Terfenadine

471.67

471.67

256-710-8

758627|665802

DTXSID2023642

C29494

White to off-white crystalline powder|Crystals from acetone

R - Respiratory system

2933399090

43.7

7.1

Solid

1.1±0.1 g/cm3

146.5-148.5 °C

626.8±55.0 °C at 760 mmHg

306.9±30.2 °C

1.580

H2O: 0.001 g/100 mL (30 ºC);chloroform: soluble 250 mg plus 5 ml of solvent, clear to very slightly hazy, colorless to faintly yellow

2-8°C

9.4X10-15 mm Hg at 25 deg C (est)

LD50 orally in mice: >2000 mg/kg (Carr, Meyer)

Henry's Law constant = 2.1X10-13 atm-cu m/mol at 25 °C (est)

pKa = 8.91 (tertiary nitrogen) (EST)

229.8 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|226.8 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|226.3 Ų [M+H]+

Hydroxyl radical reaction rate constant = 1.4X10-10 cu cm/molecule-sec at 25 °C (est)

NONH for all modes of transport

2

24/25

TM4969000

P273, P501

H413

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.

Hoechst Marion Roussel, the manufacturer of Seldane and Seldane-D announced that as of February 1, 1998, it will withdraw all single-entity (Seldane) and fixed combination (Seldane-D) preparations of terfenadine from the US market. This announcement was preceded by a declaration of the US Food and Drug administration (FDA) in January 1997 of the agency's intent to withdraw all terfenadine preparations from the US since continued marketing of terfenadine, which interacts with numerous drugs and is potentially cardiotoxic, was no longer necessary because of the availability of a single-entity preparation of fexofenadine (Allegra), the pharmacologically active metabolite of terfenadine that does not share the cardiotoxic and drug interaction potentials of the parent drug. As a result of fexofenadine availability (both as a single entity and fixed combination preparation) as alternatives, Hoechst Marion Roussel concluded that the benefits of continued availability of terfenadine preparations did not outweigh the risks.|The following drug products were withdrawn or removed from the market because such drug products or components of such drug products were found to be unsafe or not effective. The following drug products may not be compounded under the exemptions provided by section 503A(a) of the Federal Food, Drug, and Cosmetic Act: ... All drug products containing terfenadine.

H413 (97.44%): May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]|P273, and P501|Aggregated GHS information provided by 40 companies from 3 notifications to the ECHA C&L Inventory.

Mild (e.g., headache, nausea, confusion), but adverse cardiac events including cardiac arrest, ventricular arrhythmias including torsades de pointes and QT prolongation have been reported. LD50=mg/kg (orally in mice)

Prolongation of the QT interval and QT interval corrected for rate (QTc) and, rarely, serious cardiovascular effects, including arrhythmias (eg, ventricular tachycardia, atypical ventricular tachycardia (torsades de pointes)), cardiac arrest, palpitations, syncope, and death, have been reported in patients receiving recommended dosages of terfenadine concomitantly with ketoconazole. Ketoconazole can markedly inhibit the metabolism of terfenadine, probably via inhibition of the cytochrome P-450 microsomal enzyme system resulting in increased plasma concentrations of unchanged terfenadine (to measurable levels) and reduced clearance of the active carboxylic acid metabolite fexofenadine.|Erythromycin and clarithromycin may alter the metabolism of terfenadine. In some individuals, concommitant administration of erythromycin and terfenadine has resulted in increased plasma concentrations of both unchanged terfenadine and fexofenadine. ...Rarely, cardiac arrest and death have been reported in patients receiving erythromycin and terfenadine concomitantly. Therefore, terfenadine is contraindicated in patients receiving clarithromycin, erythromycin, or troleandomycin.|Some evidence indicates that mibefradil may alter the pharmacokinetics of terfenadine. Increased plasma concentrations (up to 40 ng/mL) of terfenadine were reported in a study in healthy individuals receiving 60 mg of terfenadine twice daily and mibefradil 50 or 100 mg daily. These increases of plasma unchanged terfenadine concentrations were associated with a 12% prolongation in mean QT interval corrected for rate (QTc). Since prolongation of the QTc interval may be associated with life-threatening arrhythmias and death, concomitant use of terfenadine and mibefradil is contraindicated.|In vitro, ritonavir has been shown to inhibit the metabolism of terfenadine, but the clinical importance of this in vitro finding is not known. Pending further accumulation of data, the manufacturer of terfenadine states that concomitant administration of terfenadine and human immunodeficiency virus (HIV) protease inhibitors (eg, indinavir, nelfinavir, ritonavir, saquinavir) is not recommended ... because of the theoretical risk that the HIV protease inhibitor could produce substantially increased plasma concentrations of unchanged terfenadine resulting in potentially serious and/or life-threatening adverse effects.|For more Interactions (Complete) data for TERFENADINE (13 total), please visit the HSDB record page.

