Adult: As monotherapy or in combination with metformin: Initially, 0.5 mg. Patient transferring from another hypoglycaemic agent: Initially, 1mg. All doses taken 30 minutes before each main meal. May adjust dose at intervals of 1-2 weeks, up to max 4 mg per dose. Max: 16 mg daily.
Severe CrCl 20-40 mL/min: Initially, 0.5 mg before meals, adjust according to patient’s requirement.
Should be taken with food. Usually taken w/in 15 min of the meal but time may vary from immediately before to 30 min before the meal.
Diabetic ketoacidosis with or without coma, type 1 diabetes mellitus. Concomitant use with gemfibrozil.
Hepatic and severe renal impairment. Pregnancy and lactation.
Significant: Severe hypoglycaemia, acute coronary syndrome (e.g. MI). Gastrointestinal disorders: Abdominal pain, diarrhoea. Musculoskeletal and connective tissue disorders: Arthralgia, back pain. Nervous system disorders: Headache. Respiratory, thoracic and mediastinal disorders: Upper respiratory tract infection, sinusitis, bronchitis.
This drug may cause dizziness due to hypoglycaemia, if affected, do not drive or operate machinery.
Monitor FBS periodically and during dose adjustment; HbA1C at least twice yearly.
Symptoms: Hypoglycaemic reactions (e.g. dizziness, sweating, tremor, headache, seizure, loss of consciousness or coma). Management: Mild hypoglycaemic symptoms without loss of consciousness or neurologic findings may be treated with oral glucose and adjustments in drug dosage and/or meal patterns. Severe hypoglycaemia should be treated with IV glucose. Closely monitor patient for a minimum of 24-48 hours.
Increased metabolism with CYP3A4 inducers (e.g. rifampicin, barbiturates, carbamazepine). Enhanced effect with NSAIDs and other highly protein bound drugs (e.g. salicylates, sulphonamides, phenylbutazone, oral anticoagulants and hydantoins). Increased plasma concentration with ketoconazole, fluconazole, itraconazole and erythromycin. Potentially Fatal: Enhanced and prolonged effect with gemfibrozil.
Description: Mechanism of Action: Repaglinide is a short-acting meglitinide analogue which lowers blood glucose by blocking ATP-dependent K channels in the β-cell membrane resulting to depolarisation. This leads to the opening of Ca channels. The resulting Ca influx stimulates the release of insulin from the pancreatic β-cells. Pharmacokinetics: Absorption: Rapidly and completely absorbed from the gastrointestinal tract. Bioavailability: Approx 56%. Time plasma peak concentration: Within 1 hour. Distribution: Volume of distribution: 31 L. Plasma protein binding: >98% to albumin. Metabolism: Extensively metabolised in the liver by the CYP3A4 and CYP2C8 via oxidation; further metabolised by uridine diphosphate glucuronosyltransferase 1A1 (UGT1AI) enzyme via glucuronidation. Excretion: Via faeces (approx 90%, <2% as unchanged drug); urine (approx 8%, 0.1% as unchanged drug). Elimination half-life: Approx 1 hour.
A10BX02 - repaglinide ; Belongs to the class of other blood glucose lowering drugs excluding insulins. Used in the treatment of diabetes.
Anon. Repaglinide. AHFS Clinical Drug Information [online]. Bethesda, MD. American Society of Health-System Pharmacists, Inc. https://www.ahfscdi.com. Accessed 16/11/2018.Anon. Repaglinide. Lexicomp Online. Hudson, Ohio. Wolters Kluwer Clinical Drug Information, Inc. https://online.lexi.com. Accessed 16/11/2018.Buckingham R (ed). Repaglinide. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 16/11/2018.Joint Formulary Committee. Repaglinide. British National Formulary [online]. London. BMJ Group and Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 05/03/2019.Repaglinide (Sandoz Inc). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed/. Accessed 16/11/2018.