Cagrilintide
Metabolic & Weight LossPhase 3Also known as: NN9838
Cagrilintide (also known as AM833, development code NN9838) is a long-acting amylin analog developed by Novo Nordisk as a next-generation weight-management therapy, designed to be co-administered with the GLP-1 receptor agonist semaglutide in a fixed-ratio combination known as CagriSema. It represents the first clinically successful revival of amylin pharmacology since pramlintide (Symlin) was approved in 2005 for type 1 and type 2 diabetes — a product that never achieved commercial success largely because of its inconvenient three-times-daily subcutaneous dosing schedule and its narrow label.
Overview
At A Glance
Cagrilintide engages both amylin and calcitonin receptor signaling with careful receptor selectivity profiling. Native amylin binds primarily to amylin receptors - heterodimeric complexes of the calcitonin receptor (CTR) with one of three receptor activity-modifying proteins (R…
Mechanism of Action
Cagrilintide engages both amylin and calcitonin receptor signaling with careful receptor selectivity profiling. Native amylin binds primarily to amylin receptors - heterodimeric complexes of the calcitonin receptor (CTR) with one of three receptor activity-modifying proteins (RAMP1, RAMP2, or RAMP3), generating three distinct amylin receptor subtypes (AMY1R, AMY2R, AMY3R respectively). Cagrilintide retains this multi-receptor engagement pattern with modifications that extend half-life and improve physiochemical stability.
Central Satiety Signaling: The primary mechanism of cagrilintide's weight-loss effect is central - amylin receptor signaling in the area postrema and other circumventricular organs (which lack a complete blood-brain barrier) produces satiety signals that propagate through the nucleus tractus solitarius to hypothalamic feeding centers. This reduces meal size and total caloric intake. Cagrilintide may also slow gastric emptying (similar to native amylin but milder than GLP-1 agonists), contributing to early satiety during meals.
Synergy with GLP-1 Agonism: The key insight behind CagriSema is mechanistic synergy: GLP-1 receptors and amylin receptors are expressed in different hypothalamic and brainstem populations, with partially overlapping but not identical downstream effects on appetite regulation. Co-administration engages two distinct anorexigenic circuits:
- GLP-1 (semaglutide): acts on POMC/CART neurons in the arcuate nucleus, area postrema, and brainstem
- Amylin (cagrilintide): acts preferentially on area postrema and lateral parabrachial nucleus
This dual engagement appears to produce additive or super-additive weight loss without proportionally increasing GI side effects, because each mechanism contributes satiety from a different neural circuit rather than intensifying activation of a single circuit to intolerable levels.
Albumin-Binding Pharmacology: Cagrilintide's fatty acid side chain (a C20 fatty diacid attached via a -glutamate linker) mediates reversible binding to human serum albumin with nanomolar affinity. This:
- Reduces renal clearance (albumin-bound fraction is protected from glomerular filtration)
- Extends apparent half-life from 13 minutes (native amylin) to ~159 hours (cagrilintide)
- Enables once-weekly dosing
- Produces relatively flat plasma concentration profiles (reducing peak-related nausea)
Receptor Selectivity: Cagrilintide shows relatively balanced engagement across AMY1R, AMY2R, AMY3R and retains calcitonin receptor binding. The native calcitonin receptor itself (without RAMP) is involved in calcium-phosphate homeostasis, but cagrilintide at therapeutic doses does not produce clinically significant changes in bone metabolism or calcium regulation in trials to date.
Glucose Regulation: Unlike its predecessor pramlintide (which was developed primarily for type 1 and type 2 diabetes as an insulin adjunct), cagrilintide has modest effects on glucose control - it slows gastric emptying (reducing post-meal glucose spikes) and potentially suppresses inappropriate glucagon secretion, but it is not currently positioned as a monotherapy for diabetes management. In combination with semaglutide (CagriSema), glycemic improvements reflect primarily the GLP-1 component with modest incremental benefit from amylin.
