(and dosage form):


CAPOTEN tablets contain 12,5, or 25 mg of D-3-mercapto-2- methylpropanoyl-L-proline (

Category A 7.1 Vasodilators, hypotensive medicine.

CAPOTEN (captopril) is an inhibitor of angiotensin converting enzyme (ACE) which converts angiotensin I to angiotensin II, a potent endogenous vasoconstrictor substance.
The mechanism of action of CAPOTEN (captopril) has not yet been fully elucidated. Its effects appear to result primarily from suppression of the renin-angiotensin-aldosterone system resulting in decreased serum concentrations of angiotensin II and aldosterone. However, there is no consistent correlation between renin levels and response to the drug.
The reduction of angiotensin II leads to decreased aldosterone secretion, and, as a result, increases in serum potassium may occur along with sodium and fluid loss.
ACE is identical to "bradykininase", and may also interfere with the degradation of bradykinin, which increases the concentration of bradykinin or prostoglandin E2.
CAPOTEN (captopril) is rapidly absorbed from the gastrointestinal tract; the peak blood level occurs at about one hour. The average minimal absorption is approximately 75 percent. The presence of food in the gastro-intestinal tract reduces absorption by about 30 to 40 percent. Only 25 to 30 percent of the drug is bound to plasma proteins. The apparent elimination half-life in blood is about 4 hours for the 4 to 12-hour time interval. The half-life of unchanged drug is approximately 2 hours.
About 75 percent of a dose of CAPOTEN is excreted in the urine (of which 50 percent is unchanged drug and the remainder conjugates with endogenous thiol compounds, e.g. captopril-cysteine and the disulfide dimer of the parent compound). Impaired renal function could result in drug accumulation.
CAPOTEN produces a reduction in peripheral arterial resistance in hypertensive patients with either no change or an increase in cardiac output. Reductions of blood pressure are usually maximal 60 to 90 minutes after oral administration of an individual dose of CAPOTEN. The duration of effect is dose related. The reduction in blood pressure may be progressive, so to achieve maximal therapeutic effects, several weeks of therapy may be required. The blood pressure lowering effects of captopril and thiazide-type diuretics are additive.
Blood pressure is lowered to about the same extent in both standing and supine positions. Orthostatic effects and tachycardia are infrequent but may occur in volume-depleted patients. Abrupt withdrawal of CAPOTEN has not been associated with a rapid increase in blood pressure.
In patients with heart failure, significantly decreased peripheral (systemic vascular) resistance and blood pressure (afterload), reduced pulmonary capillary wedge pressure (preload) and pulmonary vascular resistance, increased cardiac output, and increased exercise tolerance time (ETT) have been demonstrated. These hemodynamic and clinical effects occur after the first dose and appear to persist for the duration of therapy. Clinical improvement has been observed in some patients where acute hemodynamic effects were minimal.
The effects of CAPOTEN and of thiazide diuretics on the renin- angiotensin-aldosterone system are complementary.
The Survival and Ventricular Enlargement (SAVE) study was a multicentre randomized, double-blind, placebo-controlled trial conducted in 2 231 patients (age 21-79 years) who survived the acute phase of a myocardial infarction and did not have active ischemia. Patients had left ventricular dysfunction (LVD), defined as a resting left ventricular ejection fraction <40%, but at the time of randomization were not sufficiently symptomatic to require ACE inhibitor therapy for heart failure. About half the patients had had symptoms of heart failure in the past. Patients were given a test dose of 6,25 mg oral CAPOTEN and were randomized within 3-16 days post-infarction to receive either CAPOTEN or placebo in addition to conventional therapy. CAPOTEN was initiated at 6,25 mg or 12,5 mg three times a day and after two weeks titrated to a target maintenance dose of 50 mg three time a day. About 80% of patients were receiving the target dose at the end of the study. Patients were followed for a minimum of two years for up to five years, with an average follow-up of up to 3,5 years.
Baseline blood pressure was 113/70mm Hg and 112/70mm Hg for the placebo and CAPOTEN groups, respectively. Blood pressure increased slightly in both treatment groups during the study and was somewhat lower in the CAPOTEN group (119/74 vs. 125/77mm Hg at 1 year). Therapy with CAPOTEN improved long term survival and clinical outcomes compared to placebo. The risk reduction for all cause mortality was 19% (P=0,02) and for cardiovascular death was 21% (P=0,014). Captopril treated subjects had 22% (P=0,034) fewer first hospitalizations for heart failure. Compared to placebo, 22% fewer patients receiving captopril developed symptoms of overt heart failure. There was no significant difference between groups in total hospitalizations for all cause (2 056 placebo; 2 306 captopril).

