluadom (1.0 mg/kg) [25].

References