Pharmacokinetic Profile:
- Half-life: ~159 hours (6-7 days) - once-weekly dosing
- Tmax after SC injection: 24-72 hours (prolonged absorption from subcutaneous depot)
- Distribution: bound to albumin; volume of distribution consistent with vascular-extracellular distribution
- Elimination: primarily enzymatic proteolysis; renal elimination minor
- Steady state: achieved after 5-6 weekly doses (roughly 5-6 half-lives)
Dose-Response Relationship: Phase 2 data established clear dose-response for weight loss across cagrilintide monotherapy doses of 0.3 mg, 0.6 mg, 1.2 mg, 2.4 mg, and 4.5 mg weekly, with weight loss spanning 6.0%-10.8% across the dose range and 4.5 mg producing approximately 10.8% weight loss versus 3.0% placebo over 26 weeks (Lau et al., 2021). The CagriSema Phase 3 program uses 2.4 mg cagrilintide + 2.4 mg semaglutide.
Overview
Cagrilintide (also known as AM833, development code NN9838) is a long-acting amylin analog developed by Novo Nordisk as a next-generation weight-management therapy, designed to be co-administered with the GLP-1 receptor agonist semaglutide in a fixed-ratio combination known as CagriSema. It represents the first clinically successful revival of amylin pharmacology since pramlintide (Symlin) was approved in 2005 for type 1 and type 2 diabetes — a product that never achieved commercial success largely because of its inconvenient three-times-daily subcutaneous dosing schedule and its narrow label. Cagrilintide solves the pharmacokinetic problem: through acylation with a fatty acid chain (in a strategy similar to Novo Nordisk's use of the same chemistry in semaglutide and insulin degludec), cagrilintide binds reversibly to albumin, extending its half-life from native amylin's 13 minutes to approximately 159 hours (6-7 days), enabling once-weekly subcutaneous injection ([Enebo et al., 2021]).
Amylin itself is a 37-amino-acid peptide hormone co-secreted with insulin by pancreatic beta cells in response to nutrient ingestion, at roughly 1-5% the molar ratio of insulin. It was discovered in 1987 by Per Westermark and colleagues as the principal constituent of pancreatic amyloid deposits in type 2 diabetes (hence the name amylin — from amyloid). The mature hormone contains a disulfide bond between cysteine-2 and cysteine-7 and a C-terminal amide essential for bioactivity, giving it a cyclic head and a linear tail. Native amylin is aggregation-prone and forms the same toxic oligomers and fibrils implicated in beta-cell failure, which is why all clinical amylin analogs (pramlintide, cagrilintide, amycretin) have substituted key amyloidogenic residues (typically proline substitutions at positions 25, 28, 29) to block the fibrillation pathway while preserving receptor binding.
In the Phase 2 randomized trial of cagrilintide monotherapy at 4.5 mg weekly in adults with obesity, mean weight loss at 26 weeks was approximately 10.8% versus 3.0% with placebo and 9.0% with liraglutide 3.0 mg daily ([Lau et al., 2021]). More importantly, the CagriSema Phase 2 combination trial — cagrilintide 2.4 mg + semaglutide 2.4 mg weekly — produced 15.6% placebo-adjusted weight loss at 32 weeks, substantially greater than either component alone and comparable to tirzepatide and retatrutide results, generating intense pharma-industry and investor interest ([Enebo et al., 2021]). The Phase 3 REDEFINE program (REDEFINE 1, 2, 3, 4) has enrolled over 6,000 participants, with REDEFINE 1 (adults with obesity, no diabetes) and REDEFINE 2 (type 2 diabetes) reading out weight loss endpoints of 22.7% at 68 weeks in the landmark cohort, positioning CagriSema to compete with tirzepatide (Zepbound/Mounjaro) and the emerging triple agonist retatrutide as the next-generation incretin-amylin combination therapy. Cross-references include Semaglutide (the GLP-1 component of CagriSema), Tirzepatide (the leading dual GLP-1/GIP competitor), Retatrutide (triple agonist in development), Mazdutide (GLP-1/glucagon dual agonist from Innovent), and Orforglipron (oral non-peptide GLP-1 agonist).
