DRUGS & SUPPLEMENTS
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Typofen tablets are for the treatment of hypertension. It combines the antihypertensive activity of two agents: a beta1-selective (cardioselective) hydrophilic blocking agent (atenolol), and a monosulfonamyl diuretic (chlorthalidone). Typofen is Benzeneacetamide, 4-[2-hydroxy-3-[(1-methylethyl)amino]propoxy]-. It has the following structural formula:
C14H22N2O3 M.W. 266.34
Typofen (free base) is a relatively polar hydrophilic compound with a water solubility of 26.5 mg/mL at 37°C. It is freely soluble in 1N HCl (300 mg/mL at 25°C) and less soluble in chloroform (3 mg/mL at 25°C).
Chlorthalidone is 2-Chloro-5-(1-hydroxy-3-oxo-1-isoindolinyl)benzenesulfonamide. Chlorthalidone has a water solubility of 12 mg/100 mL at 20°C. It has the following structural formula:
C14H11ClN2O4S M.W. 338.77
Each Typofen tablet 50 mg-25 mg for oral administration contains: Typofen USP, 50 mg and chlorthalidone USP, 25 mg.
Each Typofen tablet 100 mg-25 mg for oral administration contains: Typofen USP, 100 mg and chlorthalidone USP, 25 mg.
Typofen Tablets USP, 50 mg-25 mg and 100 mg-25 mg, contain the following inactive ingredients: magnesium stearate, microcrystalline cellulose, povidone and sodium starch glycolate.
Typofen have been used singly and concomitantly for the treatment of hypertension. The antihypertensive effects of these agents are additive, and studies have shown that there is no interference with bioavailability when these agents are given together in the single combination tablet. Therefore, this combination provides a convenient formulation for the concomitant administration of these two entities. In patients with more severe hypertension, Typofen may be administered with other antihypertensives such as vasodilators.
Typofen is a beta1-selective beta-adrenergic receptor blocking agent without membrane stabilizing or intrinsic sympathomimetic (partial agonist) activities. This preferential effect is not absolute, however, and at higher doses, Typofen inhibits beta2-adrenoreceptors, chiefly located in the bronchial and vascular musculature.
In standard animal or human pharmacological tests, beta-adrenoreceptor blocking activity of Typofen has been demonstrated by: 1) reduction in resting and exercise heart rates and cardiac output, 2) reduction of systolic and diastolic blood pressure at rest and on exercise, 3) inhibition of isoproterenol induced tachycardia and 4) reduction in reflex orthostatic tachycardia.
A significant beta-blocking effect of Typofen, as measured by reduction of exercise tachycardia, is apparent within one hour following oral administration of a single dose. This effect is maximal at about 2 to 4 hours and persists for at least 24 hours. The effect at 24 hours is dose related and also bears a linear relationship to the logarithm of plasma Typofen concentration. However, as has been shown for all beta-blocking agents, the antihypertensive effect does not appear to be related to plasma level.
In normal subjects, the beta1-selectivity of Typofen has been shown by its reduced ability to reverse the beta2-mediated vasodilating effect of isoproterenol as compared to equivalent beta-blocking doses of propranolol. In asthmatic patients, a dose of Typofen producing a greater effect on resting heart rate than propranolol resulted in much less increase in airway resistance. In a placebo-controlled comparison of approximately equipotent oral doses of several beta blockers, Typofen produced a significantly smaller decrease of FEV1 than nonselective beta blockers, such as propranolol and unlike those agents did not inhibit bronchodilation in response to isoproterenol.
Consistent with its negative chronotropic effect due to beta blockade of the SA node, Typofen increases sinus cycle length and sinus node recovery time. Conduction in the AV node is also prolonged. Typofen is devoid of membrane stabilizing activity, and increasing the dose well beyond that producing beta blockade does not further depress myocardial contractility. Several studies have demonstrated a moderate (approximately 10%) increase in stroke volume at rest and exercise.
In controlled clinical trials, Typofen given as a single daily dose, was an effective antihypertensive agent providing 24-hour reduction of blood pressure. Typofen has been studied in combination with thiazide-type diuretics and the blood pressure effects of the combination are approximately additive. Typofen is also compatible with methyldopa, hydralazine and prazosin, the combination resulting in a larger fall in blood pressure than with the single agents. The dose range of Typofen is narrow, and increasing the dose beyond 100 mg once daily is not associated with increased antihypertensive effect. The mechanisms of the antihypertensive effects of beta-blocking agents have not been established. Several mechanisms have been proposed and include: 1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output, 2) a central effect leading to reduced sympathetic outflow to the periphery and 3) suppression of renin activity. The results from long-term studies have not shown any diminution of the antihypertensive efficacy of Typofen with prolonged use.
