Amara/Amara-4

Amara/Amara-4

glimepiride

Manufacturer:

Synmedic

Distributor:

Corbridge

Marketer:

Ambica
Full Prescribing Info
Contents
Glimepiride.
Description
Amara: Each uncoated tablet contains: Glimepiride USP 2 mg.
Amara-4: Each tablet contains: Glimepiride 4 mg.
Action
Pharmacotherapeutic group: Amara-4: Blood glucose lowering drugs, excl. insulins: Sulfonamides, urea derivatives.
Pharmacology: Pharmacodynamics: Amara: Mode of Action: Both in healthy persons and in patients with type 2 diabetes mellitus, Glimepiride decreases blood glucose concentrations, mainly by stimulating insulin release from pancreatic beta cells. This effect is based predominantly on an improved responsiveness of the pancreatic beta cells to the physiological glucose stimulus. While achieving an equivalent reduction in blood glucose, the administration of low doses of Glimepiride to animals and healthy volunteers causes the release of smaller amounts of insulin compared with Glibenclamide. This fact points to the existence of extrapancreatic (insulin-sensitizing and insulin-mimetic) effects of Glimepiride.
Moreover, compared to other sulfonylureas, Glimepiride has less effect on the cardiovascular system. It reduces platelet aggregation (animal and in vitro data) and leads to a marked reduction in the formation of atherosclerotic plaques (animal data).
Insulin release: Like all sulfonylureas, Glimepiride regulates insulin secretion by interacting with the ATP-sensitive potassium channel in the beta cell membrane. Unlike other sulfonylureas, Glimepiride binds specifically to a 65 kDa protein located in the membrane of the beta cell. This interaction of Glimepiride with its binding protein determines the probability of the ATP-sensitive potassium channel being open or closed.
Glimepiride closes the potassium channel. This induces depolarization of the beta cell and results in opening of voltage-sensitive calcium channels and influx of calcium into the cell. Finally, the rise in intracellular calcium concentration activates the release of insulin through exocytosis.
Glimepiride associates with and dissociates from its binding protein much more rapidly and, hence, frequently than glibenclamide. It is assumed that this characteristic high exchange rate of Glimepiride with the binding protein is responsible for its pronounced glucose sensitizing effect and for protecting the beta cells from desensitization and premature exhaustion.
Insulin-sensitizing effect: Glimepiride augments the normal action of insulin on peripheral glucose uptake (human and animal data).
Insulin-mimetic effects: Glimepiride mimics the action of insulin on peripheral glucose uptake and hepatic glucose output.
Peripheral glucose uptake occurs by transport into the muscle and fat cells. Glimepiride directly increases the number of glucose transport molecules in the plasma membranes of muscle and fat cells. The increased influx of glucose causes an activation of the glycosylphosphatidylinositol-specific phospholipase C. As a result, cellular cAMP levels decrease, causing a reduction in activity of protein kinase A; this in turn results in a stimulation of the metabolism of the glucose.
Glimepiride inhibits hepatic glucose output by increasing the concentration of fructose-2,6 bisphosphate which inhibits gluconeogenesis.
Effects on platelet aggregation and formation of atherosclerotic plaques: Glimepiride reduces platelet aggregation in vitro and in vivo. This effect is probably the result of a selective inhibition of cyclooxygenase, which is responsible for the formation of thromboxane A, an important endogenous platelet aggregation factor.
Glimepiride significantly reduces the formation of atherosclerotic plaques in animals. The underlying mechanism has still to be elucidated.
Cardiovascular effects: Through ATP-sensitive potassium channels (see previously mentioned), sulfonylureas also affect the cardiovascular system. Compared with conventional sulfonylureas, Glimepiride has significantly less effect on the cardiovascular system (animal data). This may be explained by the specific nature of its interaction with the binding protein of the ATP-sensitive potassium channel.
Pharmacodynamic Characteristics: In healthy persons, the minimum effective oral dose is approx. 0.6 mg. The effect of Glimepiride is dose-dependent and reproducible. The physiological response to acute physical exercise, i.e., reduction of insulin secretion, is still present under Glimepiride.
There was no significant difference in effect regardless of whether the drug was given 30 minutes or immediately before a meal. In diabetic patients, good metabolic control over 24 hours can be achieved with one single dose. Moreover, in a clinical study, good metabolic control was even achieved in 12 out of 16 patients with renal insufficiency (creatinine clearance 4 to 79 mL/min).
