Alderos F
Alderos F Uses, Dosage, Side Effects, Food Interaction and all others data.
Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. Fenofibrate is rapidly hydrolyzed after oral ingestion to its pharmacologically active form, fenofibric acid. The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα)
It lowers lipid levels by activating peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII (an inhibitor of lipoprotein lipase activity), which increases lipolysis and elimination of triglyceride-rich particles from plasma. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly
PPARα also increases apoproteins AI and AII, reduces VLDL- and LDL-containing apoprotein B, and increases HDL-containing apoprotein AI and AII. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Fenofibrate is a fibrate that activates peroxisome proliferator activated receptor alpha (PPARα) to alter lipid metabolism and treat primary hypercholesterolemia, mixed dyslipidemia, and severe hypertriglyceridemia. Fenofibrate requires once daily dosing and has a half life of 19-27 hours so its duration of action is long. Fenofibrate capsules are given at a dose of 50-150mg daily so the therapeutic index is wide. Patients should be counselled about the risk of rhabdomyolysis, myopathy, and cholelithiasis when taking fibrates.
Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a precursor of sterols, including cholesterol.The primary site of action of rosuvastatin is the liver, the target organ for lowering cholesterol. Rosuvastatin increases the number of hepatic LDL receptors on the cell surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.
Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD. Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality. Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack. Evidence has shown that even for low-risk individuals (with 19,20
Skeletal Muscle Effects
Trade Name | Alderos F |
Generic | Fenofibrate + Rosuvastatin |
Type | Tablet |
Therapeutic Class | |
Manufacturer | Alde Medi Impex |
Available Country | India |
Last Updated: | September 19, 2023 at 7:00 am |
![Alderos F Alderos F](https://www.medicinesfaq.com/media/png/alderos-f.png)
Uses
Fenofibrate is used for an adjunct to diet and other non pharmacological treatment (e.g. exercise, weight reduction) for the following:
- Treatment of severe hypertriglyceridemia with or without low HDL cholesterol.
- Mixed hyperlipidemia when a statin is contraused or not tolerated.
- Mixed hyperlipidemia in patients at high cardiovascular risk in addition to a statin when triglycerides and HDL cholesterol are not adequately controlled
Primary hypercholesterolemia (type IIa including heterozygous familial hypercholesterolemia), mixed dyslipidemia (type IIb), or homozygous familial hypercholesterolemia in patients who have not responded adequately to diet and other appropriate measures; prevention of cardiovascular events in patients at high risk of a first cardiovascular event.
Alderos F is also used to associated treatment for these conditions: Mixed Dyslipidemias, Primary Hypercholesterolemia, Severe Hypertriglyceridemia, Severe Fredrickson Type IV Hypertriglyceridemia, Severe Fredrickson Type V HypertriglyceridemiaAtherosclerosis, Atherosclerotic Cardiovascular Diseases, Cardiovascular Disease (CVD), Cardiovascular Events, Dysbetalipoproteinemia, Heterozygous Familial Hypercholesterolemia, High Blood Pressure (Hypertension), High Cholesterol, Homozygous Familial Hypercholesterolemia, Hypertension,Essential, Hypertriglyceridemias, Major Adverse Cardiovascular Events, Mixed Dyslipidemias, Postoperative Thromboembolism, Primary Hypercholesterolemia, Primary Hyperlipidemia, Cardiovascular Primary Prevention, Lipid-Lowering Therapy
How Alderos F works
Fenofibrate activates peroxisome proliferator activated receptor alpha (PPARα), increasing lipolysis, activating lipoprotein lipase, and reducing apoprotein C-III. PPARα is a nuclear receptor and its activation alters lipid, glucose, and amino acid homeostasis. Activation of PPARα activates transcription of gene transcription and translation that generates peroxisomes filled with hydrogen peroxide, reactive oxygen species, and hydroxyl radicals that also participate in lipolysis. This mechanism of increased lipid metabolism is also associated with increased oxidative stress on the liver. In rare cases this stress can lead to cirrhosis and chronic active hepatitis.
Rosuvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Rosuvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL.
In vitro and in vivo animal studies also demonstrate that rosuvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins. This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response.
Statins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation.
