Cagrilintide long-acting amylin analog peptide vial - 99% purity lab-tested for research
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Cagrilintide

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A long-acting amylin receptor agonist investigated for weight management. Synergistic with GLP-1 agonists - the CagriSema combination (cagrilintide + semaglutide) shows 15.6% weight loss.

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SKU: cagrilintide
Purity: >99% (HPLC Verified)
Form: Lyophilized Powder
Storage: Store at -20°C
CAS Number: 1415456-99-3
For Research Use Only.
All products are sold strictly for laboratory and research purposes. Products are not intended for human use or consumption of any kind.

The statements presented on this website have not been evaluated by the Food and Drug Administration (FDA). The products of this company are not intended to diagnose, treat, cure, or prevent any medical condition or disease.

What is Cagrilintide?

Cagrilintide is a long-acting amylin receptor agonist developed by Novo Nordisk for metabolic research applications. This investigational peptide mimics the natural hormone amylin (also known as islet amyloid polypeptide or IAPP), which plays a crucial role in glucose homeostasis and satiety regulation[1].

Unlike native amylin, which has an extremely short half-life of minutes, cagrilintide has been engineered for once-weekly subcutaneous administration through strategic amino acid substitutions and fatty acid acylation. This extended pharmacokinetic profile makes it particularly suitable for long-term metabolic research studies[2].

Cagrilintide (Long-Acting Amylin Analog)

  • Amino acid sequence modified from native human amylin[3]
  • Fatty acid acylation extends half-life to approximately 7 days[2]
  • Selective amylin receptor agonist (AMY1, AMY2, AMY3)[4]
  • Delays gastric emptying and reduces food intake[5]
  • Suppresses postprandial glucagon secretion[6]
  • Synergistic effects with GLP-1 receptor agonists[7]

CagriSema: The Synergistic Combination

One of the most significant developments in cagrilintide research is its combination with semaglutide (a GLP-1 receptor agonist), known as CagriSema. This fixed-ratio combination leverages complementary mechanisms of action to produce superior metabolic effects compared to either agent alone[7]:

Study Treatment Mean Weight Loss Duration
STEP 1[8] Semaglutide 2.4 mg -14.9% 68 weeks
REDEFINE 1[7] CagriSema (2.4 mg/2.4 mg) -15.6% 32 weeks
Phase 2[9] Cagrilintide 2.4 mg -10.8% 32 weeks

The CagriSema combination demonstrates that dual targeting of amylin and GLP-1 receptors produces additive or synergistic effects, representing a promising avenue for advanced metabolic research[7].

Molecular & Chemical Information

Property Cagrilintide
Molecular Formula C₁₉₁H₂₉₀N₅₀O₅₆S (approximate)
Molecular Weight ~4326 Da
CAS Number 1415456-99-3
Half-Life ~155 hours (6.5 days)[2]
Receptor Target Amylin receptors (AMY1, AMY2, AMY3)
Modification Fatty acid acylated analog of human amylin
Administration Route Subcutaneous injection

Background: Amylin's Physiological Role

Amylin is a 37-amino acid peptide hormone co-secreted with insulin from pancreatic β-cells in response to nutrient ingestion. In healthy individuals, amylin:insulin molar ratio is approximately 1:100[10].

Amylin's primary physiological functions include[11]:

  • Slowing gastric emptying: Delays the rate at which food enters the small intestine, reducing post-meal glucose spikes
  • Suppressing glucagon: Inhibits inappropriate glucagon secretion during meals, preventing hepatic glucose output
  • Promoting satiety: Acts on area postrema in the brainstem to reduce food intake

In type 2 diabetes, amylin secretion is impaired alongside insulin deficiency, contributing to postprandial hyperglycemia and dysregulated satiety[12]. Cagrilintide was developed to restore and enhance these amylinomimetic effects with a more convenient dosing schedule than pramlintide (the first-generation amylin analog requiring multiple daily injections).

Development Note: Cagrilintide is currently in Phase 3 clinical trials (REDEFINE program) and has not yet received regulatory approval. Research-grade cagrilintide is provided strictly for laboratory research applications.

How Cagrilintide Works

Cagrilintide functions as a selective amylin receptor agonist, mimicking and amplifying the physiological effects of endogenous amylin. Its mechanism of action involves multiple complementary pathways that collectively regulate glucose homeostasis, gastric function, and energy balance[4].

Amylin Receptor Activation

Amylin receptors are heterodimeric complexes formed by the calcitonin receptor (CTR) paired with receptor activity-modifying proteins (RAMPs). Three principal amylin receptor subtypes exist[13]:

AMY1 Receptor

CTR + RAMP1
Primary receptor in area postrema (brainstem satiety center)[14]

AMY2 Receptor

CTR + RAMP2
Expressed in cardiovascular tissues and central nervous system[14]

AMY3 Receptor

CTR + RAMP3
Found in peripheral tissues including gastrointestinal tract[14]

Cagrilintide binds to and activates these receptors with high affinity, triggering intracellular signaling cascades involving cyclic AMP (cAMP) and calcium mobilization[4].

Delayed Gastric Emptying

One of cagrilintide's most pronounced effects is slowing the rate of gastric emptying through activation of amylin receptors in the area postrema and vagal afferent pathways[5]:

  • Central Nervous System Signaling: Activation of AMY1 receptors in the area postrema initiates vagal efferent signals that reduce gastric motility and pyloric relaxation[15]
  • Direct Peripheral Effects: AMY3 receptor activation in the stomach and proximal small intestine may contribute to local motor function regulation[16]
  • Metabolic Consequences: Delayed gastric emptying reduces the rate of glucose appearance in the bloodstream, lowering postprandial glucose excursions without increasing insulin demand[5]

In Phase 2 trials, cagrilintide demonstrated dose-dependent reductions in gastric emptying rate, with effects sustained over the week-long dosing interval[9].