LD50 Rat oral > 2000 mg/kg|LD50 Mouse oral > 2000 mg/kg|LD50 Guinea pig oral > 2000 mg/kg|LD50 Mouse oral > 5 g/kg|For more Non-Human Toxicity Values (Complete) data for TERFENADINE (6 total), please visit the HSDB record page.

70%

The excretion of terfenadine into breast milk has not been reported previously. Disposition of terfenadine was prospectively studied in four healthy lactating mothers (age, 33+/-4 years). Subjects received 60 mg terfenadine every 12 hours over a period of 48 hours to achieve steady-state milk and plasma concentrations. Milk and plasma samples were collected at 1/2, 1, 1 1/2, 2, 3, 4, 6, 8, 12, 24, and 30 hours after the last dose. Terfenadine and its active metabolite milk and plasma concentrations were quantitated by HPLC. Terfenadine was not detected in milk or plasma. Mean +/- SD active metabolite data for milk and plasma are as follows: Cmax (ng/ml), 41.0+/-16.4 for milk, 309.0+/-120.5 for plasma; tmax (hours), 4.3+/-2.4 for milk, 3.9+/-3.0 for plasma; t1/2 beta (hours), 14.2+/-5.4 for milk, 11.7+/-6.4 for plasma; AUC(0-12) (ng.hr/mL) 320.4+/-99.8 for milk, 1590.0+/-300.4 for plasma. Metabolite milk/plasma AUC(0-12) ratios ranged from 0.12 to 0.28 (mean, 0.21+/-0.07). Newborn dosage estimates based on the highest measured concentration of terfenadine metabolite in milk suggests the maximum level of newborn exposure would not exceed 0.45% of the recommended maternal weight-corrected dose. Estimated amounts consumed by the neonate after the mother is given the recommended dose of the drug are not likely to result in plasma levels producing untoward effects.

For the treatment of allergic rhinitis, hay fever, and allergic skin disorders.

Anti-Allergic Agents; Anti-Asthmatic Agents; Histamine H1 Antagonists|Antihistaminic|This study was a single center trial comparing the effects of the nonsedating antihistamine terfenadine, at a dose of 120 mg twice a day, with placebo in the treatment of rhinitis symptoms associated with the common cold. Forty-nine subjects were treated with terfenadine, 120 mg twice each day, and 48 subjects were treated with placebo twice each day for four or five days. Evaluations by both subjects and physicians suggest that terfenadine at 120 mg given twice daily marginally improved sneezing and total symptom scores at day 4. When comparing terfenadine to placebo, neither the symptoms nor signs of the common cold improved in a clinically or statistically significant manner. Terfenadine was well tolerated and had a low incidence of side effects. Terfenadine was found to be ineffective in the treatment of the signs and symptoms of the common cold.|Results of a double blind, randomized, placebo controlled, parallel study in 37 patients indicate that terfenadine, 60 mg twice a day, is significantly more effective than placebo and as effective as hydroxyzine, 25 mg four times a day in the treatment of chronic idiopathic urticaria without causing the somnolence that was associated with the use of hydroxyzine.|For more Therapeutic Uses (Complete) data for TERFENADINE (10 total), please visit the HSDB record page.

