Astemizole

458.57

458.57

272-441-9

7HU6337315

759570|329963

DTXSID9020110

C28834

White crystals

R - Respiratory system

2933990090

42.3

5.8

White powder

1.2 g/cm3

149.1 °C

627.3ºC at 760 mmHg

333.2ºC

1.623

It is soluble in DMSO (25 mg/ml ), ethanol (25 mg/ml), chloroform, methanol, and water (partly miscible).

Store at +4°C

1.5X10-12 mm Hg at 25 deg C (est)

Oral-rat LD50: >2560mg/kg; Oral-Mouse LD50: 2560 mg/kg

Combustible; burning produces toxic nitrogen oxides and fluoride fumes; human side effects include: arrhythmia, coma, nausea, vomiting, drowsiness

Henry's Law constant = 1.9X10-15 atm-cu m/mol at 25 °C (est)

pKa = 8.13 (tertiary cyclohexane nitrogen) (est)

Hydroxyl radical reaction rate constant = 3.6X10-10 cu cm/molecule-sec at 25 °C (est)

UN 2811 6.1 / PGII

3

22-36/37/38

26-36

DD8968000

Xn

Ventilated, low temperature and dry; stored separately from food materials in warehouse

P305 + P351 + P338

H315-H319-H335

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Food and Drug Administration (FDA) has determined that astemizole 10-milligram (mg) tablets (Hismanal) were withdrawn from sale for safety reasons. The Agency will not accept or approve abbreviated new drug applications (ANDA's) for astemizole 10-mg tablets.|Astemizole, used as an antihistamine drug, was approved by FDA for marketing in the United States on 12/30/88.|The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed drug products, incl astemizole, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act. /From the Prescription Drug Product List/

Barnett A, Kreutner W; Pharmacology of Non-Sedating H1 Antihistamines; Agents Actions Suppl 33: 181-96 (1991). A review of the preclinical pharmacology of non-sedating H1 antihistamines includes comparative data on potency, duration of action, side effect liability, especially CNS depressant and anticholinergic activity and new approaches that may further enhance the efficacy of these newer compounds.|Estelle F et al; Pharmacokinetic Optimization of Histamine H1 Receptor Antagonist Therapy; Clin Pharmacokinet 21 (5): 372-93 (1991)

|Warning|H315 (98.06%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 103 companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

