Semaglutide: difference between revisions
Diff·revision 11 → 12·23:17, 8 Oct 2024
Difference between revision 11 and revision 12 of Semaglutide. 3 lines changed; the page grew by 567 bytes.
| Revision 11 — 02:38, 29 Sep 2024 OrforglipronOona (talk) add the year of first marketing authorisation, with the regulator named 5,011 bytes ±0 | Revision 12 — 23:17, 8 Oct 2024 SecretagogueSol (talk) state plainly that the research-use-only form is not approved for human use 5,578 bytes +567 | ||
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| 12 | | Molar mass = 4,113.58 g·mol⁻¹ | 12 | | Molar mass = 4,113.58 g·mol⁻¹ |
| 13 | }} | 13 | }} |
| + | 14 | {{hatnote|For the oral formulation and its absorption enhancer, see [[Oral semaglutide]]. For the drug class, see [[GLP-1 receptor agonist]].}} | |
| 14 | 15 | ||
| 15 | '''Semaglutide''' is an acylated analogue of [[Glucagon-like peptide-1]] and a [[GLP-1 receptor agonist]]. Three engineering changes to the native 31-residue sequence give it a circulating half-life of about seven days: α-aminoisobutyric acid at position 8 confers resistance to [[Dipeptidyl peptidase-4]], a C-18 fatty diacid attached at Lys26 confers [[Albumin binding half-life extension|albumin binding]], and an arginine substitution at position 34 leaves a single site available for acylation.{{r|lau2015}} | 16 | '''Semaglutide''' is an acylated analogue of [[Glucagon-like peptide-1]] and a [[GLP-1 receptor agonist]]. Three engineering changes to the native 31-residue sequence give it a circulating half-life of about seven days: α-aminoisobutyric acid at position 8 confers resistance to [[Dipeptidyl peptidase-4]], a C-18 fatty diacid attached at Lys26 confers [[Albumin binding half-life extension|albumin binding]], and an arginine substitution at position 34 leaves a single site available for acylation.{{r|lau2015}} |
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| 31 | 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. | 32 | 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. |
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| + | 34 | The oral formulation is a different pharmacokinetic proposition entirely. Bioavailability is roughly 0.4–1%, achieved by co-formulation with the absorption enhancer sodium N-(8-(2-hydroxybenzoyl)amino)caprylate, and it is critically dependent on dosing in the fasting state with no more than 120 mL of water and a subsequent 30-minute fast. Deviation from those conditions changes exposure severalfold.{{r|knudsen2019}} | |
| 32 | 35 | ||
| 33 | == References == | 36 | == References == |