Forecox trek

INSTRUCTIONS FOR MEDICAL USE OF THE MEDICINAL PRODUCT FORECOX TRAC

Composition:

Active substances: 1 tablet contains rifampicin 150 mg, pyrazinamide 400 mg, ethambutol hydrochloride 275 mg, isoniazid 75 mg;

Excipients: povidone, shellac, disodium edetate, colloidal anhydrous silicon dioxide, maize starch, sodium croscarmellose, crospovidone, talc, calcium stearate, copovidone, hypromellose, castor oil, diethyl phthalate, titanium dioxide (E 171), magnesium stearate, yellow azo dye FCF (E 110).

Pharmaceutical form. Coated tablets.

Main physicochemical properties: bilayer convex capsule-shaped tablets, coated, from yellow-pink to beige-pink color, smooth on both sides.

Pharmacotherapeutic group.
Combination antituberculosis agents. ATC code J04AM06.

Pharmacological Properties.

Pharmacodynamics.

A combined antituberculosis agent, whose action is determined by its constituent components.

Rifampicin – a semi-synthetic broad-spectrum antibiotic exhibiting bacteriostatic, and at high doses bactericidal activity. It is active against M. tuberculosis (both intracellular and extracellular forms) and is a first-line antituberculosis drug. Rifampicin inhibits DNA-dependent RNA polymerase, which is responsible for bacterial genome synthesis.

Ethambutol – a chemotherapeutic agent exerting bacteriostatic effects against Mycobacterium tuberculosis strains, including those resistant to other antituberculosis agents. The mechanism of its tuberculostatic action is associated with inhibition of nucleic acid synthesis in bacterial cells. Ethambutol is active against almost all strains of M. tuberculosis, including M. bovis and M. kansasii.

INH (Isoniazid) – an antituberculosis drug, a derivative of isonicotinic acid. Isoniazid demonstrates high activity against Mycobacterium tuberculosis, particularly against rapidly dividing strains. A positive treatment outcome is observed when isoniazid is used in combination with other antituberculosis drugs. Its mechanism of action involves inhibition of mycolic acid synthesis, a key component of the bacterial cell wall. The minimal inhibitory concentration (MIC) of isoniazid against M. tuberculosis ranges from 0.05 to 0.025 mg. Resistance to isoniazid develops rapidly when it is used as monotherapy.

Pyrazinamide – active against mycobacteria resistant to first- and second-line antituberculosis drugs. It exerts bactericidal effects in an acidic environment. To exert its activity, pyrazinamide is converted into its active form—pyrazinoic acid—by enzymatic action. It penetrates well into tuberculosis lesions; its activity is not reduced in the acidic environment of caseous masses. Therefore, it should be prescribed in cases of caseous lymphadenitis, tuberculomas, and caseous-pneumonic processes. Resistance develops rapidly when pyrazinamide is used alone; hence, it should be combined with other antituberculosis drugs. The in vitro MIC of pyrazinamide is 20 mg/L. Pyrazinamide is not active against atypical mycobacteria.

Pharmacokinetics.

Pharmacokinetics has not been studied.

Clinical characteristics.

Indications.

Tuberculosis (initial phase of pulmonary and extrapulmonary disease), including in combination with other antituberculosis drugs.

Contraindications.

Hypersensitivity to the components of the drug or to other agents closely related in chemical structure (ethionamide, niacin). History of toxic drug-induced hepatitis, including due to administration of hydrazine derivatives of isonicotinic acid (e.g., phthivazide); recent infectious hepatitis (within less than 1 year), jaundice (including mechanical), acute hepatic and/or renal failure, severe impairment of liver and kidney function, pronounced atherosclerosis; severe cardiopulmonary insufficiency, gout (including acute), asymptomatic hyperuricemia, optic neuritis; cataract; diabetic retinopathy; inflammatory eye diseases, epilepsy, predisposition to seizures; severe psychoses (including in history); poliomyelitis (including previously experienced); concomitant use of saquinavir/ritonavir.

Isoniazid is contraindicated at doses exceeding 10 mg/kg during pregnancy, in III-degree cardiopulmonary insufficiency, stage II–III arterial hypertension, ischemic heart disease, neurological disorders, chronic renal failure, hepatitis during exacerbation, liver cirrhosis, bronchial asthma, psoriasis, eczema in the phase of exacerbation, hypothyroidism.