moderately toxic

LD50=2052mg/kg in mice

The effect of a standard regimen of dirithromycin, a macrolide antibiotic, on the single-dose pharmacokinetics of the H (1) receptor blocker astemizole was evaluated in a sample of 18 healthy young adults (nine males and nine females). The study was conducted in a two-way cross-over fashion after the subjects had been randomly given either dirithromycin (two 250 mg tablets) or placebo (two tablets) every morning for 10 days. On the morning of the fourth dose of either dirithromycin or placebo each subject ingested a single 30-mg oral dose (three 10-mg tablets) of astemizole. The disposition kinetics of both astemizole and its major metabolite, N-desmethylastemizole, were characterized after measuring the concentrations of both analytes in the serum fraction of serial blood samples collected for 14 days after the astemizole dose. In addition, corrected QTc intervals were estimated from electrocardiogram rhythm strips that were run 24 hours prior to the astemizole dose, 12 hours after the astemizole dose, and after the last treatment (dirithromycin or placebo) dose in both study periods. Pharmacokinetic parameters that were measured for both astemizole and N-desmethylastemizole during each treatment were: C(max), t(max), AUC (0-infinity), CL(oral), half-life, and volume of distribution (V). None of the parameters for N-desmethylastemizole was different when comparing data by ANOVA from the dirithromycin treatment period with that of the placebo treatment period. On the other hand, during dirithromycin treatment astemizole Cl(oral) was 34% slower, volume of distribution was 24% larger, and half-life was 84% longer. Generally, all QTc intervals did not appear to be affected by dirithromycin treatment. The changes in astemizole kinetics could not be attributed to its N-demethylation since the dispositional kinetics of N-desmethylastemizole were unaffected by dirithromycin. Therefore, it is difficult to ascertain the clinical significance of the changes in astemizole kinetics. Since there were no significant differences for mean QTc intervals and no effect of dirithromycin treatment on N-desmethylastemizole kinetics, it is unlikely that a standard regimen of dirithromycin would place a patient taking astemizole at an increased risk of torsade de pointes or related ventricular arrhythmias.|The effects of chemical agents on the metabolism of the antihistamine drug astemizole were investigated to evaluate drug-drug interactions. Chemical inhibitors of astemizole O-demethylation were screened using the small intestinal and liver microsomes from rabbit as an animal model for the first-pass metabolism of humans. In the rabbit small intestine, astemizole O-demethylation was clearly inhibited by ebastine, arachidonic acid, alpha-naphthoflavone, ketoconazole, tranylcypromine, troglitazone and terfenadine. In humans, these inhibitors also reduced microsomal astemizole O-demethylation in both the small intestine and liver. However, the inhibition rate of almost all these chemicals were clearly greater in the small intestine than in the liver. Thus, a different contribution of cytochrome p450 in each tissue is suggested. All the chemicals inhibited astemizole O-demethylation in recombinant CYP2J2 microsomes. The results suggest that CYP2J2 is involved in astemizole O-demethylation in both the human small intestine and liver; however, the contribution in the liver is lower than in the small intestine. The effects of the CYP2J2 inhibitors during first-pass metabolism may be more important in the small intestine than in the liver. Since all the inhibition profiles of astemizole O-demethylation were different in the liver and small intestine, involvement of another p450 in astemizole O-demethylation in human liver may be speculated. In the rabbit microsomal systems, the same metabolites found in humans were qualitatively detected and the inhibition profiles of the chemical agents in the microsomes resembled that of humans. PMID:|Concurrent use of astemizole with clarithromycin, erythromycin or troleandomycin is contraindicated; pending further evaluation, concurrent use of astemizole with other macrolide antibiotics, such as azithromycin, is not recommended.|The aim of this study was to evaluate the effects of astemizole given intraperitoneally /to mice/ singly or for 7 days on the anticonvulsant activity of antiepileptic drugs against maximal electroshock-induced convulsions in mice. The following antiepileptic drugs were administered intraperitoneally: valproate magnesium, carbamazepine, diphenylhydantoin and phenobarbital. Adverse effects were evaluated in the chimney test (motor performance) and passive avoidance task (long-term memory). Brain and plasma levels of antiepileptic drugs were measured by immunofluorescence. Astemizole (a single dose and following a 7-day treatment at 2-6 mg/kg) reduced the threshold for electroconvulsions, being without effect upon this parameter at lower doses. Astemizole (1 mg/kg) did not significantly alter the protective effect of antiepileptic drugs against maximal electroshock (after acute and 7-day administration). Also, acute astemizole (2 mg/kg) remained ineffective in this respect. Astemizole (2 mg/kg), following chronic administration, significantly reduced the protective efficacy of phenobarbital and diphenylhydantoin, reflected by an increase in their ED(50) values (50% effective dose necessary to protect 50% of animals tested against maximal electroshock) from 21.1 to 34.0 mg/kg and from 10.4 to 19.2 mg/kg, respectively. Astemizole (2 mg/kg) did not alter the protective activity of the remaining antiepileptic drugs. Moreover, astemizole (2 mg/kg) did not influence the free plasma levels and brain concentration of the studied antiepileptic drugs. Also, this H(1) receptor antagonist did not impair long-term memory or motor coordination when given acutely. However, 7-day treatment with astemizole (2 mg/kg) significantly decreased TD(50) (50% toxic dose required to induce motor impairment in 50% of animals) value of phenobarbital, being without effect on carbamazepine, valproate and diphenylhydantoin in this respect. Similarly, phenobarbital and diphenylhydantoin, administered alone at their ED(50)s against maximal electroshock, or combined with astemizole, disturbed long-term memory in mice. The results of this study indicate that astemizole may need to be used with caution in epileptic patients.|For more Interactions (Complete) data for ASTEMIZOLE (15 total), please visit the HSDB record page.

