Propranolol Hydrochloride (Propranolol Hydrochloride)

Trade Name : Propranolol Hydrochloride

West Ward Pharmaceuticals Corp.

SOLUTION

Strength 20 mg/5mL

PROPRANOLOL HYDROCHLORIDE Adrenergic beta-Antagonists [MoA],beta-Adrenergic Blocker [EPC]

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We deliver your medicines through a validated cold chain shipment process. This process is used as these medicines need to manufactured, transported and stored at very specific temperatures, utilizing thermal and refrigerated packaging methods.

We deliver your medicines through a validated cold chain shipment process. This process is used as these medicines need to manufactured, transported and stored at very specific temperatures, utilizing thermal and refrigerated packaging methods.

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  • No data
  • No data
  • Propranolol Hydrochloride is a synthetic beta-adrenergic receptor blocking agent chemically described as 2-Propanol, 1-[(1-methylethyl)amino]-3-(1-naphthalenyloxy)-, hydrochloride,(u00b1)-. Its molecular and structural formula:
  • CHNO u2022 HCl
  • Propranolol Hydrochloride USP is a stable, odorless, white to off-white crystalline powder which is readily soluble in water and ethanol. Its molecular weight is 295.81.
  • Each 5 mL of Oral Solution for oral administration contains:
  • Alcoholu2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u2026u20260.6%.
  • Inactive Ingredients
  • Propranolol Hydrochloride Oral Solution is available for oral administration containing either 20 mg per 5 mL or 40 mg per 5 mL of propranolol hydrochloride USP. The oral solution contains the following inactive ingredients: citric acid anhydrous, cru00e8me de menthe flavor, disodium edetate, methyl paraben, propylene glycol, propylparaben, purified water, saccharin sodium, sorbitol solution and strawberry flavor.
  • General
  • Propranolol is a nonselective beta-adrenergic receptor blocking agent possessing no other autonomic nervous system activity. It specifically competes with beta-adrenergic receptor agonist agents for available receptor sites. When access to beta-receptor sites is blocked by propranolol, the chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation are decreased proportionately. At dosages greater than required for beta-blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain.
  • Mechanism of Action
  • The mechanism of the antihypertensive effect of propranolol has not been established. Factors that may contribute to the antihypertensive action include: (1) decreased cardiac output, (2) inhibition of renin release by the kidneys, and (3) diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain. Although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol. Effects of propranolol on plasma volume appear to be minor and somewhat variable.
  • In angina pectoris, propranolol generally reduces the oxygen requirement of the heart at any given level of effort by blocking the catecholamine-induced increases in the heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. Propranolol may increase oxygen requirements by increasing left ventricular fiber length, end diastolic pressure, and systolic ejection period. The net physiologic effect of beta-adrenergic blockade is usually advantageous and is manifested during exercise by delayed onset of pain and increased work capacity.
  • Propranolol exerts its antiarrhythmic effects in concentrations associated with beta-adrenergic blockade, and this appears to be its principal antiarrhythmic mechanism of action. In dosages greater than required for beta-blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain.
  • The mechanism of the antimigraine effect of propranolol has not been established. Beta-adrenergic receptors have been demonstrated in the pial vessels of the brain.
  • The specific mechanism of propranololu2019s antitremor effects has not been established, but beta-2 (noncardiac) receptors may be involved. A central effect is also possible. Clinical studies have demonstrated that propranolol is of benefit in exaggerated physiological and essential (familial) tremor.
  • Absorption
  • Propranolol is highly lipophilic and almost completely absorbed after oral administration. However, it undergoes high first-pass metabolism by the liver and on average, only about 25% of propranolol reaches the systemic circulation. Peak plasma concentrations occur about 1 to 4 hours after an oral dose.
  • Administration of protein-rich foods increase the bioavailability of propranolol by about 50% with no change in time to peak concentration, plasma binding, half-life, or the amount of unchanged drug in the urine.
  • Distribution
  • Approximately 90% of circulating propranolol is bound to plasma proteins (albumin and alpha acid glycoprotein). The binding is enantiomer-selective. The S(-)-enantiomer is preferentially bound to alpha glycoprotein and the R(+)- enantiomer preferentially bound to albumin. The volume of distribution of propranolol is approximately 4 liters/kg.
  • Propranolol crosses the blood-brain barrier and the placenta, and is distributed into breast milk.