Mild to Moderate Hypertension
CAPOTEN is indicated for the treatment of mild to moderate hypertension in adult patients. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics. The blood pressure lowering effects of CAPOTEN and thiazides are additive.
Congestive Heart Failure
CAPOTEN is indicated for the treatment of patients with congestive heart failure, and when indicated, in combination with a diuretic and/or digitalis. Most controlled clinical trial experience when captopril was added, has been in patients receiving digitalis, and diuretic treatment.
Left Ventricular dysfunction after Myocardial Infarction
Captopril is indicated to improve survival following myocardial infarction in clinically stable patients with left ventricular dysfuction manifested as an ejection fraction < 40%.
Diabetic Nephropathy: CAPOTEN (captopril) is indicated for the management of diabetic nephropathy (protein urea >500 mg/day) in patients with Type I diabetes mellitus who also have retinopathy due to insulin dependant diabetes mellitus. In these patients, CAPOTEN decreases the rate of progression of renal insufficiency.

Hypersensitivity to the product or its components, or other angiotensin-converting enzyme inhibitors.
Safety and effectiveness in individuals less than 18 years of age have not been established.
Patients with a history of angioneurotic oedema relating to previous treatment with an ACE-inhibitor. (See SPECIAL PRECAUTIONS.)
Pregnancy (see warnings)
Nursing mothers: Concentrations of unchanged captopril appear in human breast milk. Caution should be exercised when Capoten is administered to a nursing woman.