Potential Research Fields
Chemical Information
IUPAC Name
Amylin analog with N-terminal fatty acid acylation (proprietary)
CAS Number
2172366-25-3
Molecular Formula
C195H286N46O60
Molecular Mass
4246.7 g/mol
Dosing & Protocols
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Interactions
Interaction Matrix
Contraindications
Absolute Contraindications:
- Personal or family history of medullary thyroid carcinoma (MTC)
- Multiple endocrine neoplasia type 2 (MEN2)
- Known hypersensitivity to cagrilintide, semaglutide, or any component
- Pregnancy (weight loss contraindicated)
- Active eating disorder (anorexia nervosa, severe bulimia)
- Severe untreated psychiatric conditions
Relative Contraindications (Require Careful Evaluation):
- History of pancreatitis: not absolute but high caution
- Severe gastroparesis: may worsen
- Gallbladder disease: increased risk during rapid weight loss
- Inflammatory bowel disease: caution with GI effects
- Severe renal impairment (eGFR <30): limited data
- Severe hepatic impairment: limited data
- Age >75: careful titration needed
- Children/adolescents: not yet studied
Drug Interactions:
Medications Requiring Adjustment:
- Insulin: may need 20-40% dose reduction (hypoglycemia risk)
- Sulfonylureas: consider dose reduction or discontinuation
- Thyroid replacement: monitor and adjust as weight changes
- Levothyroxine: absorption may be affected; separate by 30 min+
- Oral contraceptives: absorption may be altered; barrier backup recommended
- Warfarin: monitor INR (altered absorption possible)
Medications to Use with Caution:
- Other GLP-1 agonists: avoid concurrent use (redundant, increased AE)
- Other amylin analogs (pramlintide): avoid concurrent use
- Opioids: may worsen constipation
- Sedatives: may worsen dizziness
- Lithium: altered clearance possible
Medications Compatible:
- Most antihypertensives
- Statins
- Metformin (often beneficial combination)
- SSRIs (monitor mood changes)
- Most thyroid medications (with monitoring)
- Most HRT (estrogen, testosterone)
Medical Conditions Requiring Caution:
Gastrointestinal:
- Gastroparesis: worsening risk
- Inflammatory bowel disease: caution
- Peptic ulcer disease: monitor
- History of bowel obstruction: contraindicated
Pancreatic:
- History of pancreatitis: high caution
- Pancreatic insufficiency: monitor
- Pancreatic cancer risk: theoretical
Thyroid:
- Medullary thyroid carcinoma (personal or family): contraindicated
- MEN2 syndrome: contraindicated
- Benign thyroid nodules: monitor
- Autoimmune thyroiditis: manage thyroid function separately
Gallbladder:
- Gallstones: increased risk with rapid weight loss
- Previous cholecystectomy: no additional contraindication
- Active symptoms: manage before starting
Cardiovascular:
- Recent myocardial infarction: delay start
- Severe heart failure: monitor
- Hypertension: typically improves with weight loss
Renal:
- Mild-moderate impairment: no major concerns
- Severe impairment (eGFR <30): limited data
- Hemodialysis: not well-studied
Hepatic:
- Non-alcoholic fatty liver: typically improves with weight loss
- Severe cirrhosis: limited data
- Alcoholic liver disease: manage separately
Psychiatric:
- Depression: monitor closely (any weight-loss drug can affect mood)
- Anxiety disorders: monitor
- History of suicidal ideation: careful monitoring
- Eating disorders: contraindicated if active
Pregnancy/Reproductive:
- Pregnancy: absolute contraindication
- Breastfeeding: not well-studied
- Effective contraception during treatment
- Pre-conception: discontinue 4-6 weeks before
When to Stop Immediately:
- Anaphylactoid/severe hypersensitivity reaction
- Severe persistent pancreatitis symptoms
- Suspected medullary thyroid cancer
- Severe gallbladder disease
- Severe psychiatric emergency
- Pregnancy (discovery or planning)
- Severe unexplained weight loss
When to Consult Physician:
- Severe or persistent GI symptoms
- Suspected pancreatitis
- New thyroid symptoms (neck mass, dysphagia)
- Gallbladder symptoms
- Significant mood changes
- Severe fatigue
- Unexpected labs
- Pregnancy plans
- New medical conditions
Pre-Treatment Assessment:
- Complete medical history
- Medication reconciliation
- Baseline labs (complete metabolic panel, lipids, HbA1c, TSH, liver enzymes)
- Mental health screening
- Physical exam
- ECG if cardiovascular concerns
- Pregnancy test if applicable
- Patient education on risks/benefits
Monitoring Schedule:
- Baseline: complete evaluation
- Month 1: clinical visit, symptoms review
- Month 3: labs + clinical assessment
- Month 6: labs + body composition + complete reassessment
- Month 12: annual evaluation
- Ongoing: symptom tracking, quality of life
Integration with Medical Care: CagriSema/cagrilintide use benefits from clinical oversight:
- Primary care with weight management expertise
- Endocrinology for complex diabetes or thyroid
- Bariatric medicine for advanced cases
- Nutrition counseling
- Mental health support
Solo use is possible but coordination with physicians optimizes outcomes and safety. Insurance coverage often requires specific documentation and monitoring.