  • Metabolism and Elimination
  • Propranolol is extensively metabolized with most metabolites appearing in the urine. Propranolol is metabolized through three primary routes: aromatic hydroxylation (mainly 4-hydroxylation), N-dealkylation followed by further side-chain oxidation, and direct glucuronidation. It has been estimated that the percentage contributions of these routes to total metabolism are 42%, 41% and 17%, respectively, but with considerable variability between individuals. The four major metabolites are propranolol glucuronide, naphthyloxylactic acid and glucuronic acid, and sulfate conjugates of 4-hydroxy propranolol.
  • In vitro
  • Propranolol is also a substrate of CYP2C19 and a substrate for the intestinal efflux transporter, p-glycoprotein (p-gp). Studies suggest however that p-gp is not dose-limiting for intestinal absorption of propranolol in the usual therapeutic dose range.
  • In healthy subjects, no difference was observed between CYP2D6 extensive metabolizers (EMs) and poor metabolizers (PMs) with respect to oral clearance or elimination half-life. Partial clearance of 4-hydroxy propranolol was significantly higher and of naphthyloxyactic acid significantly lower in EMs than PMs.
  • The plasma half-life of propranolol is from 3 to 6 hours.
  • Enantiomers
  • Propranolol is a racemic mixture of two enantiomers, R(+) and S(-). The S(-)-enantiomer is approximately 100 times as potent as the R(+)-enantiomer in blocking beta-adrenergic receptors. In normal subjects receiving oral doses of racemic propranolol, S(-)-enantiomer concentrations exceeded those of the R(+)-enantiomer by 40 to 90% as a result of stereoselective hepatic metabolism. Clearance of the pharmacologically active S(-)-propranolol is lower than R(+)- propranolol after intravenous and oral doses.
  • Special Populations
  • Geriatric
  • Clearance of propranolol is reduced with aging due to decline in oxidation capacity (ring oxidation and side-chain oxidation). Conjugation capacity remains unchanged. In a study of 32 patients age 30 to 84 years given a single 20-mg dose of propranolol, an inverse correlation was found between age and the partial metabolic clearances to 4-hydroxypropranolol (40HP-ring oxidation) and to naphthoxylactic acid (NLA-side chain oxidation). No correlation was found between age and the partial metabolic clearance to propranolol glucuronide (PPLG-conjugation).
  • Gender
  • Race
  • Chinese subjects had a greater proportion (18% to 45% higher) of unbound propranolol in plasma compared to Caucasians, which was associated with a lower plasma concentration of alpha acid glycoprotein.
  • Renal Insufficiency:
  • Studies have reported a delayed absorption rate and a reduced half-life of propranolol in patients with renal failure of varying severity. Despite this shorter plasma half-life, propranolol peak plasma levels were 3 to 4 times higher and total plasma levels of metabolites were up to 3 times higher in these patients than in subjects with normal renal function.
  • Chronic renal failure has been associated with a decrease in drug metabolism via down regulation of hepatic cytochrome P450 activity resulting in a lower u201cfirst-passu201d clearance.
  • Propranolol is not significantly dialyzable.
  • Hepatic Insufficiency:
  • Drug Interactions
  • Interactions with Substrates, Inhibitors or Inducers of Cytochrome P-450 Enzymes:
  • Substrates or Inhibitors of CYP2D6:
  • Substrates or Inhibitors of CYP1A2:
  • Substrates or Inhibitors of CYP2C19:
  • Inducers of Hepatic Drug Metabolism:
  • Cardiovascular Drugs: n- Antiarrhythmics:n- Array
  • The metabolism of propranolol is reduced by co-administration of quinidine, leading to a two to three fold increased blood concentration and greater degrees of clinical beta-blockade.
  • The metabolism of lidocaine is inhibited by co-administration of propranolol, resulting in a 25% increase in lidocaine concentrations.
  • Calcium Channel Blockers:
  • The mean C and AUC of nifedipine are increased by 64% and 79%, respectively, by co-administration of propranolol.
  • Propranolol does not affect the pharmacokinetics of verapamil and norverapamil. Verapamil does not affect the pharmacokinetics of propranolol.
  • Non-Cardiovascular Drugs: n- Migraine Drugs:
  • Theophylline:
  • Benzodiazepines:
  • The pharmacokinetics of oxazepam, triazolam, lorazepam, and alprazolam are not affected by co-administration of propranolol.
  • Neuroleptic Drugs:
  • Co-administration of chlorpromazine with propranolol resulted in a 70% increase in propranolol plasma level.
  • Anti-Ulcer Drugs:
  • Co-administration of metoclopramide with the long-acting propranolol did not have a significant effect on propranololu2019s pharmacokinetics.
  • Lipid Lowering Drugs:
  • Co-administration of propranolol with lovastatin or pravastatin, decreased 18% to 23% the AUC of both, but did not alter their pharmacodynamics. Propranolol did not have an effect on the pharmacokinetics of fluvastatin.
  • Warfarin:
  • Alcohol:
  • Hypertension
