Semaglutide 5mg

Three changes, each with a distinct job. Health Canada's product monograph describes the molecule as having 94% sequence homology to human GLP-1, which is the arithmetic of two substitutions in 31 residues.

At the receptor itself semaglutide is a conventional agonist at GLP-1R, a class-B1 GPCR coupling through Gs to adenylyl cyclase and cAMP. Nothing about the modifications was intended to change signalling character, and the affinity data confirm the price paid: 0.38 ± 0.06 nM, roughly threefold weaker than liraglutide (Lau 2015). Duration, not potency, is the designed property.

Yes — three authorised products, and 2026 was the year the Canadian market changed shape. None of this makes the vial on this page an authorised drug; it is an unapproved research reagent, and the distinction is the whole point of the section.

The 2026 change: Canada became the first G7 country with generic semaglutide, because of a missed fee. Novo Nordisk's Canadian composition patent, CA 2,601,784 ("Acylated GLP-1 compounds"), lapsed after a maintenance payment of roughly CAD $250 went unpaid in 2019; the last payment on record was received 23 October 2018. With the supplementary term it would otherwise have run to 20 March 2028. Health Canada approved Dr. Reddy's generic semaglutide on 28 April 2026 and Apotex on 1 May 2026, and stated it was reviewing further generic submissions. Health Canada's own announcement noted that generics in Canada are commonly 45–90% cheaper than the brand.

Why that belongs on a research-peptide page: the single largest driver of grey-market GLP-1 demand has always been price and supply of the licensed product. A Canadian generic changes that calculation in Canada specifically, and it is the sort of jurisdictional fact that vendor pages written for a US audience get wrong by omission.

No. It is not on the Prohibited List. It is on the Monitoring Programme, which is a different document with different consequences. Most vendor pages in this category assert or imply a ban. That assertion is wrong, and the error is worth correcting plainly.

WADA added semaglutide to its Monitoring Programme in 2024 and has funded analytical method development for detecting GLP-1 receptor agonists in blood and dried blood spots. Monitoring exists precisely so that WADA can observe patterns of use without sanctions attaching — a substance on the Monitoring Programme is not prohibited, and a finding does not constitute an anti-doping rule violation.

That status was reaffirmed recently rather than left to inference. On 10 September 2026 WADA's Executive Committee confirmed that GLP-1 receptor agonists would not be added to the 2027 Prohibited List, keeping them on the Monitoring Programme instead. WADA's senior director for science and medicine, Professor Olivier Rabin, paired that with a caution about unsupervised use — a caution, not a prohibition.

Two honest qualifications. Monitoring status is reviewed annually and can change; "not prohibited in 2026" is not a permanent finding. And the S0 Non-Approved Substances clause catches substances with no approval from any governmental health authority for human therapeutic use — semaglutide holds authorisations from Health Canada, FDA and EMA, so S0 does not reach the molecule, though it may reach an unapproved preparation of it. Any athlete in a tested sport should obtain a written determination from their national anti-doping organisation rather than rely on any vendor's reading, including ours.

It does not support any claim of durable effect after withdrawal. This is the single most consistently omitted finding in the category and it has its own block below.

It does not support a mortality benefit in the general population. SELECT enrolled 17,604 people with established cardiovascular disease, overweight or obesity, and no diabetes, and measured major adverse cardiovascular events against placebo. Whatever it found holds only inside a narrowly defined high-risk population. It is not evidence about anyone outside it, and the trial was not designed to answer questions about primary prevention.

It does not support tolerability claims. In SELECT, 16.6% of semaglutide participants discontinued because of adverse events versus 8.2% on placebo — double, mostly gastrointestinal, in a trial where participants had strong reason to persist. Any page describing the tolerability profile as mild is contradicted by the largest dataset available.

It does not support treating weight change as fat-specific. STEP 1 measured mean body-weight change against placebo over 68 weeks in 1,961 participants without diabetes. Body weight is not body composition, and the trial's primary endpoint was weight. Claims about lean-mass preservation require body-composition endpoints that these trials largely did not prespecify.

It does not support the MASH indication as settled. The Canadian Wegovy monograph carries that indication authorised with conditions, which is Health Canada's mechanism for approving on promising but incomplete evidence pending confirmatory trials. That is a weaker status than a standard authorisation and should be described as such.

And a limit on what we can tell you: essentially all of this human evidence comes from the licensed pharmaceutical product, manufactured to a defined specification with a defined excipient package. None of it is evidence about an unformulated research peptide, and we do not present it as such.

The effect reverses, and this was measured rather than inferred. The STEP 1 trial extension followed 327 participants for a further 52 weeks after both semaglutide and placebo were stopped at week 68.

The authors also report that cardiometabolic improvements seen from week 0 to week 68 "reverted towards baseline at week 120 for most variables." The effect on those markers is a function of ongoing exposure, not a durable physiological reset.

STEP 4 is the mirror image and makes the same point from the other direction: participants who continued semaglutide after a 20-week run-in kept losing weight, while those randomised to placebo regained. Mechanistically this is unsurprising — a receptor agonist acting on an intact, feedback-regulated appetite and gastric-emptying system leaves little trace once occupancy falls. Any protocol asking about persistence needs a withdrawal arm; the compound will not answer the question on its own.

They differ sharply in quality, and collapsing them into one "GLP-1 risks" paragraph — which most pages do — destroys the distinction that matters.

