What is Amflee Combo used for?

Hypersensitivity to the active substance, benzimidazole derivatives, or any excipient of the medicinal product.

What is the active ingredient in Amflee Combo?

Fipronil + (S)-methoprenum ((S)-methoprenum, Fipronilum)

What pharmaceutical form is Amflee Combo available in?

Amflee Combo: Roztwór do nakrapiania (50 mg + 60 mg)/pipetkę 0,5 ml (przez nakrapianie)

Is Amflee Combo OTC or prescription only?

Amflee Combo is available over-the-counter (OTC) — no prescription required.

What are the side effects of Amflee Combo?

Adverse reactions were observed in approximately 5% of patients. Adverse effects are classified by frequency of occurrence according to the following categories: very common (≥ 1/10), common (≥ 1/100 to < 1/10), uncommon (≥ 1/1,000 to < 1/100), rare (≥ 1/10,000 to < 1/1,000), very rare (< 1/10,000), not known (frequency cannot be estimated from available data). Blood and lymphatic system disorders. Rare: agranulocytosis. Very rare: leucopenia, thrombocytopenia, pancytopenia. Immune system disord

Does Amflee Combo interact with other medications?

Medicinal products whose absorption is pH-dependent. Due to the profound and prolonged inhibition of hydrochloric acid secretion, pantoprazole may affect the absorption of medicinal products for which gastric pH is an important factor in their bioavailability (e.g. certain antifungal agents such as ketoconazole, itraconazole, posaconazole, or other medicinal products such as erlotinib). HIV protease inhibitors. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir),

Can Amflee Combo be used during pregnancy?

Pregnancy. Available data on the use of Nolpaza® in pregnant women indicate no embryotoxic or feto/neonatal toxicity. Reproductive toxicity was observed in animal studies. As a precaution, the use of Nolpaza® should be avoided during pregnancy. Breast-feeding. Animal studies have shown excretion of pantoprazole in breast milk. There is insufficient data on the excretion of pantoprazole in human breast milk, though such excretion has been reported. A risk to newborns/infants cannot be excluded. A

Who manufactures Amflee Combo?

Krka, d.d., Novo mesto d.o.o. (Słowenia)

What ATC class does Amflee Combo belong to?

Amflee Combo: ATC QP53AX65. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Amflee Combo

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This information is for educational purposes only. It is not intended as medical advice. Always consult a qualified healthcare professional.