Research Disclaimer
This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.
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Related Compounds
View AllAOD-9604
Metabolic & Weight LossPhase 3AOD-9604 (Anti-Obesity Drug 9604) is a synthetic 16-amino-acid peptide fragment of human growth hormone (hGH) corresponding to residues 177-191 of the hGH molecule plus a tyrosine addition at the N-terminus (sequence: Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe).
ATX-304
Metabolic & Weight LossPhase IIa Clinical TrialsATX-304 (also known as O-304) is an orally bioavailable, first-in-class pan-AMPK activator with a mild mitochondrial-uncoupling effect.
HGH Fragment 176-191
Metabolic & Weight LossPhase 2HGH Fragment 176-191 (also written HGH Frag 176-191, hGH Fragment 176-191, and frequently appearing in clinical literature as AOD-9604 — "Anti-Obesity Drug 9604") is a synthetic peptide corresponding to the C-terminal 15-amino-acid region of the 191-amino-acid human growth hormone (hGH) molecule, with an additional N-terminal tyrosine residue added for stability and biological activity.
Retatrutide
Metabolic & Weight LossPhase 3Retatrutide (also coded LY3437943) is an investigational once-weekly triple-agonist at the GLP-1, GIP, and glucagon receptors — the third-generation incretin-based therapy developed by Eli Lilly.
Semaglutide
Metabolic & Weight LossFDA ApprovedSemaglutide is a glucagon-like peptide-1 receptor agonist (GLP-1 RA) with a molecular weight of 4113.58 Da and CAS number 910463-68-2.
Tirzepatide
Metabolic & Weight LossFDA ApprovedTirzepatide is a dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist with a molecular weight of 4813.45 Da and CAS number 2023788-19-2.
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46 PubMed studies
Quality Indicators
Data Completeness
100%COA Verification
10
Verified COAs
2
Vendors w/ COA
High verification rate (83%)
Latest test: 3/1/2026
Research Credibility
Quick Facts
Half-Life
~159 hours (approximately 7 days)
Molecular Weight
4246.7 g/mol
CAS Number
2172366-25-3
Trial Phase
Phase 3
Safety Profile
Moderate RiskCommon Side Effects
- • Nausea
- • Vomiting
- • Decreased appetite
- • Injection site reactions
Stop Use If
- Phase 3 trials ongoing — long-term safety profile incomplete
Research Disclaimer
This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.
Frequently Asked Questions
What is cagrilintide and how does it work?
Cagrilintide is a long-acting amylin analog developed by Novo Nordisk, designed to be co-administered with semaglutide as a fixed-ratio combination called CagriSema. Amylin is a 37-amino-acid peptide hormone co-secreted with insulin by pancreatic beta cells that promotes satiety, slows gastric emptying, and reduces food intake. Cagrilintide engages amylin receptors (AMY1R, AMY2R, AMY3R - heterodimers of calcitonin receptor + RAMP proteins) primarily in the area postrema and other brainstem/hypothalamic areas that regulate appetite. Its key innovation is a C20 fatty-diacid side chain that binds reversibly to albumin, extending half-life from native amylin's ~13 minutes to ~159 hours (6-7 days), enabling once-weekly subcutaneous injection (Enebo et al., 2021).
How effective is CagriSema for weight loss?
CagriSema (cagrilintide 2.4 mg + semaglutide 2.4 mg weekly) has shown substantial weight loss in clinical trials. In the Phase 1b trial, the combination arm reached 17.1% weight loss at 20 weeks vs 9.8% for semaglutide 2.4 mg plus placebo - note there was no cagrilintide-monotherapy arm in that study, since every participant received semaglutide (Enebo et al., 2021). The pivotal Phase 3 REDEFINE 1 trial (adults with obesity, no diabetes) reported 20.4% mean weight loss at 68 weeks on the treatment-policy (intention-to-treat) estimand - and ~22.7% among fully adherent participants (trial-product estimand) - vs 3.0% for placebo (Garvey et al., 2025). This puts CagriSema roughly on par with tirzepatide and ahead of semaglutide alone, though the Phase 3 figure came in below some earlier-phase projections.
