Fluphenazine

437.52

437.52

200-702-9

S79426A41Z

DTXSID2023068

C47536

Dark brown viscous oil

N - Nervous system

55.2

4.2

Solid

1.3±0.1 g/cm3

<25 °C

268-274 °C @ Press: 0.5 Torr

9℃

1.579

31.06mg/L(37 ºC)

-20°C

1.11X10-10 mm Hg at 25 deg C (est)

LD50 oral in mouse: 220mg/kg

7.9None

Henry's Law constant = 6.09X10-17 atm-cu m/mol at 25 °C (est)

7.9|pKa = 7.90

198.1 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated]

Pale yellow to yellow-orange viscous liquid or oily solid /Fluphenazine enanthate/|Characteristic odor /Fluphenazine decanoate, enanthate/|Pale yellow to yellowish orange viscous liquid; soluble in acetone, benzene /Fluphenazine decanoate/|Pale yellow to yellow-orange viscous liquid; freely soluble in alc, ether, benzene, chloroform; insoluble in water /Fluphenazine enanthate/|For more Other Experimental Properties (Complete) data for Fluphenazine (6 total), please visit the HSDB record page.

6.1

UN1230 - class 3 - PG 2 - Methanol, solution

1

11-23/24/25-39/23/24/25

16-36/37-45

TL9730000

F,T

Unstable in strong light, but stable in air at room temperature. /Fluphenazine Enanthate/

P210-P260-P280-P301 + P310-P311

H225-H301 + H311 + H331-H370

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

Fluphenazine hydrochloride oral concentrate solution should not be mixed with beverages containing caffeine (eg, coffee, cola), tannic acid (eg, tea), or pectinates (eg, apple juice), since physical incompatibility may result.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including fluphenazine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.|The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including fluphenazine decanoate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Fluphenazine decanoate/

Jann MW, Richards AL; US Pharm 10 (Jan): PH1-5, H9, H12-H13 (1985). A review of the pharmacology, pharmacokinetics, dosage and side effects of haloperidol, loxapine, thiothixene and fluphenazine is presented along with the role of clinical pharmacists in the appropriate use and selection of antipsychotics in emergency medical situations and psychiatric crises.

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P271, P280, P284, P301+P310, P302+P352, P304+P340, P305+P351+P338, P310, P320, P321, P330, P332+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 204 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Engineering controls such as exhaust ventilation are recommended.|Use a NIOSH approved respirator, if it is determined to be necessary by an industrial hygiene survey involving air monitoring. In the event that a respirator is not required, an approved dust mask should be used.

Water spray, dry chemical, carbon dioxide or foam as appropriate for surrounding fire and materials.|As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing.

Wear approved respiratory protection, chemically compatible gloves and protective clothing. Wipe up spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately labeled container for disposal. Wash spill site.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.|This material is assumed to be combustible. As with all dry powders it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity.|As a general rule, when handling USP Reference Standards avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Wash thoroughly after handling.|Use safety glasses or goggles and protect exposed skin.

May cause irritation /to the eyes, skin, and mucous membranes/. Avoid inhalation. Remove to fresh air. Avoid contact. Flush /eyes/ with copious quantities of water. Avoid /skin/ contact. Flush with copious quantities of soap and water.

Liver test abnormalities have been reported to occur in up to 40% of patients on long term therapy with phenothiazines, but elevations are uncommonly above 3 times the upper limit of normal. The aminotransferase abnormalities are usually mild, asymptomatic and transient, reversing even with continuation of medication. Several instances of clinically apparent acute liver injury have been reported due to fluphenazine, which have resembled the liver injury caused by chlorpromazine and other phenothiazines. The onset of phenothiazide-related jaundice is usually within 1 to 4 weeks, and the pattern of serum enzyme elevations is typically cholestatic or mixed. Immunoallergic features (fever, rash and eosinophilia) are present in some cases, but they are usually mild and self-limited; autoantibodies are rare. Most importantly, phenothiazide induced jaundice can be prolonged and associated with vanishing bile duct syndrome. All phenothiazine antipsychotic agents are probably capable of causing cholestatic liver injury, but the frequency of hepatotoxicity appears to be far greater with chlorpromazine than with others such as fluphenazine.