Hoechst Marion Roussel, the manufacturer of Seldane and Seldane-D announced that as of February 1, 1998, it will withdraw all single-entity (Seldane) and fixed combination (Seldane-D) preparations of terfenadine from the US market. This announcement was preceded by a declaration of the US Food and Drug administration (FDA) in January 1997 of the agency's intent to withdraw all terfenadine preparations from the US since continued marketing of terfenadine, which interacts with numerous drugs and is potentially cardiotoxic, was no longer necessary because of the availability of a single-entity preparation of fexofenadine (Allegra), the pharmacologically active metabolite of terfenadine that does not share the cardiotoxic and drug interaction potentials of the parent drug. As a result of fexofenadine availability (both as a single entity and fixed combination preparation) as alternatives, Hoechst Marion Roussel concluded that the benefits of continued availability of terfenadine preparations did not outweigh the risks.|The most frequent adverse effects reported with terfenadine are sedation (eg, drowsiness, tiredness, sleepiness, fatigue) and headache, which occur in about 5-16% of patients receiving the drug. Other less frequent adverse nervous system effects include dizziness, nervousness, and weakness. Mental depression, anxiety, malaise, agitation, euphoria, fainting sensation, floating feeling, fear of dying, tingling (eg, of the extremities), insomnia, paresthesia, tremor, decreased concentrating ability, confusion, and nightmares also have occurred. Irritability, incoordination, and vertigo have been reported rarely, and seizures and exacerbation of an underlying seizure disorder also have been reported rarely, usually in association with overdosage of the drug.|Adverse GI effects reportedly occurring in about 5-8% of patients receiving terfenadine Include abdominal distress, nausea, vomiting, and a change in bowel habits (eg, constipation, diarrhea). Increased appetite and weight gain also have been reported.|Dry mouth, nose, throat, and/or lips; cough; sore throat; and epistaxis occur in less than 5% of patients receiving terfenadine.|For more Drug Warnings (Complete) data for TERFENADINE (16 total), please visit the HSDB record page.

Terfenadine, an H1-receptor antagonist antihistamine, is similar in structure to astemizole and haloperidol, a butyrophenone antipsychotic. The active metabolite of terfenadine is fexofenadine.

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.)

On the basis of a mass balance study using 14C labeled terfenadine the oral absorption of terfenadine was estimated to be at least 70%|Although at least 70% of an oral dose of terfenadine is rapidly absorbed from the GI tract following oral administration, the drug undergoes extensive (99%) first-pass metabolism in the liver and GI tract, with minimal (10 ng/mL or less)amounts of an orally administered dose of the drug generally appearing to reach systemic circulation unchanged in healthy individuals. In some cases, increased plasma terfenadine concentrations (exceeding 10 ng/mL) following oral administration of the drug were reported in apparently healthy individuals with no identifiable risk for systemic accumulation of unchanged drug; ... Considerable interindividual variations (up to five-fold) in peak plasma concentrations have been reported with the same oral dose of terfenadine, possibly resulting from interindividual differences in first-pass metabolism and/or enterohepatic circulation of the drug.|The absolute bioavailability of oral terfenadine is not known. When administered orally, terfenadine exhibits linear pharmacokinetics up to doses of 180 mg.|Food may effect the rate slightly but does not appear to effect the extent of GI absorption of terfenadine.|Following oral administration of a single 60-mg terfenadine dose (as tablet or suspension, peak plasma concentrations of the drug occur at about 1-2 hours.|For more Absorption, Distribution and Excretion (Complete) data for TERFENADINE (17 total), please visit the HSDB record page.