Rosuvastatin exerts an anti-inflammatory effect on rat mesenteric microvascular endothelium by attenuating leukocyte rolling, adherence and transmigration. The drug also modulates nitric oxide synthase (NOS) expression and reduces ischemic-reperfusion injuries in rat hearts. Rosuvastatin increases the bioavailability of nitric oxide by upregulating NOS and by increasing the stability of NOS through post-transcriptional polyadenylation. It is unclear as to how rosuvastatin brings about these effects though they may be due to decreased concentrations of mevalonic acid.
Dosage
Alderos F dosage
The dose is one 200 mg capsule per day. Dosage should be individualized according to patient response, and should be increased sequentially if necessary following repeat serum triglyceride estimations at 4 to 8 week intervals. Patients should be placed on an appropriate triglyceride-lowering diet before receiving fenofibrate, and should continue this diet during treatment with fenofibrate. Fenofibrate should be given with meals, thereby optimizing the bioavailability of the medication.
Before treatment initiation the patient should be placed on a standard cholesterol-lowering diet that should continue during treatment. The dose should be individualized according to the goal of therapy and patient response, using current consensus guidelines.
Treatment of hypercholesterolemia: Patient of Asian origin or with risk factors for myopathy or rhabdomyolysis: initially 5 mg once daily increased if necessary to max. 20 mg daily.
Prevention of cardiovascular events: Patient of Asian origin or with risk factors for myopathy or rhabdomyolysis: initially 5 mg once daily increased if necessary to max. 20 mg daily.
Pediatric Use (Hyperlipidemia including familial hypercholesterolemia):
- Child younger than 6 years: not recommended.
- Child 6–9 years: initially 5 mg daily, increased if necessary at intervals of at least 4 weeks to usual max. 10 mg once daily.
- Child 10–18 years: initially 5 mg daily, increased if necessary at intervals of at least 4 weeks to usual max. 20 mg once daily.
[Reduced dose required with concomitant atazanavir, darunavir, ezetimibe, fibrate, itraconazole, lopinavir, or tipranavir]
Use in the elderly (>70 years): A start dose of 5 mg is recommended. No dose adjustment necessary.
Renal insufficiency:Initially 5mg once daily (do not exceed 20 mg daily) if eGFR is 30-60 mL/minute/1.73 m2. Avoid if eGFR is less than 30 mL/minute/1.73 m2
Hepatic impairment:
- Child-Pugh scores of <7: no increase in systemic exposure to rosuvastatin.
- Child-Pugh scores of 8 and 9: increased systemic exposure has been observed. In these patients an assessment of renalfunction should be considered.
- Child-Pugh scores >9: no study.
Rosuvastatin is contraindicated in patients withactive liver disease.
Race: Increased systemic exposure has been seen in Asian subjects. The recommended starting dose is 5 mg for patients of Asian ancestry. The 40 mg dose is contraindicated in these patients.
Genetic polymorphisms: Specific types of genetic polymorphisms are known that can lead to increased rosuvastatin exposure. For patients who are known to have such specific types of polymorphisms, a lower daily dose of Rosuvastatin is recommended.
Dosage in patients with pre-disposing factors to myopathy: The recommended starting dose is 5 mg in patients with predisposing factors to myopathy. The 40 mg dose is contraindicated in some of these patients.
Rosuvastatin may be given at any time of day, with or without food
Side Effects
Digestive: hepatitis, cholelithiasis, cholecystitis, hepatomegaly
Musculoskeletal: myalgia, myasthenia, rhabdomyolysis
Skin and appendages: photosensitivity, eczema
Cardiovascular: peripheral edema, angina, palpitations, tachycardia, and migraine
Common or very common: Proteinuria.
Rare: Hepatitis, jaundice.
Very rare: Gynecomastia, hematuria, hepati failure, interstitial lung disease, lupus erythematosus-like reactions, pancreatitis.
Frequency not known: Alopecia, altered liver function tests, amnesia, arthralgia, asthenia, depression, dizziness, edema, fatigue, gastrointestinal disturbances, headache, hypersensitivity reactions, hyperglycemia -may be associated with the development of diabetes mellitus (particularly in those already at risk of the condition), myalgia, myopathy, myositis, paresthesia, peripheral neuropathy, pruritus, rash, rhabdomyolysis, sexual dysfunction, sleep disturbance, Stevens-Johnson syndrome, thrombocytopenia, urticaria, visual disturbance.