Glucagon Suppression

Cagrilintide suppresses inappropriate postprandial glucagon secretion from pancreatic α-cells. This effect is particularly relevant in metabolic research contexts where glucagon dysregulation contributes to hyperglycemia[6]:

Mechanism of Glucagon Suppression

The exact mechanisms remain under investigation, but evidence suggests:

  1. Direct effects on α-cells via local amylin receptor activation
  2. Indirect modulation through delayed nutrient absorption (slower gastric emptying)
  3. Central nervous system-mediated effects on α-cell function[6]

By reducing glucagon during the postprandial period, cagrilintide decreases hepatic glucose production, contributing to improved glycemic control independent of its effects on insulin secretion[6].

Satiety and Food Intake Reduction

Cagrilintide's most clinically significant effect is its potent reduction in food intake and enhancement of satiety through activation of AMY1 receptors in the area postrema[14]:

  • Brainstem Satiety Signaling: Area postrema neurons project to nucleus tractus solitarius (NTS), which integrates peripheral satiety signals and regulates feeding behavior[17]
  • Dose-Dependent Effects: Higher doses of cagrilintide produce greater reductions in ad libitum food intake and increased subjective fullness ratings[9]
  • Sustained Effect: Unlike acute satiety signals, cagrilintide's long half-life provides continuous appetite suppression between weekly doses[2]

Synergy with GLP-1 Receptor Agonists

The combination of cagrilintide with GLP-1 receptor agonists (particularly semaglutide) produces effects greater than either agent alone. This synergy operates through multiple mechanisms[7]:

Pathway Cagrilintide (Amylin Agonist) Semaglutide (GLP-1 Agonist) Combined Effect
Gastric Emptying Marked delay via area postrema Moderate delay via vagal pathways Synergistic slowing
Satiety Signaling Area postrema → NTS pathway Hypothalamic POMC/CART neurons Complementary CNS targets
Glucagon Postprandial suppression Glucose-dependent suppression Enhanced glycemic control
Insulin No direct effect Glucose-dependent secretion Preserved insulin response

The REDEFINE 1 trial demonstrated that CagriSema (cagrilintide 2.4 mg + semaglutide 2.4 mg) produced 15.6% weight loss compared to 10.8% with cagrilintide alone and historical data of ~15% with semaglutide alone, suggesting true synergy[7].

Research Insight: The complementary mechanisms of amylin and GLP-1 agonism represent a novel pharmacological approach in metabolic research, potentially offering insights into multi-hormone regulation of energy balance.

Research Applications & Contexts

Cagrilintide is being investigated across multiple research contexts focused on metabolic regulation, weight management, and glucose homeostasis. As an investigational peptide with extensive clinical trial data, it offers researchers a well-characterized tool for studying amylin receptor biology[18].

1. Obesity and Weight Management Research

The primary focus of cagrilintide research has been its profound effects on body weight reduction[9]:

Key Clinical Trial Data - Phase 2 ONWARDS 1
  • Design: 32-week, dose-ranging study in 706 adults with overweight/obesity
  • Results (Cagrilintide monotherapy):[9]
    • 0.3 mg weekly: -3.9% weight loss
    • 0.6 mg weekly: -6.0% weight loss
    • 1.2 mg weekly: -8.1% weight loss
    • 2.4 mg weekly: -10.8% weight loss
    • 4.5 mg weekly: -10.4% weight loss
  • Mechanism: Weight loss attributed primarily to reduced energy intake (-535 kcal/day at 2.4 mg dose) rather than increased energy expenditure

Research Implications: Cagrilintide provides a valuable research tool for investigating amylin receptor-mediated satiety pathways independent of GLP-1 signaling, offering insights into hormone-specific contributions to appetite regulation.

2. Combination Therapy Research (CagriSema)

The synergistic combination of cagrilintide with semaglutide represents a novel approach in multi-agonist metabolic therapeutics[7]:

REDEFINE 1 Trial Highlights
Primary Efficacy
  • CagriSema: -15.6% weight loss at 32 weeks[7]
  • Cagrilintide alone: -10.8%
  • Placebo: -2.4%
Responder Rates
  • ≥10% weight loss: 74% (CagriSema)
  • ≥15% weight loss: 52% (CagriSema)
  • ≥20% weight loss: 32% (CagriSema)

Research Applications:

  • Investigation of multi-receptor agonism strategies in metabolic regulation
  • Study of synergistic vs. additive effects in combination pharmacology
  • Exploration of complementary satiety pathway activation
  • Analysis of dose optimization in fixed-ratio combinations

3. Glucose Homeostasis and Diabetes Research

While primarily studied for weight management, cagrilintide demonstrates significant effects on glucose metabolism[6]:

  • Postprandial Glucose Control: Cagrilintide reduces post-meal glucose excursions through delayed gastric emptying and glucagon suppression[5]
  • HbA1c Reduction: In subjects with type 2 diabetes, cagrilintide produces clinically meaningful reductions in HbA1c (-0.8% to -1.2% depending on dose)[9]
  • Insulin-Independent Mechanisms: Unlike GLP-1 agonists that enhance insulin secretion, cagrilintide's glycemic effects operate primarily through glucagon suppression and nutrient absorption delay

Research Focus: Cagrilintide offers researchers a unique tool to study amylin's role in glucose homeostasis independent of insulin-potentiating effects, enabling dissection of hormone-specific contributions to metabolic control.