Although the hydroxy metabolite of Glimepiride caused a small but significant decrease in serum glucose in healthy persons, it accounts for only a minor part of the total drug effect.
Combination therapy with metformin: In patients not adequately controlled with the maximum dosage of either Glimepiride or metformin, combination therapy with both oral antidiabetic agents can be initiated.
The improvement in metabolic control in conjunction with combination treatment as compared to treatment with either medicinal product alone has been verified in two studies.
Combination therapy with insulin: In patients not adequately controlled with the maximum dosage of either Glimepiride or metformin, combination therapy with both oral antidiabetic agents can be initiated. In two studies, the combination achieved the same improvement in metabolic control as insulin alone; however, a lower average dose of insulin was required in combination therapy.
Clinical Efficacy/Clinical Studies: An active controlled clinical trial (Glimepiride up to 8 mg daily or metformin up to 2,000 mg daily) of 24 weeks duration was performed in 285 randomized children (8-17 years of age) with type 2 diabetes. Both Glimepiride and metformin exhibited a significant decrease from baseline in HbA1c.
No significant difference was observed between treatment groups. Glimepiride failed to demonstrate non-inferiority to metformin.
Following Glimepiride treatment, there were no new safety concerns noted in children compared to adult patients with type 2 diabetes mellitus. No long-term efficacy and safety data are available in paediatric patients.
Amara-4: Glimepiride is an orally active hypoglycaemic substance belonging to the sulfonylurea group. It may be used in non-insulin dependent (type 2) diabetes mellitus.
Glimepiride acts mainly by stimulating insulin release from pancreatic beta cells. As with other sulfonylureas this effect is based on an increase of responsiveness of the pancreatic beta cells to the physiological glucose stimulus. In addition, glimepiride seems to have pronounced extrapancreatic effects also postulated for other sulfonylureas.
Insulin release: Sulfonylureas regulate insulin secretion by closing the ATP-sensitive potassium channel in the beta cell membrane. Closing the potassium channel induces depolarisation of the beta cell and results - by opening of calcium channels - in an increased influx of calcium into the cell. This leads to insulin release through exocytosis.
Glimepiride binds with a high exchange rate to a beta cell membrane protein which is associated with the ATP-sensitive potassium channel but which is different from the usual sulfonylureas binding site.
Extrapancreatic activity: The extrapancreatic effects are for example an improvement of the sensitivity of the peripheral tissue for insulin and a decrease of the insulin uptake by the liver.
The uptake of glucose from blood into peripheral muscle and fat tissues occurs via special transport proteins, located in the cell membrane. The transport of glucose in these tissues is the rate limiting step in the use of glucose. Glimepiride increases very rapidly the number of active glucose transport molecules in the plasma membranes of muscle and fat cells, resulting in stimulated glucose uptake.
Glimepiride increases the activity of the glycosyl-phosphatidylinositol-specific phospholipase C, which may be correlated with the drug-induced lipogenesis and glycogenesis in isolated fat and muscle cells.
Glimepiride inhibits the glucose production in the liver by increasing the intracellular concentration of fructose-2,6-bisphosphate, which in its turn inhibits the gluconeogenesis.
General: In healthy persons, the minimum effective oral dose is approximately 0.6 mg. The effect of glimepiride is dose-dependent and reproducible. The physiological response to acute physical exercise, reduction of insulin secretion, is still present under glimepiride.
There was no significant difference in effect regardless of whether the medicinal product was given 30 minutes or immediately before a meal. In diabetic patients, good metabolic control over 24 hours can be achieved with a single daily dose.
Although the hydroxy metabolite of glimepiride caused a small but significant decrease in serum glucose in healthy persons, it accounts for only a minor part of the total drug effect.
Combination therapy with metformin: Improved metabolic control for concomitant glimepiride therapy compared to metformin alone in patients not adequately controlled with the maximum daily dosage of metformin has been shown in one study.
Combination therapy with insulin: Data for combination therapy with insulin are limited. In patients not adequately controlled with the maximum dosage of glimepiride, concomitant insulin therapy can be initiated. In two studies, the combination achieved the same improvement in metabolic control as insulin alone; however, a lower average dose of insulin was required in combination therapy.