LD50 Rat oral >2560 mg/kg|LD50 Rat sc 355 mg/kg|LD50 Rat iv 28 mg/kg|LD50 Mouse oral 2560 mg/kg|For more Non-Human Toxicity Values (Complete) data for ASTEMIZOLE (6 total), please visit the HSDB record page.

The pharmacokinetics of astemizole in individuals with renal or hepatic impairment remain to be determined. Since astemizole is extensively metabolized in the liver, elimination of the drug may be impaired in patients with substantial hepatic impairment and use of the drug in such patients should be avoided.|Possible cardiotoxic effects with hepatic function impairment, history of QT interval prolongation, or with hypokalemia.

96.7%

Astemizole was indicated for use in the relieving allergy symptoms, particularly rhinitis and conjunctivitis. It has been withdrawn from the market however due to concerns of arrhythmias.

Anti-Allergic Agents; Histamine H1 Antagonists|Antihistaminic|Products containing astemizole were withdrawn from the US and Canadian markets by the manufacturer in June 1999.|Antihistamines are indicated in the prophylactic and symptomatic treatment of perennial and seasonal allergic rhinitis, vasomotor rhinitis, and allergic conjunctivitis due to inhalant allergens and foods. /Antihistamines/ NOTE: Products containing astemizole were withdrawn from the US and Canadian markets by the manufacturer in June 1999.|For more Therapeutic Uses (Complete) data for ASTEMIZOLE (7 total), please visit the HSDB record page.

Astemizole /has/ been shown to have a number of adverse effects on the electrophysiology of the heart, including altered repolarization, notched inverted T waves, prominent TU waves, prolonged QT interval, first- and second-degree AV block, ventricular tachycardia or fibrillation, and torsades de pointes.|Astemizole /has/ been recognized in rare cases to induce the syndrome of torsades de pointes, i.e. QT interval prolongation and life-threatening ventricular tachycardia. /It/ was found to prolong cardiac repolarization when its metabolic elimination was impaired, such as by liver disease or drugs that inhibit the 3A family of cytochrome P450. In vitro studies indicate that this action is due to blockade of one or more of the cardiac potassium channels that determine the duration of the action potential.|Safe use of antihistamines during pregnancy has not been established; therefore, the drugs should not be used in women who are or may become pregnant unless the potential benefits justify the possible risks to the fetus. Some manufacturers caution that antihistamines should not be used during the third trimester because of the risk of severe reactions (e.g., seizures) to the drugs in neonates and premature infants. /Antihistamines/|Patients receiving astemizole ... should be instructed to take the drug only as needed an not to exceed the prescribed dosage. The manufacturer of astemizole states that patients should be advised not to use astemizole on an as-needed ("prn") basis for immediate relief of symptoms. In addition, while a loading-dose regimen previously was recommended when an accelerated onset of effect was sought, such a regimen no longer is recommended because of the risk of cardiotoxicity.|For more Drug Warnings (Complete) data for ASTEMIZOLE (8 total), please visit the HSDB record page.

Astemizole is a second generation H₁-receptor antagonist. It does not significantly cross the blood brain barrier and therefore does not cause drowsiness or CNS depression at normal doses.

Agents that are used to treat allergic reactions. Most of these drugs act by preventing the release of inflammatory mediators or inhibiting the actions of released mediators on their target cells. (From AMA Drug Evaluations Annual, 1994, p475) (See all compounds classified as Anti-Allergic Agents.)|A class of non-sedating drugs that bind to but do not activate histamine receptors (DRUG INVERSE AGONISM), thereby blocking the actions of histamine or histamine agonists. These antihistamines represent a heterogenous group of compounds with differing chemical structures, adverse effects, distribution, and metabolism. Compared to the early (first generation) antihistamines, these non-sedating antihistamines have greater receptor specificity, lower penetration of BLOOD-BRAIN BARRIER, and are less likely to cause drowsiness or psychomotor impairment. (See all compounds classified as Histamine H1 Antagonists, Non-Sedating.)

