53-60-1

Basic information

• Product Name: Promazine hydrochloride
• Synonyms: 10-(3-(Dimethylamino)propyl)phenothiazine monohydrochloride;10-(3-(dimethylamino)propyl)phenothiazinemonohydrochloride;10-(3-(dimethylamino)propyl)-phenothiazinhydrochloride;10-(3-(dimethylamino)propyl)-phenothiazinmonohydrochloride;10-(gamma-Dimethylamino-n-propyl)phenothiazine hydrochloride;10-(gamma-dimethylamino-n-propyl)phenothiazinehydrochloride;10H-Phenothiazine-10-propanamine, N,N-dimethyl-, monohydrochloride;chlorowodorekpromazyny
• CAS NO: 53-60-1
• Molecular Formula: C₁₇H₂₁N₂S*Cl
• Molecular Weight: 320.88
• EINECS: 200-179-7
• Product Categories: Active Pharmaceutical Ingredients;Amines;Heterocycles;Intermediates & Fine Chemicals;Pharmaceuticals;Sulfur & Selenium Compounds;SPARINE
• Mol File: 53-60-1.mol
• Article Data: 3

Chemical Properties

• Melting Point: 174-176?C
• Boiling Point: 412.7 °C at 760 mmHg
• Flash Point: 203.4 °C
• Appearance: /
• Density: 1.1435 (rough estimate)
• Vapor Pressure: 5.08E-07mmHg at 25°C
• Refractive Index: 1.6000 (estimate)
• Storage Temp.: 2-8°C
• Solubility: Chloroform (Slightly), Methanol (Slightly), Water (Slightly)
• BRN: 3753230
• CAS DataBase Reference: Promazine hydrochloride(CAS DataBase Reference)
• NIST Chemistry Reference: Promazine hydrochloride(53-60-1)
• EPA Substance Registry System: Promazine hydrochloride(53-60-1)

Safety Data

• Hazard Codes: Xn
• Statements: 22-43
• Safety Statements: 36
• WGK Germany: 3
• RTECS: SO8575000
• Hazardous Substances Data: 53-60-1(Hazardous Substances Data)

Usage

Chemical Properties

White Solid

Uses

Different sources of media describe the Uses of 53-60-1 differently. You can refer to the following data:
1. Promazine hydrochloride has been used in conductivity and surface tension measurements and for testing inhibition of feline coronavirus (FCoV) in Felis catus whole fetus-4 (fcwf-4) cells.
2. Antipsychotic. Tranquilizer.

Definition

Isomeric with promethazine hydrochloride.

Brand name

Sparine (Baxter Healthcare); Sparine (Wyeth).

General Description

Promazine hydrochloride (PMZ) belongs to the phenothiazine drug family. Promazine is a D2 dopamine receptor antagonist and has antipsychotic and anticholinergic functionality. It is used for pain management and is also used for treating hypersensitivity reactions.

Biochem/physiol Actions

D2 dopamine receptor antagonist; phenothiazine antipsychotic.

Clinical Use

Antipsychotic for agitation and restlessness

Safety Profile

Poison by ingestion, subcutaneous, intravenous, intraperitoneal, and intramuscular routes. Human systemic effects by ingestion: general anesthesia, tremors, antipsychotic effects. An addltive permitted in food for human consumption; also permitted in the feed and drinhng water of animals and/or for the treatment of food-producing animals. When heated to decomposition it emits toxic fumes of NOx, SOx, and HCl

Drug interactions

Potentially hazardous interactions with other drugs Anaesthetics: enhanced hypotensive effect. Analgesics: increased risk of convulsions with tramadol; enhanced hypotensive and sedative effects with opioids; increased risk of ventricular arrhythmias with methadone. Anti-arrhythmics increased risk of ventricular arrhythmias with anti-arrhythmics that prolong the QT interval, e.g. procainamide, disopyramide, dronedarone and amiodarone - avoid with amiodarone and dronedarone. Antibacterials: increased risk of ventricular arrhythmias with delamanid and moxifloxacin - avoid. Antidepressants: increase concentrations and additive antimuscarinic effects, notably with tricyclics; increased risk of ventricular arrhythmias with citalopram and escitalopram - avoid; increased risk of convulsions with vortioxetine. Antiepileptics: antagonised (convulsive threshold lowered). Antimalarials: avoid with artemether/lumefantrine and piperaquine with artenimol. Antipsychotics: increased risk of ventricular arrhythmias with droperidol and pimozide - avoid; increased risk of ventricular arrhythmias with risperidone. Antivirals: concentration possibly increased with ritonavir; increased risk of ventricular arrhythmias with saquinavir - avoid. Anxiolytics and hypnotics: increased sedative effects. Atomoxetine: increased risk of ventricular arrhythmias. Beta-blockers: enhanced hypotensive effect; increased risk of ventricular arrhythmias with sotalol. Cytotoxics: increased risk of ventricular arrhythmias with arsenic trioxide. Desferrioxamine: avoid concomitant use. Diuretics: enhanced hypotensive effect. Lithium: increased risk of extrapyramidal side effects and possibly neurotoxicity. Pentamidine: increased risk of ventricular arrhythmias. Anti-arrhythmics: increased risk of ventricular arrhythmias with anti-arrhythmics that prolong the QT interval - avoid with amiodarone, disopyramide and dronedarone. Antibacterials: increased risk of ventricular arrhythmias with delamanid and moxifloxacin - avoid. Antidepressants: increased level of tricyclics (possibly increased risk of ventricular arrhythmias and antimuscarinic side effects); increased risk of ventricular arrhythmias with citalopram and escitalopram - avoid; increased risk of convulsions with vortioxetine. Anticonvulsant: antagonises anticonvulsant effect. Antimalarials: avoid with artemether/lumefantrine and piperaquine with artenimol. Antipsychotics: increased risk of ventricular arrhythmias with droperidol and pimozide - avoid; increased risk of ventricular arrhythmias with risperidone. Antivirals: concentration possibly increased with ritonavir; increased risk of ventricular arrhythmias with saquinavir - avoid. Anxiolytics and hypnotics: increased sedative effects. Atomoxetine: increased risk of ventricular arrhythmias. Beta-blockers: enhanced hypotensive effect; increased risk of ventricular arrhythmias with sotalol. Cytotoxics: increased risk of ventricular arrhythmias with arsenic trioxide. Diuretics: enhanced hypotensive effect. Lithium: increased risk of extrapyramidal side effects and possibly neurotoxicity. Pentamidine: increased risk of ventricular arrhythmias.