Interaction with other medicinal products and other forms of interaction.

Active components of the drug are hepatotoxic agents; therefore, due to the increased risk of liver damage, careful monitoring of liver function is required (see section "Special precautions for use").

When used concomitantly with antacids, reduced absorption of the drug components may occur; therefore, the drug should be taken at least 1 hour before antacids.

The drug is prescribed in combination with broad-spectrum antibacterial agents, fluoroquinolones, and sulfonamides.

Ethambutol.

Pharmacological antagonism occurs with ethionamide, spermine, spermidine, and magnesium. Ethambutol and pyrazinamide act synergistically on uric acid excretion. Combined treatment with ethambutol and isoniazid, when administered concomitantly with cyclosporine A, leads to enhanced breakdown of the latter, increasing the risk of transplant rejection. Ethambutol interacts in blood with phentolamine and may lead to increased arterial pressure. When ethambutol is used concomitantly with neurotoxic agents, enhanced neurotoxic effects of ethambutol may occur, as well as increased neurotoxicity of aminoglycosides, asparaginase, ciprofloxacin, methotrexate, carbamazepine, imipenem, lithium salts, and quinine.

Ethambutol reduces the therapeutic efficacy of digoxetin. Concomitant treatment with disulfiram may increase ethambutol concentration in blood serum and enhance its toxicity. Ethanol enhances the toxic effect of ethambutol on visual organs; therefore, alcohol consumption should be avoided during treatment.

Isoniazid.

When isoniazid is administered to patients with slow inactivation of the drug who are simultaneously receiving para-aminosalicylic acid, tissue concentration of the drug may increase, thereby increasing the risk of adverse effects.

Isoniazid may slow down hepatic metabolism of certain medicinal products, which may lead to increased toxicity. These include carbamazepine, primidone, phenytoin, diazepam, triazolam, chlorzoxazone, and disulfiram.

Isoniazid may reduce the therapeutic effect of levodopa.

Concomitant use of isoniazid with glucocorticosteroids increases metabolism and elimination of isoniazid. With itraconazole, a significant reduction in its serum concentration and lack of therapeutic effect may occur. When used concomitantly with ketoconazole, the level of ketoconazole in serum may decrease; therefore, serum concentration of the drug should be monitored and dosage adjusted if necessary. With acetaminophen, toxicity of the latter increases due to generation and accumulation of toxic metabolites in the liver, potentially leading to serious adverse reactions. With theophylline, plasma concentration of theophylline increases (monitoring of theophylline levels in blood and appropriate dose adjustment are required). With valproate, plasma concentration of valproate increases, requiring dose adjustment. With stavudine, the risk of distal sensory neuropathy increases. With zalcitabine in HIV-infected patients, clearance of isoniazid doubles, requiring monitoring of isoniazid and zalcitabine concentrations to ensure treatment efficacy. With vitamin B6 and glutamic acid, the likelihood of isoniazid side effects decreases. With diphenine, antiarrhythmic properties of diphenine are enhanced. Potential interaction of isoniazid with food products containing histamine and tyramine (hard cheese, red wine, tuna, tropical fish) may lead to adverse reactions such as headache, excessive sweating, palpitations, hot flashes, and arterial hypotension.

Rifampicin.

Rifampicin is a potent inducer of hepatic microsomal enzymes (cytochrome P450) and may cause potentially dangerous drug interactions. It accelerates metabolism of endogenous substrates such as adrenal hormones, thyroid hormones, and vitamin D.

Concomitant use of rifampicin with drugs metabolized by this enzyme system may accelerate their metabolism and reduce their activity; therefore, maintaining their optimal therapeutic blood concentration requires dosage adjustment both at the start of rifampicin therapy and after its discontinuation.