Fetal/Neonatal Morbidity and Mortality:
Should a woman become pregnant while receiving an ACE-inhibitor, the treatment must be stopped promptly and switched to a different medicine. Should a woman contemplate pregnancy, the doctor should consider alternative medication.
ACE-inhibitors pass through the placenta and can be presumed to cause disturbance in fetal blood pressure regulatory mechanisms. Oligohydramnios as well as hypotension, oliguria and anuria in newborns have been reported after administration of ACE-inhibitors in the second and third trimester. Cases of defective skull ossification have been observed. Prematurity and low birth mass can occur.
Head and Neck Angioedema: Angioedema involving the extremities, face, eyes, lips, mucous membranes, tongue, glottis or larynx has been seen in patients treated with Capoten. Patients should be advised to immediately report to their physician any signs or symptoms suggesting angioedema (e.g. swelling of face, eyes, lips, tongue, larynx and extremities; difficulty in swallowing or breathing; hoarseness) and to discontinue therapy. If angioedema involves the tongue, glottis or larynx, airway obstruction may occur and be fatal. Emergency therapy including but not necessarily limited to, subcutaneous administration of a 1:1000 solution of adrenaline should be promptly instituted. Swelling confined to the face, mucous membranes of the mouth, lips and extremities has usually resolved with discontinuation of Capoten, some cases required medical therapy (see SIDE EFFECTS AND SPECIAL PRECAUTIONS).
Intestinal Angioedema:
Intestinal angioedema has been reported rarely in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases there was no prior facial angioedema and C-1 esterasae levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan, or ultrasound, or at surgery, and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the different diagnosis of patients on ACE inhibitors presenting with abdominal pain.
Anaphylactoid reactions during high-flux dialysis/lipoprotein apheresis membrane exposure: Anaphylactoid reactions have been reported in patients haemodialyzed with high-flux dialysis membranes. Anaphylactoid reactions have also been reported in patients undergoing low-density lipoprotein apheresis with dextran sulfate absorption. In these patients, consideration should be given to using a different type of dialysis membrane or a different class of medication.
Anaphylactoid reactions during desensitization: Two patients undergoing desensitization treatment with hymenoptera venom while receiving an ACE inhibitor, sustained life-threatening anaphylactoid reactions. In the same patients, these reactions were avoided when the ACE inhibitor was temporarily withheld, but they reappeared upon inadvertent rechallenge. Therefore, caution should be used in patients treated with ACE inhibitors undergoing such desensitizations procedures.
Proteinuria: Proteinuria has been seen in patients receiving Capoten, but this has been predominantly in those who had prior renal disease or in those receiving relatively high doses (in excess of 150 mg per day), or both. Alterations in renal function (as assessed by blood urea and serum creatinine) were infrequent in these patients and did not occur in those who had prior renal disease. Nephrotic syndrome (hypoalbuminemia, edema and protein excretion greater than 3 grams per day) has also occurred. In most cases, proteinuria subsided or cleared within 6 months whether or not Capoten was continued.
Membranous glomerulopathy was found in biopsies taken from some proteinuric patients. A causal relationship to Capoten has not been established.
For patients with prior renal disease or those receiving Capoten at doses greater than 150 mg per day, urinary protein estimations (dipstick) should be done prior to treatment and monthly during the first 9 months of therapy. If these show increasing amounts of urinary protein, a 24-hour quantitative determination of urinary protein should be done. If this exceeds one gram per day, the benefits and risks of continuing Capoten should be evaluated.
Neutropenia/Agranulocytosis: Neutropenia which may be fatal has occurred in patients receiving Capoten especially in those who had pre-existing impaired renal function, collagen vascular disease, immunosuppressant therapy, concomitant allopurinol or a combination of these complicating factors and in patients using higher than recommended doses.
Evaluation of the hypertensive or heart failure patient should always include assessment of renal function.
If captopril is used in patients with impaired renal function, white blood cell and differential counts should be evaluated prior to starting treatment and at approximately two-week intervals for about three months, then periodically.
In patients with collagen vascular disease or who are exposed to other medicines known to affect the white cells or immune response, particularly when there is impaired renal function, captopril should be used only after an assessment of benefit and risk, and then with caution.
All patients receiving Capoten should be told to report any signs of infection (e.g. sore throat, fever). Serious infections resulting from the neutropenia and which proved fatal occurred at recommended doses only in patients with impaired renal function. A complete white blood cell count should be done immediately when infection is present. If the infection occurs during the first three months of therapy, Capoten should be discontinued until the results of the blood count are known.
Neutropenia was noted 2½ to 13 weeks after Capoten had been started. Thus, for patients with impaired renal function, collagen vascular disease, or who are receiving immunosuppressant drugs, white blood cell and differential counts should be performed prior to therapy, every 2 weeks during the first three months of Capoten therapy and periodically thereafter. If the neutrophil count falls below 1 000/mm3 Capoten should be discontinued and the patient's course should be followed. In general, neutrophils returned to normal in about two weeks after captopril was discontinued.
Bone marrow examinations in patients with neutropenia consistently showed myeloid hypoplasia frequently accompanied by erythriod hypoplasia and decreased numbers of megakaryocytes (eg hypoplastic bone marrow and pancytopenia; anemia and thrombocytopenia was sometimes seen). Neutropenia was associated with significant alterations of peripheral red blood cell or platelet counts in some patients.
Elevations in serum potassium have been observed in patients treated with CAPOTEN. Patients at risk for the development of hyperkalemia include those with: renal insufficiency; diabetes mellitus; and those using concomitant potassium-sparing diuretics, potassium supplements or potassium-containing salt substitutes; or other drugs associated with increases in serum potassium (e.g., heparin).
Hypotension: Symptomatic hypotension may occur in hypertensive patients and may be a possible consequence of captopril use in salt/volume depleted persons (such as those treated vigorously with diuretics), patients with heart failure or those patients undergoing renal dialysis. It has also been reported in patients without known predisposing conditions. Hypotensive episodes are usually seen early during treatment but may occur after longterm use. In hypertension, the possibility of hypotensive effects with the initial doses of captopril may be reduced by discontinuing the diuretic approximately one week prior to initiation of treatment with CAPOTEN (captopril) or initiating therapy with small doses (6,25 or 12,5 mg). Alternatively, medical supervision should be provided for at least one hour after the initial dose. A transient hypotensive response is not a contraindication to further doses which can be given without difficulty once the blood pressure has increased.
In heart failure, where the blood pressure was either normal or low, transient decreases in mean blood pressure greater than 20 percent were recorded in about half of the patients. This transient hypotension is more likely to occur after any of the first several doses and is usually well tolerated, producing either no symptoms or brief mild lightheadedness, although in rare instances it has been associated with arrhythmia or conduction defects.
A starting dose of 6,25 or 12,5 mg twice or three tomes a day may minimize the hypotensive effect. Patients should be followed closely for the first two weeks of treatment and whenever the dose of CAPOTEN and/or diuretic is increased.
Hypotension is not per se a reason to discontinue CAPOTEN. Some decrease of systemic blood pressure is a common and desirable observation upon initiation of CAPOTEN treatment in heart failure. The magnitude of the decrease is greatest early in the course of treatment; this effect stabilizes within a week or two, and generally returns to pretreatment levels, without a decrease in therapeutic efficacy, within two months.       
A hypotensive episode following the initial dose of Capoten does not preclude further episodes.
Hepatic Failure: CAPOTEN has been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood. Patients receiving CAPOTEN who develop jaundice or marked elevations of hepatic enzymes should discontinue the CAPOTEN and receive appropriate medical follow-up.
Impaired Renal Function
Some patients with renal disease, particularly those with bilateral renal artery stenosis, have developed increases in blood urea and serum creatinine after reduction of blood pressure with Capoten, usually along with a diuretic. Capoten dosage reduction or discontinuation of a diuretic, or both may be required. For some of these patients, it may not be possible to normalise blood pressure and maintain adequate renal perfusion. Some patients with heart failure have experienced a reduction in renal function during long term treatment.
Pediatric Use
: Safety and effectiveness in pediatric patients have not been established. There is limited experience reported in the literature with the use of captopril in the pediatric population; dosage, on a weight basis, was generally reported to be comparable to or less than that used in adults.
Infants, especially newborns, may be more susceptible to the adverse hemodynamic effects of captopril. Excessive, prolonged and unpredictable decreases in blood pressure and associated complications, including oliguria and seizures, have been reported.
CAPOTEN (captopril tablets) should be used in pediatric patients only if other measures for controlling blood pressure have not been effective.