Muscle effects: The risk of myopathy, myositis, and rhabdomyolysis associated with statin use is rare. Although myalgia has been reported commonly in patients receiving statins, muscle toxicity truly attributable to statin use is rare. Muscle toxicity can occur with all statins, however the likelihood increases with higher doses If muscular symptoms or raised creatine kinase occur during treatment, other possible causes (e.g. rigorous physical activity, hypothyroidism, infection, recent trauma, and drug or alcohol addiction) should be excluded before statin therapy is implicated, particularly if statin treatment has previously been tolerated for more than 3 months. When a statin is suspected to be the cause of myopathy, and creatine kinase concentration is markedly elevated (more than 5 times upper limit of normal), or if muscular symptoms are severe, treatment should be discontinued. If symptoms resolve and creatine kinase concentrations return to normal, the statin should be reintroduced at a lower dose and the patient monitored closely; an alternative statin should be prescribed if unacceptable side-effects are experienced with a particular statin. Statins should not be discontinued in the event of small, asymptomatic elevations of creatine kinase. Routine monitoring of creatine kinase is unnecessary in asymptomatic patients.Statins should not be discontinued if there is an increase in the blood-glucose concentration or HbA1C as the benefits continue to outweigh the risks.
Interstitial lung disease: If patients develop symptoms such as dyspnoea, cough, and weight loss, they should seek medical attention.
Toxicity
The oral LD50 in rats is >2g/kg and in mice is 1600mg/kg. The oral TDLO in rats is 9mg/kg.
Treat patients with supportive care including monitoring of vital signs and observing clinical status. Recent overdose may be treated with inducing vomiting or gastric lavage. Due to fenofibrate's extensive protein binding, hemodialysis is not expected to be useful.
Generally well-tolerated. Side effects may include myalgia, constipation, asthenia, abdominal pain, and nausea. Other possible side effects include myotoxicity (myopathy, myositis, rhabdomyolysis) and hepatotoxicity. To avoid toxicity in Asian patients, lower doses should be considered. Pharmacokinetic studies show an approximately two-fold increase in peak plasma concentration and AUC in Asian patients (Philippino, Chinese, Japanese, Korean, Vietnamese, or Asian-Indian descent) compared to Caucasian patients.
Precaution
Increased risk of cholelithiasis, pancreatitis, skeletal muscle effects. Patient at risk of rhabdomyolysis. Renal impairment. Pregnancy.
Hypothyroidism should be managed adequately before starting treatment with a statin. Statins should be used with caution in those with a history of liver disease or with a high alcohol intake. There is little information available on a rational approach to liver-function monitoring; however, a NICE guideline1 suggests that liver enzymes should be measured before treatment, and repeated within 3 months and at 12 months of starting treatment, unless indicated at other times by signs or symptoms suggestive of hepatotoxicity. Those with serum transaminases that are raised, but less than 3 times the upper limit of the reference range, should not be routinely excluded from statin therapy. Those with serum transaminases of more than 3 times the upper limit of the reference range should discontinue statin therapy.
Statins should be used with caution in those with risk factors for myopathy or rhabdomyolysis; patients should be advised to report unexplained muscle pain. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose galactose malabsorption should not take this medicine.
Interaction
Oral Anticoagulants: Caution should be exercised when anticoagulants are given in conjunction with fenofibrate. The dosage of the anticoagulants should be reduced to maintain the prothrombin time at the desired level to prevent bleeding complications.
Resins: Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate at least 1 hour before or 4-6 hours after a bile acid binding resin to avoid impending its absorption.
Cyclosporine: Because cyclosporine can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibrate, there is a risk that an interaction will lead to deterioration.
Cyclosporine: Cyclosporine increased rosuvastatin exposure (AUC) 7-fold. Therefore, in patients taking cyclosporine, the dose of Rosuvastatin should not exceed 5 mg once daily.
Gemfibrozil: Gemfibrozil significantly increased rosuvastatin exposure. Due to an observed increased risk of myopathy/rhabdomyolysis, combination therapy with Rosuvastatin and gemfibrozil should be avoided. If used together, the dose of Rosuvastatin should not exceed 10 mg once daily.
Protease Inhibitors: Coadministration of rosuvastatin with certain protease inhibitors has differing effects on rosuvastatin exposure. Simeprevir, which is a hepatitis C virus (HCV) protease inhibitor, or combinations of atazanavir/ritonavir or lopinavir/ritonavir, which are HIV-1 protease inhibitors, increase rosuvastatin exposure (AUC) up to threefold. For these protease inhibitors, the dose of Rosuvastatin should not exceed 10 mg once daily. The combinations of fosamprenavir / ritonavir or tipranavir / ritonavir, which are HIV 1 protease inhibitors, produce little or no change in rosuvastatin exposure. Caution should be exercised when rosuvastatin is coadministered with protease inhibitors.
