Metabolism is influenced by concomitant administration of CYP2C9 inducers (eg, rifampicin) or inhibitors (eg, fluconazole). Potentiated blood-glucose-lowering effect w/ phenylbutazone, azapropazone & oxyfenbutazone; insulin & oral antidiabetic products eg, metformin; salicylates & p-amino-salicylic acid; anabolic steroids & male sex hormones; chloramphenicol, certain long-acting sulfonamides, tetracyclines, quinolone antibiotics & clarithromycin; coumarin anticoagulants; fenfluramine; disopyramide; fibrates; ACE inhibitors; fluoxetine, MAOIs; allopurinol, probenecid, sulfinpyrazone; sympatholytics; cyclophosphamide, trophosphamide & iphosphamides; miconazole, fluconazole; pentoxifylline (high-dose parenteral); tritoqualine. Weakened blood-glucose-lowering effect w/ oestrogens & progestogens; saluretics, thiazide diuretics; thyroid-stimulating agents, glucocorticoids; phenothiazine derivatives, chlorpromazine; adrenaline & sympathicomimetics; nicotinic acid (high dosages) & nicotinic acid derivatives; laxatives (long-term use); phenytoin, diazoxide; glucagon, barbiturates & rifampicin; acetazolamide. H
2 antagonists, β-blockers, clonidine & reserpine may lead to either potentiated or weakened blood-glucose-lowering effect. Reduced or absent signs of adrenergic counter-regulation to hypoglycaemia w/ sympatholytic medicinal products eg, β-blockers, clonidine, guanethidine & reserpine. Potentiated or weakened hypoglycaemic action w/ alcohol. Potentiated or weakened effects of coumarin derivatives. Reduced GIT absorption w/ colesevelam.