Dosage must be individualised. See WARNINGS regarding hypotension in salt and volume depleted patients. CAPOTEN should be taken one hour before food intake. If possible, discontinue the patient's previous antihypertensive therapy for one week before initiating CAPOTEN. If CAPOTEN is being started in a patient already receiving a diuretic, CAPOTEN therapy should be initiated under close medical supervision.
Hypertension: The initial dose of CAPOTEN is 25 mg two or three times a day. If a satisfactory reduction of blood pressure has not been achieved after two weeks the dose of CAPOTEN may be increased to 50 mg two or three times a day. If after an additional two weeks a further reduction in blood pressure is desirable, a diuretic may be added. For patients already receiving a diuretic, the initial dose of CAPOTEN should be lower and administered with care. The dose of CAPOTEN in mild to moderate hypertension must not exceed 150 mg per day. When CAPOTEN is used alone, concomitant sodium restriction may be beneficial. CAPOTEN may be used advantageously in conjunction with other anti-hypertensive agents.
Congestive Heart Failure: Capoten therapy must be started under close medical supervision. It should be added to conventional treatment with diuretic (and digitalis where indicated). In patients with either normal or low blood pressure, who have been vigorously treated with diuretics and who may be hyponatremic and/or hypovolemic, a starting dose of 6,25 mg or 12,5 mg three times a day may minimise the duration of any transient hypotensive effect. (See WARNINGS). This dosage may be increased over a period of one to two weeks to 75 - 300  mg per day. For most patients the usual initial daily dosage is 25 mg three times a day. After a dose of 50 mg three times a day is reached, further increases in dosage should be delayed, where possible, for at least two weeks to determine if a satisfactory response occurs. Most patients studied have had a satisfactory clinical improvement at 50 or 100 mg three times a day.
Left Ventricular Dysfunction After Myocardial Infarction: Therapy may be initiated as early as three days following a myocardial infarction. After an initial dose of 6,25 mg, captopril therapy should be increased to 12,5 mg three times daily as tolerated. Captopril should then be increased as tolerated to 75 mg a day in divided doses during the next several days and to a final target dose of 150 mg daily in divided doses over the next several weeks.
If symptomatic hypotension occurs, a dosage reduction may be required. Subsequent attempts at achieving the target dose of 150 mg should be based on the patient's tolerance to captopril.
Captopril may be used in patients with other post-myocardial infarction therapies, e.g., thrombolytics, aspirin, beta blockers.
Diabetic Nephropathy: In patients with diabetic nephropathy with or without hypertension, the recommended daily dose of captopril is 75 to 100 mg in divided doses.
If further blood pressure reduction is required, other antihypertensive agents such as diuretics, beta adrenoceptor blockers, centrally acting agents or vasodilators may be used in conjunction with captopril.
Dosage Adjustment in Renal Impairment: (See PRECAUTIONS - General, Hyperkalemia)
CAPOTEN (captopril) is excreted primarily by the kidneys. Excretion rates are reduced in patients with impaired renal function. These patients will take longer to reach steady-state captopril levels and will reach higher steady-state levels for a given daily dose than patients with normal renal function. Therefore, these patients may respond to smaller or less frequent doses.
Accordingly, for patients with significant renal impairments, initial daily dosage of CAPOTEN (captopril) should be reduced, and smaller increments utilized for titration, which should be quite slow (one to two week intervals). After the desired therapeutic effect has been achieved, the dose should be slowly back titrated to determine the minimal effective dose.
The following maximum daily doses are suggested as a guide to minimise drug accumulation.
More than