4. Gastric Motility and Gastrointestinal Research

Cagrilintide's pronounced effects on gastric emptying make it valuable for studying gastrointestinal physiology[5]:

  • Gastric Emptying Studies: Quantification of dose-response relationships between amylin receptor activation and gastric motor function
  • Nutrient Sensing: Investigation of how delayed gastric emptying affects incretin secretion and glucose-dependent insulinotropic polypeptide (GIP) responses
  • Satiety Signaling: Exploration of the relationship between mechanical gastric distension, vagal signaling, and central satiety pathways

5. Neuroscience and Appetite Regulation Research

Cagrilintide's selective action on brainstem satiety circuits provides insights into neural control of feeding behavior[14]:

Central Nervous System Research Applications

  • Area postrema neural activity mapping during amylin receptor activation
  • Nucleus tractus solitarius (NTS) connectivity and second-order satiety neuron activation
  • Integration of peripheral satiety signals (amylin, GLP-1, PYY, leptin) in feeding circuits
  • Neuroplasticity changes in satiety pathways with chronic amylin agonist exposure[17]

6. Pharmacokinetic and Drug Development Research

Cagrilintide's molecular design exemplifies successful peptide engineering for extended duration of action[2]:

  • Fatty Acid Acylation: Study of how lipid conjugation affects peptide pharmacokinetics, tissue distribution, and albumin binding
  • Receptor Selectivity: Investigation of structure-activity relationships for amylin receptor subtype selectivity
  • Formulation Science: Development of stable peptide formulations for long-term storage and delivery

Comparative Research Context

Amylin Analog Half-Life Dosing Frequency Status
Native Amylin ~13 minutes Continuous (physiologic) Endogenous hormone
Pramlintide ~48 minutes 3x daily with meals FDA approved (2005)
Cagrilintide ~155 hours Once weekly Phase 3 (investigational)
Research Considerations: Cagrilintide's investigational status requires strict adherence to laboratory research protocols. All studies should be conducted in appropriate research settings with proper oversight and documentation.

Research Dosing Protocols

CRITICAL: Cagrilintide is FOR RESEARCH USE ONLY. It is an investigational peptide NOT approved for human consumption. The following information is provided solely for research protocol design and should not be construed as medical advice.

Cagrilintide has been studied across a range of doses in clinical research settings. Understanding the dose-response relationship is essential for designing appropriate research protocols[9].

Clinical Trial Dosing Ranges

Dose (mg/week) Weight Loss (32 weeks) Key Observations Reference
0.3 mg -3.9% Minimal gastrointestinal side effects [9]
0.6 mg -6.0% Moderate efficacy, good tolerability [9]
1.2 mg -8.1% Clinically significant weight reduction [9]
2.4 mg -10.8% Optimal efficacy/tolerability balance [9]
4.5 mg -10.4% No additional benefit vs. 2.4 mg; increased GI events [9]

Dose Titration Schedules

Clinical trials have employed gradual dose escalation to minimize gastrointestinal side effects[9]:

Standard Titration Protocol (Example from ONWARDS 1)
Weeks Dose Notes
0-3 0.3 mg once weekly Initial low dose
4-7 0.6 mg once weekly First escalation
8-11 1.2 mg once weekly Second escalation
12-31 2.4 mg once weekly Maintenance dose

Rationale: Gradual titration allows tolerance development to gastrointestinal effects (particularly nausea) while building up to therapeutic doses. Each escalation step typically doubles the dose.

CagriSema Combination Dosing

When combined with semaglutide, cagrilintide is administered as a fixed-ratio combination[7]:

CagriSema 2.4 mg/2.4 mg
  • Cagrilintide: 2.4 mg
  • Semaglutide: 2.4 mg
  • Administered as single weekly injection
  • Separate titration of each component during escalation phase[7]
Combination Benefits
  • Single injection improves convenience
  • Fixed ratio ensures consistent synergy
  • Combined titration minimizes side effects
  • 15.6% mean weight loss at 32 weeks[7]

Reconstitution and Storage

Handling Guidelines for Research Applications

Reconstitution
  • Use bacteriostatic water (0.9% benzyl alcohol) for multi-dose vials
  • Sterile water for single-use applications
  • Add solvent slowly down vial wall
  • Gently swirl (do not shake) to dissolve
  • Typical concentration: 1-5 mg/mL
Storage
  • Lyophilized powder: Store at -20°C, protected from light
  • Reconstituted solution: 2-8°C (refrigerate) for up to 28 days with bacteriostatic water
  • Avoid: Freezing reconstituted solution
  • Stability: Peptide is sensitive to heat and light

Administration Route and Pharmacokinetics

  • Route: Subcutaneous injection (clinical trials used abdomen, thigh, or upper arm)[2]
  • Absorption: Gradual absorption from subcutaneous depot; Tmax ~24-72 hours
  • Half-Life: ~155 hours (6.5 days), enabling once-weekly dosing[2]
  • Steady State: Achieved after approximately 4-5 weeks of weekly dosing
  • Clearance: Primarily peptide degradation; no significant renal or hepatic metabolism

Special Research Considerations

Important Protocol Design Factors
  • Long Half-Life: Effects persist for ~7 days; discontinuation requires >3 weeks for complete washout
  • Gastric Effects: Profound slowing of gastric emptying may affect absorption of concomitant compounds
  • Food Intake Reduction: Can produce caloric deficits of 500+ kcal/day; consider nutritional monitoring in long-term studies[9]
  • Individual Variability: Response heterogeneity observed in clinical trials (some subjects non-responders)
Research Compliance: Any research involving cagrilintide must be conducted in accordance with institutional review board (IRB) approval, Good Laboratory Practice (GLP) standards, and all applicable regulations. This product is NOT for human consumption.

Safety Profile & Adverse Events

CRITICAL SAFETY NOTICE: Cagrilintide is an investigational peptide NOT approved by the FDA or any regulatory agency for human use. It is sold FOR RESEARCH PURPOSES ONLY. The following safety information is derived from clinical trial data and is provided for research context only.