  • In a retrospective, uncontrolled study, 107 patients with diastolic blood pressure 110 to 150 mmHg received propranolol 120 mg t.i.d. for at least 6 months, in addition to diuretics and potassium, but with no other antihypertensive agent. Propranolol contributed to control of diastolic blood pressure, but the magnitude of the effect of propranolol on blood pressure cannot be ascertained.
  • Anginan- Pectoris
  • In a double-blind, placebo-controlled study of 32 patients of both sexes, aged 32 to 69 years, with stable angina, propranolol 100 mg t.i.d. was administered for 4 weeks and shown to be more effective than placebo in reducing the rate of angina episodes and in prolonging total exercise time.
  • Atrial Fibrillation
  • In a report examining the long-term (5 to 22 months) efficacy of propranolol, 10 patients, aged 27 to 80, with atrial fibrillation and ventricular rate >120 beats per minute despite digitalis, received propranolol up to 30 mg t.i.d. Seven patients (70%) achieved ventricular rate reduction to <100 beats per minute.
  • Myocardial Infarction
  • The Beta-Blocker Heart Attack Trial (BHAT) was a National Heart, Lung and Blood Institute-sponsored multicenter, randomized, double-blind, placebo-controlled trial conducted in 31 U.S. centers (plus one in Canada) in 3,837 persons without history of severe congestive heart failure or presence of recent heart failure; certain conduction defects; angina since infarction, who had survived the acute phase of myocardial infarction. Propranolol was administered at either 60 or 80 mg t.i.d. based on blood levels achieved during an initial trial of 40 mg t.i.d. Therapy with propranolol, begun 5 to 21 days following infarction, was shown to reduce overall mortality up to 39 months, the longest period of follow-up. This was primarily attributable to a reduction in cardiovascular mortality. The protective effect of propranolol was consistent regardless of age, sex, or site of infarction. Compared with placebo, total mortality was reduced 39% at 12 months and 26% over an average follow-up period of 25 months. The Norwegian Multicenter Trial in which propranolol was administered at 40 mg q.i.d. gave overall results which support the findings in the BHAT.
  • Although the clinical trials used either t.i.d. or q.i.d. dosing, clinical, pharmacologic, and pharmacokinetic data provide a reasonable basis for concluding that b.i.d. dosing with propranolol should be adequate in the treatment of postinfarction patients.
  • Migraine
  • In a 34-week, placebo-controlled, 4-period, dose-finding crossover study with a double-blind randomized treatment sequence, 62 patients with migraine received propranolol 20 to 80 mg 3 or 4 times daily. The headache unit index, a composite of the number of days with headache and the associated severity of the headache, was significantly reduced for patients receiving propranolol as compared to those on placebo.
  • Essential Tremor
  • In a 2 week, double-blind, parallel, placebo-controlled study of 9 patients with essential or familial tremor, propranolol, at a dose titrated as needed from 40 to 80 mg t.i.d. reduced tremor severity compared to placebo.
  • Hypertrophic Subaortic Stenosis
  • In an uncontrolled series of 13 patients with New York Heart Association (NYHA) class 2 or 3 symptoms and hypertrophic subaortic stenosis diagnosed at cardiac catheterization, oral propranolol 40 to 80 mg t.i.d. was administered and patients were followed for up to 17 months. Propranolol was associated with improved NYHA class for most patients.
  • Pheochromocytoma
  • In an uncontrolled series of 3 patients with norepinephrine-secreting pheochromocytoma who were pretreated with an alpha-adrenergic blocker (prazosin), perioperative use of propranolol at doses of 40 to 80 mg t.i.d. resulted in symptomatic blood pressure control.
  • Hypertension
  • Propranolol hydrochloride is indicated in the management of hypertension. It may be used alone or used in combination with other antihypertensive agents, particularly a thiazide diuretic. Propranolol is not indicated in the management of hypertensive emergencies.
  • Angina Pectoris Due to Coronary Atherosclerosis
  • Propranolol hydrochloride is indicated to decrease angina frequency and increase exercise tolerance in patients with angina pectoris.
  • Atrial Fibrillation
  • Propranolol hydrochloride is indicated to control ventricular rate in patients with atrial fibrillation and a rapid ventricular response.
  • Myocardial Infarction
  • Propranolol hydrochloride is indicated to reduce cardiovascular mortality in patients who have survived the acute phase of myocardial infarction and are clinically stable.
  • Migraine
  • Propranolol hydrochloride is indicated for the prophylaxis of common migraine headache. The efficacy of propranolol in the treatment of a migraine attack that has started has not been established, and propranolol is not indicated for such use.
  • Essential Tremor