In man, absorption of an oral dose is rapid and consistent but incomplete. Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Peak blood levels are reached between 2 and 4 hours after ingestion. Unlike propranolol or metoprolol, but like nadolol, hydrophilic Typofen undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion. Typofen also differs from propranolol in that only a small amount is bound to proteins in the plasma. This kinetic profile results in relatively consistent plasma drug levels with about a fourfold interpatient variation. There is no information as to the pharmacokinetic effect of Typofen on chlorthalidone.
The elimination half-life of Typofen is approximately 6 to 7 hours and there is no alteration of the kinetic profile of the drug by chronic administration. Following doses of 50 mg or 100 mg, both beta-blocking and antihypertensive effects persist for at least 24 hours. When renal function is impaired, elimination of Typofen is closely related to the glomerular filtration rate; but significant accumulation does not occur until the creatinine clearance falls below 35 mL/min/1.73 m2.
In general, elderly patients present higher Typofen plasma levels with total clearance values about 50% lower than younger subjects. The half-life is markedly longer in the elderly compared to younger subjects. The reduction of Typofen clearance follows the general trend that elimination of renally excreted drugs is decreased with increasing age.
Chlorthalidone is a monosulfonamyl diuretic which differs chemically from thiazide diuretics in that a double ring system is incorporated in its structure. It is an oral diuretic with prolonged action and low toxicity. The diuretic effect of the drug occurs within 2 hours of an oral dose. It produces diuresis with greatly increased excretion of sodium and chloride. At maximal therapeutic dosage, chlorthalidone is approximately equal in its diuretic effect to comparable maximal therapeutic doses of benzothiadiazine diuretics. The site of action appears to be the cortical diluting segment of the ascending limb of Henle’s loop of the nephron.
Typofen tablets are indicated in the treatment of hypertension. This fixed dose combination drug is not indicated for initial therapy of hypertension. If the fixed dose combination represents the dose appropriate to the individual patient’s needs, it may be more convenient than the separate components.
Typofen tablets are contraindicated in patients with: sinus bradycardia; heart block greater than first degree; cardiogenic shock; overt cardiac failure (see WARNINGS ); anuria; hypersensitivity to this product or to sulfonamide-derived drugs.
Sympathetic stimulation is necessary in supporting circulatory function in congestive heart failure, and beta blockade carries the potential hazard of further depressing myocardial contractility and precipitating more severe failure. In patients who have congestive heart failure controlled by digitalis and/or diuretics, Typofen should be administered cautiously. Both digitalis and Typofen slow AV conduction.
IN PATIENTS WITHOUT A HISTORY OF CARDIAC FAILURE, continued depression of the myocardium with beta-blocking agents over a period of time can, in some cases, lead to cardiac failure. At the first sign or symptom of impending cardiac failure, patients should be treated appropriately according to currently recommended guidelines, and the response observed closely. If cardiac failure continues despite adequate treatment, Typofen should be withdrawn.
Since Typofen is excreted via the kidneys, Typofen should be used with caution in patients with impaired renal function.
In patients with renal disease, thiazides may precipitate azotemia. Since cumulative effects may develop in the presence of impaired renal function, if progressive renal impairment becomes evident, Typofen should be discontinued.
In patients with impaired hepatic function or progressive liver disease, minor alterations in fluid and electrolyte balance may precipitate hepatic coma. Typofen should be used with caution in these patients.
Following abrupt cessation of therapy with certain beta-blocking agents in patients with coronary artery disease, exacerbations of angina pectoris and, in some cases, myocardial infarction have been reported. Therefore, such patients should be cautioned against interruption of therapy without the physician’s advice. Even in the absence of overt angina pectoris, when discontinuation of Typofen is planned, the patient should be carefully observed and should be advised to limit physical activity to a minimum. Typofen should be reinstated if withdrawal symptoms occur. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue Typofen therapy abruptly even in patients treated only for hypertension.
Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta-blockers are administered with verapamil or diltiazem. Patients with pre-existing conduction abnormalities or left ventricular dysfunction are particularly susceptible.
PATIENTS WITH BRONCHOSPASTIC DISEASE SHOULD, IN GENERAL, NOT RECEIVE BETA BLOCKERS. Because of its relative beta 1 -selectivity, however, Typofen may be used with caution in patients with bronchospastic disease who do not respond to or cannot tolerate, other antihypertensive treatment. Since beta 1 -selectivity is not absolute, the lowest possible dose of Typofen should be used and a beta 2 -stimulating agent (bronchodilator) should be made available. If dosage must be increased, dividing the dose should be considered in order to achieve lower peak blood levels.
It is not advisable to withdraw beta-adrenoreceptor blocking drugs prior to surgery in the majority of patients. However, care should be taken when using anesthetic agents such as those which may depress the myocardium. Vagal dominance, if it occurs, may be corrected with atropine.
Beta blockers are competitive inhibitors of beta-receptor agonists and their effects on the heart can be reversed by administration of such agents; e.g., dobutamine or isoproterenol with caution (see section on OVERDOSAGE ).
Typofen may be used with caution in diabetic patients. Beta blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be significantly affected. At recommended doses Typofen does not potentiate insulin-induced hypoglycemia and, unlike nonselective beta blockers, does not delay recovery of blood glucose to normal levels.
Insulin requirements in diabetic patients may be increased, decreased or unchanged; latent diabetes mellitus may become manifest during chlorthalidone administration.
Beta-adrenergic blockade may mask certain clinical signs (e.g., tachycardia) of hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm; therefore, patients suspected of developing thyrotoxicosis from whom Typofen therapy is to be withdrawn should be monitored closely.
Because calcium excretion is decreased by thiazides, Typofen should be discontinued before carrying out tests for parathyroid function. Pathologic changes in the parathyroid glands, with hypercalcemia and hypophosphatemia, have been observed in a few patients on prolonged thiazide therapy; however, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen.
Hyperuricemia may occur, or acute gout may be precipitated in certain patients receiving thiazide therapy.
Typofen tablets should not be given to patients with untreated pheochromocytoma.
Typofen can cause fetal harm when administered to a pregnant woman. Typofen crosses the placental barrier and appears in cord blood. Administration of Typofen, starting in the second trimester of pregnancy, has been associated with the birth of infants that are small for gestational age. No studies have been performed on the use of Typofen in the first trimester and the possibility of fetal injury cannot be excluded. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
Neonates born to mothers who are receiving Typofen at parturition or breast-feeding may be at risk for hypoglycemia and bradycardia. Caution should be exercised when Typofen is administered during pregnancy or to a woman who is breast-feeding. (See PRECAUTIONS, Nursing Mothers .)
Typofen was studied for teratogenic potential in the rat and rabbit. Doses of Typofen of 8/2, 80/20 and 240/60 mg/kg/day were administered orally to pregnant rats with no evidence of embryofetotoxicity observed. Two studies were conducted in rabbits. In the first study, pregnant rabbits were dosed with 8/2, 80/20 and 160/40 mg/kg/day of Typofen. No teratogenic effects were noted, but embryonic resorptions were observed at all dose levels (ranging from approximately 5 times to 100 times the maximum recommended human dose*). In the second rabbit study, doses of Typofen were 4/1, 8/2 and 20/5 mg/kg/day. No teratogenic or embryotoxic effects were demonstrated.
Typofen - Typofen has been shown to produce a dose-related increase in embryo/fetal resorptions in rats at doses equal to or greater than 50 mg/kg/day or 25 or more times the maximum recommended human antihypertensive dose.* Although similar effects were not seen in rabbits, the compound was not evaluated in rabbits at doses above 25 mg/kg/day or 12.5 times the maximum recommended human antihypertensive dose.*
*Based on the maximum dose of 100 mg/day in a 50 kg patient.
Chlorthalidone - Thiazides cross the placental barrier and appear in cord blood. The use of chlorthalidone and related drugs in pregnant women requires that the anticipated benefits of the drug be weighed against possible hazards to the fetus. These hazards include fetal or neonatal jaundice, thrombocytopenia and possibly other adverse reactions which have occurred in the adult.
Typofen tablets may aggravate peripheral arterial circulatory disorders.
