This product is a box of 10 vials.
What Is Semaglutide ?
Semaglutide is a version of the naturally occurring GLP-1, a peptide that lowers blood sugar levels and boosts insulin release. Studies show Semaglutide may also improve heart, liver, and lung function while helping to slow or prevent Alzheimer's disease effects. Research with Semaglutide indicates it can greatly reduce appetite by slowing stomach emptying and decreasing gut movement. Glucagon-Like Peptide-1 (GLP-1) analogs have been shown to trigger insulin and block glucagon release in a way that depends on glucose levels.
Sequence:Â HXEGTFTSDVSSYLEGQAAK-OH.steric diacid-EFIAWLVRGRG
Molecular Formula:Â C187H291N45O59
Molecular Weight:Â 4113.64Â g/mol
PubChem CID: 56843331
CAS Number: 910463-68-2
Synonyms:Â Semaglutide, Oxempic, Rybelsus, NN9535
Sample Dosing Schedule:
Serious Warning: Please dose this product responsibly. If you're new to the product, or haven't taken it in some time, you need to start small. Skipping to a high dose too soon will cause incredibly unpleasant & long-lasting side effects. Most users will not need to progress through to the highest dosage level to achieve substantial results.
| Week 1 through 4 | 0.25mg per week | Initial onboarding dose |
| Week 5 through 8 | 0.5mg per week | Dose Escalation (if needed) |
| Week 9 through 12 | 1mg per week | Dose Escalation (if needed) |
| Week 13 through 16 | 1.7mg per week | Dose Escalation (if needed) |
| Week 17+ | 2.4mg per week | Maximum indicated dose |
GLP-1, which stands for glucagon-like peptide-1, is a short, naturally occurring peptide hormone that's only 30-31 amino acids long. Its main job is to lower blood sugar by naturally increasing insulin release. It also helps protect beta cell insulin stores by encouraging insulin gene activity and has been linked to protective effects in the brain and central nervous system. In the digestive system, GLP-1 greatly reduces appetite by slowing stomach emptying and gut movement. Early studies suggest GLP-1 affects the heart, fat, muscles, bones, liver, lungs, and kidneys too.
The main focus of GLP-1 research has been on treating or preventing diabetes and controlling appetite. Secondary research looks at possible heart benefits from the peptide. More recent, and less developed, studies explore how GLP-1 might fight off brain diseases. This newer area is growing quickly, especially since the peptide has been found to slow or stop the buildup of amyloid beta plaques in Alzheimer's disease.
Incretin Effect
One of the most important effects of GLP-1 is called the "incretin effect." Incretins are metabolic hormones released by the digestive tract that lower blood sugar levels. GLP-1 is one of the two key hormones (the other is GIP) that trigger this effect in rodent studies. Even though GIP levels are about 10 times higher than GLP-1, evidence shows GLP-1 is more powerful, especially when blood sugar is very high.
A GLP-1 receptor on pancreatic beta cells shows that GLP-1 directly triggers insulin release from the pancreas. When combined with sulfonylurea drugs, GLP-1 boosts insulin enough to cause mild low blood sugar in up to 40% of people. Increased insulin release leads to effects like more protein building, less protein breakdown, and better amino acid uptake by muscles.
Beta Cell Protection
Animal studies suggest GLP-1 can promote the growth and increase of pancreatic beta cells. It may also help create new beta cells from early cells in the pancreatic duct lining. Research shows GLP-1 blocks beta cell death. Overall, these effects shift the balance toward more beta cell growth, hinting that the peptide could help treat diabetes and protect the pancreas from damage that hurts beta cells.
In one strong study, GLP-1 blocked beta cell death caused by high inflammatory signals. Mouse models of type 1 diabetes show GLP-1 protects islet cells from destruction and might prevent type 1 diabetes from starting.
Appetite
Mouse studies suggest giving GLP-1 or similar versions into the brain can reduce the urge to eat and cut food intake. GLP-1 seems to boost feelings of fullness, indirectly reducing hunger. Recent clinical studies in mice show that twice-daily GLP-1 receptor drugs cause steady, ongoing weight loss. Over time, this leads to big improvements in heart risk factors and lower hemoglobin A1C levels, which measure diabetes severity and blood sugar control from treatment.
Cardiovascular Benefits
GLP-1 receptors are spread throughout the heart and help improve heart function in some cases by raising heart rate and lowering left ventricular end-diastolic pressure. That pressure drop matters because high levels link to heart enlargement, changes in heart structure, and eventual heart failure.
Recent evidence suggests GLP-1 could reduce overall damage from a heart attack. It seems to boost glucose uptake in heart muscle, helping stressed cells get needed nutrients to keep working and avoid death. This glucose boost happens without insulin.
Large doses of GLP-1 in dogs improve left ventricular performance and lower blood vessel resistance. This can reduce blood pressure and ease heart strain. In turn, it helps cut long-term high blood pressure effects like heart structure changes, vessel thickening, and heart failure. Giving GLP-1 after heart injury has consistently boosted heart performance in animal models and patients.
Brain Health
Some evidence suggests GLP-1 can improve learning and protect neurons from diseases like Alzheimer's. In one study, GLP-1 boosted associative and spatial learning in mice and even fixed learning problems in mice with gene defects. Rats with extra GLP-1 receptors in certain brain areas learn and remember much better than normal ones.
More mouse research shows GLP-1 protects against toxic neuron damage, fully shielding rat models from glutamate-caused cell death. The peptide can even encourage nerve growth in lab cells. Researchers hope further GLP-1 studies will show how to stop or reverse some brain diseases.
GLP-1 and its analog exendin-4 reduce amyloid-beta levels in mouse brains, as well as the precursor protein in neurons. Amyloid-beta forms the main plaques in Alzheimer's, which link to disease severity even if not proven to cause it. It's unclear if blocking amyloid-beta buildup protects against Alzheimer's, but this research offers a promising hint for intervening in mild cognitive issues before full Alzheimer's develops.
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