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Semaglutide

Semaglutide (development code NN9535, OG217SC for oral) is a synthetic, linear peptide analogue of human glucagon-like peptide-1 (GLP-1) with approximately 94% sequence homology. It acts as a selective, long-acting GLP-1 receptor agonist and is one of the most extensively studied incretin-based therapeutics for metabolic research, including type 2 diabetes mellitus and obesity.


Chemical Profile

Property Value
CAS Number 910463-68-2
IUPAC Name (2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-4-carboxybutanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-6-(2,6-dioxo-3-piperidinyl)hexanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-6-(2,6-dioxo-3-piperidinyl)hexanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]acetyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-3-methylbutanoyl]amino]-5-(diaminomethylideneamino)pentanamide
Amino Acid Sequence H-Aib-E-G-T-F-T-S-D-V-S-S-Y-L-E-G-Q-A-A-K-E-F-I-A-W-L-V-R-G-R-G-C18 diacid
Sequence (1-Letter) HXEGTFTSDVSSYLEGQAAKEFIAWLVKGRG (with C18 fatty diacid at Lys26)
Molecular Formula C₁₈₇H₂₉₁N₄₅O₅₉
Molecular Weight 4113.58 g/mol
Purity (HPLC) ≥ 98%

Semaglutide at a Glance

  • Class: Selective GLP-1 receptor agonist
  • Developed by: Novo Nordisk
  • Research Status: Widely studied GLP-1 receptor agonist with extensive published literature
  • Route: Subcutaneous injection (weekly) or oral (daily)
  • Half-life: Approximately 7 days (SC); ~1 week (oral)
  • CAS: 910463-68-2
  • MW: 4113.58 Da
  • Key Feature: Most published GLP-1 receptor agonist in the research literature

Mechanism of Action

Semaglutide is a 31-amino-acid GLP-1 analogue with two amino acid substitutions compared to native GLP-1(7-37): Aib (α-aminoisobutyric acid) at position 8 for DPP-4 resistance, and Arg at position 34 (replacing Lys). A C18 fatty diacid chain attached to Lys26 enables albumin binding, extending the circulating half-life to approximately 7 days.

GLP-1 Receptor Activation Pathway

Component Detail
Primary Target GLP-1 receptor (GLP-1R)
Receptor Class Class B G-protein-coupled receptor (GPCR)
G-Protein Coupling Gαs → adenylyl cyclase activation → cAMP production
Downstream Signaling PKA, EPAC2, CREB, PI3K/Akt, MAPK/ERK
β-Arrestin Recruitment Yes — modulates receptor desensitization

Physiologic Effects

Effect Mechanism Outcome
Glucose-dependent insulin secretion GLP-1R activation in pancreatic β-cells Improved glycemic control, HbA1c reduction
Glucagon suppression GLP-1R activation in α-cells Reduced hepatic gluconeogenesis
Delayed gastric emptying Vagal GLP-1R signaling Reduced postprandial glucose excursions
Appetite suppression GLP-1R in hypothalamus (arcuate nucleus) Reduced caloric intake, weight loss
β-cell protection Anti-apoptotic signaling via PKA/CREB Potential preservation of β-cell mass
Cardiovascular protection Direct myocardial GLP-1R effects Reduced MACE in cardiovascular outcome trials
Neuroprotection GLP-1R in CNS Emerging research in neurodegeneration

Pharmacology

Parameter Value
Half-life (t½) ~7 days (165–168 h) — SC; ~1 week — oral
Time to Peak (Tmax) 12–24 h post-dose (SC); 1–3 h (oral)
Bioavailability ~89% (SC); ~1% (oral)
Volume of Distribution (Vd) ~0.3 L/kg
Protein Binding ~99% (albumin)
Metabolism Proteolytic degradation (no CYP involvement)
Route of Administration Subcutaneous (weekly) or oral (daily)
Elimination Renal (peptide fragments) and fecal
Duration of Action ~1 week (SC)