Less than
40 - 21
20 - 11
Capoten is removed by haemodialysis. (Note: See WARNINGS: Anaphylactoid Reaction during high-flux dialysis). When concomitant diuretic therapy is required, a loop diuretic (e.g. furosemide), rather than a thiazide diuretic, is preferred in these patients with impaired renal function.

Dermatologic: A rash may occur which is dose related. The rash is usually pruritic and maculopapular, sometimes with fever, arthralgia, and eosinophilia, but rarely urticarial and generally occurs during the first 4 weeks of treatment. It usually is self-limited and reversible and may respond to antihistamine therapy. Pruritus with or without rash, flushing, a reversible pemphigoid-like lesion, photosensitivity, angioedema (life-threatening and fatal) may occur.
Gastro-Intestinal: A reversible taste impairment has occurred. Loss of mass may be associated with loss of taste. Stomatitis, resembling aphthous ulcers, have been reported.
Elevation of liver enzymes has been noted in patients receiving the drug although no causal relationship has been found. Cases of hepatocellular injury with secondary cholestasis have been reported in association with Capoten administration. Gastric irritation and abdominal pain may occur.
Renal: Proteinuria (see WARNINGS).
Renal insufficiency, renal failure, nephrotis syndrome, polyuria, oligieria and urinary frequency.
Elevations of blood urea and creatinine (See PRECAUTIONS). Increase in the serum potassium concentrations and acidosis. (See WARNINGS).
Haematologic: Anemia, thrombocytopenia, pancytopenia and neutropenia/agranulocytosis have been reported (See WARNINGS).
Respiratory: Irritating cough, fatal angioneurotic oedema.
Cardiovascular: Hypotension may occur during Capoten therapy in patients with heart failure, renin-dependent hypertension or who are significantly volume depleted. (See WARNINGS). Tachycardia, chest pain, and palpitations have been observed. Other events which have occurred include angina pectoris, myocardial infarction, Raynaud's syndrome, and congestive heart failure. Tachycardia has been observed in volume-depleted patients.
Anaphylactoid Reactions: During haemodialysis (See WARNINGS).
Other: Paraesthesias of the hands, serum sickness, bronchospasm and lymphadenopathy have been reported. Angioedema of the face, eyes, lips, mucous membranes, tongue, glottis or larynx and the extremities may occur. CAPOTEN should be stopped immediately and patients should never be exposed again to any ACE-inhibitor.
Other clinical adverse effects reported since the medicine was marketed are listed below. Incidence or causal relationship cannot be accurately determined.
General: Asthenia, gynecomastia
Cardiovascular: Cardiac arrest, cerebrovascular accident/insufficiency, rhythm disturbances, orthostatic hypotension, syncope
Dermatologic: Bullous pemphigus, erythema multiforme (including Stevens-Johnson syndrome), exfoliative dermatitis
Gastrointestinal: Pancreatitis, glossitis, dyspepsia
Hematologic: including aplastic and haemolytic
Hepatobiliary: Jaundice, hepatitis, including rare cases of hepatic necrosis, cholestasis
Metabolic: Symptomatic hyponatremia
Musculoskeletal: Myalgia, myasthenia
Nervous/Psychiatric: Ataxia, confusion, depression, nervousness, somnolence
Respiratory: Bronchospasm, eosinophilic pneumonitis, rhinitis
Special Senses: Blurred vision
Urogenital: Impotence
A syndrome has been reported which may included: fever, myalgia, arthralgia, interstitial nephritis, vasculitis, rash or other dermatologic manifestations, eosinophilia and an elevated erythrocyte sedementation rate.
Altered Laboratory Findings
Serum Electrolytes: Hyperkalemia, especially in patients with renal impairment.
Hyponatremia, particularly in patients receiving a low sodium diet or concomitant diuretics.
Blood Urea, Serum Creatinine: Transient elevations of blood urea or serum creatinine, especially in volume or salt depleted patients or those with renovascular hypertension may occur.
Hematologic: A positive Anti-DNA Antibodies test has been reported.
Liver Function Tests: Elevations of liver transaminases, alkaline phosphatase, and serum bilirubin have occurred.

