$89.99
Buy Cagrilintide Peptide 10 mg Online from SourceTides. AM833 | NNC0174-0833 | CAS 1415456-99-3 | DACRA (Dual Amylin and Calcitonin Receptor Agonist) | MW ~4,409 Da | C₁₉₄H₃₁₂N₅₄O₅₉S₂ | 37 AA | ≥99% HPLC | Disulfide Cys2–Cys7 confirmed | C20 fatty diacid confirmed | Endotoxin <1 EU/mg (LAL) | Full CoA | Lyophilised | Dry-ice cold chain.
Long-acting lipidated amylin analog (Novo Nordisk). Half-life 159–195 h (once-weekly SC). AMY1R + AMY3R primary weight loss receptors (eBioMedicine 2025 RAMP-KO validation). Phase 3 REDEFINE 1: 11.8% monotherapy; 22.7% CagriSema (68 weeks) — largest Phase 3 obesity trial result. NDA submitted FDA December 2025. Not WADA-prohibited. For in-vitro laboratory research use only. Not for human consumption.
Buy Cagrilintide Peptide 10 mg Online | AM833 | Long-Acting Amylin Analog | DACRA | ≥99% Purity | CoA | SourceTides
Buy Cagrilintide Peptide 10 mg Online from SourceTides.
Cagrilintide (AM833; NNC0174-0833; NN9838; CAS 1415456-99-3) is Novo Nordisk’s investigational long-acting lipidated amylin analog — a Dual Amylin and Calcitonin Receptor Agonist (DACRA) developed as the most advanced amylin-based compound in clinical development for obesity.
Its 37-amino acid backbone is derived from pramlintide (not native human amylin), deliberately designed to avoid native amylin’s fatal pharmacological flaw: a propensity to form toxic amyloid fibrils that makes it unsuitable as a drug.
Three amino acid substitutions (N14E, V17R, P37Y) eliminate fibril formation while preserving full AMY/CTR receptor agonist activity.
A C20 eicosanedioic fatty diacid attached at the N-terminus via a γ-glutamic acid linker enables reversible serum albumin binding — extending half-life from pramlintide’s 50 minutes to 159–195 hours (approximately 7 days), making once-weekly SC dosing possible.
Cagrilintide activates the amylin receptor family (AMY1R, AMY2R, AMY3R) — heterodimeric complexes of the calcitonin receptor (CTR) with receptor activity-modifying proteins (RAMP1, RAMP2, RAMP3) — and the calcitonin receptor (CTR) directly.
The primary weight-loss mediators are AMY1R and AMY3R, confirmed in RAMP1/3-knockout mouse models (eBioMedicine 2025).
These receptors are concentrated in the area postrema and hypothalamus — the brainstem satiety circuits that regulate food intake and energy homeostasis.
The clinical evidence is the most extensive of any amylin analog in research.
Phase 3 REDEFINE 1 (monotherapy sub-analysis; 68 weeks): 11.8% mean body weight reduction vs 2.3% placebo, with 31.6% of participants achieving ≥15% weight loss.
Combined with semaglutide as CagriSema: 22.7% mean body weight reduction at 68 weeks — the largest weight loss result from any Phase 3 obesity trial to date.
Novo Nordisk submitted the CagriSema NDA to the FDA in December 2025; a decision is expected in late 2026.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.
Cagrilintide Peptide 10 mg — Technical Specifications
| Parameter | Specification |
|---|---|
| INN / Common Name | Cagrilintide |
| Development Codes | AM833; NNC0174-0833; NN9838; GLXC-26801 |
| CAS Number | 1415456-99-3 |
| PubChem CID | 167312356 |
| DrugBank | DB18887 |
| Molecular Formula | C₁₉₄H₃₁₂N₅₄O₅₉S₂ |
| Molecular Weight | ~4,409 Da |
| Peptide Backbone | 37 amino acids; based on pramlintide (not native human amylin); Cys2–Cys7 disulfide bridge retained; N-terminal lipidation |
| Key Amino Acid Substitutions | N14E (Asn→Glu); V17R (Val→Arg); P37Y (Pro→Tyr); Pro substitutions at positions 25, 28, 29 retained from pramlintide — all prevent amyloid fibril formation while maintaining receptor affinity |
| Lipidation | C20 eicosanedioic fatty diacid attached at N-terminus via γ-glutamic acid (γ-Glu) linker; enables reversible serum albumin binding; extends half-life from ~50 min (pramlintide) to 159–195 hours |
| Disulfide Bridge | Cys2–Cys7 intramolecular disulfide bridge; creates N-terminal ring structure essential for amylin receptor binding conformation; must remain intact (cyclic form) for activity |
| Half-Life | 159–195 hours (~7–8 days); enables once-weekly SC dosing; comparable to semaglutide weekly formulation; dramatically extended vs pramlintide (50 min) and native amylin (15 min) |
| Receptor Targets | Non-selective agonist: AMY1R (CTR + RAMP1); AMY2R (CTR + RAMP2); AMY3R (CTR + RAMP3); CTR (calcitonin receptor) directly; primary in-vivo weight loss mediated by AMY1R and AMY3R (eBioMedicine 2025) |
| Mechanism Class | DACRA — Dual Amylin and Calcitonin Receptor Agonist; satiety signalling via area postrema (brainstem) and hypothalamus; distinct from GLP-1R mechanism |