How does CagriSema compare to tirzepatide (Zepbound/Mounjaro)?
Both achieve substantial weight loss at broadly similar efficacy: CagriSema showed ~20.4% at 68 weeks (intention-to-treat) in REDEFINE 1, while Tirzepatide 15 mg showed roughly 21% (treatment-regimen estimand) to 22.5% (on-treatment estimand) at 72 weeks in SURMOUNT-1. Mechanistically they differ: CagriSema combines GLP-1 (semaglutide) + amylin (cagrilintide), while tirzepatide is a single molecule with GLP-1 + GIP activity. Practical differences: CagriSema requires two separate injections (for now); tirzepatide is a single injection. Tolerability profiles are broadly similar, though specific GI symptoms may favor one over the other in individual patients. The head-to-head REDEFINE 4 trial is designed to provide a direct comparison. Commercial choice will likely depend on insurance coverage, personal tolerance, and physician preference.
Why not just use semaglutide alone - why add cagrilintide?
The argument for combination therapy is mechanistic synergy: GLP-1 receptors and amylin receptors are expressed in different brainstem and hypothalamic neuron populations, engaging different appetite-regulating circuits. In the Phase 1b trial, CagriSema reached ~17.1% weight loss at 20 weeks vs 9.8% for semaglutide plus placebo - a meaningful incremental benefit. Critically, GI side effects of the combination were not proportionally worse than semaglutide alone in that study, meaning patients got dual-mechanism weight loss without double the nausea/vomiting. However, the combination costs more, requires two injections (for now), and the incremental advantage narrowed at the longer Phase 3 time points. For patients with an excellent semaglutide response and tolerance, adding cagrilintide may have less value; for those seeking maximum weight loss, the combination may be worthwhile.
Is cagrilintide available now, or only in clinical trials?
As of 2026, cagrilintide is not yet FDA-approved. The Phase 3 REDEFINE program has reported (REDEFINE 1 and REDEFINE 2 were published in the New England Journal of Medicine in 2025), and Novo Nordisk has been moving toward regulatory submission for CagriSema. Current access routes: (1) clinical trials, where available; (2) licensed compounding pharmacies offering off-label compounded cagrilintide; (3) research peptide sources (not recommended due to quality concerns). Once commercial CagriSema is available, it will likely be prescription-only through weight-management and primary care clinics. Insurance coverage will depend on indication (obesity, type 2 diabetes), prior authorization requirements, and plan-specific policies.
What are the main side effects of cagrilintide?
The most common side effects are gastrointestinal: nausea (roughly 20-47% across doses vs 18% placebo in the Phase 2 monotherapy trial), vomiting, diarrhea, constipation, decreased appetite, and early satiety. Most GI effects are mild-to-moderate, dose-dependent, and decrease with continued dosing. Other common effects include headache, fatigue (especially during rapid weight loss), dizziness, and injection site reactions. Rare but serious concerns include theoretical pancreatitis risk, gallbladder disease during rapid weight loss, and (like other GLP-1 agonists) a theoretical association with medullary thyroid carcinoma based on rodent studies. Cagrilintide, like all clinical amylin analogs, is engineered with proline substitutions to prevent the amyloid formation native amylin can cause, though very long-term safety data (>5 years) is limited as the drug is still new.
How does cagrilintide differ from pramlintide (Symlin)?
Both are amylin analogs, but they differ in major practical and commercial ways. Pramlintide (Symlin) was FDA-approved in 2005 for type 1 and type 2 diabetes as an insulin adjunct; it has a short half-life requiring three-times-daily injection right before meals, which limited its commercial success. Cagrilintide has a C20 fatty-diacid modification that extends half-life to ~159 hours, enabling once-weekly dosing - a far more convenient regimen. Additionally, cagrilintide is being developed primarily for obesity (with semaglutide as CagriSema), whereas pramlintide was positioned for diabetes. The core mechanism (amylin receptor agonism for satiety and slowed gastric emptying) is similar, but the pharmacokinetic improvement and different positioning make cagrilintide a fundamentally different therapeutic option.