Hepatic|Although the exact metabolic fate of terfenadine is not clearly established, the drug is extensively metabolized in the liver by cytochrome P-450 microsomal enzyme system including CYP3A4 and to a lesser extent in the GI mucosa by CYP3A, principally via oxidation of the terminal methyl group to fexofenadine and via N-dealkylation of the substituted butanol side chain to a piperidine carbinol derivative (alpha,alpha-diphenyl-4-piperidinemethanol). Small amounts of other hydroxylated metabolites also have been detected, but their exact structures have not been elucidated.|It has been suggested that fexofenadine, the main metabolite of terfenadine, may be responsible for the antihistaminic effect of terfenadine since only minimal amounts (10 ng/mL or less) of unchanged drug usually are detected in plasma following oral administration of terfenadine in healthy individuals. The piperidine carbinol derivative lacks both in vivo and in vitro antihistaminic activity.|Terfenadine (Seldane) undergoes extensive metabolism to form azacyclonol and terfenadine alcohol. Terfenadine alcohol is subsequently metabolized to azacyclonol and terfenadine acid. Although testosterone 6 beta-hydroxylation (CYP3A(4)) has been shown to be the principal enzyme involved in the first step in terfenadine's biotransformation (formation of azacyclonol and terfenadine alcohol), the enzymes catalyzing the subsequent metabolic steps in the conversion of terfenadine alcohol to azacyclonol and terfenadine acid have not been identified. The purpose of these studies was to determine the role of cytochrome P450 isoforms in the biotransformation of terfenadine and terfenadine alcohol. To this end, both terfenadine and its alcohol were incubated with 10 individual human liver microsomal samples that have been characterized for major isozyme activities. The metabolites and parent drugs were quantified by HPLC. The formation of azacyclonol and terfenadine alcohol from terfenadine is confirmed to be catalyzed predominantly by CYP3A(4) isozyme, and the ratio of the rate of terfenadine alcohol formation to that of azacyclonol is 3:1. Involvement of the CYP3A(4) in terfenadine metabolism was further confirmed by the following studies: a) inhibition of terfenadine alcohol formation by ketoconazole and troleandomycin, two specific inhibitors of CYP3A(4), and b) time course of terfenadine alcohol formation by cloned human CYP3A(4). When terfenadine alcohol was used as substrate, both the terfenadine acid and azacyclonol formation were also catalyzed by CYP3A(4) isozyme. However, the rate of formation of the terfenadine acid metabolite is almost 9 times faster than that of azacyclonol. The net ratio of terfenadine acid to azacyclonol is 2:1.

3.5 hours|Following multiple oral dosing of 60 mg of terfenadine twice daily, steady-state mean elimination half-lives of unchanged terfenadine and the carboxylic acid metabolite (fexofenadine) were 16.4 and 20.2 hours, respectively.|Elimination half-life: 20.3 hr