Coumarin Anticoagulants: Rosuvastatin significantly increased INR in patients receiving coumarin anticoagulants. Therefore, caution should be exercised when coumarin anticoagulants are given in conjunction with Rosuvastatin. In patients taking coumarin anticoagulants and Rosuvastatin concomitantly, INR should be determined before starting Rosuvastatin and frequently enough during early therapy to ensure that no significant alteration of INR occurs.
Niacin: The risk of skeletal muscle effects may be enhanced when Rosuvastatin is used in combination with lipid-modifying doses (>1 g/day) of niacin; caution should be used when prescribing with Rosuvastatin.
Fenofibrate: When Rosuvastatin was coadministered with fenofibrate, no clinically significant increase in the AUC of rosuvastatin or fenofibrate was observed. Because it is known that the risk of myopathy during treatment with statins is increased with concomitant use of fenofibrates, caution should be used when prescribing fenofibrates with Rosuvastatin.
Colchicine: Cases of myopathy, including rhabdomyolysis, have been reported with statins, including rosuvastatin, coadministered with colchicine, and caution should be exercised when prescribing Rosuvastatin with colchicine
Volume of Distribution
The volume of distribution of fenofibrate is 0.89L/kg, and can be as high as 60L.
Rosuvastatin undergoes first-pass extraction in the liver, which is the primary site of cholesterol synthesis and LDL-C clearance. The mean volume of distribution at steady-state of rosuvastatin is approximately 134 litres.
Elimination Route
A single 300mg oral dose of fenofibrate reaches a Cmax of 6-9.5mg/L with a Tmax of 4-6h in healthy, fasting volunteers.
In a study of healthy white male volunteers, the absolute oral bioavailability of rosuvastatin was found to be approximately 20% while absorption was estimated to be 50%, which is consistent with a substantial first-pass effect after oral dosing. Another study in healthy volunteers found that the peak plasma concentration (Cmax) of rosuvastatin was 6.06ng/mL and was reached at a median of 5 hours following oral dosing. Both Cmax and AUC increased in approximate proportion to dose. Neither food nor evening versus morning administration was shown to have an effect on the AUC of rosuvastatin. Many statins are known to interact with hepatic uptake transporters and thus reach high concentrations at their site of action in the liver.
Breast Cancer Resistance Protein (BCRP) is a membrane-bound protein that plays an important role in the absorption of rosuvastatin, particularly as CYP3A4 has minimal involvement in its metabolism. Evidence from pharmacogenetic studies of c.421C>A single nucleotide polymorphisms (SNPs) in the gene for BCRP has demonstrated that individuals with the 421AA genotype have reduced functional activity and 2.4-fold higher AUC and Cmax values for rosuvastatin compared to study individuals with the control 421CC genotype. This has important implications for the variation in response to the drug in terms of efficacy and toxicity, particularly as the BCRP c.421C>A polymorphism occurs more frequently in Asian populations than in Caucasians. Other statin drugs impacted by this polymorphism include fluvastatin and atorvastatin.
Genetic differences in the OATP1B1 (organic-anion-transporting polypeptide 1B1) hepatic transporter have also been shown to impact rosuvastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C SNP showed that rosuvastatin AUC was increased 1.62-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals. Other statin drugs impacted by this polymorphism include simvastatin, pitavastatin, atorvastatin, and pravastatin.
For patients known to have the above-mentioned c.421AA BCRP or c.521CC OATP1B1 genotypes, a maximum daily dose of 20mg of rosuvastatin is recommended to avoid adverse effects from the increased exposure to the drug, such as muscle pain and risk of rhabdomyolysis.
Half Life
Fenofibric acid, the active metabolite of fenofibrate, has a half life of 23 hours. Fenofibrate has a half life of 19-27 hours in healthy subjects and up to 143 hours in patients with renal failure.
The elimination half-life (t½) of rosuvastatin is approximately 19 hours and does not increase with increasing doses.
Clearance
The oral clearance of fenofibrate is 1.1L/h in young adults and 1.2L/h in the elderly.
