Promazine (brand name Sparine among others), is used as a short-term add-on treatment for psychomotor agitation. Its approved uses in people is limited, but is used as a tranquilizer in veterinary medicine. It has weak antipsychotic effects but is generally not used to treat psychoses.
It acts similar to chlorpromazine and causes sedation. It has predominantly anticholinergic side effects, though extrapyramidal side effects are not uncommon. It belongs to the typical antipsychotic and phenothiazine class of drugs.
Promazine was approved for medical use in the United States in the 1950s, although it is no longer commercially available there. |
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InChI=1S/C17H20N2S/c1-18(2)12-7-13-19-14-8-3-5-10-16(14)20-17-11-6-4-9-15(17)19/h3-6,8-11H,7,12-13H2,1-2H3 |
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Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
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dopaminergic antagonist
A drug that binds to but does not activate dopamine receptors, thereby blocking the actions of dopamine or exogenous agonists.
H1-receptor antagonist
H1-receptor antagonists are the drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine.
muscarinic antagonist
A drug that binds to but does not activate muscarinic cholinergic receptors, thereby blocking the actions of endogenous acetylcholine or exogenous agonists.
serotonergic antagonist
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or serotonergic agonists.
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
Any EC 3.4.21.* (serine endopeptidase) inhibitor that interferes with the action of prolyl oligopeptidase (EC 3.4.21.26).
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dopaminergic antagonist
A drug that binds to but does not activate dopamine receptors, thereby blocking the actions of dopamine or exogenous agonists.
H1-receptor antagonist
H1-receptor antagonists are the drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine.
muscarinic antagonist
A drug that binds to but does not activate muscarinic cholinergic receptors, thereby blocking the actions of endogenous acetylcholine or exogenous agonists.
serotonergic antagonist
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or serotonergic agonists.
phenothiazine antipsychotic drug
antiemetic
A drug used to prevent nausea or vomiting. An antiemetic may act by a wide range of mechanisms: it might affect the medullary control centres (the vomiting centre and the chemoreceptive trigger zone) or affect the peripheral receptors.
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View more via ChEBI Ontology
N,N-dimethyl-3-(10H-phenothiazin-10-yl)propan-1-amine
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promazina
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ChemIDplus
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promazine
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ChEBI
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promazinum
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ChemIDplus
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10-(3-(Dimethylamino)propyl)phenothiazine
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ChemIDplus
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N-(3-Dimethylaminopropyl)phenothiazine
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ChemIDplus
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N-Dimethylamino-1-methylethyl thiodiphenylamine
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ChemIDplus
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Promazine
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KEGG COMPOUND
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244925
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Reaxys Registry Number
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Reaxys
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58-40-2
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CAS Registry Number
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ChemIDplus
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Peltonen I, Männistö PT (2011) Effects of diverse psychopharmacological substances on the activity of brain prolyl oligopeptidase. Basic & clinical pharmacology & toxicology 108, 46-54 [PubMed:20825390] [show Abstract] Prolyl oligopeptidase (POP) has been connected to learning, memory and mood. Changes in serum or plasma POP activity have been linked to psychiatric disorders. POP has been thought to interfere in these conditions by cleaving neuroactive peptides or via the phosphatidylinositol second messenger system. However, little is known about the possible POP inhibition of commonly used psychoactive drugs. In this study, we measured the effects of various psychotropic drugs, including antidepressants, antipsychotics, mood stabilisers and anxiolytics, on the activity of the rat brain homogenate POP. Of the 38 compounds tested, 18 inhibited POP by at least 20% at 10 μM (buspirone, chlorpromazine, citalopram, clozapine, desipramine, duloxetine, escitalopram, flupenthixol, imipramine, ketanserin, lamotrigine, levomepromazine, prazosin, prochlorperazine, promazine, risperidone ritanserin and thioridazine). Thioridazine and valproate (VPA) acted at therapeutic plasma levels. Kinetically, VPA was a