Impaired Renal Function
Heart Failure: Some patients may develop stable elevations of blood urea nitrogen and serum creatinine upon long-term treatment with captopril. A few patients, generally those with severe preexisting renal disease, required discontinuation of treatment due to progressively increasing creatinine; subsequent improvement probably depends upon the severity of the underlying renal disease.
Capoten should be used only with extreme caution in patients with aortic stenosis because of the potentially harmful consequences of reduced coronary perfusion secondary to the reduced blood pressure.
Capoten may cause a false-positive urine test for acetone.
Hyperkalemia (See WARNINGS)
Cough: ACE inhibitor-induced cough should be considered as part of the differential diagnosis of cough.
Surgery/Anaesthesia: In patients undergoing major surgery or during anaesthesia with agents that produce hypotension, Capoten will block angiotensin II formation secondary to compensatory renin release. This may lead to hypotension which can be corrected by volume expansion.

Patients on Diuretic Therapy:
Patients on diuretics and especially those in whom diuretic therapy was recently instituted, as well as those on severe dietary salt restrictions or dialysis, may experience a precipitous reduction of blood pressure often within the first hour after receiving the initial dose of captopril.
Agents Having Vasodilator Activity: Nitroglycerin or other nitrates or other drugs having vasodilator activity should be administered cautiously, and at low dosage.
Agents Affecting Sympathetic Activity: The sympathetic nervous system may be especially important in supporting blood pressure in patients receiving captopril alone or with diuretics. Therefore, agents affecting sympathetic activity (e.g., ganglionic blocking agents or adrenergic neuron blocking agents) should be used with caution.
Agents Increasing Serum Potassium: Since captopril decreases aldosterone production, elevation of serum potassium may occur. Potassium-sparing diuretics such as spironolactone, triamterene, or amiloride, or potassium supplements are generally contra-indicated and should be given only for documented hypokalemia, and then with caution, since they may lead to a significant increase of serum potassium. Salt substitutes containing potassium should also be used with caution.
Inhibitors of endogenous prostaglandin synthesis: It has been reported that indomethacin may reduce the antihypertensive effect of Capoten, especially in cases of low renin hypertension. Other nonsteroidal anti-inflammatory agents (e.g. aspirin) may also have this effect.
Lithium: Increased serum lithium levels and symptoms of lithium nephrotoxicity have been reported in patients receiving concomitant lithium and ACE inhibitor therapy. These drugs should be coadministered with caution and frequent monitoring of serum lithium levels is recommended. If a diuretic is also used, it may increase the risk of lithium toxicity.
Drug/Laboratory Test Interaction: Capoten may cause a false-positive urine test for acetone.

In the event of overdosage, hypotension would be the most important problem. Volume expansion with an intravenous infusion of normal saline is the treatment of choice. Captopril is removed by haemodialysis. (See WARNINGS) Treatment is symptomatic and supportive.

CAPOTEN HS A slightly mottled, white, flat capsule shaped tablet with a bisect bar on one side and the other face may bear the word ‘SQUIBB’ and the number 450.
CAPOTEN 25 mg A slightly mottled, white 6,5 mm square tablet, biconvex, quadrisected on one face; the other face may bear the word 'SQUIBB' and the number 452.

HS                Blister packs of 90 tablets.
25 mg Blister packs of 60 tablets.

Store at room temperature not exceeding 25°C.
Protect from excessive moisture, heat and light.

CAPOTEN HS         V/7.1/302
CAPOTEN 25 mg         N/7.1/84

47 Van Buuren Road,
Bedfordview. 2008.

JUNE 1997

*Authorised User of the TM CAPOTEN

Updated on this site: July 2005
Source: Pharmaceutical Industry

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