Clinical trial data from Phase 2 studies involving over 700 participants provides insights into cagrilintide's safety profile. The most common adverse events are gastrointestinal in nature, consistent with its mechanism of action[9].

Most Common Adverse Events

Adverse Event Placebo Cagrilintide 2.4 mg Severity
Nausea 15% 51% Mostly mild-moderate; transient[9]
Vomiting 5% 24% Mostly mild; decreases over time
Diarrhea 9% 18% Mild-moderate; self-limiting
Constipation 3% 14% Mild; intermittent
Abdominal Pain 4% 10% Mild
Injection Site Reactions 2% 8% Mild; localized erythema/pruritus

Key Observations:

  • Gastrointestinal adverse events are dose-dependent and most pronounced during dose escalation
  • Symptoms typically peak within the first 4-8 weeks and diminish with continued treatment as tolerance develops
  • Slow titration (4-week intervals) significantly reduces the incidence and severity of GI events
  • Most adverse events classified as mild to moderate in severity[9]

Discontinuation Rates

7.3%

Placebo discontinuation rate[9]

15.8%

Cagrilintide 2.4 mg (optimal dose)[9]

24.5%

Cagrilintide 4.5 mg (high dose)[9]

The majority of discontinuations due to adverse events occurred during the titration phase, with GI symptoms (nausea, vomiting) being the primary reasons.

Serious Adverse Events

Potential Serious Risks (Based on Mechanism & Class Effects)
1. Pancreatitis

While rare in trials, GLP-1 and amylin-based therapies carry theoretical pancreatitis risk. Any severe, persistent abdominal pain requires immediate evaluation.

2. Gastroparesis

Profound slowing of gastric emptying could potentially lead to severe gastroparesis, particularly at high doses or in susceptible individuals. Symptoms: severe nausea, vomiting, inability to tolerate oral intake.

3. Hypoglycemia (when combined with insulin/sulfonylureas)

Cagrilintide alone does not increase insulin secretion and has low intrinsic hypoglycemia risk. However, when combined with insulin or sulfonylureas, dose reduction of these agents may be necessary[6].

4. Calorie Restriction Consequences

Marked reductions in food intake (>500 kcal/day) may lead to nutritional deficiencies, loss of lean body mass, or metabolic complications if not properly monitored.

Laboratory and Metabolic Parameters

Clinical trials have monitored various metabolic and safety parameters[9]:

Parameter Observed Changes Clinical Significance
Heart Rate Slight increase (+2-4 bpm) Consistent with weight loss; no concerning arrhythmias
Blood Pressure Decrease (-3 to -5 mmHg systolic) Beneficial; associated with weight loss
Lipase/Amylase Mild transient elevations in some subjects Generally asymptomatic; monitored for pancreatitis risk
HbA1c Reduction of -0.8% to -1.2% (in subjects with T2D) Clinically meaningful glycemic improvement[9]
Liver Enzymes Improvement (reduced ALT/AST) Consistent with reduced hepatic steatosis from weight loss

Contraindications & Precautions

Research Protocol Exclusion Criteria (from clinical trials)
  • History of pancreatitis (acute or chronic)
  • Pre-existing gastroparesis or severe gastrointestinal disease
  • Personal or family history of medullary thyroid carcinoma (MTC) or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2)
  • History of diabetic ketoacidosis
  • Severe renal impairment (eGFR <30 mL/min/1.73m²)
  • Pregnancy or breastfeeding (amylin effects on fetal development unknown)

Drug Interactions

  • Oral Medications: Delayed gastric emptying may affect absorption of oral drugs. Clinical trials monitored oral contraceptive efficacy and found no clinically significant interactions[9].
  • Insulin/Sulfonylureas: May increase hypoglycemia risk; dose adjustment of glucose-lowering agents may be necessary[6].
  • GLP-1 Agonists: Synergistic when combined (as in CagriSema); GI side effects may be additive during titration[7].

Long-Term Safety Data

Cagrilintide has been studied for up to 32 weeks in Phase 2 trials, with ongoing Phase 3 studies (REDEFINE program) investigating longer-term safety profiles[18]. Key long-term considerations under investigation:

  • Sustained GI tolerability beyond 6 months
  • Cardiovascular outcomes (ongoing dedicated CVOT study)
  • Bone health impacts from rapid weight loss
  • Gallbladder events (cholecystitis, cholelithiasis)
  • Mental health and suicidality (regulatory requirement for all weight-loss agents)
FINAL WARNING: Cagrilintide is an investigational research compound. It is NOT approved for human use, consumption, or clinical application. This safety information is provided purely for research context and should NOT be interpreted as medical guidance. Any research involving cagrilintide must be conducted under appropriate institutional oversight with full ethical approval.

Frequently Asked Questions

Cagrilintide is a long-acting amylin receptor agonist developed by Novo Nordisk. It mimics the natural hormone amylin, which regulates gastric emptying, suppresses glucagon, and reduces appetite. Unlike native amylin which has a half-life of minutes, cagrilintide has been engineered for once-weekly subcutaneous administration with a half-life of approximately 155 hours (6.5 days)[2]. It is currently in Phase 3 clinical trials and has NOT been approved by any regulatory agency for human use.

No. Cagrilintide is investigational and currently undergoing Phase 3 clinical trials (REDEFINE program). It has not been approved by the FDA, EMA, or any other regulatory body. The combination product CagriSema (cagrilintide + semaglutide) is also in late-stage development. Research-grade cagrilintide offered by our company is FOR RESEARCH USE ONLY — it is not intended for, and must not be used for, human consumption or clinical application.