Metabolism

Promazine undergoes considerable first-pass metabolism in the gut wall. It is also extensively metabolised in the liver and is excreted in the urine and faeces in the form of numerous active and inactive metabolites.

InChI:InChI=1/C17H20N2S.ClH/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;1H

Upstream product

• 69-09-0 chlorpromazine hydrochloride 
• 56-81-5 glycerol 
• 67-56-1 methanol 
• 71-23-8 propan-1-ol 
• 64-17-5 ethanol 
• 67-63-0 isopropyl alcohol 
• 92-84-2 10H-phenothiazine 
• 6300-04-5 3-dimethylaminopropionic acid 

Downstream Products

• 58-40-2 promazine 
• 2095-20-7 Norpromazine 
• 146-21-4 promazine sulfoxide 

Relevant articles and documents

Systematic Study of the Effects of Experimental Parameters on the Beam-induced Dehalogenation of Chlorpromazine in Liquid Secondary Ion Mass Spectrometry

The effect of experimental parameters such as time of irradiation, analyte concentration, primary beam density, matrix selection and matrix additives on the beam-induced dehalogenation of chlorpromazine in liquid secondary ion mass spectrometry (LSIMS) was investigated.It was found that dehalogenation of chlorpromazine in glycerol increased with increasing time of irradiation, analyte concentration and primary beam density.These results were compared with those obtained using 4-chlorophenylalanine ethyl ester and the differences observed were rationalized in terms of compound surface activity.Evidence is given that matrix selection is the key experimental parameter affecting the extent of beam-induced degalogenation of chlorpromazine in LSIMS.Of the eleven matrices used, the greatest extent of degalogenation was observed in glycerol.Sulfur-containing matrices consistently exhibited a lower extent of dehalogenation than oxygen-containing aliphatic matrices, implying that sulfur is implicated in mitigating the reduction process.Dehalogenation was totally inhibited in 2-hydroxyethyl disulfide, 4-hydroxybenzenesulfonic acid and 3-nitrobenzyl alcohol.Similarly, the use of matrix additives such as 3-nitrobenzyl alcohol and trifluoroacetic acid was found to be useful in inhibiting the extent of dehalogenation occurring in glycerol.

Photodegradation of 2-chloro substituted phenothiazines in alcohols

The mechanisms that trigger the phototoxic response to 2- chlorophenothiazine derivatives are still unknown. To better understand the relationship between the molecular structure of halogenated phenothiazines and their phototoxic activity, their photophysics and photochemistry were studied in several alcohols. The photodestruction quantum yields were determined under anaerobic conditions using monochromatic light (313 nm). Absorption- and emission-spectroscopy, 1H- and 13C-NMR and GC-MS were used to characterize the photoproducts and reference compounds. An electron transfer mechanism had been previously proposed by Bunce et al. (J. Med. Chem. 22, 202-204) to explain the large difference between the photodestruction quantum yield of 2-chlorpromazine (φ = 0.46) and 2-chlorphenothiazine (φ = 0.20). According to these authors, the alkylamino chain transfers an electron to the phenothiazine moiety. Our results demonstrate that this mechanism is incorrect, because the photodestruction quantum yields of all chlorinated derivatives of this study are the same under the same conditions of solvent and irradiation wavelength. The quantum yield has no dependence on the 10-substituent, but it depends on the solvent. The percentage of each photoproduct, on the other hand, strongly depends on that substituent, but not very much on the solvent. Finally, it is demonstrated that the phototoxic effect of chlorinated phenothiazines is not related to the photodechlorination, although both processes share the same transient.