  • Propranolol hydrochloride is indicated in the management of familial or hereditary essential tremor. Familial or essential tremor consists of involuntary, rhythmic, oscillatory movements, usually limited to the upper limbs. It is absent at rest, but occurs when the limb is held in a fixed posture or position against gravity and during active movement. Propranolol causes a reduction in the tremor amplitude, but not in the tremor frequency. Propranolol hydrochloride is not indicated for the treatment of tremor associated with Parkinsonism.
  • Hypertrophic Subaortic Stenosis
  • Propranolol hydrochloride improves NYHA functional class in symptomatic patients with hypertrophic subaortic stenosis.
  • Pheochromocytoma
  • Propranolol hydrochloride is indicated as an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine-secreting tumors.
  • Propranolol hydrochloride is contraindicated in: 1) cardiogenic shock; 2) sinus bradycardia and greater than first degree block; 3) bronchial asthma; and 4) in patients with known hypersensitivity to propranolol hydrochloride.
  • Angina Pectoris
  • There have been reports of exacerbation of angina and, in some cases, myocardial infarction, following abrupt discontinuance of propranolol therapy. Therefore, when discontinuance of propranolol is planned, the dosage should be gradually reduced over at least a few weeks and the patient should be cautioned against interruption or cessation of therapy without the physicianu2019s advice. If propranolol therapy is interrupted and exacerbation of angina occurs, it usually is advisable to reinstitute propranolol therapy and take other measures appropriate for the management of angina pectoris. Since coronary artery disease may be unrecognized, it may be prudent to follow the above advice in patients considered at risk of having occult atherosclerotic heart disease who are given propranolol for other indications.
  • Hypersensitivity and Skin Reactions
  • Hypersensitivity reactions, including anaphylactic/anaphylactoid reactions, have been associated with the administration of propranolol (see ).
  • Cutaneous reactions, including Stevens-Johnson Syndrome, toxic epidermal necrolysis, exfoliative dermatitis, erythema multiforme, and urticaria, have been reported with use of propranolol (see ).
  • Cardiac Failure
  • Sympathetic stimulation may be a vital component supporting circulatory function in patients with congestive heart failure, and its inhibition by beta-blockade may precipitate more severe failure. Although beta-blockers should be avoided in overt congestive heart failure, some have been shown to be highly beneficial when used with close follow-up in patients with a history of failure who are well compensated and are receiving additional therapies, including diuretics as needed. Beta-adrenergic blocking agents do not abolish the inotropic action of digitalis on heart muscle.
  • In Patients without a History of Heart Failure
  • Nonallergic Bronchospasm (e.g., Chronic Bronchitis, Emphysema)
  • In general, patients with bronchospastic lung disease should not receive beta-blockers. Propranolol should be administered with caution in this setting since it may provoke a bronchial asthmatic attack by blocking bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-receptors.
  • Major Surgery
  • Chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery, however the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and surgical procedures.
  • Diabetes and Hypoglycemia
  • Beta-adrenergic blockade may prevent the appearance of certain premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia, especially in labile insulin-dependent diabetics. In these patients, it may be more difficult to adjust the dosage of insulin.
  • Propranolol therapy, particularly when given to infants and children, diabetic or not, has been associated with hypoglycemia, especially during fasting as in preparation for surgery. Hypoglycemia has been reported in patients taking propranolol after prolonged physical exertion and in patients with renal insufficiency.
  • Thyrotoxicosis
  • Beta-adrenergic blockade may mask certain clinical signs of hyperthyroidism. Therefore, abrupt withdrawal of propranolol may be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm. Propranolol may change thyroid-function tests, increasing T and reverse T and decreasing T.
  • Wolff-Parkinson-White Syndrome
  • Beta-adrenergic blockade in patients with Wolf-Parkinson-White Syndrome and tachycardia has been associated with severe bradycardia requiring treatment with a pacemaker. In one case, this result was reported after an initial dose of 5 mg propranolol.
  • Pheochromocytoma
  • Blocking only the peripheral dilator (beta) action of epinephrine with propranolol leaves its constrictor (alpha) action unopposed. In the event of hemorrhage or shock, there is a disadvantage in having both beta and alpha blockade since the combination prevents the increase in heart rate and peripheral vasoconstriction needed to maintain blood pressure.
  • General
  • Propranolol should be used with caution in patients with impaired hepatic or renal function. Propranolol is not indicated for the treatment of hypertensive emergencies.