| Key Metabolic Effects | Appetite suppression and satiety via AMY1R/AMY3R brainstem circuits; gastric emptying delay; glucagon suppression; dose-dependent body weight reduction; additive with GLP-1R agonism via complementary neural circuits |
| Developer | Novo Nordisk A/S; CagriSema NDA submitted FDA December 2025; PDUFA decision expected late 2026 |
| Physical Form | White lyophilised powder; hygroscopic |
| Purity | ≥99% (RP-HPLC); disulfide bridge integrity confirmed (ESI-MS; −2 Da vs linear form); C20 fatty acid modification confirmed by mass; identity confirmed by charge-state deconvolution MS (MW ~4409 Da) |
| Endotoxin | <1 EU/mg (LAL chromogenic assay) |
| Solubility | Soluble in sterile water and PBS pH 7.4; may require gentle warming to 37°C with slow rotation for complete dissolution due to C20 fatty acid modification; do not vortex |
| Storage — Lyophilised | −20°C long-term (18–24 months); 2–8°C short-term; protect from moisture and light; equilibrate sealed vial to room temperature before opening |
| Storage — Reconstituted | 2–8°C up to 7 days; −20°C for longer; avoid freeze-thaw; aliquot before freezing; do not expose to reducing agents (DTT, β-ME, TCEP) which break the Cys2–Cys7 disulfide |
| Certificate of Analysis | Lot-specific CoA with every order; HPLC + ESI-MS (~4409 Da; disulfide intact; C20 confirmed) + endotoxin |
| WADA Status | Not listed on 2024–2025 WADA Prohibited List; not prohibited |
What Is Cagrilintide?
Amylin is a 37-amino acid peptide co-secreted with insulin from pancreatic beta cells.
It is released into the portal circulation in response to meals and acts on area postrema and hypothalamic amylin receptors to reduce food intake, slow gastric emptying, suppress glucagon secretion, and produce satiety.
In type 2 diabetes, amylin secretion is deficient — the same beta cell failure that reduces insulin secretion simultaneously eliminates amylin’s meal-related satiety signalling.
Native human amylin cannot be used as a drug because it forms toxic amyloid fibrils at physiological concentrations — a property responsible for the islet amyloid deposits found in type 2 diabetes.
Pramlintide (Symlin), the only approved amylin analog, solved the fibrillation problem by replacing three amino acids with prolines at positions 25, 28, and 29 — prolines break the beta-sheet structure required for fibril formation.
Pramlintide is clinically effective but its 50-minute half-life requires three injections per day, which limited its commercial success.
Cagrilintide is Novo Nordisk’s engineering solution to pramlintide’s limitations.
Starting from the pramlintide backbone (which already has anti-fibril proline substitutions), three additional substitutions (N14E, V17R, P37Y) further stabilise the sequence against degradation and aggregation.
The N-terminal C20 eicosanedioic fatty diacid chain — attached via a γ-glutamic acid linker — enables reversible binding to serum albumin, dramatically extending half-life.
The result is a once-weekly amylin analog that out-performs liraglutide 3.0 mg in monotherapy weight loss (10.8% vs ~4–5%) and produces additive weight loss with semaglutide that exceeds either drug alone.
The REDEFINE 1 Phase 3 results (CagriSema combination; 22.7% weight loss at 68 weeks) represent the largest weight loss ever reported from a Phase 3 obesity trial.
When you buy Cagrilintide Peptide 10 mg from SourceTides, you access research-grade AM833/NNC0174-0833 with disulfide bridge integrity confirmed and C20 fatty acid modification verified.
Why Amylin + GLP-1 Combination Outperforms Either Alone
Complementary Neural Satiety Circuits
GLP-1 receptors (GLP-1R) and amylin receptors (AMY1R/AMY3R) are expressed on different neuronal populations within the brainstem and hypothalamus.
GLP-1R-expressing neurons are concentrated in the nucleus of the solitary tract (NTS) and arcuate nucleus.
AMY1R/AMY3R-expressing neurons are concentrated in the area postrema — a circumventricular organ outside the blood-brain barrier that can detect circulating hormones directly.
Because the two receptor systems signal through partly distinct neural circuits, their satiety signals summate rather than saturate each other.
Activating both simultaneously produces more satiety signalling than either receptor system alone can generate — explaining why CagriSema combination therapy consistently produces more weight loss than either semaglutide or cagrilintide monotherapy.
This additive mechanism is mechanistically distinct from the GLP-1R/GIPR combination in Tirzepatide, which combines two receptors in the same incretin circuit family.