Rifampicin accelerates metabolism of antiarrhythmic drugs (e.g., disopyramide, mexiletine, quinidine, propafenone, tocainide); β-blockers (e.g., bisoprolol, propranolol); calcium channel blockers (e.g., diltiazem, nifedipine, verapamil, nimodipine, isradipine, nicardipine, nisoldipine); cardiac glycosides (digoxetin, digoxin); antiepileptic, anticonvulsant drugs (e.g., phenytoin, carbamazepine); psychotropic agents — antipsychotics (e.g., haloperidol, aripiprazole), tricyclic antidepressants (e.g., amitriptyline, nortriptyline), anxiolytics and hypnotics (e.g., diazepam, benzodiazepines, zopiclone, zolpidem), barbiturates; antithrombotic agents (vitamin K antagonists), indirect anticoagulants; prothrombin time should be monitored daily or as frequently as needed to determine the required anticoagulant dose; antifungal agents (e.g., terbinafine, fluconazole, itraconazole, ketoconazole, voriconazole); antiviral agents (e.g., saquinavir, indinavir, efavirenz, amprenavir, nelfinavir, atazanavir, lopinavir, nevirapine); antibacterial agents (e.g., chloramphenicol, clarithromycin, dapsone, doxycycline, fluoroquinolones, telithromycin); corticosteroids (for systemic use); antiestrogens (e.g., tamoxifen, toremifene, gestrinone); systemic hormonal contraceptives, estrogens, progestogens (alternative non-hormonal contraception should be recommended to patients using oral contraceptives during rifampicin therapy); thyroid hormones (e.g., levothyroxine); clofibrate; oral antidiabetic agents (sulfonylureas and their derivatives, e.g., chlorpropamide, tolbutamide, thiazolidinediones); immunosuppressants (e.g., cyclosporine, sirolimus, tacrolimus); cytostatics (e.g., imatinib, erlotinib, irinotecan); losartan; methadone, narcotic analgesics; praziquantel; quinine; riluzole; selective 5-HT3 receptor antagonists (e.g., ondansetron); statins metabolized by CYP3A4 (e.g., simvastatin); theophylline; diuretics (e.g., eplerenone).

Other interactions.

Concomitant use of rifampicin with atovaquone reduces atovaquone concentration and increases rifampicin concentration in serum; with ketoconazole — serum concentrations of both drugs are reduced; with enalapril — concentration of enalaprilat, the active metabolite of enalapril, is reduced (dose adjustment of enalapril may be required depending on clinical status); with probenecid and co-trimoxazole — rifampicin blood levels increase; with saquinavir/ritonavir — increased risk of hepatotoxicity, this combination is contraindicated; with sulfasalazine — plasma concentration of sulfapyridine decreases, possibly due to disruption of intestinal bacterial flora responsible for conversion of sulfasalazine into sulfapyridine and mesalazine; with halothane, isoniazid — increased risk of hepatotoxicity (concomitant use of rifampicin and halothane should be avoided). Cases of severe liver injury, including fatal outcomes, have been reported in patients receiving daily rifampicin and pyrazinamide for two months; this combination should only be used under careful monitoring and if potential benefit outweighs the risk of hepatotoxicity and fatal outcome; with clozapine, flecainide — increased toxic effect on bone marrow; with para-aminosalicylic acid preparations containing bentonite (aluminum hydrosilicate) — to ensure adequate blood concentrations, the interval between administration should be at least 4 hours; with ciprofloxacin, clarithromycin — possible increase in rifampicin blood concentration; cases of lupus-like syndrome have been reported with concomitant use of rifampicin.

Laboratory and diagnostic tests.

During treatment with rifampicin, bromsulfalein testing should not be used, as rifampicin alters bromsulfalein excretion parameters, potentially leading to false impressions of impaired function. Microbiological methods for determining serum concentrations of folic acid and vitamin B12 should also be avoided.

Cross-reactivity and false-positive screening test results for opioids using the KIMS method or quantitative immunoassay methods may occur; confirmatory tests (e.g., gas chromatography/mass spectrometry) are recommended.

Pyrazinamide.

Concomitant use of pyrazinamide and ethionamide increases the risk of liver damage, especially in diabetic patients. During treatment with this combination, liver function should be monitored regularly. If any signs of impaired liver function occur, treatment with this drug combination should be discontinued.

Pyrazinamide reduces cyclosporine metabolism and thereby decreases cyclosporine serum levels. In patients receiving cyclosporine, cyclosporine serum levels should be monitored from the start of pyrazinamide therapy and after its discontinuation.

Pyrazinamide may reduce the effectiveness of drugs used to treat gout and agents promoting uric acid excretion (allopurinol, colchicine, probenecid, sulfinpyrazone). This may increase serum uric acid levels in patients with gout receiving pyrazinamide. Dose adjustments of these drugs may be necessary to control hyperuricemia when gout medications and uricosuric agents are used concomitantly with pyrazinamide.

Concomitant use of pyrazinamide with allopurinol may reduce metabolism of pyrazinamide metabolites. However, pyrazinamide metabolism itself is not significantly altered.