Special populations: Paediatric population: An active controlled clinical trial (glimepiride up to 8 mg daily or metformin up to 2,000 mg daily) of 24 weeks duration was performed in 285 children (8-17 years of age) with type 2 diabetes.
Both glimepiride and metformin exhibited a significant decrease from baseline in HbA1c (glimepiride -0.95 (se 0.41); metformin -1.39 (se 0.40)). However, glimepiride did not achieve the criteria of non-inferiority to metformin in mean change from baseline of HbA1c. The difference between treatments was 0.44% in favour of metformin. The upper limit (1.05) of the 95% confidence interval for the difference was not below the 0.3% non-inferiority margin.
Following glimepiride treatment, there were no new safety concerns noted in children compared to adult patients with type 2 diabetes mellitus. No long-term efficacy and safety data are available in paediatric patients.
Pharmacokinetics: Amara: The primary mechanism of action of Glimepiride in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells. In addition, extrapancreatic effects may also play a role in the activity of sulfonylureas such as Glimepiride. This supported by both pre-clinical and clinical studies demonstrating that the Glimepiride administration can lead to increased sensitivity of peripheral tissues to insulin. This findings are consistent with the results of a long term randomized, placebo-controlled trial in which Glimepiride therapy improved postprandial insulin/C-peptide levels responses and overall glycemic controlled without producing clinically meaningful increased in fasting insulin/C-peptide levels. However, as with other sulfonylureas, the mechanism by which Glimepiride lowers blood glucose during long-term administration has not been clearly established.
Amara-4: Absorption: The bioavailability of glimepiride after oral administration is complete. Food intake has no relevant influence on absorption, only the absorption rate is slightly diminished. Maximum serum concentrations (Cmax) are reached approx 2.5 hours after oral intake (mean 0.3 μg/mL during multiple dosing of 4 mg/daily) and there is a linear relationship between dose and both Cmax and AUC (area under the time concentration curve).
Distribution: Glimepiride has a very low distribution volume (approx. 8.8 litres), which is roughly equal to the albumin distribution space, high protein binding (>99%) and a low clearance (approx. 48 ml/min).
In animals, glimepiride is excreted in milk. Glimepiride is transferred to the placenta. Passage of the blood-brain barrier is low.
Biotransformation and Elimination: Mean dominant serum half-life, which is of relevance for the serum concentrations under multiple-dose conditions, is about 5 to 8 hours. After high doses, slightly longer half-lives were noted.
After a single dose of radiolabelled glimepiride, 58% of the radioactivity was recovered in the urine, and 35% in the faeces. No unchanged substance was detected in the urine. Two metabolites most probably resulting from hepatic metabolism (major enzyme is CYP2C9) were identified both in urine and faeces: the hydroxy derivative and the carboxy derivative. After oral administration of glimepiride, the terminal half-lives of these metabolites were 3 to 6 and 5 to 6 hours respectively.
Comparison of single and multiple once-daily dosing revealed no significant differences in pharmacokinetics, and the intra individual variability was very low. There was no relevant accumulation.
Special populations: Pharmacokinetics were similar in males and females, as well as in young and elderly (above 65 years) patients. In patients with low creatinine clearance, there was a tendency for glimepiride clearance to increase and for average serum concentrations to decrease, most probably resulting from a more rapid elimination because of lower protein binding.
Renal elimination of the two metabolites was impaired. Overall no additional risk of accumulation is to be assumed in such patients.
Pharmacokinetics in five non-diabetic patients after bile duct surgery were similar to those in healthy persons.
Paediatric population: A fed study investigating the pharmacokinetics, safety, and tolerability of a 1 mg single dose of glimepiride in 30 paediatric patients (4 children aged 10-12 years and 26 children aged 12-17 years) with type 2 diabetes showed mean AUC(0-last), Cmax and t1/2 similar to that previously observed in adults.
Mechanism of Action: Glimepiride distinctly lowers the blood glucose level by both the defects associated with Type 2 diabetes, by stimulating pancreatic beta cells to produce more insulin, and induce increased activity of peripheral insulin intra cellular receptor.
Clinical Pharmacology: With Glimepiride GI absorption is complete with no interference of meals. Significant absorption of glimepiride is seen within one hour, and distributed throughout the body, bound to the plasma protein to an extent of 99.5% and it is metabolised by oxidative biotransformation and 60% is excreted in the urine, and the remaining is excreted in the faeces.