The GLP-1R + AMY1R/AMY3R combination spans two fundamentally different neuroendocrine circuits — making the additivity both more predictable and potentially more durable than within-family combinations.
Glucagon Suppression: Both Mechanisms Contribute
Both GLP-1R and amylin receptor activation suppress glucagon secretion from pancreatic alpha cells.
GLP-1R does so through direct somatotroph and indirect insulin-mediated inhibition of alpha cells.
Amylin receptors suppress glucagon through neural circuits — the area postrema amylin receptor signal travels to the hypothalamus, which then modulates alpha-cell secretion via autonomic pathways.
The dual glucagon suppression in CagriSema may contribute to the combination’s glycaemic efficacy in T2D beyond the weight-loss benefit.
For research design: this dual glucagon suppression pathway is a clean endpoint for comparing GLP-1R-only (semaglutide), amylin-only (cagrilintide), and combination CagriSema in OGTT-based glucagon suppression studies.
Amylin Receptor Pharmacology: How Cagrilintide Signals
Amylin receptors are heterodimeric complexes consisting of the calcitonin receptor (CTR) combined with one of three receptor activity-modifying proteins (RAMP1, RAMP2, RAMP3):
AMY1R = CTR + RAMP1 | AMY2R = CTR + RAMP2 | AMY3R = CTR + RAMP3.
CTR alone (without RAMPs) is the calcitonin receptor.
All three AMY receptors and CTR couple to Gs proteins, activating adenylyl cyclase → cAMP → PKA cascades — the same second messenger pathway used by GLP-1R.
Despite this shared second messenger, cagrilintide and GLP-1 agonists activate different cell populations in different brain regions, which is why their combination is additive rather than redundant.
The landmark 2025 eBioMedicine study (PMC12270663) — using RAMP1/RAMP3 double-knockout mice (which cannot form AMY1R or AMY3R) — definitively established that cagrilintide’s weight loss is mediated specifically by AMY1R and AMY3R, not by CTR or AMY2R alone.
Cagrilintide produced 3.4 g weight loss in wild-type mice but failed to reduce body weight in the RAMP1/3-KO mice, confirming AMY1R/AMY3R dependence.
This is the first study to map cagrilintide’s in-vivo receptor specificity with genetic precision — and it has direct implications for research design (RAMP1/3-KO mice are the definitive control for cagrilintide receptor attribution studies).
Cagrilintide vs Pramlintide: What Changed and Why
| Property | Native Amylin | Pramlintide (Symlin) | Cagrilintide (AM833) |
|---|---|---|---|
| Fibril formation | Yes — toxic; forms islet amyloid deposits in T2D | Eliminated (Pro25/28/29 substitutions) | Eliminated (pramlintide substitutions + N14E/V17R/P37Y) |
| Half-life | ~15 min | ~50 min | 159–195 h (~7–8 days) |
| Dosing frequency | Not used as drug | 3× daily injections | Once-weekly SC |
| Lipidation | No | No | C20 eicosanedioic fatty diacid via γ-Glu linker (N-terminal) |
| Weight loss (monotherapy) | Not studied clinically | ~2–3 kg in T2D studies | 10.8% at 26 weeks (Phase 2); 11.8% at 68 weeks (Phase 3) |
| Combination therapy | — | Adjunct to insulin only | CagriSema: 22.7% weight loss (Phase 3; 68 weeks) |
| Regulatory status | — | FDA-approved (Symlin) for T1D/T2D adjunct to insulin | CagriSema NDA submitted Dec 2025; decision ~late 2026 |
Cagrilintide Clinical Evidence
| Trial / Study | Design | Key Finding | Source |
|---|---|---|---|
| Phase 2 dose-finding (Lau 2021) — Monotherapy | RCT (LANCET Diabetes & Endocrinology 2021); multiple doses; 26 weeks; adults with obesity (no T2D) | Dose-dependent weight loss: 4.5 mg → 10.8% at 26 weeks; surpassed liraglutide 3.0 mg comparator; established dose-response and efficacy safety profile for once-weekly amylin monotherapy | Lau et al. 2021 — Lancet Diabetes Endocrinol — PMID: 34197737 |