Zidovudine may substantially reduce pyrazinamide serum levels and increase the risk of anemia.

Pyrazinamide interferes with Acetest® and Ketostix® tests by coloring samples reddish-brown.

Pyrazinamide may interfere with serum iron determination using the Ferrochel® II instrument.

Concomitant use with drugs that block tubular secretion may reduce their excretion and enhance toxic reactions. It enhances the antituberculosis effect of ofloxacin and lomefloxacin.

Concomitant use of pyrazinamide and phenytoin may increase phenytoin serum concentration, potentially causing phenytoin intoxication symptoms.

If adverse effects from the central nervous system (ataxia, hyperreflexia, nystagmus, tremor) occur during concomitant use of pyrazinamide and phenytoin, the drugs should be discontinued, serum phenytoin concentration determined, and phenytoin dosage adjusted accordingly.

Pyrazinamide may enhance the effect of hypoglycemic agents.

Special precautions.

The drug should be prescribed with caution to patients with mild to moderate hepatic or renal impairment. Monitoring of liver and kidney function parameters should be performed weekly during the first 2 weeks and then every 2 weeks for the following 6 weeks (thymol test, bilirubin levels, serum glutamic-oxaloacetic transaminase, ALT and AST, as well as determination of serum uric acid). Caution is also advised in patients with stage II–III arterial hypertension, ischemic heart disease, neurological disorders, acute hepatitis, liver cirrhosis, porphyria, bronchial asthma, psoriasis, exacerbation-phase eczema, hypothyroidism, chronic alcoholism, patients receiving other potentially hepatotoxic drugs, elderly patients, and debilitated patients. If signs of hepatotoxicity or nephrotoxicity occur, the drug should be discontinued. To reduce the toxic effects of pyrazinamide, methionine, lipocaine, glucose, and vitamin B₁₂ should be administered.

Alcoholic beverages should not be consumed during treatment with this drug. Alcohol increases the hepatotoxic effect and reduces the drug's efficacy.

The risk of hepatotoxicity increases in patients aged 35 years and older, particularly in females, slow acetylators, HIV-infected patients, those with malnutrition, and patients with pre-existing neuropathy.

The drug should be used cautiously in patients with diabetes mellitus (a positive glucosuria test may occur in diabetic patients).

Pyridoxine should be prescribed to patients at risk of developing neuropathy or pyridoxine deficiency (diabetic patients, chronic alcoholics, patients with hypotrophy, renal insufficiency, pregnant women, and HIV-infected individuals).

Visual acuity, refraction, visual fields, intraocular pressure, and fundus should be systematically monitored before and during treatment. Ophthalmological monitoring should be performed daily in patients with renal impairment. The drug should not be prescribed if visual function cannot be assessed (e.g., in critically ill patients or those with psychiatric disorders).

Ophthalmological monitoring should be performed for each eye separately and together, as visual acuity changes may be unilateral or bilateral. If visual disturbances occur, treatment should be discontinued to prevent optic nerve atrophy. Visual changes are usually reversible and resolve within several weeks after discontinuation of treatment, although in some cases resolution may take several months. In rare cases, visual changes are irreversible due to optic nerve atrophy. Patients should be instructed to inform their physician about any visual changes. Hydroxocobalamin or cyanocobalamin should be administered if visual disturbances occur. Vision typically recovers within several weeks or even months.

Treatment with this drug requires continuous monitoring of peripheral blood parameters, liver and kidney function, blood glucose, prothrombin levels, uric acid levels, and consultations with an ophthalmologist and neurologist.

Treatment should be discontinued if serum liver enzyme levels increase more than threefold or if bilirubin levels rise. Treatment should be immediately stopped at the first signs of hepatitis (malaise, fatigue, nausea, anorexia). The drug may increase serum urate concentrations due to reduced renal excretion of uric acid. The drug should be used cautiously in patients with elevated serum uric acid levels.

To reduce adverse effects, pyridoxine hydrochloride (orally or intramuscularly), glutamic acid, thiamine chloride or thiamine bromide (intramuscularly), or sodium ATP salt should be co-administered with the drug.

The drug should not be taken with food, as bioavailability may be reduced when taken together with meals.

It should be remembered that the drug's metabolites may discolor urine, saliva, and other biological fluids to an orange-red color.

