Fonazine - CAS 7456-24-8
Catalog number: 7456-24-8
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Histamine Receptor
Dimetotiazine is a histamine H1 receptor antagonist. It is a phenothiazine drug used for the treatment of migraine.
Fonazine; Dimetotiazine; Dimethothiazine; Dimetiotazine; Banistyl; Dimethodin; fonazine mesylate; fonazine monomesylate ;Migristene; Promaquid;10-(2-(Dimethylamino)propyl)-N,N-dimethylphenothiazine-2-sulfonamide;7455-39-2(Dimetotiazine Mesilate)
Soluble in DMSO
-20℃ Freezer
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Canonical SMILES:
1.Effects of KB-2796 on plasma extravasation following antidromic trigeminal stimulation in the rat.
Hashimoto M;Yamamoto Y;Takagi H Res Commun Mol Pathol Pharmacol. 1997 Jul;97(1):79-94.
We investigated the effects of KB-2796 (1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)piperazine dihydrochloride), a novel calcium channel blocker, on neurogenic inflammation caused by electrical stimulation in the trigeminal ganglion and on cutaneous reactions induced by inflammatory mediators in rats, by measuring plasma extravasation. Neurogenic inflammation was inhibited by pretreatment with capsaicin (25 mg/kg, s.c.) but not indomethacin (10 mg/kg, i.p.), while phosphoramidon (2.5 mg/kg, i.v.) augmented it. KB-2796 (0.1-1 mg/kg, i.v.) significantly inhibited neurogenic inflammation in a dose dependent manner, without affecting histamine-, bradykinin- or substance P-induced cutaneous reactions. Dimetotiazine (0.3 and 1 mg/kg, i.v.), flunarizine (1 mg/kg, i.v.), mepyramine (1 mg/kg, i.v.) and sumatriptan (1 mg/kg, i.v.) significantly inhibited neurogenic inflammation. However, these compounds also showed complete or partial inhibition of histamine-, bradykinin- or substance P-induced reactions. Nifedipine (0.1 mg/kg, i.v.) did not show marked effects on neurogenic inflammation and cutaneous reactions. The present experiments indicate that neurogenic inflammation is presumably mediated not only by neuropeptides released from trigeminal nerve endings but also by secondarily released histamine, and that KB-2796 like sumatriptan may inhibit neurogenic inflammation caused by trigeminal nerve stimulation probably through inhibition of neuropeptide release but its inhibition may be distinct from the calcium blocking action of the 1,4-dihydropyridine type.
2.Enhancement of the cyclic motor activity of the ovine small intestine by lysergic acid derivatives. Mechanism and significance.
Ruckebusch Y Gastroenterology. 1984 Nov;87(5):1049-55.
The effects of a variety of substances influencing the initiation of cyclic motor events at the gastroduodenal junction were studied in conscious sheep. A significant and long-lasting decrease in the frequency of cyclic events from approximately 100 min to 30-40 min was elicited by the intraduodenal bulb administration of the lysergic acid derivatives methylergonovine and methysergide. This effect was dose-dependent and occurred with smaller dosages than those effective when administered parenterally or more distal in the jejunum. Intraluminal administration of cyproheptadine, fonazine, and metergoline into the duodenal bulb increased the interval between phase III activity. At higher dosages, however, cyproheptadine and metergoline reduced the spiking activity of the antroduodenal junction, without significantly changing the cycle duration of the migrating myoelectric complex on the duodenal bulb or jejunum. After administration of cyproheptadine, fonazine, and metergoline, the cycling activity of the duodenojejunum was irregular for 1-2 days. These findings are compatible with a resetting of the enteric biological clock at a faster rhythm and suggest a selective action via an enteric serotoninergic mechanism involved in the normal pacing of the cyclic motor events of the gut.
3.Comparative effects of selected phenothiazine tranquilizers and antihistaminics on bacterial cells and possible interactions with antibiotics.
Shibl AM;Hammouda Y;Al-Sowaygh I J Pharm Sci. 1984 Jun;73(6):841-3.
Evaluation of the antibacterial effect of phenothiazine antihistaminics (trimeprazine, promethazine, and fonazine) and phenothiazine tranquilizers (promazine, chlorpromazine, triflupromazine, and propiomazine) on Staphylococcus aureus showed that tranquilizers were more active [minimum inhibitory concentration (MIC) 0.5-1.6 micrograms/mL] than antihistaminics (MIC greater than 1.6 micrograms/mL). The antibacterial activity was found to correlate with both the rate of adsorption of these drugs on the bacterial cells and the surface tension of their solutions. Phenothiazine tranquilizers caused rapid and extensive leakage of potassium ions from bacterial cells, while phenothiazine antihistaminics produced relatively slower leakage of these ions. A study of the effect of the phenothiazines on the antibacterial activity of some antibiotics showed that all phenothiazines produced a synergistic effect with erythromycin and an antagonistic effect with tobramycin. Variable effects were observed with chloramphenicol, and no effect was observed with penicillin. Results were explained on the basis of structural characteristics of the phenothiazines.
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CAS 7456-24-8 Fonazine

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