| Phase 1b (CagriSema combination; semaglutide + cagrilintide) | Placebo-controlled RCT; 20 weeks; overweight/obese participants + 2.4 mg semaglutide background | Cagrilintide 1.2 mg + semaglutide 2.4 mg: 15.7% weight loss; Cagrilintide 2.4 mg + semaglutide 2.4 mg: 17.1% weight loss at 20 weeks vs semaglutide + placebo 9.8%; additive effect confirmed; warranted Phase 3 | Enebo et al. 2021 — Lancet — PMID: 34587388 |
| REDEFINE 1 — Phase 3 monotherapy sub-analysis (EASD 2025) | Sub-analysis of Phase 3 REDEFINE 1; 68 weeks; adults with obesity (no T2D); once-weekly cagrilintide 2.4 mg + lifestyle intervention | 11.8% mean body weight reduction vs 2.3% placebo; 31.6% of participants achieved ≥15% weight loss vs 4.7% placebo; first Phase 3 data for any long-acting amylin analog monotherapy; generally well tolerated; GI side effects mostly temporary | Novo Nordisk / EASD September 2025 |
| REDEFINE 1 — Phase 3 CagriSema (Novo Nordisk; 2025) | Phase 3 RCT; 68 weeks; n=3,417; adults with obesity (no T2D) | 22.7% mean body weight reduction with CagriSema (cagrilintide 2.4 mg + semaglutide 2.4 mg) vs 3.0% placebo — the largest weight loss ever reported in any Phase 3 obesity RCT; NDA submitted FDA December 2025 | Novo Nordisk REDEFINE 1 top-line results 2025 |
| REDEFINE 2 — Phase 3 CagriSema in T2D (2025) | Phase 3 RCT; 68 weeks; overweight/obese adults with T2D | 13.7% mean body weight reduction with CagriSema; significant HbA1c reduction; dual metabolic and weight outcomes; supports NDA for T2D indication | Novo Nordisk REDEFINE 2 results 2025 |
| AMY1R/AMY3R receptor validation (eBioMedicine 2025) | Preclinical (RAMP1/3-KO mice; high-fat diet; 3 nmol/kg cagrilintide SC) | Cagrilintide: −3.4 g body weight in WT mice (P<0.005); no weight loss in RAMP1/3-KO mice — confirms AMY1R and AMY3R are obligatory in-vivo receptors for cagrilintide’s weight loss; CTR/AMY2R insufficient alone; first genetic receptor specificity validation for cagrilintide | PMC12270663 — eBioMedicine 2025 |
| Structural basis (Nat Commun 2025) | Cryo-EM structures of cagrilintide bound to CTR and AMY1R | Amylin-like binding mode confirmed; distinct conformational dynamics at calcitonin-family receptors vs other peptide ligands; structural basis for non-selective CTR + AMYR agonism characterised at atomic resolution; foundation for next-generation selective amylin analog design | Nat Commun 2025 — Cagrilintide cryo-EM structures |
Cagrilintide in the Obesity Peptide Landscape
| Compound | Mechanism | Peak Phase 3 Weight Loss | Best Research Use | SourceTides |
|---|---|---|---|---|
| Semaglutide | GLP-1R mono-agonist | ~15% (STEP-1; 68 weeks) | GLP-1R monotherapy reference; comparison against AMY receptor pathway | Buy Semaglutide |
| Tirzepatide | GLP-1R + GIPR dual | ~22.5% (SURMOUNT-1; 72 weeks) | GLP-1R/GIPR comparison; incretin dual agonism vs amylin pathway | Buy Tirzepatide |
| Retatrutide | GLP-1R + GIPR + GCGR triple | 24.2% (Phase 2; 48 weeks) | Triple incretin axis; compare vs amylin/GLP-1 combination | Buy Retatrutide |
| Mazdutide | GLP-1R + GCGR dual | Phase 3 (China; ongoing) | OXM-derived dual agonism; NAFLD/MAFLD; GLP-1/glucagon axis | Buy Mazdutide |
| Cagrilintide (this product) | AMY1R + AMY3R + CTR (DACRA) | 11.8% monotherapy; 22.7% CagriSema (Phase 3; 68 weeks) | Amylin receptor pharmacology; brainstem satiety circuits; GLP-1/amylin additive mechanism; novel combination therapy research | Buy Cagrilintide |
| Trinity-X | GLP-1R + GIPR + GCGR triple | No published standalone data | Triple incretin axis; compare vs amylin/GLP-1 combination in DIO models | Buy Trinity-X |
| GLP-1 (native) | GLP-1R (endogenous) | Minimal (t½ ~2 min) | GLP-1R receptor pharmacology reference; incretin biology comparison | Buy GLP-1 |
What Is Cagrilintide Used for in Research?