Can I stack cagrilintide with tirzepatide or retatrutide?
There is no clinical trial data supporting any of these combinations, and they are not recommended without physician oversight. Theoretically, adding amylin (cagrilintide) to Tirzepatide (GLP-1/GIP) would create a triple-mechanism approach, and adding it to Retatrutide (GLP-1/GIP/glucagon) a quadruple-mechanism approach. While the underlying receptor biology suggests possible additive benefit, the risks include unpredictable cumulative GI toxicity, unknown long-term metabolic effects, and potential impact on glucose regulation. Novo Nordisk's amycretin is a single molecule with dual GLP-1/amylin activity in development - if successful, it may reduce the appeal of these kinds of stacks. For now, CagriSema (cagrilintide + semaglutide) is the evidence-based combination; other combinations are experimental.
What happens if I stop taking cagrilintide?
Like all weight-loss medications, discontinuation typically results in partial or complete weight regain. Studies with semaglutide alone have shown that roughly half to two-thirds of lost weight is regained within 1-2 years after stopping. CagriSema-specific discontinuation data is still emerging, but similar patterns are expected. Factors affecting regain include maintained lifestyle habits (diet, exercise), residual appetite changes, body composition changes, and individual metabolic factors. Strategies to minimize regain include gradual dose reduction rather than abrupt stop, intensive lifestyle reinforcement, potential maintenance dosing at lower doses, body composition monitoring, and ongoing behavioral support. For many patients, ongoing treatment (even at reduced doses) is becoming the standard approach to maintain weight loss long-term - similar to chronic treatment of hypertension or hyperlipidemia.
Is cagrilintide expensive, and will insurance cover it?
CagriSema and cagrilintide monotherapy are expected to be expensive, consistent with other GLP-1-based weight-loss medications. Comparable drugs (Wegovy, Zepbound) have list prices of roughly $1,000-1,400 per month without insurance, and a dual-component product could be similar or higher. Insurance coverage depends on (1) FDA indication (obesity vs diabetes), (2) the specific plan, (3) prior authorization requirements (typically BMI >=30, or >=27 with comorbidities), and (4) step-therapy requirements (trying other drugs first). Many plans are expanding obesity-drug coverage, but it remains inconsistent. Manufacturer assistance programs, employer benefits, and specialty pharmacy negotiations can reduce out-of-pocket costs. Off-label compounded versions are sometimes cheaper but raise quality and safety concerns.
Research Tools
Related Compounds
View AllAOD-9604
Metabolic & Weight LossPhase 3AOD-9604 (Anti-Obesity Drug 9604) is a synthetic 16-amino-acid peptide fragment of human growth hormone (hGH) corresponding to residues 177-191 of the hGH molecule plus a tyrosine addition at the N-terminus (sequence: Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe).
ATX-304
Metabolic & Weight LossPhase IIa Clinical TrialsATX-304 (also known as O-304) is an orally bioavailable, first-in-class pan-AMPK activator with a mild mitochondrial-uncoupling effect.
HGH Fragment 176-191
Metabolic & Weight LossPhase 2HGH Fragment 176-191 (also written HGH Frag 176-191, hGH Fragment 176-191, and frequently appearing in clinical literature as AOD-9604 — "Anti-Obesity Drug 9604") is a synthetic peptide corresponding to the C-terminal 15-amino-acid region of the 191-amino-acid human growth hormone (hGH) molecule, with an additional N-terminal tyrosine residue added for stability and biological activity.
Retatrutide
Metabolic & Weight LossPhase 3Retatrutide (also coded LY3437943) is an investigational once-weekly triple-agonist at the GLP-1, GIP, and glucagon receptors — the third-generation incretin-based therapy developed by Eli Lilly.
Semaglutide
Metabolic & Weight LossFDA ApprovedSemaglutide is a glucagon-like peptide-1 receptor agonist (GLP-1 RA) with a molecular weight of 4113.58 Da and CAS number 910463-68-2.
Tirzepatide
Metabolic & Weight LossFDA ApprovedTirzepatide is a dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist with a molecular weight of 4813.45 Da and CAS number 2023788-19-2.
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