Indications/Uses
Amara: Glimepiride is indicated for the treatment of type 2 diabetes mellitus, when diet, physical exercise and weight reduction alone are not adequate.
Amara-4: It is used for the treatment of Type 2 diabetes mellitus.
Dosage/Direction for Use
Amara: Given by mouth in a dose of 1 to 2 mg daily, initially may be increased if necessary to 4 mg daily for maintenance. Or as prescribed by the physician.
Amara-4: Glimepiride is given by mouth in a dose of 1 to 2 mg daily, which may be increased if necessary to 4 mg daily for maintenance. Or as prescribed by the physician.
Overdosage
Signs and Symptoms: Amara: Acute overdosage as well as long-term treatment with too high dose of Glimepiride may lead to severe life-threatening hypoglycemia.
Amara-4: After ingestion of an overdosage hypoglycaemia may occur, lasting from 12 to 72 hours, and may recur after an initial recovery. Symptoms may not be present for up to 24 hours after ingestion. In general observation in hospital is recommended. Nausea, vomiting and epigastric pain may occur. The hypoglycaemia may in general be accompanied by neurological symptoms like restlessness, tremor, visual disturbances, coordination problems, sleepiness, coma and convulsions.
Management: Amara: As soon as an overdose of Glimepiride has been discovered, a physician must be notified without delay.
The patient must immediately take sugar, if possible in the form of glucose, unless a physician has already undertaken responsibility for treating the overdose.
Careful monitoring is essential until the physician is confident that the patient is out of danger. It must be remembered that hypoglycemia may recur after initial recovery.
Admission to hospital may sometimes be necessary even as a precautionary measure. In particular, significant overdoses and severe reactions with signs such as loss of consciousness or other serious neurological disorders are medical emergencies and require immediate treatment and admission to hospital.
If, for example, the patient is unconscious, an intravenous injection of concentrated glucose solution is indicated (for adults starting with 40 mL of 20% solution, for example). Alternatively in adults, administration of glucagon, e.g. in doses of 0.5 to 1 mg I.V., S.C. or I.M., may be considered.
In particular, when treating hypoglycemia due to accidental intake of Glimepiride in infants and young children, the dose of glucose given must be very carefully adjusted in view of the possibility of producing dangerous hyperglycemia, and must be controlled by close monitoring of blood glucose. Patients who have ingested life-threatening amounts of Glimepiride require detoxification (e.g. by gastric lavage and medicinal charcoal).
After acute glucose replacement has been completed it is usually necessary to give an intravenous glucose infusion in lower concentration so as to ensure that the hypoglycemia does not recur. The patient's blood glucose level should be carefully monitored for at least 24 hours. In severe cases with a protracted course, hypoglycemia, or the danger of slipping back into hypoglycemia, may persist for several days.
Amara-4: Treatment primarily consists of preventing absorption by inducing vomiting and then drinking water or lemonade with activated charcoal (adsorbent) and sodium-sulphate (laxative). If large quantities have been ingested gastric lavage is indicated, followed by activated charcoal and sodium-sulphate. In case of (severe) overdosage hospitalisation in an intensive care department is indicated. Start the administration of glucose as soon as possible, if necessary by a bolus intravenous injection of 50 mL of a 50% solution, followed by an infusion of a 10% solution with strict monitoring of blood glucose. Further treatment should be symptomatic.
In particular when treating hypoglycaemia due to accidental intake of glimepiride in infants and young children, the dose of glucose given must be carefully controlled to avoid the possibility of producing dangerous hyperglycaemia. Blood glucose should be closely monitored.
Contraindications
Amara: Hypersensitivity to Glimepiride, other sulfonylureas, other sulfonamides or any of the excipients. Insulin dependent (type I) diabetes mellitus (e.g., for the treatment of diabetics with a history of ketoacidosis) or diabetic precoma or coma.
Amara-4: Glimepiride is contraindicated in patients with the following conditions: hypersensitivity to glimepiride, other sulfonylureas or sulfonamides or to any of the excipients; insulin dependent diabetes; diabetic coma; ketoacidosis; severe renal or hepatic function disorders.
In case of severe renal or hepatic function disorders, a change over to insulin is required.
Warnings
Amara: In the initial weeks of treatment the risk of hypoglycemia may be increased and necessitates especially careful monitoring. Glucose levels in blood and urine must be checked regularly, as should additionally the proportion of glycated hemoglobin.
