| Class | Oral hypoglycaemic |
|---|---|
| Chemistry |
Second generation sulfonylurea |
| Routes of administration |
Oral only |
| Absorption |
Absorption can be rapid and complete with appropriate solubilising excipients. If it were absorbed completely, it would have 95% oral bioavailability, as only 5% is lost to first pass metabolism. |
| Solubility |
pKa=5.5; terrible solubility in either water or lipid |
| Distribution |
VOD= 0.2-0.45 L/kg; 99.9% protein bound |
| Metabolism |
Extensive hepatic metabolism; two major metabolites are also active |
| Elimination |
Weakly active metabolites are excreted in urine (50%) and in faeces (50%) via bile |
| Time course of action |
Half life 15 hrs |
| Target receptor |
Sulfonylurea receptors (SUR1 and SUR2), which form a part of the ATP-sensitive potassium channel complex on pancreatic β-cells |
| Mechanism of action |
By binding to the ATP-sensitive K channel, sulfonylureas act like ATP (i.e. same as a rise in blood glucose), closing the channel and stopping the efflux of potassium from the cell, which promotes depolarisation. The depolarisation then leads to insulin release |
| Clinical effects |
Hypoglycaemia, but also: |
| Literature reference |
Coppack, 1990 |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology | |
| Related SAQs |