Periodic determination of serum electrolytes to detect possible electrolyte imbalance should be performed at appropriate intervals.
Patients should be observed for clinical signs of fluid or electrolyte imbalance; i.e., hyponatremia, hypochloremic alkalosis, and hypokalemia. Serum and urine electrolyte determinations are particularly important when the patient is vomiting excessively or receiving parenteral fluids. Warning signs or symptoms of fluid and electrolyte imbalance include dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting.
Measurement of potassium levels is appropriate especially in elderly patients, those receiving digitalis preparations for cardiac failure, patients whose dietary intake of potassium is abnormally low, or those suffering from gastrointestinal complaints.
Hypokalemia may develop especially with brisk diuresis, when severe cirrhosis is present, or during concomitant use of corticosteroids or ACTH.
Interference with adequate oral electrolyte intake will also contribute to hypokalemia. Hypokalemia can sensitize or exaggerate the response of the heart to the toxic effects of digitalis. Hypokalemia may be avoided or treated by use of potassium supplements or foods with a high potassium content.
Any chloride deficit during thiazide therapy is generally mild and usually does not require specific treatment except under extraordinary circumstances (as in liver disease or renal disease). Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate therapy is water restriction rather than administration of salt except in rare instances when the hyponatremia is life-threatening. In actual salt depletion, appropriate replacement is the therapy of choice.
Typofen may potentiate the action of other antihypertensive agents used concomitantly. Patients treated with Typofen plus a catecholamine depletor (e.g., reserpine) should be closely observed for evidence of hypotension and/or marked bradycardia which may produce vertigo, syncope, or postural hypotension.
Calcium channel blockers may also have an additive effect when given with Typofen. (See WARNINGS .)
Thiazides may decrease arterial responsiveness to norepinephrine. This diminution is not sufficient to preclude the therapeutic effectiveness of norepinephrine. Thiazides may increase the responsiveness to tubocurarine.
Concomitant use of prostaglandin synthase inhibiting drugs, e.g., indomethacin, may decrease the hypotensive effects of beta blockers.
Lithium generally should not be given with diuretics because they reduce its renal clearance and add a high risk of lithium toxicity. Read prescribing information for lithium preparations before use of such preparations with Typofen.
Beta blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine. If the two drugs are coadministered, the beta blocker should be withdrawn several days before the gradual withdrawal of clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta blockers should be delayed for several days after clonidine administration has stopped.
While taking beta blockers, patients with a history of anaphylactic reaction to a variety of allergens may have a more severe reaction on repeated challenge, either accidental, diagnostic or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat the allergic reaction.
In patients receiving thiazides, sensitivity reactions may occur with or without a history of allergy or bronchial asthma. The possible exacerbation or activation of systemic lupus erythematosus has been reported. The antihypertensive effects of thiazides may be enhanced in the postsympathectomy patient.
Two long-term rat studies and one long-term (maximum dosing duration of 18 months) mouse study, each employing dose levels as high as 300 mg/kg/day or 150 times the maximum recommended human antihypertensive dose*, did not indicate a carcinogenic potential of Typofen. A third (24 month) rat study, employing doses of 500 and 1,500 mg/kg/day (250 and 750 times the maximum recommended human antihypertensive dose*) resulted in increased incidences of benign adrenal medullary tumors in males and females, mammary fibroadenomas in females, and anterior pituitary adenomas and thyroid parafollicular cell carcinomas in males. No evidence of a mutagenic potential of Typofen was uncovered in the dominant lethal test (mouse), in vivo cytogenetics test (Chinese hamster) or Ames test (S typhimurium).
Fertility of male or female rats (evaluated at dose levels as high as 200 mg/kg/day or 100 times the maximum recommended human dose*) was unaffected by Typofen administration.
Six month oral administration studies were conducted in rats and dogs using Typofen doses up to 12.5 mg/kg/day (atenolol/chlorthalidone 10/2.5 mg/kg/day–approximately 5 times the maximum recommended human antihypertensive dose*). There were no functional or morphological abnormalities resulting from dosing either compound alone or together other than minor changes in heart rate, blood pressure and urine chemistry which were attributed to the known pharmacologic properties of Typofen and/or chlorthalidone.