Terfenadine competes with histamine for binding at H1-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle. This reversible binding of terfenadine 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, CNS depression is minimal.|... Terfenadine appears to have a dual effect on histamine H1-receptors. In vitro studies indicate that terfenadine competitively antagonizes the actions of histamine at concentrations of 15-47 ng/mL, while a relatively irreversible antagonism occurs at higher concentrations (ie, 150-470 ng/mL). Experimental evidence indicates that the drug exhibits a specific and selective antagonism of histamine H1-receptors and that the drug slowly binds to the H1-receptor and forms a stable complex from which it subsequently slowly dissociates. These finding suggest that the prolonged and generally irreversible nature of terfenadin's antagonism of histamine results principally from the drugs slow dissociation from the H1-receptors.|Unlike many other antihistamines, terfenadine does not possess appreciable anticholinergic or antiserotonergic effects at usual antihistaminic doses in pharmacologic studies. However, in clinical trials there was no difference in the frequency of anticholinergic-like effects (eg, dryness of the nose, mouth, throat and/or lips)observed with terfenadine or other antihistamines (ie, chlopheniramine, clemastine, dexchlorpheniramine). Terfenadine also does not exhibit any appreciable alpha or beta-adrenergic blocking activity or histamine H2-receptor antagonism.|Terfenadine has increased urinary bladder capacity in individuals with normal bladder function and in some patients with neurogenic bladder and overactive detrusor muscle function, probably via a histamine H1-antagonist effect on the detrusor muscle; this effect appears to vary diurnally, being maximal at night.|The mechanism of the cardiotoxic effects of certain "nonsedating" antihistamines including terfenadine currently is not understood, and would appear to be contrary to what would be expected from studies on cardiac histamine H1-receptors; therefore, the possibility that H3-receptors (mediating a regulatory feedback mechanism) may be involved has been suggested. Limited evidence from animal models using terfenadine suggests that the cardiotoxic effects of the drug may result at least in part from blockade of the potassium channel involved in repolarization of cardiac cells (ie, blockade of the delayed rectifier potassium current IK). In some animal studies using fexofenadine, no blockade of the potassium channel involved in repolarization of cardiac cells was observed which may indicate a lack of fexofenadine-induced cardiotoxicity. In addition,in in vitro studies using fexofenadine, no effect was observed on delayed rectifier potassium channel cloned from human heart at fexofenadine concentrations up to 1.0X10-5M. Unlike with other antihistamines, anticholinergic and/or local anesthetic effects appear to be unlikely cause of the cardiac effects of certain "nonsedating" antihistamines, including terfenadine.|Basophils in mononuclear cell populations were challenged with allergens, anti-immunoglobulin E (anti-IgE), C5a or formyl-methyl-leucyl-phenylalanine (FMLP), with or without a short pre-incubation with interleukin-3 (IL-3), in the presence of increasing concentrations of terfenadine. At doses of 0.1-1 ug/mL, terfenadine inhibits histamine release and generation of the sulfidoleukotrienes, leukotriene C4, D4 and E4 in basophils challenged with an IgE-dependent trigger. At concentrations above 10 ug/mL, however, terfenadine induces the histamine release but abolishes the formation of leukotrienes, and this may be due to a cytotoxic effect. In eosinophils, by contrast, terfenadine appears to inhibit the production of leukotrienes by eosinophils, triggered by FMLP only at concentrations above 10 ug/mL (which are toxic to basophils at least). In a double-blind, placebo-controlled study, 15 allergic patients were given skin challenges with specific allergen and with histamine, before and at 3 days, 2 and 4 weeks after treatment with terfenadine (120 mg/day for 3 days). The skin reactions were evaluated visually and followed kinetically by thermography. Terfenadine caused a significant decrease in both the immediate and late-phase reactions. Late-phase reactions to histamine were shown with thermography in some of the patients tested.

Treatment of terfenadine overdosage generally involves symptomatic and supportive care. Because of the risk of adverse cardiovascular effects, ECG monitoring is recommended for at least 24 hours following acute overdosage of terfenadine or for as long as QTc is prolonged. ... Administration of activated charcoal may be useful in preventing absorption of terfenadine. Appropriate therapy should be instituted if hypotension and/or cardiac arrhythmias occur. Antiarrhythmic agents that can prolong QT interval (eg, class 1A agents) should be avoided in treating overdosage-associated arrhythmias in which prolongation of QTc interval is a manifestation. While arrhythmias may resolve spontaneously following discontinuance of terfenadine, when necessary, therapy for ventricular tachycardia with associated QT prolongation (eg, torsades de pointes) can include temporary atrial or ventricular pacing, IV magnesium sulfate, IV isoproterenol, and/or DC cardioversion (for initial management of sustained, symptomatic runs).|Limited data indicate that the carboxylic acid metabolite of terfenadine (fexofenadine) is not completely removed by hemoperfusion or hemodialysis.|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/