| Research Field | Application | Why Cagrilintide |
|---|---|---|
| Amylin receptor pharmacology | AMY1R/AMY2R/AMY3R receptor binding; cAMP signalling; β-arrestin recruitment; receptor internalisation; CTR vs AMY receptor selectivity; cryo-EM structural studies | Most clinically advanced amylin receptor agonist; cryo-EM structures available for CTR and AMY1R complexes (Nat Commun 2025); AMY1R/AMY3R genetic receptor validation (eBioMedicine 2025); definitive pharmacological tool for amylin receptor research with full clinical trial context |
| Obesity and body composition | DIO rodent models; body weight reduction; amylin-pathway satiety vs GLP-1-pathway satiety; food intake; energy expenditure; fat mass vs lean mass | Once-weekly dosing (7-day half-life) simplifies DIO protocol design; RAMP1/3-KO mouse model enables clean receptor attribution; compare cagrilintide monotherapy vs Semaglutide monotherapy to isolate amylin vs GLP-1 contributions to body weight |
| GLP-1 + amylin combination mechanism | Additive vs synergistic satiety; neural circuit mapping; hypothalamic gene expression; area postrema vs NTS receptor distributions; combination mechanistic studies | Studying cagrilintide alone and combined with Semaglutide in identical DIO protocols directly recapitulates the published CagriSema Phase 3 data — the most directly relevant preclinical research framework for the combination’s clinical evidence base |
| Brainstem satiety circuit research | Area postrema AMY1R/AMY3R signalling; arcuate nucleus vs NTS food intake regulation; c-Fos activation mapping; neuropeptide Y (NPY) and POMC circuits; energy homeostasis | Amylin receptors in the area postrema are outside the blood-brain barrier — making cagrilintide uniquely accessible to the CNS from systemic injection; maps satiety circuits distinct from GLP-1R NTS pathways |
| Type 2 diabetes research | OGTT; glucagon suppression; HbA1c-proxy endpoints; beta cell function; amylin deficiency models; GLP-1/amylin co-secretion biology | T2D involves dual amylin AND insulin deficiency; cagrilintide provides amylin replacement; REDEFINE 2 Phase 3 T2D data (13.7% weight loss) provides the clinical reference; studied alongside Semaglutide, Tirzepatide, and Glucagon in metabolic research panels |
| Gastric emptying research | Gastric emptying rate; meal-stimulated satiety; post-prandial glucose excursion; GLP-1/amylin gastric emptying comparison | Both amylin and GLP-1 slow gastric emptying via different mechanisms; comparing cagrilintide vs semaglutide for gastric emptying delay isolates the contribution of each pathway to meal processing and glycaemic control |
| GH axis + amylin interaction | GH/IGF-1 lean mass preservation during weight loss; GH axis + amylin pathway interaction; body composition during caloric restriction | Studied alongside Ipamorelin and Sermorelin for lean mass preservation protocols — GH axis support during cagrilintide-driven weight loss; equivalent to CagriSema lean mass protocols |
| Novel combination therapy design | Amylin + GLP-1 + GCGR triple axis; cagrilintide + mazdutide; cagrilintide + retatrutide; novel three-pathway obesity combinations beyond CagriSema | Cagrilintide’s area-postrema amylin pathway is additive to GLP-1R agonism; combining with Mazdutide (GLP-1R + GCGR) or Retatrutide (GLP-1R + GIPR + GCGR) explores whether three-pathway amylin + incretin combinations could exceed CagriSema |
Cagrilintide Pharmacokinetics and Research Design
| Parameter | Value / Notes | Research Implication |
|---|---|---|
| Plasma half-life | 159–195 hours (~7–8 days); albumin-binding via C20 fatty diacid N-terminal chain | Once-weekly SC dosing is validated; in rodent studies, dose once weekly; measure metabolic endpoints weekly; steady-state plasma concentration reached at ~4–5 weeks of weekly dosing |
| Rodent in-vivo dose (preclinical) | 3 nmol/kg SC (eBioMedicine 2025 RAMP-KO study); 0.1–30 nmol/kg SC dose range published (Kruse 2021 J Med Chem); once-weekly dosing for chronic studies | Start at 3–10 nmol/kg SC once weekly in DIO mouse; measure body weight, food intake, fasting glucose weekly; compare WT vs RAMP1/3-KO to confirm AMY1R/AMY3R dependence; include semaglutide arm for GLP-1R comparison |
| In-vitro receptor assay | 1–1000 nM for AMY1R/AMY3R/CTR cAMP accumulation, β-arrestin, receptor internalisation assays in HEK293 cells expressing each receptor | Express each receptor (AMY1R = CTR + RAMP1; AMY2R = CTR + RAMP2; AMY3R = CTR + RAMP3; CTR alone) separately in HEK293; measure cAMP for each; compare selectivity profile; include pramlintide and salmon calcitonin as reference agonists |
| Reconstitution note (C20 fatty acid) | C20 fatty diacid modification may require 37°C gentle rotation for complete dissolution; same protocol as Mazdutide and Semaglutide | Dissolve in sterile PBS pH 7.4 at 37°C with slow end-over-end rotation for 15–30 min; filter through 0.22 µm; do not vortex or sonicate; do not add reducing agents (breaks Cys2–Cys7 disulfide) |
| Disulfide bridge protection | Cys2–Cys7 disulfide bridge; same QC principle as AOD-9604, Oxytocin, AHK-Cu | Avoid DTT, β-ME, TCEP in all buffers; verify disulfide integrity from CoA (ESI-MS: MW ~4409 Da cyclic vs MW ~4411 Da linearised); use non-reducing gel conditions for PAGE analysis |
| Key metabolic endpoints | Body weight; food intake; fasting glucose; OGTT; glucagon suppression; gastric emptying (Evans blue or acetaminophen method); c-Fos in area postrema (immunohistochemistry for receptor attribution) | c-Fos immunohistochemistry in area postrema is the classical neuroanatomical readout for amylin receptor activation — measure 2 hours post-dose; compare cagrilintide (area postrema activation) vs semaglutide (NTS/arcuate activation) to map circuit differences |
Cagrilintide Quality Control at SourceTides
Every batch of Cagrilintide Peptide 10 mg from SourceTides undergoes these tests before release.