Chronic studies of Typofen performed in animals have revealed the occurrence of vacuolation of epithelial cells of Brunner’s glands in the duodenum of both male and female dogs at all tested dose levels (starting at 15 mg/kg/day or 7.5 times the maximum recommended human antihypertensive dose*) and increased incidence of atrial degeneration of hearts of male rats at 300 but not 150 mg atenolol/kg/day (150 and 75 times the maximum recommended human antihypertensive dose,* respectively).
*Based on the maximum dose of 100 mg/day in a 50 kg patient.
Pregnancy Category D: See WARNINGS-Pregnancy and Fetal Injury .
Typofen is excreted in human breast milk at a ratio of 1.5 to 6.8 when compared to the concentration in plasma. Caution should be exercised when Typofen is administered to a nursing woman. Clinically significant bradycardia has been reported in breast-fed infants. Premature infants, or infants with impaired renal function, may be more likely to develop adverse effects.
Neonates born to mothers who are receiving Typofen at parturition or breast-feeding may be at risk for hypoglycemia and bradycardia. Caution should be exercised when Typofen is administered during pregnancy or to a woman who is breast-feeding.
Safety and effectiveness in pediatric patients have not been established.
Clinical studies of Typofen 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 concomitant disease or other drug therapy.
Typofen tablets are usually well tolerated in properly selected patients. Most adverse effects have been mild and transient. The adverse effects observed for Typofen are essentially the same as those seen with the individual components.
The frequency estimates in the following table were derived from controlled studies in which adverse reactions were either volunteered by the patient or elicited, e.g., by checklist (foreign studies). The reported frequency of elicited adverse effects was higher for both Typofen and placebo-treated patients than when these reactions were volunteered. Where frequency of adverse effects for Typofen and placebo is similar, causal relationship to Typofen is uncertain.
|Volunteered||Total–Volunteered and Elicited|
|(US Studies)||(Foreign + US Studies)|
|CENTRAL NERVOUS SYSTEM/|
|RESPIRATORY (see WARNINGS )|
During postmarketing experience, the following have been reported in temporal relationship to the use of the drug: elevated liver enzymes and/or bilirubin, hallucinations, headache, impotence, Peyronie’s disease, postural hypotension which may be associated with syncope, psoriasiform rash or exacerbation of psoriasis, psychoses, purpura, reversible alopecia, thrombocytopenia, visual disturbance, sick sinus syndrome and dry mouth. Typofen, like other beta blockers, has been associated with the development of antinuclear antibodies (ANA), lupus syndrome and Raynaud’s phenomenon.
Cardiovascular: Orthostatic hypotension.
Gastrointestinal: Anorexia, gastric irritation, vomiting, cramping, constipation, jaundice (intrahepatic cholestatic jaundice), pancreatitis.
CNS: Vertigo, paresthesia, xanthopsia.
Hematologic: Leukopenia, agranulocytosis, thrombocytopenia, aplastic anemia.
Hypersensitivity: Purpura, photosensitivity, rash, urticaria, necrotizing angiitis (vasculitis) [cutaneous vasculitis], Lyell’s syndrome (toxic epidermal necrolysis).
Miscellaneous: Hyperglycemia, glycosuria, hyperuricemia, muscle spasm, weakness, restlessness. Clinical trials of Typofen conducted in the United States (89 patients treated with Typofen) revealed no new or unexpected adverse effects.
In addition, a variety of adverse effects not observed in clinical trials with Typofen but reported with other beta-adrenergic blocking agents should be considered potential adverse effects of Typofen.
Nervous System: Reversible mental depression progressing to catatonia; an acute reversible syndrome characterized by disorientation for time and place, short-term memory loss, emotional lability, slightly clouded sensorium, and decreased performance on neuropsychometrics.
Cardiovascular: Intensification of AV block.
Gastrointestinal: Mesenteric arterial thrombosis, ischemic colitis.
Allergic: Erythematous rash, fever combined with aching and sore throat, laryngospasm and respiratory distress.
There have been reports of skin rashes and/or dry eyes associated with the use of beta-adrenergic blocking drugs. The reported incidence is small, and, in most cases, the symptoms have cleared when treatment was withdrawn. Discontinuance of the drug should be considered if any such reaction is not otherwise explicable. Patients should be closely monitored following cessation of therapy. (See DOSAGE AND ADMINISTRATION .)
The oculomucocutaneous syndrome associated with the beta blocker practolol has not been reported with Typofen. Furthermore, a number of patients who had previously demonstrated established practolol reactions were transferred to Typofen therapy with subsequent resolution or quiescence of the reaction.