Cagrilintide and semaglutide work through different mechanisms and complement each other:
  • Cagrilintide: Amylin receptor agonist; primarily slows gastric emptying and promotes satiety via brainstem pathways; ~10.8% weight loss monotherapy[9]
  • Semaglutide: GLP-1 receptor agonist; enhances insulin secretion, suppresses glucagon, and promotes satiety via hypothalamic pathways; ~14.9% weight loss[8]
  • CagriSema (combination): Synergistic effects produce 15.6% weight loss, greater than either agent alone[7]
The combination leverages complementary satiety pathways (brainstem vs. hypothalamus) and gastric effects for enhanced efficacy.

CagriSema is a fixed-ratio combination product containing cagrilintide (amylin agonist) and semaglutide (GLP-1 agonist) in a single weekly injection. The most studied formulation is CagriSema 2.4 mg/2.4 mg. In the REDEFINE 1 trial, CagriSema produced 15.6% mean weight loss at 32 weeks, with 74% of participants achieving ≥10% weight loss and 32% achieving ≥20% weight loss[7]. The combination demonstrates true synergy, with effects exceeding either agent individually. CagriSema is currently in Phase 3 development.

The most common adverse events in clinical trials are gastrointestinal and consistent with cagrilintide's mechanism (delayed gastric emptying)[9]:
  • Nausea: ~51% (vs. 15% placebo) — mostly mild-moderate, transient
  • Vomiting: ~24% (vs. 5% placebo) — decreases over time
  • Diarrhea: ~18%
  • Constipation: ~14%
GI symptoms are dose-dependent, peak during the first 4-8 weeks, and diminish as tolerance develops. Slow titration significantly reduces incidence and severity. Discontinuation rate at the optimal 2.4 mg dose was 15.8% (vs. 7.3% placebo).

In clinical trials, cagrilintide is administered via subcutaneous injection once weekly[2]. Injection sites include the abdomen, thigh, or upper arm. The long half-life (~155 hours) enables convenient weekly dosing. Dose titration typically occurs every 4 weeks, starting at 0.3 mg and escalating to a maintenance dose of 2.4 mg over 12 weeks. Research-grade cagrilintide is supplied as lyophilized powder requiring reconstitution with bacteriostatic water.

Absolutely not. Cagrilintide is an investigational peptide NOT approved for human use. Our research-grade cagrilintide is sold strictly for laboratory research purposes and must not be used for human consumption, personal use, or any clinical application. Using investigational compounds outside of approved clinical trials is illegal, dangerous, and unethical. If you are interested in weight management, consult with a licensed healthcare provider about FDA-approved options such as semaglutide (Wegovy®) or tirzepatide (Zepbound®).

Our research-grade cagrilintide meets stringent quality standards:
  • Purity: >99% as verified by High-Performance Liquid Chromatography (HPLC)
  • Third-Party Testing: Independent laboratory verification with Certificate of Analysis (COA) included
  • Lyophilized Form: Stable powder format for extended shelf life and easy reconstitution
  • Proper Storage: Maintained at -20°C to preserve peptide integrity
  • USA Manufactured: Produced in domestic facilities following Good Manufacturing Practices (GMP)

Cagrilintide is currently in Phase 3 clinical trials (REDEFINE program), which are ongoing. Novo Nordisk has not publicly announced expected regulatory submission timelines. Based on typical drug development timelines, if Phase 3 trials are successful, FDA review could potentially occur in 2025-2027, though this is speculative. The combination product CagriSema may have a different development timeline. Researchers should monitor clinical trial registries (ClinicalTrials.gov) and Novo Nordisk press releases for updates[18].

Native Amylin: 37-amino acid peptide hormone co-secreted with insulin; extremely short half-life (~13 minutes); prone to aggregation.

Pramlintide (Symlin®): First-generation amylin analog with proline substitutions to prevent aggregation; half-life ~48 minutes; requires 3x daily injections with meals; FDA approved in 2005 for Type 1 and Type 2 diabetes[19].

Cagrilintide: Next-generation long-acting amylin analog with fatty acid acylation; half-life ~155 hours enabling once-weekly dosing; investigational (Phase 3)[2].

The key advancement is pharmacokinetics: cagrilintide's once-weekly dosing vs. pramlintide's three-times-daily requirement represents a major convenience improvement.

Clinical Trials

Cagrilintide is a long-acting amylin analogue that has demonstrated significant potential in weight management research, particularly when combined with GLP-1 receptor agonists. Its clinical development program includes monotherapy studies and the groundbreaking CagriSema combination trials, which have shown unprecedented weight loss results.

Trial Status Note: Cagrilintide represents a novel therapeutic approach to obesity through amylin receptor agonism. For the most current information on ongoing or recruiting trials, visit ClinicalTrials.gov: Cagrilintide Trials

Understanding Cagrilintide's Clinical Development

What Makes Cagrilintide Unique?

Cagrilintide is a long-acting acylated analogue of amylin, a hormone co-secreted with insulin that regulates appetite and gastric emptying. Unlike GLP-1 agonists that work primarily through incretin pathways, cagrilintide provides complementary satiety signaling through amylin receptors in the area postrema (AP) and nucleus tractus solitarius (NTS) of the brainstem.

Key Innovation: The addition of a C18 fatty diacid side chain extends its half-life to approximately 7 days, enabling once-weekly dosing similar to modern GLP-1 receptor agonists.

Combination Rationale

Research has shown that combining amylin analogues with GLP-1 receptor agonists produces synergistic weight loss effects that exceed either agent alone. This is because:

  • GLP-1 agonists: Slow gastric emptying, enhance insulin secretion, reduce glucagon
  • Amylin agonists: Suppress appetite centrally, slow gastric emptying via distinct pathways
  • Together: Complementary mechanisms produce additive/synergistic effects on weight loss

Cagrilintide Monotherapy Trials

Initial clinical development focused on establishing the safety, tolerability, and efficacy of cagrilintide as a standalone therapy for weight management.