For a 37-amino acid lipidated peptide with a disulfide bridge, two QC elements are critical: the Cys2–Cys7 disulfide confirmation and the C20 fatty acid modification verification — both confirmed by MS.
| Test | Method | Specification | Why It Matters |
|---|---|---|---|
| Purity | RP-HPLC (C18; UV 220 nm) | ≥99% peak area purity | 37-AA lipidated peptides are susceptible to deletion sequences and incomplete lipidation; ≥99% confirms full-length, fully lipidated sequence dominates |
| Identity + Disulfide + C20 Confirmation | ESI-MS (charge-state deconvolution); non-reducing conditions for disulfide; MW ~4409 Da expected | MW ~4409 Da confirmed (cyclic disulfide; −2 Da vs linearised form); C20 fatty diacid moiety confirmed by mass; disulfide intact | Three critical structure confirmations in one MS analysis: (1) correct full-length sequence mass; (2) disulfide bridge intact (active for receptor binding); (3) C20 lipid present (active for albumin-mediated half-life extension) |
| Endotoxin | LAL chromogenic assay | <1 EU/mg | LPS activates inflammatory signalling in beta cells, hypothalamic neurons, and area postrema cells — directly confounding glucagon, food intake, and amylin receptor signalling endpoints |
| Appearance | Visual inspection | White lyophilised powder; no discolouration, aggregation, or amyloid-like cloudiness | Amyloid fibril formation (though designed to be prevented by the Pro substitutions) would manifest as cloudiness or visible aggregates; white powder confirms amyloid-free active form |
| Certificate of Analysis | Lot-specific PDF | HPLC + MS (~4409 Da; Cys2–Cys7 disulfide confirmed; C20 lipid confirmed) + endotoxin + dates | The three-item MS confirmation (correct mass + disulfide + C20 lipid) is the unique CoA element for cagrilintide; mandatory documentation for any receptor pharmacology or in-vivo study reporting cagrilintide as the test article |
Cagrilintide Regulatory Status
| Jurisdiction | Status | Notes |
|---|---|---|
| USA (FDA) | Not approved as standalone; CagriSema (cagrilintide + semaglutide) NDA submitted December 2025; PDUFA decision expected late 2026; not a DEA controlled substance | Novo Nordisk submitted the CagriSema NDA to the FDA in December 2025. Standalone cagrilintide NDA not yet submitted. Not a scheduled or controlled substance. SourceTides supplies research-grade for laboratory use only. |
| EU / UK / Australia / Canada | Not approved in any jurisdiction; not a controlled substance; research compound | No marketing authorisation in any jurisdiction. Regulatory submissions for CagriSema expected following FDA decision. Not a controlled substance. See the SourceTides shipping policy. |
| WADA | Not listed on 2024–2025 WADA Prohibited List; not prohibited | No performance-enhancing classification. Verify annually at wada-ama.org. |
Peer-Reviewed References
| # | Citation | Link |
|---|---|---|
| 1 | Kruse T et al. (2021). Development of cagrilintide, a long-acting amylin analogue. J Med Chem. 64(15):11183–11194. [Medicinal chemistry design; preclinical pharmacology; dose-response; PK in rats; key structural decisions for clinical candidate selection] | PubMed PMID: 34296896 — J Med Chem 2021 |
| 2 | Lau DCW et al. (2021). Efficacy and safety of once-weekly cagrilintide 4.5 mg in people with overweight and obesity. Lancet Diabetes Endocrinol. 9(8):563–573. PMID: 34197737. [Phase 2 dose-finding; 10.8% weight loss at 26 weeks] | PubMed PMID: 34197737 — Lancet Diabetes Endocrinol 2021 |
| 3 | Enebo LB et al. (2021). Safety, tolerability, pharmacokinetics, and pharmacodynamics of cagrilintide with semaglutide. Lancet. 397:1535–1548. PMID: 34587388. [Phase 1b CagriSema combination; 17.1% weight loss at 20 weeks] | PubMed PMID: 34587388 — Lancet 2021 |
| 4 | Larsen AT et al. (2025). Cagrilintide lowers bodyweight through brain amylin receptors 1 and 3. eBioMedicine. PMC12270663. [RAMP1/3-KO mouse validation; AMY1R/AMY3R confirmed as obligatory weight loss receptors; CTR/AMY2R insufficient] | PMC12270663 — eBioMedicine 2025 |
| 5 | Structural and dynamic features of cagrilintide binding to CTR and AMY1R. Nat Commun. 2025. [Cryo-EM structures at 2.68–3.26 Å; amylin-like binding mode; distinct conformational dynamics] | Nature Communications 2025 |
| 6 | Wikipedia: Cagrilintide. CAS 1415456-99-3; formula; Phase 3 REDEFINE results; CagriSema NDA. | Wikipedia: Cagrilintide |
Frequently Researched Alongside Cagrilintide
These compounds are most commonly studied alongside Cagrilintide in metabolic, obesity, amylin receptor, and combination therapy research:
