Semaglutide: difference between revisions
Diff·revision 7 → 8·21:05, 14 Aug 2024
Difference between revision 7 and revision 8 of Semaglutide. 9 lines changed; the page grew by 891 bytes.
| Revision 7 — 06:52, 31 Jul 2024 FlowTrialFraser (talk) add category for the drug class 3,912 bytes +734 | Revision 8 — 21:05, 14 Aug 2024 BatchNumberBede (talk) rm the equipotency claim — the cited paper does not make it 4,803 bytes +891 | ||
|---|---|---|---|
| 5 | | Routes = Subcutaneous weekly; oral daily | 5 | | Routes = Subcutaneous weekly; oral daily |
| 6 | | First approval = 2017 (type 2 diabetes) | 6 | | First approval = 2017 (type 2 diabetes) |
| + | 7 | <!-- Identifiers --> | |
| + | 8 | | CAS Number = 910463-68-2 | |
| + | 9 | | Molecular formula = {{math|C_{187}H_{291}N_{45}O_{59}}} | |
| + | 10 | | Molar mass = 4,113.58 g·mol⁻¹ | |
| 7 | }} | 11 | }} |
| 8 | 12 | ||
| ⋮ | ⋮ | ||
| 19 | 23 | ||
| 20 | The spacer does real work. It holds the peptide far enough from the albumin surface that the receptor-binding N-terminus remains accessible while the fatty acid is buried in the albumin binding site, so the albumin-bound fraction is a genuine reservoir rather than a sequestered pool. The terminal carboxylate of the diacid raises albumin affinity substantially over a monoacid.{{r|knudsen2019}} | 24 | The spacer does real work. It holds the peptide far enough from the albumin surface that the receptor-binding N-terminus remains accessible while the fatty acid is buried in the albumin binding site, so the albumin-bound fraction is a genuine reservoir rather than a sequestered pool. The terminal carboxylate of the diacid raises albumin affinity substantially over a monoacid.{{r|knudsen2019}} |
| + | 25 | ||
| + | 26 | == Pharmacokinetics == | |
| + | 27 | Subcutaneous bioavailability is approximately 89% and is not materially affected by injection site. The terminal half-life of about 165 hours supports weekly dosing, with steady state reached after four to five weeks — which is why titration steps are held for four weeks and why a dose change is not fully expressed for a month.{{r|lau2015}} | |
| + | 28 | ||
| + | 29 | Elimination is by proteolysis and β-oxidation of the fatty-acid chain rather than by a single organ pathway, and neither renal nor hepatic impairment requires dose adjustment in the studied ranges. There is no clinically significant cytochrome-mediated interaction, though delayed [[Gastric emptying|gastric emptying]] can alter the absorption rate of concomitant oral drugs. | |
| 21 | 30 | ||
| 22 | == References == | 31 | == References == |