Research Evidence

Preclinical Research

Study Model Findings Reference
Lau et al. 2015 DPP-4 stability assay Albumin binding extends half-life > 100 h vs 2 min for native GLP-1 DOI: 10.1021/acs.jmedchem.5b00726
Kapitza et al. 2017 Zucker diabetic fatty rats Dose-dependent HbA1c reduction and weight loss DOI: 10.1111/dom.12885
Secher et al. 2014 Rodent brain mapping GLP-1R activation in arcuate nucleus mediates appetite suppression DOI: 10.1172/JCI72434
Jensen et al. 2018 DIO mice 15% body weight reduction at pharmacological doses DOI: 10.1016/j.physbeh.2018.03.020

Published Research (Selected Trials)

Trial Phase Dose Duration Primary Outcome Reference
SUSTAIN-1 Phase 3a 0.5, 1.0 mg 30 weeks HbA1c −1.5% (1.0 mg) vs placebo NCT02054897
SUSTAIN-6 Phase 3b 0.5, 1.0 mg 104 weeks 26% reduction in MACE (CVOT) DOI: 10.1056/NEJMoa1607141
STEP-1 Phase 3 2.4 mg 68 weeks 14.9% mean body weight reduction DOI: 10.1056/NEJMoa2032183
STEP-2 Phase 3 2.4 mg 68 weeks 9.6% weight loss (T2D + obesity) DOI: 10.1016/S0140-6736(21)02713-6
PIONEER-6 Phase 3a 14 mg (oral) 104 weeks Cardiovascular safety (oral semaglutide) DOI: 10.1056/NEJMoa1913163
SELECT Phase 3 2.4 mg 208 weeks 20% reduction in MACE (CV outcomes) DOI: 10.1056/NEJMoa2307563

Dosing Reference

Parameter Recommendation
Dosage Range (Research) 0.25–2.4 mg, once weekly (SC)
Reconstitution Solvent Bacteriostatic water (0.9% benzyl alcohol)
Reconstitution Volume 1–2 mL per vial
Final Concentration 1–2.5 mg/mL
Storage (Lyophilized) −20°C, protected from light
Storage (Reconstituted) 2–8°C for up to 14 days
Administration Subcutaneous injection (abdomen, thigh, upper arm)
Do Not Use If solution is cloudy or contains particulates

Safety Profile

Category Adverse Events / Observations
Most Common Nausea (20–44%), diarrhea (13–28%), vomiting (5–15%), constipation (7–12%)
Gastrointestinal Abdominal pain, dyspepsia, flatulence — dose-dependent tolerability
Serious (Rare) Pancreatitis (0.1–0.3%), gallbladder disease (0.5–1.5%), retinopathy complications
Cardiovascular Heart rate increase (2–4 bpm); reduced MACE in CVOT
Contraindications For research use only; not for human or veterinary application
Regulatory Note Thyroid C-cell findings observed in rodent studies
Drug Interactions Delayed gastric emptying may affect absorption of oral medications
Hypoglycemia Risk Low as monotherapy; increased with sulfonylureas/insulin
Immunogenicity Anti-drug antibodies in ~1–3% of study subjects
Pregnancy Not recommended; limited human data

Physicochemical Properties

Property Value
Physical State White to off-white lyophilized powder
Solubility (Water) Freely soluble (> 50 mg/mL)
Solubility (Bacteriostatic Water) Soluble (> 20 mg/mL)
logP (Octanol/Water) ~4.5
pKa (Predominant) ~4.1 (carboxylic acid groups)
Isoelectric Point (pI) ~4.8
Stability (Lyophilized) ≥ 36 months at −20°C
Stability (Solution) 14 days at 2–8°C
pH (Reconstituted) 7.0–8.0
Appearance (Solution) Clear, colorless solution