- Semaglutide — FDA-approved GLP-1R mono-agonist; the direct CagriSema partner and the most important research comparator; studying cagrilintide alone and combined with semaglutide in identical DIO protocols directly recapitulates the Phase 3 REDEFINE design — the only preclinical framework with direct Phase 3 clinical correlation for this combination
- Tirzepatide — FDA-approved GLP-1R + GIPR dual agonist; studied alongside cagrilintide in comparative obesity research where incretin dual agonism (GLP-1R + GIPR) vs amylin/GLP-1 combination (DACRA + GLP-1R) are compared for weight loss, lean mass preservation, and glycaemic outcomes
- Retatrutide — GLP-1R + GIPR + GCGR triple agonist; studied alongside cagrilintide to compare incretin triple agonism vs amylin/GLP-1 combination; cagrilintide targets AMY receptors (area postrema), retatrutide targets incretin receptors (pancreas, adipose, liver) — a genuinely different combination strategy
- Mazdutide — GLP-1R + GCGR dual agonist; studied with cagrilintide in novel three-axis combination research: cagrilintide (AMY1R/AMY3R) + mazdutide (GLP-1R + GCGR) covers amylin, GLP-1, and glucagon receptor pathways simultaneously — a potential advance beyond CagriSema
- Trinity-X — GLP-1R + GIPR + GCGR tri-agonist; studied alongside cagrilintide to compare incretin-only triple agonism vs amylin pathway addition; does adding amylin receptor activation produce further improvement beyond triple incretin agonism?
- Glucagon — Endogenous GCGR agonist; studied alongside cagrilintide in glucagon suppression assays — both cagrilintide (via neural AMY receptor pathway) and GLP-1 (direct alpha cell) suppress glucagon; comparing cagrilintide vs glucagon in identical models maps the neural vs direct alpha cell glucagon suppression pathways
- GLP-1 — Endogenous GLP-1R agonist; studied alongside cagrilintide in incretin biology research comparing area-postrema amylin satiety vs NTS/arcuate GLP-1R satiety at the circuit level
- Ipamorelin 10 mg — Selective GH secretagogue; studied with cagrilintide in body composition research where GH/IGF-1 lean mass preservation (Ipamorelin) is combined with amylin-mediated fat mass reduction (cagrilintide) — the GH axis + amylin combination for optimal body composition
- Sermorelin 10 mg — GHRH agonist; studied with cagrilintide in obesity + sarcopenia protocols where GH axis anabolic support (Sermorelin) and amylin satiety (cagrilintide) produce fat loss without lean mass compromise
- AOD-9604 Peptide — hGH fragment; direct adipocyte lipolysis via β₃-AR; studied with cagrilintide to combine amylin-mediated satiety (appetite suppression) with direct adipocyte fat mobilisation (AOD-9604) — complementary input/output body fat reduction mechanisms
- Kisspeptin-10 10 mg — GnRH pulse generator; studied alongside cagrilintide in metabolic-reproductive neuroendocrinology research where hypothalamic energy sensing (amylin pathway) interacts with reproductive axis (Kisspeptin/GnRH) — relevant to obesity-related hypogonadism models
- NAD⁺ Injectable — Sirtuin substrate; mitochondrial metabolism; studied with cagrilintide in comprehensive metabolic ageing panels combining amylin pathway satiety (cagrilintide) and mitochondrial metabolic enhancement (NAD⁺) for weight loss + metabolic health outcomes
- LIPO-C Injectable — Multi-nutrient hepatic lipotropic; studied alongside cagrilintide in metabolic syndrome protocols where amylin-driven appetite suppression (cagrilintide) is combined with hepatic lipid metabolism support (LIPO-C methionine/choline)
Frequently Asked Questions
You can buy Cagrilintide Peptide 10 mg (AM833; NNC0174-0833; CAS 1415456-99-3) directly from SourceTides.
Every order includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity), ESI-MS identity confirmation (MW ~4409 Da; Cys2–Cys7 disulfide intact; C20 fatty diacid modification confirmed), and LAL endotoxin result (<1 EU/mg). All vials are lyophilised white powder and dispatched on dry-ice cold chain.
See the SourceTides shipping policy for dispatch details.
Pramlintide (Symlin) is the only approved amylin analog — approved as an adjunct to insulin in T1D and T2D. It works by replacing amylin’s three most amyloidogenic amino acids with prolines (positions 25, 28, 29) to prevent fibril formation, but its plasma half-life is only ~50 minutes, requiring three subcutaneous injections per day. Its weight loss effect is modest (~2–3 kg in trials).