Alertness and reactions may be impaired due to hypo- or hyperglycemia. This may affect the ability to operate a vehicle or heavy machinery.
Special Precautions
Amara: Factors favouring hypoglycaemia include: Unwillingness or (more commonly in older patients) incapacity of the patient to cooperate; undernourishment, irregular mealtimes or skipped meals; imbalance between physical exertion and carbohydrate intake; alterations of diet; consumption of alcohol, especially in combination with skipped meals; impaired renal function; severe impairment of liver function; overdosage with Glimepiride; certain uncompensated disorders of the endocrine system affecting carbohydrate metabolism or counter regulation of hypoglycaemia (as for example in certain disorders of thyroid function and in anterior pituitary or corticoadrenal insufficiency); concurrent administration of certain other medicines, treatment with Glimepiride in the absence of any indication.
If such risk factors for hypoglycaemia are present, it may be necessary to adjust the dosage of Glimepiride or the entire therapy. This also applies whenever illness occurs during therapy or the patient's lifestyle changes.
Those symptoms of hypoglycaemia which reflect the body's adrenergic counter-regulation may be milder or absent where hypoglycaemia develops gradually, in the elderly, and where there is autonomic neuropathy or where the patient is receiving concurrent treatment with beta-blockers, clonidine, reserpine, guanethidine or other sympatholytic drugs.
Hypoglycaemia can almost always be promptly controlled by immediate intake of carbohydrates (glucose or sugar).
It is known from other sulfonylureas that, despite initially successful countermeasures, hypoglycaemia may recur. Patients must, therefore, remain under close observation.
Severe hypoglycaemia further requires immediate treatment and follow-up by a physician and, in some circumstances, in-patient hospital care.
Treatment of patients with G6PD-deficiency with sulfonylurea agents can lead to hemolytic anaemia.
Since Glimepiride belongs to the class of sulfonylurea agents, caution should be used in patients wtih G6PD-deficiency and a non-sulfonylurea alternatives should be considered.
Driving a Vehicle or Performing Other Hazardous Tasks: Alertness and reactions may be impaired due to hypo- or hyperglycaemia, especially when beginning or after altering treatment or when Glimepiride is not taken regularly. This may, for example, affect the ability to drive or to operate machinery.
Amara-4: Glimepiride must be taken shortly before or during a meal.
When meals are taken at irregular hours or skipped altogether, treatment with "Glimepiride Tablets" may lead to hypoglycaemia. Possible symptoms of hypoglycaemia include: headache, ravenous hunger, nausea, vomiting, lassitude, sleepiness, disordered sleep, restlessness, aggressiveness, impaired concentration, alertness and reaction time, depression, confusion, speech and visual disorders, aphasia, tremor, paresis, sensory disturbances, dizziness, helplessness, loss of self-control, delirium, cerebral convulsions, somnolence and loss of consciousness up to and including coma, shallow respiration and bradycardia. In addition, signs of adrenergic counter-regulation may be present such as sweating, clammy skin, anxiety, tachycardia, hypertension, palpitations, angina pectoris and cardiac arrhythmias.
The clinical picture of a severe hypoglycaemic attack may resemble that of a stroke.
Symptoms can almost always be promptly controlled by immediate intake carbohydrates (sugar). Artificial sweeteners have no effect.
It is known from other sulfonylureas that, despite initially successful countermeasures, hypoglycaemia may recur.
Severe hypoglycaemia or prolonged hypoglycaemia, only temporarily controlled by the usual amounts of sugar, require immediate medical treatment and occasionally hospitalisation.
Factors favouring hypoglycaemia include: unwillingness or (more commonly in older patients) incapacity of the patient to cooperate; undernutrition, irregular mealtimes or missed meals or periods of fasting; alterations in diet; imbalance between physical exertion and carbohydrate intake; consumption of alcohol, especially in combination with skipped meals; impaired renal function; serious liver dysfunction; overdosage with Glimepiride Tablets; certain uncompensated disorders of the endocrine system affecting carbohydrate metabolism or counter regulation of hypoglycaemia (as for example in certain disorders of thyroid function and in anterior pituitary or adrenocortical insufficiency); concurrent administration of certain other medicinal products.
Treatment with glimepiride tablets requires regular monitoring of glucose levels in blood and urine. In addition, determination of the proportion of glycosylated haemoglobin is recommended.