/HUMAN EXPOSURE STUDIES/ A possible hypersensitivity reaction, manifested as exacerbation of an existing dermatologic condition has been reported in one patient receiving terfenadine. Stevens-Johnson syndrome, which recurred on rechallenge, also has been reported in at least one patient receiving terfenadine.|/SIGNS AND SYMPTOMS/ Several cases of terfenadine overdosage have been reported to date. Signs and Symptoms following acute overdosage of the drug generally have been absent or mild (eg, headache, nausea, confusion). However potentially serious cardiac adverse effects, including arrhythmias (eg, ventricular tachycardia, atypical ventricular tachycardia (torsades de pointes)). Arrest, and prolongation of the QT interval corrected for rate (QTc), occasionally have been reported in patients receiving terfenadine doses of 306 mg or more; such cardiotoxic effects are even more likely at doses exceeding 600 mg. In addition, prolongation of in the QTc interval of up to 30% have been reported in patients receiving terfenadine dosages of 300 mg twice daily; such prolongations also have been reported in patients receiving lower dosages of the drug. Seizures and syncope also have been associated with terfenadine overdosages.|/CASE REPORTS/ One patient (a 16 year old female) who intentionally ingested 1.5 g of terfenadine and underwent gastric lavage 1 hour after ingestion had a complete and uneventful recovery except for a decrease in blood pressure from 110/60 to 90/50 mm Hg 3 hours after ingestion.|/CASE REPORTS/ ...Atypical ventricular tachycardia (torsades de pointes) developed 15 hr after acute ingestion of about 3.4 g of terfenadine, 7 g of cephalexin, and 1.2 g of ibuprofen; the arrhythmia progressed to ventricular fibrillation which was responsive to cardiovesion and lidocain. Two tonic-clonic seizures reportedly occurred prior to admission and quinidine-like cardio-toxic effects, including QT-interval prolongation and widened, notched T waves were noted following admission in a patient who ingested an unknown quantity of terfenadine; plasma concentrations of unchanged drug and its carboxylic acid metabolite (fexofenadine) in this patient were 43 and 1504 ng/mL, respectively, upon admission and 26.5 and 389 ng/mL, respectively, 9 hours after admission. Although not clearly established, it was suggested that the seizures observed in this patient may have resulted from terfenadine-induced cardiotoxicity.|For more Human Toxicity Excerpts (Complete) data for TERFENADINE (10 total), please visit the HSDB record page.

alpha-(4-(1,1-Dimethylethyl)phenyl)-4-(hydroxydiphenylmethyl)-1-piperdinebutanol

Oral tablets, 60 mg, Seldane, Hoechst Marion Roussel.|Oral tablets extended-release core (pseudoephedrine hydrochloride only), 60 mg with Pseudoephedrine Hydrochloride 120 mg, Seldane-D, Hoechst Marion Roussel. /Terfenadine Combinations/|Trade name: Teldane (Hoechst Marion Roussel)

Withdrawn from US market, January, 1997.

Toxicological screening of drugs by microbore high-performance liquid chromatography with photodiode-array detection and ultraviolet spectral library searches.|Reversed-phase high-performance liquid chromatographic analysis of terfenadine at a wavelength of 254 nm. The concn range 0.1-0.8 mg/ml. The relative std deviation was 0.47% and the recovery was 100.4-104.44%.|Analyte: terfenadine; matrix: blood (plasma); procedure: high-performance liquid chromatography with mass spectrometry detection; limit of quantitation: 200 pg/mL|Analyte: terfenadine; matrix: blood (plasma); procedure: high-performance liquid chromatography with mass spectrometry detection; limit of quantitation: 100 pg/mL|For more Analytic Laboratory Methods (Complete) data for TERFENADINE (6 total), please visit the HSDB record page.

Determination of the metabolites of terfenadine in human urine by thermospray liquid chromatography-mass spectrometry.|Determination of terfenadine and terfenadine acid metabolite in plasma using solid-phase extraction and high-performance liquid chromatography with fluorescence detection. For terfenadine, the validated quantitation range of this method is 10.0-84.2 ng/ml with relative standard deviation of 5.7-30%. For terfenadine acid metabolite, the relative standard deviation of 4.1-24%.

Pharmaceuticals