Cagrilintide 20mg Perte de poids
Coupe-faim longue durée.
Le coupe-faim de longue durée. Analogue de l'amyline avec demi-vie prolongée à 7 jours. Cagrilintide ralentit la vidange gastrique et active les voies de satiété centrale. Associé au Semaglutide (le duo CagriSema, en phase 3), il pousse la perte de poids au-delà du Semaglutide seul. Le complément stratégique des protocoles modernes.
Product information
Cagrilintide 20mg is the extended-protocol format for long cohorts and CagriSema combinations over prolonged duration. The molecule is strictly identical to the 5mg or 10mg versions: only the total lyophilized peptide quantity per vial changes. 20mg enables the full 0.3-4.5mg weekly escalation (9mg consumed over 10 weeks) followed by a 2.4mg maintenance phase over an additional 4 to 5 weeks — 14 to 15 weeks of single-subject follow-up. Alternatively: supply 2 subjects in parallel through the full escalation phase. Cost per mg reduced by about 35% versus 10mg. Long-acting synthetic analog of human amylin developed by Novo Nordisk. Our Cagrilintide 20mg batch is solid-phase synthesized, HPLC purity of at least 98%, lyophilized under inert atmosphere. Stock in France, discreet shipping the next day, 3 to 7 business days in the EU. Reference choice to reproduce REDEFINE designs or CagriSema combinations documented in phase 2 over extended duration.
01Mechanism of action
Cagrilintide is a long-acting synthetic analog of human amylin, designed by Novo Nordisk to overcome the pharmacokinetic limitations of pramlintide (short half-life, multi-daily administration). The molecule is modified by acylation with a C18 fatty acid chain on the Lys22 residue, which maximizes serum albumin binding and extends plasma half-life to approximately 7 days in humans, compatible with weekly administration.
At the receptor level, Cagrilintide simultaneously activates the calcitonin receptor (CTR) and the amylin receptor complexes (AMY1, AMY2, AMY3) formed by association of CTR with receptor activity-modifying proteins (RAMPs). This signaling, distinct from that of GLP-1, produces an anorexigenic effect through complementary neuronal pathways: activation of catecholaminergic neurons in the solitary tract (NTS), modulation of satiety circuits in the hypothalamus, and GLP-1-independent slowing of gastric emptying.
In preclinical DIO (Diet-Induced Obesity) models, animals treated with Cagrilintide alone have shown a 11 to 13% weight reduction over 4 weeks, with preservation of lean mass. The most striking effect documented in the literature remains the synergy observed in co-administration with Semaglutide (CagriSema): full addition of anorexigenic effects, weight reduction exceeding 20% in clinical phase 2 at 32 weeks (Frias et al., Lancet 2023). This synergy has opened an entire field of exploration on amylin + GLP-1 combination that neither molecule alone can achieve.
Cagrilintide also modulates bone markers and calcium metabolism via the calcitonin pathway, which is the subject of parallel studies on bone mineral density and post-menopausal fractures. These avenues remain exploratory but broaden the research scope beyond pure energy metabolism.
Cagrilintide is a synthetic analogue of human amylin (hIAPP, Islet Amyloid Polypeptide, 37 aa, 3904 Da), a peptide hormone co-secreted with insulin by pancreatic β-cells whose sequence is closely conserved with calcitonin. Native human amylin shows amyloidogenic propensity (Aβ-like fibril formation in diabetic pancreatic islets) requiring stabilising modifications: cagrilintide incorporates (1) Pro25, Pro28, Pro29 substitutions (inherited from pramlintide) blocking β-sheet propensity and fibrillisation, (2) an Arg18 substitution improving solubility, and (3) a C20 diacid acylation (eicosanedioic acid) on Lys8 via γ-Glu/OEG linker, conferring reversible plasma albumin binding responsible for its exceptional half-life (~180 hours, compatible with weekly administration). Pharmacologically, cagrilintide activates hybrid receptors AMY1R, AMY2R, AMY3R (calcitonin-receptor + RAMP1/2/3 complexes), the amylin/CGRP receptor family, and more weakly the calcitonin receptor CTR. Signalling pathways include adenylate cyclase activation (cAMP), glucagon suppression, slowed gastric emptying, and central action on arcuate hypothalamic nucleus (POMC/CART neurons) for satiety.
Similar peptides
Against Semaglutide (GLP-1 mono-agonist), Cagrilintide acts through a completely distinct pathway (amylin and calcitonin receptors). In monotherapy, its weight efficacy is slightly inferior (10-11% vs 15% in phase 2 at comparable dose), but its tolerance profile is gentler, its gastrointestinal effects less pronounced, and it modulates complementary neuronal circuits. The main interest of Cagrilintide is not to be better than Semaglutide solo, but to open the possibility of a synergistic combination.
Against Tirzepatide (dual GIP/GLP-1 agonist), Cagrilintide is clearly less powerful in monotherapy (10% vs 22%). The interest lies elsewhere: Cagrilintide engages no incretin receptor, making it an ideal orthogonal tool to dissect the contribution of the amylin pathway independently of the incretin axis. In combination with a GLP-1 or GIP/GLP-1 agonist, Cagrilintide brings an additive effect because it relies on distinct receptors.
Against Retatrutide (triple agonist), same logic: Cagrilintide is less powerful solo (10% vs 24%) but represents a complementary non-redundant pharmacological lever. Preclinical research programs are actively exploring triple-agonist + amylin combinations.
Strategic conclusion: choose Cagrilintide when the experimental design involves exploring the pure amylin pathway, or when the design incorporates co-administration with an incretin agonist to reproduce the CagriSema synergy documented in phase 2. Cagrilintide in monotherapy is a research tool more than a standalone therapeutic candidate.
Cagrilintide stands out among other amylin agonists by its extended half-life. Compared to pramlintide (Symlin, FDA-authorised amylin analogue for T1D/T2D US, 48 min half-life, 3x/day injectable), cagrilintide extends half-life to ~180h thanks to C20 acylation, allowing weekly administration compatible with chronic obesity model studies. Compared to pure GLP-1R agonists (semaglutide, liraglutide), cagrilintide targets a complementary pathway (amylin/CGRP) with distinct satiety and glucagon suppression mechanisms, justifying CagriSema combination development in clinical research. Compared to GLP-1/GIP co-agonists (tirzepatide) or GLP-1/GIP/GCGR (retatrutide), cagrilintide shares no pathway but may theoretically be additive with these co-agonists (study not yet reported). Compared to davalintide (AC2307, amylin/calcitonin chimera), cagrilintide has a more selective amylin-like profile while preserving residual calcitonin receptor activity (involved in central satiety effects).