  • Beta-adrenergic receptor blockade can cause reduction of intraocular pressure. Patients should be told that propranolol may interfere with the glaucoma screening test. Withdrawal may lead to a return of increased intraocular pressure.
  • While taking beta-blockers, patients with a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge, either accidental, diagnostic, or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat allergic reaction.
  • Clinical Laboratory Tests
  • In patients with hypertension, use of propranolol has been associated with elevated levels of serum potassium, serum transaminases and alkaline phosphatase. In severe heart failure, the use of propranolol has been associated with increases in Blood Urea Nitrogen.
  • Drug Interactions
  • Caution should be exercised when propranolol is administered with drugs that have an effect on CYP2D6, 1A2, or 2C19 metabolic pathways. Co-administration of such drugs with propranolol may lead to clinically relevant drug interactions and changes on its efficacy and/or toxicity (see in ).
  • Cardiovascular Drugs: n- Antiarrhythmics:
  • Quinidine increases the concentration of propranolol and produces greater degrees of clinical beta-blockade and may cause postural hypotension.
  • Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with u03b2-blockers such as propranolol.
  • The clearance of lidocaine is reduced with administration of propranolol. Lidocaine toxicity has been reported following co-administration with propranolol.
  • Caution should be exercised when administering propranolol with drugs that slow A-V nodal conduction, e.g. lidocaine and calcium channel blockers.
  • Digitalis Glycosides:
  • Calcium Channel Blockers:
  • There have been reports of significant bradycardia, heart failure, and cardiovascular collapse with concurrent use of verapamil and beta-blockers.
  • Co-administration of propranolol and diltiazem in patients with cardiac disease has been associated with bradycardia, hypotension, high-degree heart block, and heart failure.
  • ACE Inhibitors:
  • The antihypertensive effects of clonidine may be antagonized by beta-blockers. Propranolol should be administered cautiously to patients withdrawing from clonidine.
  • Alpha-Blockers:
  • Postural hypotension has been reported in patients taking both beta-blockers and terazosin or doxazosin.
  • Reserpine:
  • Inotropic Agents:
  • Isoproterenol and Dobutamine:
  • Non-Cardiovascular Drugs: n- Nonsteroidal Anti-Inflammatory Drugs:
  • Administration of indomethacin with propranolol may reduce the efficacy of propranolol in reducing blood pressure and heart rate.
  • Antidepressants:
  • Anesthetic Agents:
  • Warfarin:
  • Neuroleptic Drugs:
  • Thyroxine:
  • Alcohol:
  • Carcinogenesis, Mutagenesis, Impairment of Fertility
  • In dietary administration studies in which mice and rats were treated with propranolol hydrochloride for up to 18 months at doses of up to 150 mg/kg/day, there was no evidence of drug-related tumorigenesis. On a body surface area basis, this dose in the mouse and rat is, respectively, about equal to and about twice the maximum recommended human oral daily dose (MRHD) of 640 mg propranolol hydrochloride. In a study in which both male and female rats were exposed to propranolol hydrochloride in their diets at concentrations of up to 0.05% (about 50 mg/kg body weight and less than the MRHD), from 60 days prior to mating and throughout pregnancy and lactation for two generations, there were no effects on fertility. Based on differing results from Ames Tests performed by different laboratories, there is equivocal evidence for a genotoxic effect of propranolol hydrochloride in bacteria ( strain TA 1538).
  • Pregnancy
  • Pregnancy Category C
  • In a series of reproductive and developmental toxicology studies, propranolol hydrochloride was given to rats by gavage or in the diet throughout pregnancy and lactation. At doses of 150 mg/kg/day, but not at doses of 80 mg/kg/day (equivalent to the MRHD on a body surface area basis), treatment was associated with embryotoxicity (reduced litter size and increased resorption rates) as well as neonatal toxicity (deaths). Propranolol hydrochloride also was administered (in the feed) to rabbits (throughout pregnancy and lactation) at doses as high as 150 mg/kg/day (about 5 times the maximum recommended human oral daily dose). No evidence of embryo or neonatal toxicity was noted.
  • There are no adequate and well-controlled studies in pregnant women. Intrauterine growth retardation, small placentas, and congenital abnormalities have been reported in neonates whose mothers received propranolol during pregnancy. Neonates whose mothers received propranolol at parturition have exhibited bradycardia, hypoglycemia, and/or respiratory depression. Adequate facilities for monitoring such infants at birth should be available. Propranolol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
  • Nursing Mothers
  • Propranolol is excreted in human milk. Caution should be exercised when propranolol is administered to a nursing woman.
  • Pediatric Use
  • Safety and effectiveness of propranolol in pediatric patients have not been established.
