Semaglutide
Stylized molecular signature · scaled by MW
~145–168 h in humans (SC, terminal). Long t½ driven by C18 fatty-diacid linker at Lys26 binding plasma albumin and resistance to DPP-4 via Aib8 substitution. Lau et al., J Med Chem 2015.
Profiled for reference only.
Semaglutide is indexed here for literature reference. Peptide Plus does not list this compound at the time of this page generation. Peptide Plus remains the seller of record for any compound listed on alphapeptide.store — we do not ship, store, or handle product.
How it’s studied.
Semaglutide is a 31-residue GLP-1 receptor agonist with ~94% homology to native human GLP-1(7-37). An Aib8 substitution confers DPP-4 resistance, while a γGlu-2xOEG-C18-diacid moiety on Lys26 enables non-covalent albumin binding that extends the circulating half-life. Activation of the pancreatic β-cell GLP-1R increases glucose-dependent insulin secretion via Gαs-cAMP-PKA/EPAC2 signaling; central GLP-1R activation in the arcuate and brainstem reduces food intake. Studied for metabolic, cardiovascular, and neurodegeneration endpoints.
Semaglutide (NN9535) is a fatty-acid-acylated GLP-1 analog engineered by Novo Nordisk for once-weekly subcutaneous dosing. The Aib8 substitution blocks DPP-4 cleavage and a fatty-diacid moiety on Lys26 binds serum albumin, producing a ~165-hour terminal half-life — among the longest of any approved peptide therapeutic. It is the most-studied incretin agonist of the decade, with applications spanning glycemic, cardiometabolic, hepatic, and CNS research.
- 01
Glycemic regulation models in T2D research
- 02
Body-weight and adiposity studies in DIO rodent models
- 03
Cardiovascular outcome surrogates (LDL, blood pressure, hsCRP)
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Emerging neuroprotection research (Alzheimer's, Parkinson's models)
Reported in literature: 0.25 mg weekly titrated to 1.0–2.4 mg weekly SC (clinical research, not for human use)
Verify each value in primary literature.
Pre-filled defaults for Semaglutide.
- Concentration
- 2.50mg/mL
- Draw on U-100
- 10units
- Volume / dose
- 0.100mL
- Doses / vial
- 20
Assumes 27-gauge insulin syringe, U-100 markings. Verify before use.
Open in calculatorCo-factors and supporting compounds.
Well-studiedCompounds identified in published research as sharing pathways with Semaglutide, or studied alongside it in trials. Reference material only — not a recommendation, not medical advice. Citations link to PubMed.
Vitamin B12 (cobalamin)
Methylcobalamin or cyanocobalaminDelayed gastric emptying + reduced food intake impair release and absorption of food-bound B12; concurrent metformin compounds the absorption interference
Cobalamin deficits have been reported to increase over time in GLP-1 RA users in a 2026 narrative review of micronutrient deficiencies. The mechanism proposed is reduced dietary intake under sustained satiety plus delayed gastric emptying interfering with B12 release from food protein. The signal mirrors the long-documented metformin-B12 association; the two drugs are frequently co-prescribed in type 2 diabetes, and co-administration of metformin with GLP-1 RAs has been independently associated with lower serum B12 in cross-sectional analyses. Studied alongside the drug primarily through observational pharmacovigilance rather than dedicated supplementation RCTs.
Dietary protein (with resistance training)
Whole-food proteinPharmacologic weight loss drives concomitant lean mass loss; dietary protein supplies amino acid substrate for muscle protein synthesis, which resistance training amplifies
Semaglutide treatment is associated with reductions in absolute lean body mass — exploratory analysis of STEP 1 reported a -9.7% change in absolute lean mass over 68 weeks, with the lean-to-fat ratio nonetheless improving because fat mass loss was larger. The SEMALEAN prospective cohort showed an initial 3 kg lean mass loss at 7 months that stabilized through 12 months, with handgrip strength rising and sarcopenic-obesity prevalence falling from 49% to 33%. Reviews of GLP-1 RA sarcopenia consistently describe high protein intake and resistance training as the principal mitigation strategies studied alongside the drug class.
Vitamin D3 + calcium
Cholecalciferol + calciumReduced food intake under satiety lowers both vitamin D and calcium intake; rapid weight loss independently accelerates bone resorption, compounding the bone-related downstream effect
Vitamin D deficiency is the most commonly observed micronutrient abnormality in GLP-1 RA users in the 2026 Urbina narrative review, rising from 7.5% at 6 months to 13.6% at 12 months. Calcium intake was below estimated requirements in more than 60% of users in the same analysis. Both deficits are mechanistically relevant to bone mineral density loss, which has been independently reported in DXA-based studies of semaglutide users — declines documented at the total hip, femoral neck and lumbar spine, particularly in patients without diabetes where weight loss drove the bone signal. Studied alongside the drug through observational deficiency surveillance.
Semaglutide is the best-studied molecule in this group for cofactor signals; most of the GLP-1 RA class literature is dominated by semaglutide cohorts.