competitive inhibitor, thioridazine a non-competitive inhibitor and ketanserin a mixed type inhibitor. Being lipophilic, many of the psychoactive compounds are present in the brain at several-times higher concentrations than in plasma. At concentrations reported to be reached in the brain, chlorpromazine, clozapine, desipramine, imipramine, prochlorperazine and promazine inhibited POP by 30-50% suggesting that they could inhibit POP in vivo. However, when studied ex vivo, a single dose of 10 mg/kg thioridazine caused a deep sedation in the mice but did not inhibit the activity of POP. In conclusion, compared with conventional POP inhibitors, all psychopharmacological compounds tested are very weak inhibitors in vitro, and we doubt that their POP inhibition would be therapeutically meaningful. | Rossi R, De Giorgio F, Benucci G, Oliva A, Fucci N (2009) Acute intoxication by triazolam and promazine: a case report. Medicine, science, and the law 49, 65-68 [PubMed:19306624] [show Abstract] A fatality due to ingestion of triazolam and promazine is reported. Triazolam is a benzodiazepine widely prescribed as a hypnotic drug for the treatment of sleep disorders. Promazine is a neuroleptic drug. There is no previous evidence in the literature of death due to an overdose related to the contemporaneous intake of these two drugs. In this report the authors present the case of a 76-year-old woman who was found deceased at home with no evidence of trauma or asphyxia; near the body several empty pharmaceutical boxes containing triazolam and promazine were noticed. Toxicological analyses were performed and drug levels measured by means of gas chromatography coupled with mass spectrometry. The triazolam concentration in each specimen was as follows: blood 1100ng/ml; gastric content 1300ng/ml; the promazine concentration in blood and in gastric content was 3450ng/ml and 5800ng/ ml respectively. Based on the autopsy findings, patient history and toxicological results, the cause of death was determined to be acute intoxication due to the effect of triazolam and promazine and the manner of suicide. | Barnard DL, Day CW, Bailey K, Heiner M, Montgomery R, Lauridsen L, Jung KH, Li JK, Chan PK, Sidwell RW (2008) Is the anti-psychotic, 10-(3-(dimethylamino)propyl)phenothiazine (promazine), a potential drug with which to treat SARS infections? Lack of efficacy of promazine on SARS-CoV replication in a mouse model. Antiviral research 79, 105-113 [PubMed:18423639] [show Abstract] Phenothiazine and derivatives were tested for inhibition of SARS-CoV replication. Phenothiazine slightly inhibited SARS-CoV replication in a neutral red (NR) uptake assay. Adding a propylamino group to give promazine reduced virus yields (VYR assay) with an EC(90)=8.3+/-2.8 microM, but without selectivity. Various substitutions in the basic phenothiazine structure did not promote efficacy. Phenazine ethosulfate was the most potent compound by VYR assay (EC(90)=6.1+/-4.3 microM). All compounds were toxic (IC(50)=6.6-74.5 microM) except for phenoxathiin (IC(50)=858+/-208 microM) and 10-(alpha-diethylamino-propionyl) phenothiazine.HCl (IC(50)=195+/-71.2 microM). Consequently, none were selective inhibitors of SARS-CoV replication (SI values <1-3.3 microM). These data portended the poor efficacy of promazine in a SARS-CoV mouse lung replication model. Intraperitoneal treatment with promazine using a prophylactic (-4h)/therapeutic regimen of 1, 10, or 50mg/(kg day) did not reduce virus lung titers at day 3, yet prolonged virus replication to 14 days. Similar therapeutic promazine doses were not efficacious. Thus, promazine did not affect SARS-CoV replication in vitro or in vivo, nor were any other phenothiazines efficacious in reducing virus replication. Therefore, treating SARS infections with compounds like promazine is not warranted. | Varga JM, Kalchschmid G, Klein GF, Fritsch P (1991) Mechanism of allergic cross-reactions--I. Multispecific binding of ligands to a mouse monoclonal anti-DNP IgE antibody. Molecular immunology 28, 641-654 [PubMed:1650428] [show Abstract] A recently developed solid-phase binding assay was used to investigate the specificity of ligand binding to a mouse monoclonal anti-dinitrophenyl IgE [IgE(aDNP)]. All DNP-amino acids, that were tested, inhibited the binding of radio-labeled IgE(aDNP) to DNP covalently attached to polystyrene microtiter plates; however, the concentration for 50% inhibition varied within four orders of magnitude, DNP-L-serine being the most, DNP-proline the least potent inhibitor. In addition to DNP analogues a large number (2074) of drugs and other compounds were tested for their ability to compete with DNP for the binding site of IgE(aDNP). At the concentrations used for screening 59% of the compounds had no significant inhibition; 19% inhibited the binding of IgE(aDNP) more than 50%. Several families of compounds (tetracyclines, polymyxines, phenotiazines, salicylates and quinones) of effective competitors were found. Within these families change in the functional groups attached to the "family stem" had major effects on the affinity of ligand binding. The occurrence frequencies of interactions of ligands with IgE(aDNP) is in good agreement with a semi-empirical model for multispecific antibody-ligand interactions. |
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