  • Bronchospasm and congestive heart failure have been reported coincident with the administration of propranolol therapy in pediatric patients.
  • Geriatric Use
  • Clinical studies of propranolol did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
  • The following adverse events were observed and have been reported in patients using propranolol.
  • Cardiovascular:
  • Central Nervous System:
  • Gastrointestinal:
  • Allergic:
  • Respiratory:
  • Hematologic:
  • Autoimmune:
  • Skin and Mucous Membranes:
  • Genitourinary:
  • Propranolol is not significantly dialyzable. In the event of overdosage or exaggerated response, the following measures should be employed:
  • General
  • Supportive Therapy
  • The electrocardiogram, pulse, blood pressure, neurobehavioral status and intake and output balance must be monitored. Isoproterenol and aminophylline may be used for bronchospasm.
  • General
  • Because of the variable bioavailability of propranolol, the dose should be individualized based on response.
  • Hypertension
  • The usual initial dosage is 40 mg propranolol twice daily, whether used alone or added to a diuretic. Dosage may be increased gradually until adequate blood pressure control is achieved. The usual maintenance dosage is 120 mg to 240 mg per day. In some instances a dosage of 640 mg a day may be required. The time needed for full antihypertensive response to a given dosage is variable and may range from a few days to several weeks.
  • While twice-daily dosing is effective and can maintain a reduction in blood pressure throughout the day, some patients, especially when lower doses are used, may experience a modest rise in blood pressure toward the end of the 12-hour dosing interval. This can be evaluated by measuring blood pressure near the end of the dosing interval to determine whether satisfactory control is being maintained throughout the day. If control is not adequate, a larger dose, or 3-times-daily therapy may achieve better control.
  • Angina Pectoris
  • Total daily doses of 80 mg to 320 mg propranolol, when administered orally, twice a day, three times a day, or four times a day, have been shown to increase exercise tolerance and to reduce ischemic changes in the ECG. If treatment is to be discontinued, reduce dosage gradually over a period of several weeks. (See .)
  • Atrial Fibrillation
  • The recommended dose is 10 mg to 30 mg propranolol three or four times daily before meals and at bedtime.
  • Myocardial Infarction
  • In the Beta-Blocker Heart Attack Trial (BHAT), the initial dose was 40 mg t.i.d., with titration after 1 month to 60 mg to 80 mg t.i.d. as tolerated. The recommended daily dosage is 180 mg to 240 mg propranolol per day in divided doses. Although a t.i.d. regimen was used in the BHAT and a q.i.d. regimen in the Norwegian Multicenter Trial, there is a reasonable basis for the use of either a t.i.d. or b.i.d. regimen (see ). The effectiveness and safety of daily dosages greater than 240 mg for prevention of cardiac mortality have not been established. However, higher dosages may be needed to effectively treat co-existing diseases such as angina or hypertension (see above).
  • Migraine
  • The initial dose is 80 mg propranolol daily in divided doses. The usual effective dose range is 160 mg to 240 mg per day. The dosage may be increased gradually to achieve optimum migraine prophylaxis. If a satisfactory response is not obtained within four to six weeks after reaching the maximum dose, propranolol therapy should be discontinued. It may be advisable to withdraw the drug gradually over a period of several weeks.
  • Essential Tremor
  • The initial dosage is 40 mg propranolol twice daily. Optimum reduction of essential tremor is usually achieved with a dose of 120 mg per day. Occasionally, it may be necessary to administer 240 mg to 320 mg per day.
  • Hypertrophic Subaortic Stenosis
  • The usual dosage is 20 mg to 40 mg propranolol three or four times daily before meals and at bedtime.
  • Pheochromocytoma
  • The usual dosage is 60 mg propranolol daily in divided doses for three days prior to surgery as adjunctive therapy to alpha-adrenergic blockade. For the management of inoperable tumors, the usual dosage is 30 mg daily in divided doses as adjunctive therapy to alpha-adrenergic blockade.
  • Propranolol Hydrochloride Oral Solution
  • 20 mg per 5 mL oral solution is supplied as a (strawberry-mint flavor) clear, colorless to slightly colored viscous solution.
  • NDC 0054-3727-63: Bottle of 500 mL
  • 40 mg per 5 mL oral solution is supplied as a (strawberry-mint flavor) clear, colorless to slightly colored, viscous solution.
  • NDC 0054-3730-63: Bottle of 500 mL
  • Storage
  • Store at 20u00b0 to 25u00b0C (68u00b0 to 77u00b0F). [See USP Controlled Room Temperature.] Dispense in a tight, light-resistant, child-resistant container as defined in USP/NF.
  • Distr. by: n
  • Pharmaceuticals Corp.
  • Eatontown, NJ 07724
  • 4071708//08 Revised May 2017
  • No data
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Comparator Sourcing for Clinical Trials