Women of reproductive age should use reliable contraceptive methods (oral hormonal contraceptives combined with additional non-hormonal contraceptive methods) during treatment with this drug.

Pyrazinamide inhibits renal excretion of urates, which may result in hyperuricemia, usually without signs of gout. Pyrazinamide should be used cautiously in patients with a history of gout.

Pyrazinamide should be administered cautiously in diabetic patients due to difficulties in maintaining desired blood glucose concentrations.

In patients with renal insufficiency, accumulation of the drug in the body may occur.

Skin and subcutaneous tissue disorders

During post-marketing surveillance, severe cutaneous adverse reactions (SCARs) associated with ethambutol use have been reported, including Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS), which may be life-threatening or fatal.

Patients should be informed about the signs and symptoms of these reactions, and skin reactions should be carefully monitored during treatment.

If signs or symptoms suggestive of these reactions occur, ethambutol should be discontinued immediately, and alternative treatment should be considered (if necessary).

Ethambutol treatment must never be resumed in patients who have experienced a serious reaction such as SJS, TEN, or DRESS while receiving ethambutol.

In children, skin rashes may be mistakenly attributed to the primary infection or another infectious process; therefore, physicians should consider the possibility of an ethambutol-related reaction in children who develop rash and fever during ethambutol therapy.

Use during pregnancy or breastfeeding.

The drug is contraindicated during pregnancy.

Breastfeeding should be discontinued during treatment with this drug.

Ability to affect reaction speed when driving or operating machinery.

Due to possible reduction in visual acuity and adverse neurological reactions during treatment, patients should refrain from driving or operating machinery during treatment.

Dosage and Administration

The daily dose is determined according to the patient's body weight. For patients weighing 30–39 kg – 2 tablets; 40–54 kg – 3 tablets; 55–70 kg – 4 tablets; more than 70 kg – 5 tablets. The tablets should be taken once daily with a full glass of water, for a duration of 2–3 months.

Children

The safety and efficacy of Forecox Trek in children have not been established; therefore, the administration of Forecox Trek is not recommended in this age group.

Overdose

Symptoms: dizziness, headache, increased fatigue, drowsiness, polyneuritis, optic neuritis (which may lead to blindness), deterioration of visual acuity, blurred vision, development of neurological disturbances, seizures, confusion, stupor, hallucinations (including visual), lethargy, dysarthria, indistinct speech, disorientation, hyperreflexia, peripheral polyneuropathy, loss of appetite, nausea, vomiting, diarrhea, abdominal pain, respiratory depression, dyspnea, asystole, hepatomegaly, jaundice, liver function abnormalities, increased plasma levels of bilirubin and liver transaminases, brownish-red or orange discoloration of the skin, oral mucosa, sclera, urine, saliva, sweat, mucus, and feces proportional to the ingested dose, allergic reactions, elevated body temperature, leukopenia, thrombocytopenia, acute hemolytic anemia, renal failure, asymptomatic hyperuricemia, periorbital or facial edema, pruritus, pulmonary edema, metabolic acidosis, hyperglycemia, glucosuria, ketonuria, coma. Respiratory distress syndrome or other adverse reactions may develop over time.

Treatment: discontinue the drug, induce vomiting or perform gastric lavage, administer enterosorbents, monitor liver function and determine serum urate levels. Intravenous infusion of Ringer's solution, Sorbilact, or Reosorbilact should be administered, and forced diuresis should be carried out. Vitamins of group B are prescribed. Monitor and take measures to support vital functions; resuscitation procedures should be performed if necessary. There is no specific antidote.

Forced diuresis, peritoneal dialysis, or hemodialysis are indicated. In life-threatening conditions, exchange blood transfusion is indicated.

Side effects.

Eye disorders: optic neuritis (unilateral or bilateral), manifested by impaired perception of red and green colors, narrowing of visual fields, decreased visual acuity up to complete blindness; development of central or peripheral scotoma; retinal hemorrhage; optic nerve atrophy.

Immune system disorders: anaphylactic reactions/anaphylaxis, including anaphylactic shock; angioneurotic edema; bronchospasm; interstitial pneumonitis; lymphadenopathy; vasculitis; rheumatoid syndrome.