An increase in insulin dosage or decrease in chlorpromazine dosage may be necessary to maintain control of blood glucose levels in patients receiving insulin ... Other phenothiazines that may increase blood glucose levels include fluphenazine ... .|Concurrent use of imipramine and chlorpromazine may result in increased serum levels of either drug. ... Chlorpromazine inhibits the metabolism of imipramine and nortriptyline. Similar precaution should be observed when other ... phenothiazines are used concurrently ... . /Phenothiazines/|A drug interaction involving ascorbic acid and fluphenazine hydrochloride was reported in a 23 yr old male manic depressive patient. During 13 days patient received replacement ascorbic acid steady state fluphenazine hydrochloride plasma levels declined 25% from baseline. This reduction was associated with escalation of manic behavior. Mechanism by which ascorbic acid replacement lowers fluphenazine hydrochloride plasma levels might involve not only liver enzyme induction but also interactions at the absorptive phase. /Fluphenazine hydrochloride/|QT interval-prolonging medications, including cisapride, erythromycin, and quinidine /may produce/ additive QT interval prolongation increasing the risk of developing cardiac arrhythmias when /concurrently administered with phenothiazines/. /Phenothiazines/|For more Interactions (Complete) data for Fluphenazine (31 total), please visit the HSDB record page.

LD50 Rat ip 100 mg/kg|LD50 Rat sc 640 mg/kg|LD50 Mouse oral 220 mg/kg|LD50 Mouse ip 89 mg/kg|LD50 Mouse iv 51 mg/kg

Phenothiazines ... may appear in milk of nursing mothers... /phenothiazines, human, oral, im/

For management of manifestations of psychotic disorders.

Fluphenazine is a phenothiazine and antipsychotic agent which is no longer in common use. Fluphenazine can cause mild and transient serum enzyme elevations and has been linked to rare instances of clinically apparent cholestatic liver injury.

Antipsychotic Agents

Antipsychotic Agents, Phenothiazine; Dopamine Antagonists|Fluphenazine hydrochloride is indicated in the management of manifestations of psychotic disorders. /Included in US product label/|Fluphenazine hydrochloride has not been shown effective in the management of behavioral complications in patients with mental retardation. /Included in US product label/|Variability in response to antipsychotic drug treatment may be caused by variable patient compliance, interactions with other drugs, pharmacokinetic variations and variations in concentration-response relationships at the receptor level. Pharmacokinetic variations may in some cases be compensated by individual dosage adjustments based on plasma drug level measurements. The interpatient variability in response to certain time-course of drug concentrations at the receptor site could hitherto only be assessed by clinical judgement. New methods for in vivo assessment of receptor occupancy hold promise for possible measurement of parameters accounting for at least part of the interindividual variation in drug response at the receptor level. Monitoring of fluphenazine, perphenazine, thiothixene and sulpiride plasma levels by specific chemical assay methods seems to offer some guidance to individualization of drug doses. Definite therapeutic plasma level ranges have not been established for chlorpromazine and haloperidol. However, monitoring plasma levels of chlorpromazine or haloperidol might be of value when drug-induced toxicity is suspected, and as a means of controlling patient compliance.|For more Therapeutic Uses (Complete) data for Fluphenazine (6 total), please visit the HSDB record page.

/Fluphenazine/ should never be given intravenously.|... Extrapyramidal reactions ... fairly common, usually 3 types ... Parkinsonian-like syndrome ... dystonia and dyskinesia, including torticollis, tics, and other involuntary muscle movements ... akathisia, shown by restlessness ... hyperreflexia, reported in newborn ... ./Phenothiazines/|12 patients, 24-62 yr old, developed tardive dyskinesia after receiving fluphenazine from 1-2 months to 10 years. First signs of tardive dyskinesia are reversible and length of time symptoms persist prior to discontinuing is more important than age.|Inappropriate antidiuretic hormone secretion most likely related with fluphenazine enanthate therapy in schizophrenic patient 2 days following im dose of 50 mg patient was admitted to hospital. /Fluphenazine Enanthate/|For more Drug Warnings (Complete) data for Fluphenazine (47 total), please visit the HSDB record page.

Phenothiazines produce varying degrees of sedation without hypnosis or anesthesia in normal and psychotic patients; however, the drugs potentiate the CNS depressant actions of sedatives, hypnotics, and anesthetics. Tolerance to the sedative effects develops over a period of days or weeks during long-term therapy. /Phenothiazine General Statement/|In general, phenothiazines do not produce psychic dependence; however, gastritis, nausea and vomiting, dizziness, and tremulousness have been reported following abrupt cessation of high dose therapy.

Fluphenazine is a trifluoro-methyl phenothiazine derivative intended for the management of schizophrenia and other psychotic disorders. Fluphenazine has not been shown effective in the management of behaviorial complications in patients with mental retardation.