Rapidly absorbed from the gastrointestinal tract.|Protein binding: 96%|Time to peak concentration: Within 1 hour.|It is not known whether astemizole is distributed into human breast milk. Astemizole is distributed into the milk of dogs.|Following concomitant administration of astemizole with food, oral bioavailability of the drug is decreased by 60%.

Almost completely metabolized in the liver and primarily excreted in the feces.|Orally administered astemizole is well absorbed but undergoes an extensive first-pass metabolism to O-desmethylastemizole. Desmethylastemizole is formed in the human microsomal systems of the small intestine as well as the liver, which suggests the role of cytochromes P450 (P450s) in the first-pass metabolism of astemizole. Human P450s involved in the O-demethylation of astemizole have, however, not been identified, and the involvement of twelve known drug-metabolizing P450s were denied. During the course of the P450 identification study, higher activities of the astemizole O-demethylation in the rabbit small intestine than in the liver (about 3-fold) were found. These data suggest the possible involvement of CYP2J, since P450 included in this subfamily is dominantly expressed in the small intestine of rabbits. ...|... Three metabolites of astemizole were detected in a /human/ liver microsomal system, i.e. desmethylastemizole (DES-AST), 6-hydroxyastemizole (6OH-AST) and norastemizole (NOR-AST) at the ratio of 7.4:2.8:1. Experiments with recombinant P450s and antibodies indicate a negligible role for CYP3A4 on the main metabolic route of astemizole, i.e. formation of DES-AST, although CYP3A4 may mediate the relatively minor metabolic routes to 6OH-AST and NOR-AST. Recombinant CYP2D6 catalyzed the formation of 6OH-AST and DES-AST. Studies with human liver microsomes, however, suggest a major role for a mono P450 in DES-AST formation. ...|Second-generation, relatively nonsedating histamine H1-receptor antagonists (H1-RA) are extensively used worldwide for the symptomatic treatment of allergic rhinoconjunctivitis and chronic urticaria. Information about the pharmacokinetics and pharmacodynamics of these medications, while still incomplete, is now sufficient to permit optimisation of therapy. Published pharmacokinetic and pharmacodynamic information on these H1-RA is summarised here, and areas where more data are required are delineated. Serum concentrations of most second-generation H1-RA are relatively low, and are usually measured by radioimmunoassay. After oral administration, peak concentrations are observed within 2 or 3 h. Bioavailability has not been well studied, due to the lack of intravenous formulations. Most H1-RA are metabolised in the hepatic cytochrome P450 system: terfenadine, astemizole, loratadine, azelastine, and ebastine have 1 or more active metabolites which are present in serum in higher concentrations than the respective parent compound, and therefore can be measured by high performance liquid chromatography. Cetirizine, an active metabolite of the first generation H1-receptor antagonist hydroxyzine, is not further metabolised to any great extent in vivo, and is eliminated via renal excretion. Levocabastine is also eliminated primarily by excretion. Serum elimination half-life values differ greatly from 1 H1-RA to another, and are 24 h or less for terfenadine, astemizole, loratadine, cetirizine, azelastine and ebastine, and the active metabolites of terfenadine, loratadine and ebastine. The active metabolite of azelastine (demethylazelastine) has a serum elimination half-life value of about 2 days, while that of astemizole (demethyl-astemizole) has a value of 9.5 days. From the few published studies in which the apparent volumes of distribution of the second-generation H1-RA have been calculated, it appears that tissue distribution is extensive. In children, the half-lives of H1-RA are generally shorter than are found in adults; there is no published information on the pharmacokinetics of astemizole, loratadine, azelastine, or ebastine in children. In some elderly adults, terfenadine, loratadine and cetirizine may have longer half-lives than in young healthy adults. There is little published data on the pharmacokinetics of the second-generation H1-RA in patients with impaired hepatic function. The half-life of cetirizine is prolonged in those with impaired renal function. There is a paucity of information on the pharmacokinetics of H1-RA in neonates, in pregnancy or during lactation.|The antiallergic effects of astemizole and its metabolites were studied in rats and guinea pigs. All of the metabolites of astemizole tested were more active than the parent compound in inhibiting contraction of the ileum and bronchoconstriction induced by histamine in guinea pigs. Desmethylastemizole was about the same as astemizole in inhibiting mepyramine binding in guinea pig cerebellum. In heterologous passive cutaneous anaphylaxis (PCA) and homologous PCA, the metabolites caused almost equipotent inhibition to that seen with astemizole. No H2-antagonistic activity was seen with astemizole or desmethylastemizole.|Astemizole has known human metabolites that include 2-(4-hydroxyphenyl)acetaldehyde, 6-Hydroxyastemizole, 6-desmethylastermizole, and norastemizole.