Pharmacodynamics. Mechanism of action. Pantoprazole is a substituted benzimidazole that inhibits the secretion of hydrochloric acid in the stomach by specifically blocking the proton pumps of parietal cells. Pantoprazole is converted to its active form in the acidic environment of parietal cells, where it inhibits the H⁺/K⁺-ATPase enzyme, thereby blocking the final step of hydrochloric acid production in the stomach. The inhibition is dose-dependent and affects both basal and stimulated acid secretion. Most patients achieve symptom relief within 2 weeks. Treatment with pantoprazole, as with other proton pump inhibitors (PPIs) and H2-receptor antagonists, reduces gastric acidity and thus increases gastrin secretion proportionally to the reduction in acidity. The increase in gastrin secretion is reversible. Since pantoprazole binds to the enzyme distally to the cell receptor, it can inhibit hydrochloric acid secretion regardless of stimulation by other substances (acetylcholine, histamine, gastrin). The effect is the same with oral and intravenous administration. Fasting gastrin levels increase during pantoprazole treatment. In most cases, during short-term use, they do not exceed the upper limit of normal. During long-term treatment, gastrin levels double in most cases. Excessive increases occur only in isolated cases. As a consequence, in a small number of cases during long-term treatment, a mild to moderate increase in specific endocrine (ECL) cells in the stomach is observed (similar to adenomatoid hyperplasia). However, according to studies conducted to date, the formation of neuroendocrine tumour precursor cells (atypical hyperplasia) or neuroendocrine tumours of the stomach, which were found in animal studies, has not been observed in humans. Based on the results of animal studies, an effect of long-term (more than one year) treatment with pantoprazole on endocrine parameters of the thyroid gland cannot be excluded. During treatment with antisecretory medicinal products, serum gastrin levels increase in response to decreased acid secretion. In addition, due to the decrease in gastric acidity, chromogranin A (CgA) levels increase. Elevated CgA levels may interfere with investigations for neuroendocrine tumours. Available published data suggest that PPI therapy should be discontinued between 5 days and 2 weeks before CgA measurements. This allows CgA levels to return to the normal range, which may be falsely elevated after PPI treatment. Pharmacokinetics. Absorption. Pantoprazole is rapidly absorbed, and peak plasma concentrations are achieved after a single oral dose of 40 mg. The mean peak serum concentration of approximately 2–3 µg/ml is reached approximately 2.5 hours after administration; the concentration remains at a steady level after repeated dosing. Pharmacokinetic properties do not change after single or repeated administration. In the dose range of 10 to 80 mg, plasma pharmacokinetics of pantoprazole are linear after both oral and intravenous administration. The absolute bioavailability of the tablets is approximately 77%. Concomitant food intake does not affect AUC (area under the concentration-time curve) or peak serum concentration and, therefore, bioavailability. Only the variability of the lag time increases with concomitant food intake. Distribution. Serum protein binding of pantoprazole is approximately 98%. The volume of distribution is approximately 0.15 L/kg. Biotransformation. The substance is metabolised almost exclusively in the liver. The main metabolic pathway is demethylation via CYP2C19 followed by sulphate conjugation; other metabolic pathways include oxidation via CYP3A4. Elimination. The terminal elimination half-life is approximately 1 hour and the clearance is 0.1 L/h/kg. A few cases of delayed elimination were noted. Due to the specific binding of pantoprazole to the proton pumps of parietal cells, the half-life does not correlate with the much longer duration of action (inhibition of acid secretion). The majority of pantoprazole metabolites are excreted renally (approximately 80%), the remainder is excreted in the faeces. The main metabolite in both serum and urine is desmethylpantoprazole conjugated with sulphate. The half-life of the main metabolite (approximately 1.5 hours) is not much longer than that of pantoprazole. Special patient populations. Poor metabolisers. Approximately 3% of Europeans lack functional CYP2C19 enzyme activity and are referred to as poor metabolisers. In these individuals, pantoprazole metabolism is probably catalysed mainly by CYP3A4. After a single dose of 40 mg pantoprazole, the mean area under the plasma concentration-time curve was approximately 6-fold higher in poor metabolisers than in subjects with functionally active CYP2C19 enzyme (extensive metabolisers). The mean peak plasma concentration was increased by approximately 60%. These findings do not affect the dosing of pantoprazole. Renal impairment. No dose reduction is recommended when pantoprazole is administered to patients with impaired renal function (including patients on dialysis). As in healthy subjects, the half-life of pantoprazole is short. Only very small amounts of pantoprazole are dialysed. Although the main metabolite has a moderately longer half-life (2–3 hours), elimination is still rapid, so accumulation does not occur. Hepatic impairment. Although in patients with liver cirrhosis (Child-Pugh classes A and B) the half-life increases to 7–9 hours and AUC increases 5- to 7-fold, the peak serum concentration increases only slightly — by 1.5-fold compared to healthy volunteers. Elderly patients. A slight increase in AUC and Cmax in elderly volunteers compared to younger volunteers is also of no clinical significance.