Skin and subcutaneous tissue disorders: skin rashes (including measles-like, maculopapular dermatitis, purpura, or exfoliative dermatitis); hyperemia; urticaria; pruritus; toxic epidermal necrolysis; Stevens-Johnson syndrome; erythema multiforme; possible exacerbation of systemic lupus erythematosus symptoms or development of lupus-like syndrome; hot flushes; pemphigoid (bullous) reaction; acne; photosensitization; dermatitis, including toxic-allergic dermatitis; frequency unknown – drug-induced eosinophilia with systemic symptoms (DRESS) (see section "Special precautions").

Nervous system disorders: dizziness; headache; depression; confusion; disorientation; hallucinations; seizures; increased frequency of seizures in patients with epilepsy; ataxia; myasthenia; peripheral neuropathy; peripheral neuritis; paresthesia; limb numbness; paralysis; hyperreflexia; toxic encephalopathy; memory disorders; sleep disturbances; insomnia; somnolence; mood changes; irritability; increased excitability; euphoria; intracerebral hemorrhage; hearing loss and tinnitus in patients with renal insufficiency.

Blood and lymphatic system disorders: neutropenia; leukopenia; thrombocytopenia; eosinophilia; anemia, including hemolytic and aplastic anemia, sideroblastic anemia; methemoglobinemia; erythrocyte vacuolization; agranulocytosis; thrombocytopenic purpura; hypercoagulation; tendency to thrombosis; splenomegaly; porphyria; increased serum iron concentration.

Musculoskeletal and connective tissue disorders: arthralgia, joint swelling, joint stiffness, myalgia, rhabdomyolysis, gout attacks, arthritis.

Respiratory system disorders: lung infiltrates with or without eosinophilia, pneumonitis, dyspnea, shortness of breath, dry cough.

Cardiovascular system disorders: pericarditis, myocarditis, arterial hypertension/hypotension, palpitations, chest pain and pain in the cardiac area, worsening of myocardial ischemia in elderly patients, sensation of heat, facial hyperemia.

Gastrointestinal disorders: loss of appetite or decreased appetite, metallic taste in the mouth, dyspeptic symptoms, heartburn, dry mouth, stomatitis, nausea, vomiting, diarrhea, constipation, pain/discomfort in the epigastric area/abdomen, peptic ulcer/deterioration of peptic ulcer, acute pancreatitis, erosive gastritis, pseudomembranous colitis.

Hepatobiliary disorders: liver damage/liver function impairment; elevated levels of liver transaminases, alkaline phosphatase, thymol test; hepatitis; discomfort in the right hypochondrium; jaundice; fulminant hepatic failure which may lead to necrosis (especially in patients aged over 35 years); hyperbilirubinemia; jaundice; bilirubinuria; hepatomegaly; possible development of acute liver atrophy, dose-dependent.

Renal and urinary disorders: interstitial nephritis; dysuria; acute renal failure; elevated levels of urea and creatinine; nephron necrosis; myoglobinuric renal failure due to rhabdomyolysis; hemoglobinuria; urinary retention (in men); hematuria; dysuria; pain during urination.

Metabolic and nutritional disorders: uric acid diathesis; gout exacerbation; hyperuricemia; pyridoxine deficiency affecting the conversion of tryptophan to nicotinic acid; pellagra; acidosis.

Endocrine disorders: gynecomastia in men, menorrhagia in women, Cushing's syndrome, menstrual cycle disturbances, adrenal insufficiency in patients with impaired adrenal function, hyperglycemia.

General disorders: increased body temperature; chills; influenza-like syndrome; weakness; edema; malaise; tendency to bleeding and hemorrhages; herpes; lacrimation; orange-red discoloration of urine, feces, saliva, sputum, sweat, mucus; candidiasis; withdrawal syndrome which may occur upon discontinuation of the drug, including headache, insomnia, irritability, nervousness.

Shelf life. 3 years.

Storage conditions.

For tablets in blisters:

Store at a temperature not exceeding 25°C in the original packaging.

Keep out of reach of children.

For tablets in strips:

Store at a temperature not exceeding 30°C in the original packaging.

Keep out of reach of children.

Packaging.

6 tablets per strip, 10 strips per cardboard box.

28 tablets per blister, 24 blisters per cardboard box.

Prescription category. Prescription only.

Manufacturer.

Macleods Pharmaceuticals Limited.

Manufacturer's address and place of business.

Phase II, Plot No. 12, 15, 21, 23, 24, 25, 26, 27, 28 and 30, Survey No. 366, Premier Industrial Estate, Kachigam, Daman, 396210, India.