1 day|Elimination: Astemizole (plus hydroxylated metabolites) - Mutiple doses, biphasic with an initial half life of 7 to 9 days (with plasma concentrations being reduced by 75% within this phase) and a terminal half life of about 19 days.|With multiple doses: 7 to 9 days (initial); 19 days (terminal).|The active metabolite of astemizole (demethyl-astemizole) has a value of 9.5 days.

Astemizole competes with histamine for binding at H₁-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle. This reversible binding of astemizole to H₁-receptors suppresses the formation of edema, flare, and pruritus resulting from histaminic activity. As the drug does not readily cross the blood-brain barrier and preferentially binds at H1 receptors in the peripehery rather than within the brain, CNS depression is minimal. Astemizole may also act on H₃-receptors, producing adverse effects.|Antihistamines are effective therapy against histamine-mediated conditions, including seasonal and perennial allergic rhinitis and chronic urticaria. They may also have a therapeutic role to play in asthma. Until recently all antihistamines produced some degree of drowsiness, as well as having anticholinergic side effects. Several non-sedating antihistamines have now been developed. Evidence suggests that their freedom from central nervous system effects is due to their lack of penetration of the blood brain barrier. They also have no appreciable binding to cholinergic receptors. Two of these non-sedating antihistamines, terfenadine and astemizole, have novel binding characteristics with the histamine H1 receptor, exhibiting irreversible binding at higher concentrations. In humans astemizole has a remarkably long half-life of elimination, on the order of 12 to 18 days for metabolites. Clinical trials have demonstrated that these newer antihistamines are as effective as classical antihistamines and that they have no greater incidence of central nervous system or anticholinergic side effects than placebo.|QT interval prolongation and torsade de pointes are associated with astemizole intake and have been ascribed to block the repolarizing K+ currents, specifically the rapidly activating component of the delayed rectifier iKr. ... The perforated patch clamp recording technique was used to study the effects of desmethylastemizole (20 nmol/liter) on action potentials and iKr in isolated rabbit ventricular myocytes. Desmethylastemizole produced action potential prolongation and the induction of plateau early afterdepolarizations. Under voltage clamp conditions, desmethylastemizole suppressed iKr amplitude by approximately 65%. The drug E-4031 (100 nmol/liter), which selectively blocks iKr, had a similar effect on current amplitude. Desmethylastemizole, the major astemizole metabolite, blocks the repolarizing K+ current iKr with high affinity. The clinical observation of QT prolongation and torsade de pointes found with astemizole intake may principally be caused by the proarrhythmic effects of its metabolite desmethylastemizole.|Astemizole /has/ been recognized in rare cases to induce the syndrome of torsades de pointes, i.e. QT interval prolongation and life-threatening ventricular tachycardia. /It/ was found to prolong cardiac repolarization when its metabolic elimination was impaired, such as by liver disease or drugs that inhibit the 3A family of cytochrome P450. In vitro studies indicate that this action is due to blockade of one or more of the cardiac potassium channels that determine the duration of the action potential.

