Promazine

< 25 °C

< 25 °C

Promazine HCl is maximally stable at pH 6.5 /Promazine HCl/

OXIDIZES UPON PROLONGED EXPOSURE TO AIR & ACQUIRES BLUE OR PINK COLOR /HYDROCHLORIDE/

RABBIT, RAT, & SHEEP TRIALS INDICATE IT MAY HELP REDUCE TOXIC EFFECTS OF CARBON TETRACHLORIDE. ... HAS INCR TOXICITY OF ORGANOPHOSPHORUS OR OTHER ACETYLCHOLINESTERASE INHIBITORS & PROCAINE.

...PHENOTHIAZINES...MAY PRODUCE ADDITIVE HYPOTENSIVE EFFECTS WITH PROPRANOLOL. /PHENOTHIAZINES/

...OTHER ANTIPSYCHOTIC DRUGS ... MAY BLOCK ANTIHYPERTENSIVE EFFECTS OF GUANETHIDINE ... /PHENOTHIAZINES/

Additive QT interval prolongation may increase the risk of ventricular tachycardia when /probucol is used with phenothiazines/. /Phenothiazines/

For more Interactions (Complete) data for PROMAZINE (31 total), please visit the HSDB record page.

It has predominantly anticholinergic side effects, though extrapyramidal side effects are not uncommon either. Other effects include endocrine effects (such as gynaecomastia and menstrual disturbance), sensitivity to sunlight and haemolytic anaemia (A308, L1149).

Promazine is an antagonist at types 1, 2, and 4 dopamine receptors, 5-HT receptor types 2A and 2C, muscarinic receptors 1 through 5, alpha(1)-receptors, and histamine H1-receptors. Promazine's antipsychotic effect is due to antagonism at dopamine and serotonin type 2 receptors, with greater activity at serotonin 5-HT2 receptors than at dopamine type-2 receptors. This may explain the lack of extrapyramidal effects. Promazine does not appear to block dopamine within the tubero-infundibular tract, explaining the lower incidence of hyperprolactinemia than with typical antipsychotic agents or risperidone. Antagonism at muscarinic receptors, H1-receptors, and alpha(1)-receptors also occurs with promazine.

HIGH DOSES...FOR PROLONGED PERIODS...STAR-SHAPED OPACITIES...IN ANTERIOR PORTION OF LENS...VISUAL IMPAIRMENT...EPITHELIAL KERATOPATHY, LACRIMATION...PIGMENTARY RETINOPATHY /CHRONIC TOXICITY, HYDROCHLORIDE/

LONG-TERM ADMIN OF HIGH DOSES...MAY RESULT IN PIGMENT DEPOSITIONS IN...BODY TISSUES...BRAIN, HEART, LIVER, KIDNEYS, RETINA..CORNEA /& SKIN, USUALLY YELLOWISH-BROWN BUT MAY BECOME GREYISH-PURPLE/. OCULAR CHANGES...DEPOSITION OF FINE PARTICULATE MATTER IN LENS & CORNEA /CHRONIC TOXICITY, HYDROCHLORIDE/

Sudden and unexpected deaths have occurred in patients receiving phenothiazines, especially during long-term administration of the drugs. In some patients, sudden death appeared to result from asphyxia (secondary to failure of the cough reflex) or cardiac arrest. /Phenothiazines/

In general, overdosage of phenothiazines may be expected to produce effects that are extensions of common adverse effects; severe extrapyramidal reactions, hypotension, and sedation have been the principal effects reported. CNS depression progressing to coma with areflexia may occur; patients with early or mild intoxication may experience restlessness, confusion, and excitement. Other reported effects associated with acute phenothiazine overdosage have included tachycardia, ECG changes and cardiac arrhythmias, hypothermia, miosis, tremor, muscle twitching, spasm or rigidity, seizures, muscular hypotonia, ileus, dry mouth, difficulty in swallowing or breathing, cyanosis, and respiratory and/or vasomotor collapse, possibly with sudden apnea. /Phenothiazines/

...CERTAIN DEGREE OF BOTH LEUKOPENIA & LYMPHOCYTOSIS WAS REPORTED... SYMPTOMS OF OVERDOSAGE ARE DROP IN BLOOD PRESSURE, RESPIRATORY DEPRESSION & CIRCULATORY COLLAPSE.