Comparator Sourcing for Clinical Trials

GNH India brings over 10 years of experience in Comparator

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Name Patient Supply

Name Patient Supply

Today, the exact cause for many rare diseases remains unknown

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Validated Cold Chain Shipment

Validated Cold Chain Shipment

With shifting of pharma industry from synthetic molecules to biologic

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Clinical Trials Supply

Clinical Trials Supply

STOP SOURCING..... START SMART SOURCING...... COME STRAIGHT TO THE SOURCE

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Dossiers and Stability Studies

Dossiers and Stability Studies

STABILITY STUDIES STABILITY, BA / BE STUDIES Due to our active

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Pharmaceutical Contract Manufacturing

Pharmaceutical Contract Manufacturing

GNH Provides Contract Manufacturing services for: Generic Medicines with following

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Pricing

Pricing

PRICING POLICY Terms of sales are typically prepaid, unless otherwise

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Disclaimer

Please see the Legal Notice for detailed terms and disclaimers. The Legal Notice governs the use of this Website and by accessing and using this Website you agree to be bound by and accept the Legal Notice.

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General

64020 Products

GNH India Brings to over 64036 Product SKUs from India all at 1 place with easy access and global deliveries.

US NDC

71247 Products

GNH India Brings to over 71252 Product SKUs from India all at 1 place with easy access and global deliveries.

Canadian DIN

51046 Products

GNH India Brings to over 51047 Product SKUs from India all at 1 place with easy access and global deliveries.

Swiss Drugs

150 Products

GNH India Brings to over 150 Product SKUs from India all at 1 place with easy access and global deliveries.

NZ Drugs

13296 Products

GNH Brings to over 13298 Product SKUs from India all at 1 place with easy access and global deliveries.

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