Cagrilintide starts from the pramlintide backbone and adds three further engineering improvements. Three additional amino acid substitutions (N14E, V17R, P37Y) further stabilise the peptide. A C20 eicosanedioic fatty diacid is attached at the N-terminus via a γ-glutamic acid linker — enabling reversible serum albumin binding that extends the half-life from 50 minutes to 159–195 hours (~7 days). The result is a once-weekly amylin analog that produced 10.8% weight loss at 26 weeks in Phase 2 (vs ~2–3 kg for pramlintide) and 22.7% weight loss combined with semaglutide in Phase 3.
Cagrilintide is effectively pramlintide redesigned for once-weekly dosing and meaningful obesity treatment — the compound that finally realises the clinical potential that amylin biology has always promised.
Semaglutide activates GLP-1 receptors concentrated in the nucleus of the solitary tract (NTS) and arcuate nucleus — brainstem and hypothalamic satiety circuits that reduce food intake and body weight.
Cagrilintide activates amylin receptors (AMY1R, AMY3R) concentrated in the area postrema — a circumventricular organ in the brainstem that sits outside the blood-brain barrier and can directly detect circulating hormones. Area postrema AMY receptor activation generates a satiety signal through circuits that are partly distinct from the GLP-1R circuits activated by semaglutide.
Because the two receptor systems activate different neuronal populations and partly different downstream circuits, their satiety signals sum together rather than competing for the same signalling bottleneck. The 2021 Phase 1b data confirmed this: semaglutide alone = 9.8% weight loss at 20 weeks; adding cagrilintide 2.4 mg produced 17.1% — nearly double. The Phase 3 CagriSema: 22.7% at 68 weeks vs ~15% for semaglutide alone in STEP-1. The clinical data matches the mechanistic prediction from circuit anatomy.
This was definitively answered in the 2025 eBioMedicine study (PMC12270663) using RAMP1/RAMP3 double-knockout mice.
Amylin receptors are heterodimers: CTR (calcitonin receptor) + RAMP1 = AMY1R; CTR + RAMP2 = AMY2R; CTR + RAMP3 = AMY3R. RAMP1/RAMP3-knockout mice cannot form AMY1R or AMY3R — they have CTR and AMY2R only.
In wild-type mice, cagrilintide (3 nmol/kg SC) produced 3.4 g body weight loss. In RAMP1/3-KO mice, cagrilintide produced no body weight reduction. The conclusion: AMY1R and AMY3R are obligatory for cagrilintide’s in-vivo weight loss. CTR and AMY2R are insufficient. This has a direct research design implication: RAMP1/3-KO mice are the definitive cagrilintide receptor attribution control — every in-vivo cagrilintide study that claims AMY receptor-mediated effects should include this KO model or a pharmacological AMY1R/AMY3R antagonist arm.
Novo Nordisk submitted the New Drug Application (NDA) for CagriSema (cagrilintide 2.4 mg + semaglutide 2.4 mg; co-formulated) to the FDA in December 2025. Based on the FDA’s standard 10-month review timeline for priority review NDAs, a PDUFA decision date is expected in late 2026.
The NDA is supported by the Phase 3 REDEFINE programme: REDEFINE 1 (22.7% weight loss in non-diabetic adults with obesity; n=3,417; 68 weeks) and REDEFINE 2 (13.7% weight loss in T2D; 68 weeks). These are the largest weight reduction results ever submitted for an obesity NDA.
Standalone cagrilintide monotherapy NDA has not been submitted as of May 2026. SourceTides supplies research-grade cagrilintide for in-vitro laboratory research use only — not as a pharmaceutical preparation or substitute for CagriSema.
Cagrilintide is not a controlled substance in any of these jurisdictions. It is not DEA-scheduled in the USA, not controlled under the Misuse of Drugs Act 1971 in the UK, and not a CDSA controlled substance in Canada. In Australia, it is not a scheduled substance — verify current TGA status for institutional compliance.
Cagrilintide (as standalone) has not been approved as a pharmaceutical drug in any jurisdiction. CagriSema NDA is under FDA review. Cagrilintide is not WADA-prohibited.
SourceTides supplies for in-vitro laboratory research use only. See the SourceTides shipping policy for jurisdiction-specific details.
SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways.
For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.
All SourceTides products, including Cagrilintide Peptide 10 mg (AM833; CAS 1415456-99-3), are for in-vitro laboratory research use only.
CagriSema NDA has been submitted to the FDA (December 2025) but Cagrilintide is not approved by the FDA, EMA, TGA, or Health Canada as a standalone drug.
These products are not for human consumption.
By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable regulations.
| Weight | 0.01 lbs |
|---|---|
| Dimensions | 5 × 5 × 5 in |
| Purity | ≥99% HPLC, C20 Fatty Diacid Confirmed (ESI-MS ~4409 Da), Cys2–Cys7 Disulfide Intact |
| Receptor Targets | |
| Form | Lyophilised Powder (once-weekly; C20 albumin-binding; t½ ~7 days) |
| CAS Number | 1415456-99-3 |
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