Regular hepatic and haematological monitoring (especially leucocytes and thrombocytes) are required during treatment with glimepiride tablets.
In stress-situations (e.g. accidents, acute operations, infections with fever etc) a temporary switch to insulin may be indicated.
No experience has been gained concerning the use of glimepiride tablets in patients with severe impairment of liver function or dialysis patients. In patients with severe impairment of renal or liver function change over to insulin is indicated.
Treatment of patients with G6PD-deficiency with sulfonylurea agents can lead to hemolytic anaemia. Since glimepiride belongs to the class of sulfonylurea agents, caution should be used in patients with G6PD-deficiency and a non-sulfonylurea alternative should be considered.
Glimepiride Tablets contains lactose monohydrate. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Sulfonylurea should not be used with Type I diabetes mellitus.
Use In Pregnancy & Lactation
Pregnancy: Amara: Glimepiride must not be taken during pregnancy. Otherwise there is risk of harm to the child. The patient must change over to insulin during pregnancy.
Patients planning a pregnancy must inform their physician.
It is recommended that such patients change over to insulin.
Amara-4: Risk related to the diabetes: Abnormal blood glucose levels during pregnancy are associated with a higher incidence of congenital abnormalities and perinatal mortality. So the blood glucose level must be closely monitored during pregnancy in order to avoid the teratogenic risk. The use of insulin is required under such circumstances. Patients who consider pregnancy should inform their physician.
Risk related to glimepiride: There are no adequate data from the use of glimepiride in pregnant women. Animal studies have shown reproductive toxicity which likely was related to the pharmacologic action (hypoglycaemia) of glimepiride.
Consequently, glimepiride should not be used during the whole pregnancy. In case of treatment by glimepiride, if the patient plans to become pregnant or if a pregnancy is discovered, the treatment should be switched as soon as possible to insulin therapy.
Lactation: Amara: To prevent possible ingestion with the breast milk and possible harm to the child, Glimepiride must not be taken by breastfeeding women. If necessary the patient must change over to insulin, or must stop breastfeeding.
Amara-4: The excretion in human milk is unknown. Glimepiride is excreted in rat milk. As other sulfonylureas are excreted in human milk and because there is a risk of hypoglycaemia in nursing infants, breastfeeding is advised against during treatment with glimepiride.
Adverse Reactions
Amara: Hypoglycemia, temporary visual impairment, gastrointestinal disturbances. Rarely thrombocytopenia, leucopenia, haemolytic anaemia. Occasionally allergic or pseudoallergic reactions like itching, urticaria or rashes. In isolated cases allergic vasculitis, photosensitivity or a disease in serum sodium may occur.
Amara-4: Gastrointestinal disturbances such as nausea, vomiting, heartburn, anorexia and diarrhea.
Increased appetite and weight gain may occur. Skin rashes and pruritus may occur and photosensitivity has been reported.
Drug Interactions
Amara: An increased hypoglycemic effect has occurred or might be expected with ACE Inhibitors, alcohol, allopurinol some analgesics (notably azapropazone, phenylbutazone and the salicylates), azoles, antifungals, (fluconazole, ketoconazole and miconazole), chloramphenicol, cimetidine, clofibrate and related compounds, coumarin anticoagulants, halofenate, heparin, MAOI's, octreotide (also this may also produce hyperglycemia), ranitidine, sulphinpyrazone, sulphonamides (including co-trimoxazole), tetracyclines, tricyclic antidepressants, and thyroid hormones.
Amara-4: With NSAID's e.g., Salicylates, Sulphonamides, Chloramphenicol, Coumadin and Probenecid may potentiate the hypoglycemic action of Glimepiride Thiazides, other diuretic, phenothiazines, thyroid products, oral contraceptives and phenytoin tend to produce hyperglycemic.
Storage
Store at temperatures not exceeding 30ºC.
MIMS Class
Antidiabetic Agents
ATC Classification
A10BB12 - glimepiride ; Belongs to the class of sulfonylureas. Used in the treatment of diabetes.
Presentation/Packing
Amara: Tab 2 mg (light pink, circular, biconvex shaped, uncoated, having breakline on one side and plain on the other side) x 30's.
Amara-4: Tab 4 mg (pink coloured flat, "8" shaped scored on both sides, uncoated) x 100's.
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