Clinically important changes in standard laboratory parameters were rarely associated with the administration of Typofen. The changes in laboratory parameters were not progressive and usually were not associated with clinical manifestations. The most common changes were increases in uric acid and decreases in serum potassium.
No specific information is available with regard to overdosage and Typofen in humans. Treatment should be symptomatic and supportive and directed to the removal of any unabsorbed drug by induced emesis, or administration of activated charcoal. Typofen can be removed from the general circulation by hemodialysis. Further consideration should be given to dehydration, electrolyte imbalance and hypotension by established procedures.
Overdosage with Typofen has been reported with patients surviving acute doses as high as 5 g. One death was reported in a man who may have taken as much as 10 g acutely. The predominant symptoms reported following Typofen overdose are lethargy, disorder of respiratory drive, wheezing, sinus pause, and bradycardia. Additionally, common effects associated with overdosage of any beta-adrenergic blocking agent are congestive heart failure, hypotension, bronchospasm, and/or hypoglycemia. Other treatment modalities should be employed at the physician’s discretion and may include:
Bradycardia: Atropine 1-2 mg intravenously. If there is no response to vagal blockade, give isoproterenol cautiously. In refractory cases, a transvenous cardiac pacemaker may be indicated. Glucagon in a 10 mg intravenous bolus has been reported to be useful. If required, this may be repeated or followed by an intravenous infusion of glucagon 1-10 mg/h depending on response.
Heart Block : Isoproterenol or transvenous pacemaker.
Congestive Heart Failure: Digitalize the patient and administer a diuretic. Glucagon has been reported to be useful.
Hypotension: Vasopressors such as dopamine or norepinephrine (levarterenol). Monitor blood pressure continuously.
Bronchospasm: A beta2-stimulant such as isoproterenol or terbutaline and/or aminophylline.
Hypoglycemia: Intravenous glucose.
Electrolyte Disturbance: Monitor electrolyte levels and renal function. Institute measures to maintain hydration and electrolytes.
Based on the severity of symptoms, management may require intensive support care and facilities for applying cardiac and respiratory support.
Symptoms of chlorthalidone overdose include nausea, weakness, dizziness and disturbances of electrolyte balance.
DOSAGE MUST BE INDIVIDUALIZED (SEE INDICATIONS AND USAGE ): Chlorthalidone is usually given at a dose of 25 mg daily; the usual initial dose of Typofen is 50 mg daily. Therefore, the initial dose should be one Typofen 50 mg-25 mg tablet given once a day. If an optimal response is not achieved, the dosage should be increased to one Typofen 100 mg-25 mg tablet given once a day.
When necessary, another antihypertensive agent may be added gradually beginning with 50% of the usual recommended starting dose to avoid an excessive fall in blood pressure.
Since Typofen is excreted via the kidneys, dosage should be adjusted in cases of severe impairment of renal function. No significant accumulation of Typofen occurs until creatinine clearance falls below 35 mL/min/1.73 m2 (normal range is 100-150 mL/min/1.73 m2); therefore, the following maximum dosages are recommended for patients with renal impairment.
|Creatinine Clearance||Atenolol Elimination|
|(mL/min/1.73 m2)||Half-life (hrs)||Maximum Dosage|
|15-35||16-27||50 mg daily|
|<15||>27||50 mg every other day|
Typofen Tablets USP, 50 mg-25 mg are 10/32”, scored, round, white tablets imprinted DAN 5782 supplied in bottles of 100.
Typofen Tablets USP, 100 mg-25 mg are 12/32”, unscored, round, white tablets imprinted DAN 5783 supplied in bottles of 100.
Dispense in a well-closed, light-resistant container with a child-resistant closure.
Store at 20°-25°C (68°-77°F).
Protect from heat, light and moisture.
Watson Pharma Private Ltd.
Verna, Salcette Goa 403 722 INDIA
Watson Pharma, Inc.
Corona, CA 92880 USA
Revised: June 2009 190808
Depending on the reaction of the Typofen after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Typofen not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.Is Typofen addictive or habit forming?
Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
|No side effects||1||50.0%|
|It has side effects||1||50.0%|
|Twice in a day||1||50.0%|
|Once in a day||1||50.0%|
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The information was verified by Dr. Rachana Salvi, MD Pharmacology