Treatment of astemizole-induced torsades de pointes includes discontinuing use of astemizole, intravenous administration of magnesium sulfate and isoproterenol, temporary cardiac pacing, and, when necessary, direct current cardioversion. A cardiac cause of syncope or convulsions must not be overlooked, especially in patients taking H1 antagonists because they often have these symptoms before hospitalization or detection of torsades de pointes (or both).|Children poisoned with astemizole need emergency medical evaluation, a 12-lead electrocardiogram with calculation of the corrected QT interval, and continuous cardiac monitoring for 24 hr.|Maintain an open airway and assist ventilation if necessary. Treat coma, hyperthermia, and atypical ventricular tachycardia if they occur. Monitor the patient for at least 6 to 8 hours after ingestion.There is no specific antidote for antihistamine overdose. As for anticholinergic poisoning, physostigmine has been used for treatment of severe delirium or tachycardia. However because antihistamine overdose carry a greater risk for seizures physostigmine is not recommended routinely. Sodium bicarbonate may be useful for myocardial depression and QRS interval prolongation after massive diphenhydramine overdose. Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. Because of slowed gastrointestinal motility, gut decontamination procedures may be helpful even in late-presenting patients. Hemodialysis, hemoperfusion, peritoneal dialysis, and repeat dose activated charcoal are not effective in removing antihistamines.|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/|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/

/CASE REPORTS/ A 14-year-old female who intentionally ingested 270 mg of astemizole and developed torsade de pointes, a form of polymorphic ventricular tachycardia that is associated with prolongation of the QTc interval /was reported/. She was successfully treated with magnesium sulfate infusion and had an uneventful recovery over a period of 36 hours. This case illustrates that astemizole overdose is not benign and should be considered in the differential diagnosis of ventricular tachyarrhythmias. Use of high-dose Astemizole may not be advisable for patients who are at risk for prolongation of the QTc interval.|/CASE REPORTS/ 6 cases of accidental astemizole poisoning in children have been reported to the Finnish Poison Information Center. The children were aged 1 year 7 months to 3 years 4 months and had taken doses of 2.5 to 16.7 mg/kg, at least twelve times that recommended. In 2 children the overdose was verified by measurement of drug concentrations. Despite measures to prevent drug absorption, prolonged QTc-interval, a sign of cardiac toxicity, was found in all 5 children on whom an electrocardiogram was available for analysis, and severe ventricular arrhythmias developed in 1.|/CASE REPORTS/ Five cases of astemizole (Hismanal) overdose causing prolonged corrected QT interval, ventricular dysrhythmias, and atrioventricular heart block are reported in 5 children (ages 1.5-11 yr). Cardiotoxic effects lasted an average of 2.5 days. Children poisoned with astemizole need emergency medical evaluation, a 12-lead electrocardiogram with calculation of the corrected QT interval, and continuous cardiac monitoring for 24 hr.|/CASE REPORTS/ Astemizole, a relatively new H1 blocker, has been reported to cause ventricular arrhythmias in the poisoned patient. Two cases of astemizole poisoning /were presented/, one with asystole followed by ventricular fibrillation occurring 11 hours after ingestion treated with defibrillation and one with an isolated finding of a prolonged corrected QT interval. Electrocardiogram monitoring to detect conduction defects can identify patients at risk of developing life-threatening arrhythmias.|For more Human Toxicity Excerpts (Complete) data for ASTEMIZOLE (11 total), please visit the HSDB record page.

Alermizol

Trade names: Histmanol (Janssen), Cilergil (Cilag), Almizol (Nobel).

High performance liquid chromatographic determination of astemizole in pharmaceutical dosage forms. The recovery and relative std. deviation were 100.44-102.09 and 0.4471-1.4531%.|Analyte: astemizole; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: astemizole; matrix: chemical purity; procedure: liquid chromatography with detection at 278 nm and comparison to standards|Analyte: astemizole; matrix: pharmaceutical preparation (tablet); procedure: thin-layer chromatography with comparison to standards (chemical identification)|For more Analytic Laboratory Methods (Complete) data for ASTEMIZOLE (6 total), please visit the HSDB record page.

A TLC procedure has been developed for the detn of astemizole in plasma as the free and as protein-bound substance.|Radioimmunoassay procedures for the determination of the determination of astemizole and metabolites in human human plasma.