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. (See all compounds classified as Antipsychotic Agents.)|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. (See all compounds classified as Dopamine Antagonists.)

Fluphenazine hydrochloride is rapidly absorbed from the GI tract and from parenteral sites. Following oral or im administration of fluphenazine hydrochloride, the onset of action usually occurs within 1 hour; the duration of action is 6-8 hours. Following administration of a single dose of fluphenazine hydrochloride in one limited study, peak serum fluphenazine concentrations were reached within 1.5-2 or 0.5 hours following im or oral administration, respectively.|Esterification of fluphenazine slows the rate of release of the drug from fatty tissues, thus prolonging the drug's duration of action; administration of the esters in a sesame oil vehicle further delays their rate of release. Following im administration of fluphenazine decanoate in sesame oil, the onset of action occurs within 24-72 hours; the duration of action is usually 1-6 weeks, with an average of 2 weeks.|Phenothiazines are highly bound to plasma proteins.|The distribution and metabolic fate of fluphenazine have not been fully elucidated. Fluphenazine reportedly crosses the blood-brain barrier; radioactivity was present in CSF following im administration of radiolabeled fluphenazine decanoate in 2 individuals.|For more Absorption, Distribution and Excretion (Complete) data for Fluphenazine (7 total), please visit the HSDB record page.

In dogs and rhesus monkeys, the major fecal metabolite, 7-hydroxyfluphenazine, was isolated and identified by mass spectrometric and NMR measurements, involving synthetic 7- and 8-hydroxyfluphenazines. 7-hydroxyfluphenazine is present in bile of treated dogs and rhesus monkeys as glucuronide.|Degradation of piperazine ring in fluphenazine in vivo leads to formation of gamma-(phenothiazinyl-10)-propylamine and of its ring substituted analogs CF3-gamma-(phenothiazinyl-10)-propylamine and C1-gamma-(phenothiazinyl-10)-propylamine.|Fluphenazine and its principal metabolites, fluphenazine sulfoxide, 7-hydroxyfluphenazine and fluphenazine conjugates were identified in human plasma, urine and feces, following im and oral administration of 25 mg of (14)C-fluphenazine dihydrochloride to patients.|Adult and newborn rats were treated with psychotropic drugs; neuroleptics (fluphenazine, benperidol, pimozide, thiotixen), an ataractic (oxazepam) and an anti- depressant (protriptyline) for periods up to one year or longer. The body weight was monitored, and brain weight, total cerebral lipid content, content of individual phospholipids, incorporation of (32)P into individual phospholipids, and the fatty acids composition of phosphatidylethanolamine were measured. The prolonged treatment with neuroleptics and an antidepressant, but not with oxazepam, produced profound, often biphasic or multiphasic changes in the biochemistry of phospholipids. These changes should be taken into account in discussion of the mechanism of action and side-effects of prolonged treatment with antidepressants and neuroleptics.|For more Metabolism/Metabolites (Complete) data for Fluphenazine (6 total), please visit the HSDB record page.|Fluphenazine has known human metabolites that include 10-{3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl}-2-(trifluoromethyl)-10H-5'-phenothiazin-5-one.

... The mean terminal half-life of fluphenazine (+ or - SD) was 16.4 + or - 13.3 hr. ...|Plasma half-life of fluphenazine after a single dose was 14.7 hours in 1 patient given hydrochloride by mouth and 14.9 and 15.3 hours in 2 patients given hydrochloride by intramuscular injection. Half-life was 3.6 and 3.7 days in 2 patients given enanthate intramuscularly and 9.6 and 6.8 days in 2 patients given the decanoate intramuscularly.

Fluphenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.|Agranulocytosis and the release of transaminase enzymes from liver cells are known consequences of neuroleptic drug use. These effects are most common with low potency neuroleptic drugs. It has been hypothesized that these effects are due to the direct toxic action of these drugs on blood and liver cells. The purpose of this study is to compare the cytotoxic effects of eight neuroleptic drugs in five different biological test systems. In all of the test systems, thioridazine, chlorpromazine, trifluoperazine, fluphenzine and thiothixene (group one drugs) were the most toxic drugs and molindone was the least toxic. Thioridazine was between 25 and 84 times more toxic than molindone. Loxapine was significantly more toxic than molindone, but less toxic than the group one drugs. Haloperidol was intermediate in toxicity between the group one drugs and loxapine. /It was/ concluded that the difference in cytotoxicity of the neuroleptic drugs observed in these experiments accounts in part for the increase in agranulocytosis and hepatotoxicity with thioridazine and chlorpromazine and for the lower incidence of these side effects with less toxic drugs. The possibility that tardive dyskinesia may be due to the cytotoxic effects of neuroleptic drugs is discussed and an experiment to test this hypothesis is suggested.|The principal pharmacologic effects of fluphenazine are similar to those of chlorpromazine. Fluphenazine is more potent on a weight basis than chlorpromazine. Fluphenazine has weak anticholinergic and sedative effects and strong extrapyramidal effects. Fluphenazine has weak antiemetic activity.|The development of phenothiazine derivatives as psychopharmacologic agents resulted from the observation that certain phenothiazine antihistaminic compounds produced sedation. In an attempt to enhance the sedative effects of these drugs, promethazine and chlorpromazine were synthesized. Chlorpromazine is the pharmacologic prototype of the phenothiazines. The pharmacology of phenothiazines is complex, and because of their actions on the central and autonomic nervous systems, the drugs affect many different sites in the body. Although the actions of the various phenothiazines are generally similar, these drugs differ both quantitatively and qualitatively in the extent to which they produce specific pharmacologic effects. /Phenothiazine General Statement/|In the CNS, phenothiazines act principally at the subcortical levels of the reticular formation, limbic system, and hypothalamus. Phenothiazines generally do not produce substantial cortical depression; however, there is minimal information on the specific effects of phenothiazines at the cortical level. Phenothiazines also act in the basal ganglia, exhibiting extrapyramidal effects. The precise mechanism(s) of action, including antipsychotic action, of phenothiazines has not been determined, but may be principally related to antidopaminergic effects of the drugs. There is evidence to indicate that phenothiazines antagonize dopamine-mediated neurotransmission at the synapses. There is also some evidence that phenothiazines may block postsynaptic dopamine receptor sites. However, it has not been determined whether the antipsychotic effect of the drugs is causally related to their antidopaminergic effects. Phenothiazines also have peripheral and/or central antagonistic activity against alpha-adrenergic, serotonergic, histaminic (H1-receptors), and muscarinic receptors. Phenothiazines also have some adrenergic activity, since they block the reuptake of monoamines at the presynaptic neuronal membrane, which tends to enhance neurotransmission. The effects of phenothiazines on the autonomic nervous system are complex and unpredictable because the drugs exhibit varying degrees of alpha-adrenergic blocking, muscarinic blocking, and adrenergic activity. The antipsychotic activity of phenothiazines may be related to any or all of these effects, but it has been suggested that the drugs' effects on dopamine are probably most important. It has also been suggested that effects of phenothiazines on other amines (eg, gamma-aminobutyric acid [GABA]) or peptides (eg, substance P, endorphins) may contribute to their antipsychotic effect. Further study is needed to determine the role of central neuronal receptor antagonism and of effects on biochemical mediators in the antipsychotic action of the phenothiazines and other antipsychotic agents. /Phenothiazine General Statement/|For more Mechanism of Action (Complete) data for Fluphenazine (17 total), please visit the HSDB record page.