Synthesis Pathway

| Parameter | Detail |

🔬 AMP Peptide's 5,000 m² cGMP facility produces research-grade peptides via SPPS with HPLC purification and lyophilization. |-----------|--------| | Method | Solid-phase peptide synthesis (SPPS), Fmoc/tBu strategy | | Resin | Rink amide MBHA resin (0.3–0.6 mmol/g loading) | | Coupling Reagents | HATU/HBTU with DIPEA (4 equiv., 2 × 30 min couplings) | | Deprotection | 20% piperidine in DMF (2 × 5 min + 1 × 15 min) | | Fatty Acid Conjugation | C18 diacid coupled to Lys26 side chain after selective Mtt deprotection | | Cleavage | TFA/TIPS/H₂O (95:2.5:2.5, 2.5 h, room temperature) | | Purification | Preparative RP-HPLC (C18, 5 μm, gradient 25–55% ACN/H₂O + 0.1% TFA) | | Salt Exchange | Lyophilization from 0.1% HCl (acetate-to-chloride exchange) | | Yield (crude) | 55–65% based on resin loading | | Yield (purified) | 18–25% after HPLC purification |


Analytical Methods

HPLC Analysis

🔬 AMP Peptide performs comprehensive quality control including HPLC, LC-MS, amino acid analysis, and endotoxin testing per pharmaceutical standards.

Parameter Condition
Column C18 reverse-phase (4.6 × 250 mm, 5 μm)
Mobile Phase A 0.1% TFA in water
Mobile Phase B 0.085% TFA in acetonitrile
Gradient 20–60% B over 25 min
Flow Rate 1.0 mL/min
Detection UV at 214 nm
Purity (AUC) ≥ 98% at UV 214 nm
Column Temperature 40°C
Injection Volume 20 μL
Retention Time ~13–15 min
Mass Spectrometry ESI-MS or MALDI-TOF, [M+H]⁺ ~4114.6 Da
Amino Acid Analysis 6N HCl hydrolysis, 110°C, 24 h, pre-column derivatization
Water Content ≤ 5% (Karl Fischer titration)
Residual Solvents ≤ 5000 ppm (GC headspace, ICH Q3C)
Endotoxin ≤ 10 EU/mg (LAL assay)

LC-MS Analysis

Parameter Condition
Ionization Electrospray (ESI+), positive mode
Mass Range m/z 500–2500
Capillary Voltage 3.5 kV
Cone Voltage 40 V
Desolvation Temp 350°C
Source Temp 120°C
Detected Mass (M+H)+ ~4114.6 Da
Charge State Distribution +3 to +7 (multiply charged)

Stability Data

Condition Duration Purity Retention
Lyophilized at −20°C 36 months ≥ 95% initial purity
Lyophilized at 2–8°C 24 months ≥ 95% initial purity
Lyophilized at 25°C/60% RH 6 months ≥ 90% initial purity
Reconstituted at 2–8°C 14 days ≥ 95% initial purity
Reconstituted at 25°C 24 h ≥ 90% initial purity
Freeze‑thaw (3 cycles, −20°C to rt) Completed ≥ 98% initial purity
Photostability (ICH Q1B, 48 h) Completed ≥ 95% initial purity

References

  1. Marso SP, et al. (2016). Semaglutide and cardiovascular outcomes in patients with type 2 diabetes (SUSTAIN-6). New England Journal of Medicine. DOI: 10.1056/NEJMoa1607141
  2. Wilding JPH, et al. (2021). Once-weekly semaglutide in adults with overweight or obesity (STEP-1). New England Journal of Medicine. DOI: 10.1056/NEJMoa2032183
  3. Lau J, et al. (2015). Discovery of semaglutide, a once-weekly GLP-1 analogue. Journal of Medicinal Chemistry. DOI: 10.1021/acs.jmedchem.5b00726
  4. Secher A, et al. (2014). The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loss. Journal of Clinical Investigation. DOI: 10.1172/JCI72434
  5. Lincoff AM, et al. (2023). Semaglutide and cardiovascular outcomes in obesity (SELECT). New England Journal of Medicine. DOI: 10.1056/NEJMoa2307563
  6. Davies M, et al. (2021). Semaglutide 2.4 mg in type 2 diabetes and obesity (STEP-2). The Lancet. DOI: 10.1016/S0140-6736(21)02713-6
  7. Husain M, et al. (2019). Oral semaglutide and cardiovascular outcomes (PIONEER-6). New England Journal of Medicine. DOI: 10.1056/NEJMoa1913163

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