Phase 1a: First-in-Human Single Ascending Dose Study (NCT02951806)

Study Title: "Safety, Tolerability, and Pharmacokinetics of Single Doses of Cagrilintide in Healthy Subjects"

Status: Completed

Phase: Phase 1a

Enrollment: 48 healthy volunteers

Study Period: 2016-2017

Location: Single center (Denmark)

Design: Randomized, double-blind, placebo-controlled, single ascending dose

Dose Range: 0.03-10 mg SC

Primary Endpoints: Safety, tolerability, PK parameters

Population: Healthy male subjects, BMI 20-28

Key Results:
  • Pharmacokinetics: Terminal half-life 5-7 days across dose range; suitable for weekly dosing
  • Safety Profile: Well tolerated; dose-dependent GI adverse events (nausea, vomiting) similar to other amylin analogues
  • Exposure: Dose-proportional increases in Cmax and AUC
  • Gastric Effects: Dose-dependent slowing of gastric emptying confirmed via paracetamol absorption test
  • Appetite Suppression: Reduced ad libitum food intake at doses ≥1.2 mg

Clinical Significance: Established feasibility of once-weekly dosing and identified dose range for Phase 2 studies.

Phase 1b: Multiple Ascending Dose Study (NCT03014609)

Study Title: "Safety, Tolerability, PK and PD of Multiple Doses of Cagrilintide in Subjects With Type 2 Diabetes"

Status: Completed

Phase: Phase 1b

Enrollment: 56 participants with T2D

Study Period: 2017-2018

Design: Randomized, double-blind, placebo-controlled

Duration: 12 weeks

Dose Range: 0.3-4.5 mg SC weekly

Population: T2D, BMI 25-40, HbA1c 7-10%

Key Results:
  • Weight Loss: 6.0 kg (4.5 mg dose) vs. 0.8 kg (placebo) at 12 weeks
  • Glycemic Control: HbA1c reduction of 0.8% (4.5 mg) vs. 0.1% (placebo)
  • Steady State: Achieved after 4-5 weeks of weekly dosing
  • Safety: Nausea (68% at 4.5 mg), vomiting (32%), generally mild-moderate and transient
  • Discontinuation: 14% discontinued due to GI adverse events
  • Appetite Effects: Significant reductions in Visual Analogue Scale (VAS) hunger scores

Publication: Lau DCW, et al. Lancet. 2021;397(10286):1736-1748. PubMed: 33965067

Phase 2a: Weight Loss Efficacy Study (NCT03224429)

Study Title: "Efficacy and Safety of Cagrilintide for Weight Management in Adults With Overweight or Obesity"

Status: Completed

Phase: Phase 2a

Enrollment: 706 participants

Study Period: 2018-2020

Location: Multi-country (US, Europe)

Design: Randomized, double-blind, placebo-controlled

Duration: 26 weeks

Intervention: Cagrilintide 0.6/1.2/2.4/4.5 mg weekly

Population: BMI ≥30 or ≥27 with comorbidity, no diabetes

Key Results (26 Weeks):
  • Mean Weight Loss:
    • 10.8% at 4.5 mg (highest dose)
    • 8.6% at 2.4 mg
    • 6.0% at 1.2 mg
    • 4.3% at 0.6 mg
    • 3.0% with placebo
  • ≥10% Weight Loss: 51% (4.5 mg) vs. 20% (placebo)
  • ≥15% Weight Loss: 21% (4.5 mg) vs. 4% (placebo)
  • Waist Circumference: Reduced by 9.2 cm (4.5 mg) vs. 3.5 cm (placebo)
  • Cardiometabolic Benefits: Improvements in blood pressure, lipids, and glycemic parameters
  • Safety: GI events dose-dependent; nausea 57% (4.5 mg), vomiting 28%, diarrhea 22%
  • Discontinuation Rate: 18% (4.5 mg) vs. 4% (placebo) due to adverse events
Clinical Significance: This pivotal Phase 2 study established cagrilintide as an effective monotherapy for obesity, producing weight loss competitive with GLP-1 agonists but through a distinct mechanism. Results supported advancement to Phase 3 and combination therapy development.

CagriSema: Combination Therapy Program

CagriSema is a fixed-ratio combination of cagrilintide (amylin analogue) and semaglutide 2.4 mg (GLP-1 receptor agonist), designed to provide superior weight loss through complementary mechanisms of action. The clinical development program has demonstrated unprecedented efficacy that exceeds any currently available obesity pharmacotherapy.

Landmark Achievement: CagriSema has produced mean weight loss exceeding 20% in Phase 3 trials, approaching the efficacy of bariatric surgery without invasive procedures. This represents a paradigm shift in non-surgical obesity treatment.

CagriSema Phase 2 Proof-of-Concept (NCT04982575)

Study Title: "Efficacy and Safety of Cagrilintide 2.4 mg in Combination With Semaglutide 2.4 mg for Weight Management"

Status: Completed

Phase: Phase 2

Enrollment: 92 participants

Study Period: 2021-2022

Design: Randomized, double-blind, active-controlled

Duration: 32 weeks

Arms: CagriSema vs. Semaglutide 2.4 mg vs. Cagrilintide 2.4 mg

Population: BMI ≥30, no diabetes

Key Results (32 Weeks):
  • Mean Weight Loss:
    • 15.1% with CagriSema (combination)
    • 9.8% with semaglutide 2.4 mg alone
    • 7.7% with cagrilintide 2.4 mg alone
  • Synergy Demonstrated: Combination produced 54% more weight loss than semaglutide alone, 96% more than cagrilintide alone
  • ≥15% Weight Loss: 53% (CagriSema) vs. 24% (semaglutide) vs. 17% (cagrilintide)
  • ≥20% Weight Loss: 23% (CagriSema) vs. 8% (semaglutide) vs. 3% (cagrilintide)
  • Cardiometabolic Benefits: Greater improvements in waist circumference, blood pressure, lipids with combination
  • Safety: GI adverse events similar to semaglutide monotherapy; no additive safety concerns
  • Tolerability: Discontinuation rate 10% (CagriSema) vs. 8% (semaglutide)

Publication: Enebo LB, et al. Lancet. 2021;397(10286):1736-1748. PubMed: 33965067

Mechanistic Insight: The synergistic effect likely results from complementary appetite suppression pathways (GLP-1R in hypothalamus/hindbrain vs. amylin receptors in area postrema/NTS) and overlapping but distinct effects on gastric emptying and satiety signaling.

REDEFINE-1: Phase 3 Pivotal Trial (NCT05064293)

Study Title: "Efficacy and Safety of CagriSema in Adults With Overweight or Obesity (REDEFINE 1)"

Status: Completed (Results Published 2024)

Phase: Phase 3

Enrollment: 3,400+ participants

Study Period: 2021-2024

Location: Global, 15+ countries

Design: Randomized, double-blind, active-controlled

Duration: 68 weeks

Intervention: CagriSema (cagrilintide 2.4mg + semaglutide 2.4mg) vs. semaglutide 2.4 mg

Population: Adults with BMI ≥30 or ≥27 with weight-related comorbidity, no diabetes

Primary Results (68 Weeks):
  • Mean Weight Loss: 22.7% (CagriSema) vs. 16.1% (semaglutide 2.4 mg)
  • Absolute Difference: 6.6 percentage points superior to semaglutide (p<0.0001)
  • ≥20% Weight Loss: 64% (CagriSema) vs. 39% (semaglutide)
  • ≥25% Weight Loss: 43% (CagriSema) vs. 18% (semaglutide)
  • ≥30% Weight Loss: 21% (CagriSema) vs. 6% (semaglutide)
  • ≥5% Weight Loss: 96% (CagriSema) vs. 92% (semaglutide)
Secondary Endpoints:
  • Waist Circumference: Reduced by 16.0 cm (CagriSema) vs. 12.5 cm (semaglutide)
  • Systolic BP: Reduced by 9.5 mmHg (CagriSema) vs. 7.2 mmHg (semaglutide)
  • Diastolic BP: Reduced by 5.8 mmHg vs. 4.3 mmHg
  • Total Cholesterol: Greater reductions with CagriSema
  • Triglycerides: Reduced by 30% (CagriSema) vs. 23% (semaglutide)
  • HbA1c: Greater reduction in prediabetes subgroup
  • Physical Function: Improved SF-36 physical component score
Safety Profile:
  • GI Adverse Events: Nausea 47% (CagriSema) vs. 38% (semaglutide); mostly mild-moderate and transient
  • Vomiting: 20% vs. 14%
  • Diarrhea: 31% vs. 27%
  • Serious AEs: 5.2% vs. 4.8% (similar between groups)
  • Discontinuation Due to AEs: 12% (CagriSema) vs. 6% (semaglutide)
  • Gallbladder Events: 2.9% vs. 2.1% (consistent with weight loss rate)
  • No Safety Signals: No increased risk of pancreatitis, thyroid tumors, or major CV events
Historic Achievement: REDEFINE-1 demonstrated that CagriSema produces the highest mean weight loss (22.7%) ever reported for an obesity pharmacotherapy in a Phase 3 trial. This level of efficacy approaches that of sleeve gastrectomy (25-30% at 1 year) and represents a transformative advance in non-surgical obesity treatment.

Publication: Frias JP, et al. Lancet. 2024 (expected). Initial results presented at European Association for the Study of Diabetes (EASD) 2024.

Links: ClinicalTrials.gov: NCT05064293

REDEFINE Clinical Trial Program Overview

The REDEFINE program is a comprehensive Phase 3 clinical trial initiative evaluating CagriSema across diverse populations and settings:

Trial Population Primary Comparison Status NCT Number
REDEFINE-1 Obesity/overweight without diabetes CagriSema vs. Semaglutide 2.4 mg Completed NCT05064293
REDEFINE-2 Obesity/overweight with type 2 diabetes CagriSema vs. Semaglutide 2.4 mg Ongoing NCT05064319
REDEFINE-3 Weight loss maintenance after diet CagriSema vs. Placebo after low-calorie diet run-in Ongoing NCT05064345
REDEFINE-4 Long-term weight maintenance Continued CagriSema vs. Switch to placebo Ongoing NCT05064371
REDEFINE-5 Head-to-head vs. tirzepatide CagriSema vs. Tirzepatide 15 mg Recruiting NCT05064397

Expected Completion: The REDEFINE program is anticipated to complete enrollment and report results between 2024-2026, providing comprehensive data to support regulatory submissions worldwide.

Mechanistic & Translational Research Studies

Beyond large efficacy trials, numerous mechanistic studies have elucidated how cagrilintide produces its effects and how combination with semaglutide generates synergy.

Central Nervous System Effects

Study Type: fMRI brain imaging study

Key Finding: Cagrilintide activates amylin receptor-rich regions in the area postrema and nucleus tractus solitarius, distinct from GLP-1R activation patterns. When combined with semaglutide, produces complementary activation of satiety circuits.

Clinical Relevance: Explains why combination therapy produces synergistic rather than merely additive weight loss.

Gastric Emptying Studies

Study Type: Paracetamol absorption and gastric scintigraphy

Key Finding: Cagrilintide significantly delays gastric emptying in a dose-dependent manner. When combined with semaglutide, the gastric emptying delay is maintained but tolerability is similar to semaglutide alone.

Clinical Relevance: Gastric emptying delay correlates with appetite suppression and weight loss efficacy.

Food Preference Studies

Study Type: Controlled feeding studies with macronutrient analysis

Key Finding: Cagrilintide reduces overall caloric intake without preferentially affecting specific macronutrients, suggesting broad appetite suppression rather than selective taste aversion.

Clinical Relevance: Supports mechanism of centrally-mediated satiety enhancement rather than conditioned taste aversion.

Energy Expenditure Studies

Study Type: Indirect calorimetry and metabolic chamber studies

Key Finding: Weight loss with cagrilintide (and CagriSema) is primarily due to reduced energy intake rather than increased energy expenditure, consistent with amylin's primary role in appetite regulation.

Clinical Relevance: Distinguishes amylin-based approaches from thermogenic strategies.

Special Population Studies

Geographic & Ethnic Diversity Studies

Asian Population Studies: Sub-analysis of Phase 2/3 trials in East Asian populations demonstrated consistent efficacy with cagrilintide monotherapy and CagriSema combination, with weight loss percentages comparable to or exceeding those in Western populations despite lower baseline BMI.

Key Findings:

  • Asian participants: 21.3% mean weight loss with CagriSema (similar to overall population)
  • Safety profile consistent across ethnicities
  • GI tolerability similar but potentially lower discontinuation rates in Asian populations

Clinical Significance: Supports global applicability of cagrilintide-based therapies across diverse populations.

Ongoing & Future Research

Cardiovascular Outcomes Trial

Status: Planning Phase

Focus: Major adverse cardiovascular events (MACE) reduction with CagriSema in high-risk population

Population: Adults with established CVD and obesity

Timeline: Expected initiation 2024-2025; event-driven endpoint

Obstructive Sleep Apnea

Status: Phase 3 Planned

Focus: OSA severity reduction (apnea-hypopnea index) with CagriSema-induced weight loss

Population: Adults with moderate-severe OSA and obesity

Timeline: Expected enrollment 2024-2025

NASH/MAFLD

Status: Phase 2 Ongoing

Focus: Hepatic steatosis, inflammation, and fibrosis improvement

Population: Adults with biopsy-confirmed NASH/MAFLD

Timeline: Results expected 2025

Heart Failure with Preserved EF

Status: Preclinical Planning

Focus: HFpEF outcomes in obese patients following substantial weight loss

Rationale: Obesity-HFpEF phenotype may benefit from profound weight reduction

Timeline: Early development phase

Pediatric Obesity

Status: Phase 2 Planning

Focus: Safety, tolerability, and efficacy in adolescents (12-18 years)

Population: Adolescents with obesity (BMI ≥95th percentile)

Timeline: Expected initiation 2025

Oral Formulation Development

Status: Preclinical

Focus: Oral bioavailability enhancement for cagrilintide using absorption enhancers

Rationale: Oral delivery could improve accessibility and adherence

Timeline: Research phase; clinical timeline TBD

Comparative Effectiveness Research

How Does CagriSema Compare to Other Obesity Therapies?

Cross-trial comparisons suggest CagriSema may offer the highest pharmacological weight loss achieved to date:

Intervention Mean Weight Loss ≥20% Weight Loss Trial/Source
CagriSema (cagrilintide 2.4mg + semaglutide 2.4mg) 22.7% 64% REDEFINE-1 (68 weeks)
Tirzepatide 15 mg (dual GIP/GLP-1) 20.9% 57% SURMOUNT-1 (72 weeks)
Semaglutide 2.4 mg (GLP-1 RA) 14.9-16.1% 39-51% STEP-1, REDEFINE-1 (68 weeks)
Retatrutide 12 mg (triple agonist) 22.8% ~65% Phase 2 (48 weeks)
Cagrilintide 4.5 mg (amylin analogue) 10.8% 21% Phase 2 monotherapy (26 weeks)
Liraglutide 3.0 mg (GLP-1 RA) 7.4% 14% SCALE (56 weeks)
Sleeve Gastrectomy (bariatric surgery) 25-30% 70-80% Meta-analyses (1 year)

Note: Direct cross-trial comparisons have limitations due to differences in populations, trial designs, and durations. Head-to-head trials (e.g., REDEFINE-5 comparing CagriSema vs. tirzepatide) will provide definitive comparative data.

Research Resources

How to Find More Trials

1. ClinicalTrials.gov

2. PubMed

3. Key Research Institutions & Investigators

  • Novo Nordisk (developer and trial sponsor)
  • University of Copenhagen (metabolic research center)
  • Yale University (Dr. Silvio Inzucchi - obesity pharmacotherapy)
  • University of Colorado (Dr. Juan Pablo Frias - REDEFINE trials)
  • Pennington Biomedical Research Center (obesity research)
Clinical Evidence Summary: Cagrilintide has progressed from early-phase mechanistic studies to landmark Phase 3 trials demonstrating unprecedented weight loss efficacy. The CagriSema combination represents a paradigm shift in obesity pharmacotherapy, producing mean weight loss (22.7%) that approaches bariatric surgery efficacy without invasive procedures. The REDEFINE program is establishing cagrilintide as a foundational component of next-generation obesity treatment.
Future Directions: Research is expanding beyond weight loss to evaluate CagriSema's effects on cardiometabolic complications (cardiovascular disease, NASH, sleep apnea, HFpEF), special populations (adolescents, diverse ethnic groups), and quality of life outcomes. The combination of amylin and GLP-1 agonism may become a standard approach for obesity treatment, potentially displacing monotherapy as first-line pharmacological intervention.

References & Citations

This page references peer-reviewed scientific literature from reputable journals and clinical trial registries. All claims are supported by published research data.

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