⚠️ Warnings

Hepatic impairment. Patients with severe hepatic impairment should have their liver enzyme levels monitored regularly, particularly during long-term treatment. Treatment should be discontinued if liver enzyme levels are elevated. Combination therapy. When used in combination therapy, the instructions for medical use of the respective medicinal products should be followed. Gastric malignancy. Symptomatic response to pantoprazole treatment may mask the symptoms of gastric malignancy and delay their diagnosis. In the presence of alarm symptoms (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis, anaemia, melaena), as well as when a gastric ulcer is suspected or present, malignancy should be excluded. If symptoms persist despite adequate treatment, further investigation should be considered. HIV protease inhibitors. Co-administration of pantoprazole with HIV protease inhibitors (such as atazanavir), the absorption of which is dependent on intragastric pH, is not recommended due to significant reduction in their bioavailability (see section "Interaction with other medicinal products and other forms of interaction"). Effect on vitamin B12 absorption. Pantoprazole may reduce the absorption of vitamin B12 (cyanocobalamin) due to hypo- or achlorhydria. This should be considered in patients with reduced body weight or risk factors for decreased vitamin B12 (cyanocobalamin) absorption, particularly during long-term treatment or in the presence of relevant clinical symptoms. Long-term treatment. During long-term treatment, especially exceeding 1 year, patients should be kept under regular medical supervision. Gastrointestinal infections caused by bacteria. Treatment may slightly increase the risk of gastrointestinal infections caused by bacteria such as Salmonella and Campylobacter or C. difficile. Hypomagnesaemia. Rare cases of severe hypomagnesaemia have been reported in patients treated with PPIs such as pantoprazole for at least 3 months and, in most cases, for 1 year. The following serious clinical manifestations of hypomagnesaemia may develop insidiously: fatigue, tetany, delirium, convulsions, dizziness, and ventricular arrhythmia. Hypomagnesaemia may lead to hypocalcaemia and/or hypokalaemia (see section "Special warnings and precautions for use"). In cases of hypomagnesaemia (and hypocalcaemia and/or hypokalaemia associated with hypomagnesaemia), the condition improved in most patients following magnesium replacement therapy and discontinuation of PPI treatment. Patients requiring long-term therapy or those taking PPIs concomitantly with digoxin or medicinal products that may cause hypomagnesaemia (e.g. diuretics) should have their magnesium levels measured before starting PPI treatment and periodically during treatment. Bone fractures. Long-term treatment (more than 1 year) with high-dose proton pump inhibitors may moderately increase the risk of hip, wrist, and spine fractures, predominantly in the elderly or in the presence of other risk factors. Observational studies suggest that proton pump inhibitors may increase the overall risk of fractures by 10–40%. Some of these may be attributable to other risk factors. Patients at risk of developing osteoporosis should receive treatment in accordance with current clinical guidelines and should have adequate intake of vitamin D and calcium. Severe cutaneous adverse reactions (SCARs). Severe cutaneous adverse reactions have been reported with the use of pantoprazole, including erythema multiforme, Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS syndrome), which can be life-threatening or fatal. The frequency of these reactions is not known (see section "Adverse reactions"). Patients should be informed about the signs and symptoms of these reactions when prescribing pantoprazole, and skin reactions should be closely monitored. If symptoms suggestive of these severe cutaneous reactions appear, pantoprazole treatment should be immediately discontinued and alternative treatment considered. Subacute cutaneous lupus erythematosus. Proton pump inhibitor use has been associated with very rare cases of subacute cutaneous lupus erythematosus. If lesions occur, especially in sun-exposed areas of the skin, and if accompanied by arthralgia, the patient should seek immediate medical attention, and the physician should consider whether discontinuation of Nolpaza® is necessary. The occurrence of subacute cutaneous lupus erythematosus during prior PPI therapy may increase the risk of its development with other proton pump inhibitors. Effect on laboratory test results. Elevated chromogranin A (CgA) levels may interfere with investigations for neuroendocrine tumours. To avoid such interference, Nolpaza® treatment should be temporarily discontinued at least 5 days before CgA level measurement (see section "Pharmacodynamics"). If CgA and gastrin levels have not returned to the normal range after initial measurement, repeat measurements should be performed 14 days after discontinuation of PPI treatment. Information regarding excipients. Nolpaza® contains sorbitol. Patients with rare hereditary fructose intolerance should not take this medicinal product.

Amflee Combo

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