Treatment of phenothiazine overdosage generally involves symptomatic and supportive care. There is no specific antidote for phenothiazine intoxication; however, anticholinergic antiparkinsonian drugs may be useful in controlling extrapyramidal reactions associated with phenothiazine overdosage. Following acute ingestion of the drugs, the stomach should be emptied by gastric lavage and consideration also should be given to repeated doses of activated charcoal. If the patient is comatose, having seizures or a dystonic reaction, or lacks the gag reflex, gastric lavage may be performed if an endotracheal tube with cuff inflated is in place to prevent aspiration of gastric contents. Gastric lavage may be useful even several hours after the drug has been ingested, since GI motility may be greatly reduced following overdosage of phenothiazines. Induction of emesis should generally not be attempted, since a phenothiazine-induced dystonic reaction of the head or neck may result in aspiration of vomitus during emesis. Administration of a saline cathartic may be beneficial in enhancing evacuation of the drug from the GI tract, especially following ingestion of extended-release preparations (eg, Spansules). /Phenothiazine General Statement/|Cardiovascular monitoring should begin immediately and should include continuous ECG monitoring to detect possible arrhythmias. Treatment may include correction of electrolyte abnormalities and acid-base balance, lidocaine, phenytoin, isoproterenol, ventricular pacing, and defibrillation. Antiarrhythmic agents that can prolong the QT interval (eg, class IA [disopyramide, procainamide, quinidine] or III agents) should be avoided in treating overdosage-associated arrhythmias in which prolongation of QTc is a manifestation. Appropriate therapy (IV fluids and a vasopressor) should be instituted if hypotension occurs; epinephrine, bretylium, or dopamine should not be used. For the management of refractory hypotension, vasopressors such as phenylephrine, levarterenol, or metaraminol may be used. Appropriate therapy should be instituted if excessive sedation occurs; CNS stimulants that may cause seizures should be avoided. If seizures occur, treatment should not include barbiturates because these drugs may potentiate phenothiazine-induced respiratory depression. Hypothermia is common and sometimes difficult to control. In some patients with acute toxicity, exchange transfusions may be useful, but hemodialysis, forced diuresis, hemoperfusion, or manipulation of urine pH is of little value in enhancing elimination of phenothiazines. /Phenothiazine General Statement/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ The growth hormone (hGH) and prolactin (hPRL) response to insulin induced hypoglycaemia was studied in six alcoholics on two occasions before and after treatment with a single intramuscular injection of fluphenazine (Modecate). On both occasions blood samples were taken at intervals before and after the intravenous injection of soluble insulin (0.1 u/kg body weight). The patients were investigated on the first occasion, 2-7 days after cessation of drinking and they all demonstrated an adequate hGH response. They then received an injection of fluphenazine (Modecate 12.5 mg) and were reinvestigated 1 week later. The hGH response to hypoglycaemia was significantly impaired after treatment with fluphenazine. Basal hPRL concentrations were significantly increased and increased concentrations of hPRL in response to hypoglycaemia occurred after treatment. /Investigators/ conclude that a single injection of fluphenazine (Modecate 12.5 mg) has a marked effect on hypothalamic-pituitary mechanisms controlling hGH and hPRL release.|/SIGNS AND SYMPTOMS/ In general, overdosage of phenothiazines may be expected to produce effects that are extensions of common adverse reactions; severe extrapyramidal reactions, hypotension, and sedation have been the principal effects reported. CNS depression progressing to coma with areflexia or CNS stimulation with convulsions followed by respiratory depression may occur; patients with early or mild intoxication may experience drowsiness, restlessness, disorientation, confusion, and excitement. Other reported effects associated with acute phenothiazine overdosage have included shock (eg, ECG changes and cardiac arrhythmias), increased QT and PR intervals, non-specific ST and T wave changes, bradycardia, sinus tachycardia, bilateral bundle branch block, atrioventricular block, ventricular tachycardia, ventricular fibrillation, torsades de pointes, myocardial depression, agitation, dry skin, nasal congestion, urinary retention, oliguria, uremia, blurred vision, hypothermia, hyperthermia, mydriasis, miosis, tremor, muscle twitching, spasm or rigidity, seizures, muscular hypotonia, constipation, ileus, dry mouth, vomiting, difficulty in swallowing or breathing, cyanosis, and respiratory and/or vasomotor collapse, and pulmonary edema, possibly with sudden apnea. /Phenothiazine general Statement/|/SIGNS AND SYMPTOMS/ Geriatric patients with dementia-related psychosis treated with either conventional (first-generation) or atypical (second-generation) antipsychotic agents are at an increased risk of mortality.|/SIGNS AND SYMPTOMS/ Various ECG changes, including nonspecific, usually reversible, Q- and T-wave abnormalities have occurred in some patients receiving phenothiazines. ECG changes may resemble quinidine-like alterations or those induced by hypokalemia. Sudden death, apparently secondary to cardiac arrest, also has occurred. /Phenothiazine General Statement/|For more Human Toxicity Excerpts (Complete) data for Fluphenazine (17 total), please visit the HSDB record page.

Flufenazin

Fluphenazine Decanoate Preparations: (AHFS, 2010):|Fluphenazine Hydrochloride Preparations: (AHFS, 2010):|Anatensol, Dapotum, Lyogen, Moditen, Omca, Pacinol, Permitil, Prolixin, Siqualone, Tensofin, Valamina. /Fluphenazine dihydrochloride/

Thin-layer chromatographic method to identify fluphenazine, using a 2-solvent system of benzene & dioxane concentrated ammonia is presented.|Fluorometric determination of fluphenazine employing in situ photochemical oxidation.|Determination of sulfoxide in degraded phenothiazine formulations by difference spectrophotometry. /Phenothiazine formulations/|In presence of suitable oxidizing agent, phenothiazines develop characterisitic color that can be used for qualitative determination. /Phenothiazines/|TLC of basic drugs /including thioridazine/ on silica gel.

Determination of fluphenazine in human plasma by radioimmunoassay.|Determination of fluphenazine in plasma by ion-pair partition chromatography.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals