Labetalol

Pharmaceuticals -> Used in Switzerland

Pharmaceuticals

2.7

1.89

Breast Feeding; Lactation; Milk, Human; Antihypertensive Agents; Adrenergic Beta-Antagonists; Antiarrhythmics

Pharmaceuticals

Labetalol hydrochloride tablets should be stored in well closed containers at 2-30 °C; tablets in unit dose packages should be protected from excessive moisture. Labetalol hydrochloride injection should be stored at 2-30 °C and protected from light and freezing. Labetalol hydrochloride tablets and injection have an expiration date of 3 and 2 years, respectively, after the date of manufacture. /Labetalol hydrochloride/

Labetalol hydrochloride is most stable in solutions having a pH of 2- 4. The drug is physically and chemically compatible with the following iv solutions: 5% dextrose; 0.9% sodium chloride; 2.5% dextrose and 0.45% sodium chloride; 5% dextrose and 0.2, 0.33, or 0.9% sodium chloride; 5% dextrose and lactated Ringer's or Ringer's; lactated Ringer's; or Ringer's. Following dilution of labetalol hydrochloride injection with one of these iv solutions, solutions containing 1.25-3.75 mg/ml are stable for at least 24 hrs when refrigerated or stored at room temperature. In one study, these solutions were stable for at least 72 hrs at 4 or 25 °C. Appreciable changes in pH or osmolarity of these iv solutions did not occur following admixture of labetalol hydrochloride injection. The drug is physically and/or chemically incompatible with 5% sodium bicarbonate injection; labetalol hydrochloride solutions containing 1.25-3.75 mg/ml in 5% sodium bicarbonate have a pH of 7.6-8 and form a white precipitate, probably the free base, within 6 hrs after admixture. /Labetalol hydrochloride/

7.4

9.3

pKa = 9.3

175.2 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID0044654]

176.41 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

178.1 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]

Warning

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

P203, P261, P264, P264+P265, P271, P273, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 3 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl labetalol hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act. /Labetalol hydrochloride/

Prichard BN; Beta-blocking Agents with Vasodilating Action. J Cardiovasc Pharmacol 19 (Suppl 1): S1-4 (1992). Beta-blocking agents with vasodilating action are discussed. Drugs have been developed that in addition to blocking the beta-receptor have an important peripheral vasodilator activity. Labetalol was the first drug of this group to be developed.

Donnelly R, Macphee GJ; Clinical Pharmacokinetics and Kinetic-dynamic Relationships of Dilevalol and Labetalol. Clin Pharmacokinet 21 (2): 95-109 (1991). A review comparing the availability, metabolism, pharmacokinetics, efficacy and side effects of th vasodilatory beta-blockers labetalol and its stereoisomer, dilevalol, is presented. The effects of patient age and smoking habits on the response to hypertension therapy with these 2 drugs are included.

Jackson CD, Fishbein L; A Toxicological Review of Beta-adrenergic Blockers. Fundam Appl Toxicol 6 (3): 395-422 (1986). Eighteen beta-adrenergic blockers have been reviewed and the available literature pertaining to their potential carcinogenicity, mutagenicity, and teratogenicity has been summarized and compared.

Reproduction studies in rats or rabbits using combined oral labetalol hydrochloride and hydrochlorothiazide dosages up to about 15 and 80 times the maximum recommended human dosage, respectively, have not revealed evidence of teratogenicity, although combined oral dosages 3.5 and 20 times the maximum recommended human dosage, respectively, were maternotoxic with resultant fetotoxicity in rabbits. The combination appeared to be more toxic than either drug alone in rabbits. /Labetalol hydrochloride/

When labetalol is administered with diuretics or other hypotensive drugs, the hypotensive effect may be increased. ... When beta-adrenergic blocking agents are administered with calcium-channel blocking agents, therapeutic as well as adverse effects may be additive.

Concomitant administration of iv labetalol and halothane anesthesia results in asynergistic hypotensive effect, the degree and duration of which may be controlled by adjusting the halothane concentration; however, excessive hypotension can result in a large reduction in cardiac output and an increase in central venous pressure.

Concomitant administration of oral cimetidine has been shown to substantially increase the absolute bioavailability of oral labetalol, possibly via enhanced absorption or decreased first pass hepatic metabolism of labetalol.

For more Interactions (Complete) data for LABETALOL (10 total), please visit the HSDB record page.

Labetalol therapy has been associated with mild-to-moderate elevations of serum aminotransferase levels in up to 8% of patients, a rate far higher than with other beta-blockers. These elevations, however, are usually transient, not associated with symptoms, and can resolve even with continuation of therapy. Idiosyncratic, clinically apparent liver injury from labetalol is rare, but several instances have been reported as isolated case reports as well as in case series. The liver injury typically arises after 4 to 16 weeks of therapy and the pattern of serum enzyme elevations is usually hepatocellular with an acute hepatitis-like onset and course. Immunoallergic features (rash, fever, eosinophilia) are uncommon as is autoantibody formation. While most cases resolve rapidly once labetalol is stopped, there have been several instances of acute liver failure and death or need for emergency liver transplantation associated with labetalol use, particularly if there is a delay in its discontinuation. Labetalol is the beta-blocker with the highest apparent risk for causing clinically apparent liver injury.

Overall, labetalol is usually well tolerated. Most adverse effects are typically mild and transient. As previously described above, symptomatic postural hypotension is a potential occurrence if patients are tilted or allowed to change positions from the supine or seated position to standing too quickly. This is especially important in the post-operative period (PACU or the ward) when managing a hypertensive patient with labetalol who can otherwise ambulate to the bathroom. Increased sweating, as well as flushing, have been reported with the use of labetalol. It seems the incidence of adverse reactions after administering labetalol seems to be dose-dependent.

Oral, parenteral (intravenous injection). Completely absorbed (100%) from the gastrointestinal tract with peak plasma levels occurring 1 to 2 hours after oral administration. The absolute bioavailability of labetalol is increased when administered with food.

Supportive care and close monitoring are the staples of treatment for an overdose of beta-blockers with the addition of glucagon for severe refractory hypotension and bradycardia.

Labetalol has two asymmetric centers and therefore, exists as a molecular complex of two diastereoisomeric pairs. Dilevalol, the R,R' stereoisomer, makes up 25% of racemic labetalol. Labetalol HCl combines both selective, competitive, alpha-1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta- blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively. Beta-2-agonist activity has been demonstrated in animals with minimal beta-1-agonist (ISA) activity detected. In animals, at doses greater than those required for alpha- or beta- adrenergic blockade, a membrane stabilizing effect has been demonstrated.

In several studies in patients with hypertension and elevated plasma renin activity, long term oral administration of labetalol hydrochloride (150 mg to 2.4 g daily) has been reported to suppress plasma renin activity at rest and during exercise, and in the supine and standing positions; in most of the studies, the net suppressive effect on renin was generally proportional to basal plasma renin activity. In other studies, labetalol has been reported to have an inconsistent overall effect on resting plasma renin activity, but there was considerable interindividual variation in plasma renin activity in these studies. Following acute iv administration, labetalol has been reported to produce substantial reductions in plasma angiotensin II concentration, particularly in patients with high basal values. Although labetalol has been reported to have little, if any, effect on plasma aldosterone concentration following long term oral administration in several studies, there is some evidence that the drug may decrease plasma aldosterone concentration following oral or iv administration. Labetalol has also been reported to decrease urinary aldosterone excretion following oral administration in patients with hypertension. /Labetalol hydrochloride/

Following iv administration in one preliminary study, labetalol caused a substantial increase in serum prolactin concentration which was more marked in females than in males.

The most frequent adverse cardiovascular effect of labetalol is symptomatic orthostatic hypotension, which occurs in about 1-5% or 60% of patients following oral (alone or in fixed combination with hydrochlorothiazide) or iv administration of the drug, respectively. Orthostatic hypotension has been associated with loss of consciousness occasionally following iv administration and rarely following oral administration. Symptomatic orthostatic hypotension is likely to occur if supine patients are tilted upward or allowed to assume the upright position within 3 hr following iv administration of labetalol. Moderate hypotension occurs in about 1% of patients in the supine position who are receiving the drug iv. Following oral administration, orthostatic hypotension appears to occur more frequently during initiation of therapy, in patients receiving concomitant administration of a diuretic, and in those receiving higher dosages of the drug. ... Development or exacerbation of congestive heart failure has occurred in some patients receiving labetalol, although the drug appears to be less likely to precipitate congestive heart failure than pure beta-adrenergic blocking agents. At the first sign or symptom of impending cardiac failu re during labetalol therapy, patients should receive adequate treatment (eg, cardiac glycoside, diuretic) and should be observed closely; if cardiac failure continues, labetalol should be discontinued, gradually if possible. ... Ventricular arrhythmia (including ventricular premature contractions), edema or fluid retention, bradycardia, hypotension, syncope, chest pain, atrioventricular conduction delay, and atrioventricular block have occurred during therapy with labetalol.

Adverse nervous system effects occur with variable frequency with labetalol and most of these effects appear to be dose related. At the usual labetalol hydrochloride dosage of 200-400 mg twice daily (alone or in fixed combination with hydrochlorothiazide), most adverse nervous system effects occur in 5% or less of patients. Adverse nervous system effects of the drug include drowsiness or tiredness, dizziness or lightheadedness (often posture related), headache, fatigue, lethargy, and nightmares or vivid dreams. Paresthesia, usually mild, transient tingling of the scalp or skin, may also occur following oral (alone or in fixed combination with hydrochlorothiazide) or iv administration of the drug, usually at the beginning of therapy. Hypoesthesia or numbness and circumoral paresthesia have also occurred. Mental depression, paroniria, vertigo, somnolence, yawning, tremor, asthenia, and insomnia have also been reported. Some adverse nervous system effects such as fatigue, mental depression, and sleep disorders may occur less frequently with labetalol than with pure beta-adrenergic blocking agents. Adverse nervous system effects of labetalol may be obviated by a reduction in dosage or alteration of dosage schedule.

For more Human Toxicity Excerpts (Complete) data for LABETALOL (15 total), please visit the HSDB record page.

Benchmark Dataset for the Liver Toxicity Knowledge Base (LTKB)

labetalol

Trandate®

Beta blockers

8

most-DILI-concern

No evidence of labetalol induced mutagenesis was seen with the modified Ames test or in studies in mice and rats using dominant lethal assays.

No evidence of carcinogenesis was seen in mice receiving oral labetalol hydrochloride dosages up to 200 mg/kg daily for 18 mo or in rats receiving oral dosages up to 225 mg/kg daily for up to 113 wk in females and up to 116 wks in males. /Labetalol hydrochloride/

Reproduction studies in rats and rabbits using oral labetalol hydrochloride dosages up to about 6 and 4 times the maximum recommended human dosage, respectively, have not revealed reproducible evidence of fetal malformation; however, oral dosages approximating the maximum recommended human dosage were associated with an increased incidence of fetal resorption in both species. There was no evidence of drug related fetotoxicity in rabbits receiving iv dosages of the drug up to 1.7 times the maximum recommended human dosage. In rats, oral administration of labetalol hydrochloride at dosages 2-4 times the maximum recommended human dosage during the period of late gestation through weaning was associated with decreased neonatal survival. /Labetalol hydrochloride/

Apnea and cardiovasular collapse may appear suddenly. Hence cardiac monitoring and iv lines should be established immediately. ... Dopamine and isoproterenol are the initial drugs of choice for hypotension, and atropine for bradycardia, but these agents may not be effective. Beta-blockers may saturate beta receptors, and cardioselectivity does not influence the decision about which inotropic agent to use. ... The usual measures of decontamination are emesis/lavage, activated charcoal, and cathartics for patients who present several hr after ingestion. Patients with severe overdoses may develop severe apnea and/or seizures, and this fact indicates that the use of syrup of ipecac in this setting is dangerous. Activated charcoal and/or lavage are safer procedures in severe overdoses. ... /Isoproterenol/ is a non-selective beta-adrenergic agonist in beta-blocker overdose. ... /Glucagon/ enhances cardiac contractility. /Class II beta-Blockers/

Treatment of labetalol overdosage generally involves symptomatic and supportive care. Following acute ingestion of the drug, the stomach should be emptied immediately by inducing emesis or by gastric lavage. If the patient is comatose, having seizures, 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. Administration of activated charcoal after emesis or gastric lavage may be useful in preventing absorption of labetalol, although specific data are not available. Patients should be placed in a supine position and their legs elevated if necessary to improve blood supply to the brain. For symptomatic bradycardia, atropine or epinephrine may be given. A vasopressor (eg, norepinephrine, dopamine) may be given for severe hypotension. For heart failure, a cardiac glycoside and diuretic may be used; dopamine or dobutamine may also be useful. Glucagon may also be useful for the management of myocardial depression and hypotension. A beta-adrenergic agonist and/or a theophylline derivative may be used for bronchospasm. For seizures, diazepam may be used. Labetalol is not appreciably removed (less than 1% of a dose) by hemodialysis or peritoneal dialysis.

◉ Summary of Use during Lactation

◈ What is labetalol?

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl labetalol hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act. /Labetalol hydrochloride/

C07AG01

C - Cardiovascular system

QC - Cardiovascular system

Labetalol antagonizes various adrenergic receptors to decrease blood pressure. The duration of action is long as it is generally given twice daily, and the therapeutic window is wide as patients usually take 200-400mg twice daily. Patients susceptible to bronchospasms should not use labetalol unless they are unresponsive to or intolerant of other antihypertensives.

Labetalol non-selectively antagonizes beta-adrenergic receptors, and selectively antagonizes alpha-1-adrenergic receptors. Following oral administration, labetalol has 3 times the beta-blocking ability than alpha-blocking ability. This increases to 6.9 times following intravenous administration. Antagonism of alpha-1-adrenergic receptors leads to vasodilation and decreased vascular resistance. This leads to a decrease in blood pressure that is most pronounced while standing. Antagonism of beta-1-adrenergic receptors leads to a slight decrease in heart rate. Antagonism of beta-2-adrenergic receptors leads to some of the side effects of labetalol such as bronchospasms, however this may be slightly attenuated by alpha-1-adrenergic antagonism. Labetalol leads to sustained vasodilation over the long term without a significant decrease in cardiac output or stroke volume, and a minimal decrease in heart rate.

A specific competitive antagonist at both alpha- and beta-adrenergic receptor sites.

Class II antiarrhythmic, beta-adrenoceptor-blocking agents are membrane depressant drugs that decrease the influx of sodium and calcium ions by reducing membrane bound adenylate cyclase and cAMP. The reduction in cation transport lengthens depolarization by decreasing the amplitude and slope of the transmembrane potential. Beta-adrenoceptor-blocking agents also reduce myocardial contractility by decreasing calcium release from the sarcoplasmic reticulum (the influx of calcium couples excitation and contraction by initiating the release of calcium from the sarcoplasmic reticulum). Membrane-stabilizing activity enhances the reduction in myocardial contractility in overdose with these drugs in addition to producing a quinidinelike effect of ORS widening. A direct myocardial effect also leads to myocardial depression independent of beta-adrenergic blockade and membrane stabilization. ... beta-Blockers are classified as cardioselective based on their ability to antagonize the cardiac (beta1) but not the peripheral (beta2) receptors. However, cardioselectivity is incomplete and dose dependent and disappears at high doses. /Class II beta-Blockers/

The principal physiologic action of labetalol is to competitively block adrenergic stimulation of beta-receptors within the myocardium (beta1-receptors) and within bronchial and vascular smooth muscle (beta2-receptors) and alpha1-receptors within vascular smooth muscle. In addition to inhibiting access of endogenous or exogenous catecholamines to beta-adrenergic receptors, labetalol has been shown to exhibit some intrinsic beta2-agonist activity in animals; however, the drug exerts little, if any, intrinsic beta1-agonist activity. Labetalol does not exhibit intrinsic alpha-adrenergic agonist activity. There is some evidence from animal studies suggesting that the drug may have a vasodilating effect, possibly resulting from a direct or beta2-agonist action. In animals, at doses greater than those required for alpha- or beta-adrenergic blockade, labetalol also has a membrane stabilizing effect on the heart which is similar to that of quinidine; however, this effect is unlikely to be clinically important since it occurs only at doses higher than those required for alpha- or beta-adrenergic blockade.

The hemodynamic effects of labetalol are variable following oral or iv administration. Labetalol, unlike pure beta-adrenergic blocking agents, produces a dose dependent (at usual doses) decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined alpha- and beta-adrenergic blocking activity. Labetalol effectively reduces blood pressure in the standing or supine position, but because of the drug's alpha1-adrenergic blocking activity, the effect on blood pressure is position dependent; labetalol induced decreases in blood pressure are greater in the standing than in the supine position, and orthostatic hypotension can occur. The blunting of exercise induced increases in blood pressure by oral or iv labetalol is generally greater than that produced by pure beta-adrenergic blocking agents (eg; propranolol), but the blunting of exercise induced tachycardia produced by labetalol is generally less than that produced by pure beta-adrenergic blocking agents.

The electrophysiologic effects of labetalol are variable and appear to be mediated via the drug's myocardial beta1-adrenergic blocking activity. Labetalol may decrease conduction velocity through the atrioventricular node and increase the atrial effective refractory period, but the drug appears to have inconsistent effects on sinoatrial conduction time and the atrioventricular nodal refractory period; the decrease in atrioventricular nodal conduction velocity produced by labetalol is less than that produced by pure beta-adrenergic blocking agents. In healthy individuals and in patients with cardiac disease (eg, coronary artery disease), labetalol generally has little effect on sinus rate, intraventricular conduction, the His-Purkinje system, or duration of the QRS complex. In one study in hypertensive patients, oral labetalol therapy was associated with a substantial reduction in ventricular premature contractions, and in another study in hypertensive patients, iv labetalol rapidly restored sinus rhythm in some patients with supraventricular or ventricular arrhythmias.

Labetalol has a half life of 1.7-6.1 hours.

Plasma concentrations of labetalol appear to decline in a biphasic or possibly triphasic manner. In healthy adults and adults with hypertension, the half-life in the distribution phase has been reported to average 6-44 min and the half-life in the terminal elimination phase (t1/2beta) has been reported to average 2.5-8 hr. The variability in reported mean half-lives for the drug may have resulted in part from use of a relatively insensitive spectrofluorometric assay in some studies. The manufacturers state that the drug has a plasma elimination half-life of 5.5 or 6-8 hr following iv or oral administration, respectively. The elimination half-life of the drug appears to be unchanged in individuals with renal or hepatic impairment, but may be increased in patients with severe renal impairment (eg; creatinine clearance less than 10 ml/min) undergoing dialysis and slightly increased (but within the reported range) in geriatric individuals.

The metabolism of labetalol has not been fully described in the literature but studies in sheep show an N-dealkylation to 3-amino-1-phenyl butane. This metabolite may be further metabolized to benzylacetone and 3-amino-(4-hydroxyphenyl)butane. Labetalol in humans is mainly metabolized to glucuronide metabolites such as the O-phenyl-glucuronide and the N-glucuronide.

Labetalol is extensively metabolized in the liver and possibly in the GI mucosa following oral administration, principally by conjugation with glucuronic acid. The major metabolite is the O-alkylglucuronide, with smaller amounts of the O-phenylglucuronide and N-glucuronide being formed. Following oral administration, labetalol undergoes extensive first pass metabolism in the liver and/or GI mucosa.

Primarily hepatic, undergoes significant first pass metabolism Route of Elimination: These metabolites are present in plasma and are excreted in the urine, and via the bile, into the feces. Half Life: 6-8 hours

R5H8897N95

LABETALOL

Mechanisms of Action [MoA] - Adrenergic beta-Antagonists

Established Pharmacologic Class [EPC] - beta-Adrenergic Blocker

Labetalol is a beta-Adrenergic Blocker. The mechanism of action of labetalol is as an Adrenergic beta-Antagonist.

LABETALOL

Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.

Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.

Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.

Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.

100mg and 200mg oral doses of labetalol have a Tmax of 20 minutes to 2 hours. Bioavailability may be as low as 11% or as high as 86% and may increase in older patients or when taken with food.

Radiolabelled doses of labetalol are 55-60% recovered in the urine and 12-27% recovered in the feces.

In normotensive patients, the volume of distribution is 805L. In hypertensive patients, the volume of distribution is between 188-747L with an average of 392L.

Labetalol has a plasma clearance of approximately 1500mL/min and a whole blood clearance of 1100mL/min.

Cardioselective beta-blockers /including labetalol/ tend to be hydrophilic, whereas nonselective beta blockers tend to be lipophilic. The property of lipophilicity is an essential factor for the expression of nonselectivity. Lopophilic beta-blockers generally undergo hepatic elimination and distribute well into all body compartments, including the brain. Hydrophilic beta-blockers usually are excreted unchanged by the kidney and enter deep body compartments with difficulty. /From table/

Beta-blocker drugs are rapidly absorbed, with a bioavailability varying between 30% and 90% because of the large first-pass hepatic extraction. ... Most beta-blockers ... have apparent volumes of distribution greater than 1 l/kg /Class II beta-blockers/

MEDICATION

Use (kg) in USA (2002): 1980

For the management of hypertension (alone or in combination with other classes of antihypertensive agents), as well as chronic stable angina pectoris and sympathetic overactivity syndrome associated with severe tetanus. Labetalol is used parenterally for immediate reduction in blood pressure in severe hypertension or in hypertensive crises when considered an emergency, for the control of blood pressure in patients with pheochromocytoma and pregnant women with preeclampsia, and to produce controlled hypotension during anesthesia to reduce bleeding resulting from surgical procedures.

Oral Tablets, film coated, 100 mg, Normodyne (with parabens, scored), Schering; Trandate (with parabens: scored), Allen & Hanburys; 200 mg, Normodyne (with parabens: scored), Schering; Trandate (with parabens; scored), Allen & Hanburys; 300 mg, Normodyne (with parabens), Schering; Trandate (with aprabens; scored), Allen & Hanburys. /Labetalol hydrochloride/

Parenteral Injection, for IV use, 5 mg/ml, Normodyne (with anhydrous dextrose 15 mg/ml, edetate disodium, and parabens), Schering; Trandate (with anhydrous dextrosse 45 mg ml, edetate disodium and parabens), Allen & Hanburys. /Labetalol hydrochloride/

Oral Tablets film coated, 100 mg with Hydrochlorothiazide 25 mg, Normozide 100/25 (with parabens), Schering; Trandate HCT 9 with parabens), Allen & Hanburys; 200 mg with Hydrochlorothiazide 25 mg, Normozide 200/25 (with parabens), Schering; Trandate HCT (with parabens), Allen & Hanburys; 300 mg withHydrochlorothiazide 25 mg, Normozide 300/25 (with parabens), Schering; Trandate HCT (with parabens), Allen & Hanburys. /Labetalol Hydrochloride Combinations/