HAS PRODUCED MARKED ARRHYTHMIAS IN BOTH ANESTHETIZED & ACTIVE UNANESTHETIZED DOGS.

PROMAZINE, PHENOTHIAZINE DERIVATIVE TRANQUILIZER HAS PRODUCED REVERSIBLE OPACITY OF FRONT OF LENS IN MICE...BUT NO RELATED EFFECT HAS BEEN NOTED IN HUMAN BEINGS.

PROMAZINE WAS TESTED FOR ABILITY TO INDUCE SISTER-CHROMATID EXCHANGES WITH & WITHOUT PHOTOACTIVATION BY VISIBLE LIGHT IN CHINESE HAMSTER CELL LINE V79 CLONES. IN THE DARK IT INCREASED THE FREQUENCY OF SISTER-CHROMATID EXCHANGES.

NONE OF PHENOTHIAZINES WAS MUTAGENIC IN DARK. MUTAGENICITY WAS OBSERVED ONLY IN STRAINS OF SALMONELLA TYPHIMURIUM THAT LACKED EXCISION REPAIR OF DNA & MUTAGENICITY WAS ELEVATED IN STRAINS WITH PLASMID PKM101.

EXTRAPYRAMIDAL SYMPTOMS...RELIEVED WITH BARBITURATES, METHYLPHENIDATE HYDROCHLORIDE...ANTI-PARKINSON DRUGS...BENZTROPINE MESYLATE...TRIHEXYPHENIDYL HYDROCHLORIDE...DIPHENHYDRAMINE HYDROCHLORIDE...IN SEVERE CASES, SUPPORTIVE THERAPY...MAINTAINING CLEAR AIRWAY & ADEQUATE HYDRATION. /HYDROCHLORIDE/

Hepatic, primarily to N-desmethylpromazine and promazine sulfoxide.

YIELDS DEMETHYLPROMAZINE, PROMAZINE-N-OXIDE, & PROMAZINE SULFOXIDE IN MAN & IN RAT; YIELDS 3-HYDROXYPROMAZINE & PHENOTHIAZINE IN MAN. /FROM TABLE/

...METAB...BY OXIDATIVE PROCESSES MEDIATED LARGELY BY HEPATIC MICROSOMAL & OTHER DRUG-METABOLIZING ENZYMES. CONJUGATION WITH GLUCURONIC ACID...PROMINENT ROUTE.../PRC: REACTIONS INCL HYDROXYLATION, DEMETHYLATION, SULFOXIDE FORMATION; METABOLIC ALTERATIONS IN SIDE CHAIN MAY ALSO OCCUR/. /PHENOTHIAZINES/

Promazine has known human metabolites that include N-Desmethyl promazine and Promazine 5-sulfoxide.

Hepatic, primarily to N-desmethylpromazine and promazine sulfoxide. Absorption may be erratic and peak plasma concentrations show large interindividual differences. The metabolism occurs through oxidative processes mediated largely by hepatic microsomal and other drug metabolizing enzymes. Antoher step is the conjugaion with glucuronic acid. Other reactions include hydroxylation, demetylation, and sulfoxide formation. Moreover, metabolic alterations in side chain may also occur (A308, A631).

Drugs used to prevent NAUSEA or VOMITING.

Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.

Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.

Absorption may be erratic and peak plasma concentrations show large interindividual differences.

IV ADMIN RESULTS PEAK IN ABOUT 5 MIN, IM IN ABOUT 20-30 MIN, ORAL IN ABOUT 1-2 HR. PARENTERAL EFFECTS ARE MORE PREDICTABLE, & USUALLY REQUIRE ABOUT HALF ORAL DOSAGE FOR SOME COMPARABLE EFFECTS.