Elimination Route
5-25% of a dose of fenofibrate is eliminated in the feces, while 60-88% is eliminated in the urine. 70-75% of the dose recovered in the urine is in the form of fenofibryl glucuronide and 16% as fenofibric acid.
Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.
A study in healthy adult male volunteers found that approximately 90% of the rosuvastatin dose was recovered in feces within 72 hours after dose, while the remaining 10% was recovered in urine. The drug was completely excreted from the body after 10 days of dosing. They also found that approximately 76.8% of the excreted dose was unchanged from the parent compound, with the remaining dose recovered as the metabolites n-desmethyl rosuvastatin and rosuvastatin-5S-lactone.
Renal tubular secretion is responsible for >90% of total renal clearance, and is believed to be mediated primarily by the uptake transporter OAT3 (Organic anion transporter 1), while OAT1 had minimal involvement.
Pregnancy & Breastfeeding use
Pregnancy Category C. Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Nursing mothers: Fenofibrate should not be used in nursing mothers. Because of the potential for tumorigenicity seen in animal studies, a decision should be made whether to discontinue nursing or to discontinue the drug.
Pregnancy Category X. Teratogenic effects. Rosuvastatin is contraindicated in pregnancy and lactation. Women of child bearing potential should use appropriate contraceptive measures. If a patient becomes pregnant during use of this product, treatment should be discontinued immediately.
Rosuvastatin is excreted in the milk of rats. There are no data with respect to excretion in milk in humans
Contraindication
Fenofibrate is contraindicated in patients with-
- Hypersensitivity to fenofibrate or any component of this medication.
- Known photoallergy or phototoxic reaction during treatment with fibrates or ketoprofen.
- Severe liver dysfunction, gallbladder disease, biliary cirrhosis, severe renal disorders.
- Chronic or acute pancreatitis with the exception of acute pancreatitis due to severe hypertriglyceridemia.
- Pregnancy and lactation.
Rosuvastatin is contraindicated:
- In patients with hypersensitivity to rosuvastatin or to any of the excipients.
- In patients with active liver disease including unexplained, persistent elevations of serum transaminases and any serum transaminase elevation exceeding 3 x the upper limit of normal (ULN).
- In patients with severe renal impairment (creatinine clearance < mL/minute/1.73m2).
- In patients with myopathy.
- In patients receiving concomitant cyclosporine.
- During pregnancy and lactation and in women of childbearing potential not using appropriate contraceptive measures.
Special Warning
Geriatrics: This indicates that a similar dosage regimen can be used in the elderly, without increasing accumulation of the drug or metabolites.
Pediatrics: No data are available. Fenofibrate is not indicated for use in the pediatric population.
Gender: No pharmacokinetic difference between male and female has been observed for fenofibrate.
Renal insufficiency: The dosage of fenofibrate should be minimized in patients who have severe renal impairment, while no modification of dosage is required in patients having moderate renal impairment.
Hepatic insufficiency: No pharmacokinetic study has been conducted in patients having hepatic insufficiency.
Age and sex: There was no clinically relevant effect of age or sex on the pharmacokinetics of Rosuvastatin in adults.
Race: Pharmacokinetic studies show an increase in exposure in Asian subjects compared with Caucasians.
Severe renal impairment (not on hemodialysis): Starting dose is 5 mg, not to exceed 10 mg
Use in the elderly: Patients > 70 years: A start dose of 5 mg is recommended. No dose adjustment necessary.
Renal insufficiency: Initially 5mg once daily (do not exceed 20mg daily) if eGFR is 30–60 mL/ minute/ 1.73 m2. Avoid if eGFR is less than 30 mL /minute/ 1.73 m2.
Genetic polymorphisms: Specific types of genetic polymorphisms are known that can lead to increased rosuvastatin exposure. For patients who are known to have such specific types of polymorphisms, a lower daily dose of Rosuvastatin is recommended.
Dosage in patients with pre-disposing factors to myopathy: The recommended starting dose is 5 mg in patients with predisposing factors to myopathy. The 40 mg dose is contraindicated in some of these patients.
Acute Overdose
There is no specific treatment in the event of overdose. In the event of overdose, the patient should be treated symptomatically and supportive measures instituted as required. Haemodialysis is unlikely to be of benefit.
Storage Condition
Store at cool & dry place. Protect from light and moisture.
Keep out of the reach of children. Store below 30° C. Keep in the original package in a cool & dry place in order to protect from light and moisture.
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