Gallbladder disease: the strongest signal, and dose- and indication-dependent. He et al. pooled 76 randomised trials and 103,371 participants: gallbladder or biliary disease RR 1.37 (95% CI 1.23–1.52); cholelithiasis 1.27 (1.10–1.47); cholecystitis 1.36 (1.14–1.62). The subgroup structure is the informative part. In the 13 trials using GLP-1 agonists for weight loss, RR was 2.29 (1.64–3.18), against 1.27 (1.14–1.45) in the 63 diabetes and other trials. Higher doses gave RR 1.56 (1.36–1.78); lower doses 0.99 (0.73–1.33). Longer duration 1.40 (1.26–1.56); shorter 0.79 (0.48–1.31). A clean exposure–response gradient across three independent axes is what a real signal looks like. It is also partly confounded by rapid weight loss itself, which is an established gallstone risk factor independent of any drug.

Pancreatitis, bowel obstruction and gastroparesis: widely cited, much weaker than the citations suggest. The source is Sodhi et al., a retrospective claims-database cohort. Read the numbers rather than the headline: there were 613 semaglutide users and 4,144 liraglutide users against 654 bupropion-naltrexone comparators, and the adjusted hazard ratio for pancreatitis was 9.09 with a 95% CI of 1.25 to 66. A confidence interval spanning a 53-fold range is a statement about how few events were observed. Bowel obstruction was 4.22 (1.02–17.40); gastroparesis 3.67 (1.15–11.90); biliary disease 1.50 (0.89–2.53), not significant. The authors themselves flag the absence of dose and duration data, ICD coding misclassification, and a study population mostly with diabetes — which independently causes gastroparesis.

A subsequent reanalysis, published in Alimentary Pharmacology & Therapeutics in 2025 under the title "Some Risks of Gastrointestinal Adverse Events Associated With Glucagon-Like Peptide-1 Receptor Agonists Are Likely Explained by BMI," concluded that part of the apparent excess is attributable to baseline BMI rather than drug exposure. We could not retrieve that paper's full text and therefore quote none of its effect estimates; we cite it only for the direction of its conclusion.

The common events are not the interesting ones but they are the real ones. Health Canada's own review summary for Wegovy records gastrointestinal disorders in 73% of participants, headache in 16% and fatigue in 11%, with a 16-week dose-escalation schedule designed specifically to mitigate the GI burden. Frequent, mostly transient, and the dominant reason people stop.

This is the question a Canadian buyer actually has, almost no vendor answers it honestly, and the answer differs by country. We are not lawyers and none of this is legal advice.

United States — the window opened on a shortage and has closed. Large-scale compounding of semaglutide was lawful only while FDA listed the drug as in shortage, which permits compounders to make copies under sections 503A and 503B. FDA declared the semaglutide injection shortage resolved on 21 February 2025, with enforcement discretion ending 22 April 2025 for 503A pharmacies and 22 May 2025 for 503B outsourcing facilities. Tirzepatide had gone first: removed from the shortage list 2 October 2024, with deadlines of 18 February and 19 March 2025. On 30 April 2026 FDA went further and proposed to exclude semaglutide, tirzepatide and liraglutide from the 503B bulks list entirely, stating it "did not identify a clinical need for outsourcing facilities to compound" them from bulk substances, with comments open to 29 June 2026.

Canada — there was never a window. Canada has no shortage-triggered compounding exemption of the American kind. Health Canada's position, circulated to pharmacy regulators in June 2025, is that these activities constitute manufacturing rather than compounding, because they generally use unauthorised active pharmaceutical ingredients and duplicate an available authorised product without an unmet therapeutic need. Provincial regulators including the Alberta College of Pharmacy have stated plainly that unauthorised compounding of semaglutide-containing products is not permitted.

Why this reaches a research-reagent page. Health Canada's public advisory of 9 April 2026 on injectable peptides bought online named 14 compounds — BPC-157, CJC-1295, DSIP, Epitalon, GHK-Cu, HCG, Ipamorelin, KPV, Melanotan I and II, MOTS-C, NAD+, SS-31, TB-500 and Retatrutide. Semaglutide was not among them. That absence is a fact, not a shield: the advisory's operative sentence is that research-use-only labelling "does not make these products legal or exempt from regulatory requirements." On 11 June 2026 the Superior Court of Québec granted Health Canada a permanent injunction against a Québec online peptide retailer, barring manufacture, testing, distribution and sale of unauthorised injectable peptides and advertising through sites reachable from Canadian IP addresses. Neither action named semaglutide; both establish reasoning that does not depend on the compound.

We publish this knowing it cuts against our own interest, because the alternative is pretending a disclaimer is a legal shield when two regulators have now said it is not. So the research framing has to be real rather than decorative: we supply a reagent, publish no dosing or administration guidance, and make no human-use claims. Whether a particular purchase, import or use is lawful in your circumstances is a question for a Canadian regulatory lawyer, not for a product page.

Same compound, same supplier, different economics and different handling profile. The honest summary is that the 10 mg vial is cheaper per milligram and the 5 mg vial is easier to consume without compromise.

The argument that actually decides it is not price. One lot across an entire experiment is worth more than a small saving. If the work spans conditions that must be comparable, buy the size that covers all of them from one vial — a lot change mid-series introduces a variable you cannot control for retrospectively. If the work is exploratory and the next experiment may use something else entirely, the smaller vial wastes less.

Both vials are supplied as a single sealed fill with no excipient, and each is characterised by its own lot report, so the purity and content figures are not transferable between them. Check the number on the label against the published report for that lot specifically.

Two numbers, from one laboratory, on one lot. Janoshik Analytical, report #101805, analysis conducted January 2026: purity 99.247%, measured peptide content 6.05 mg against a 5 mg nominal fill. Report numbers are published for every lot on our lab results page.

Those two figures answer different questions and conflating them is the commonest error in reading a certificate of analysis. Purity is the proportion of chromatographic peak area attributable to the target peptide — how much of the peptide present is the intended sequence rather than truncations, deletions, des-acyl species or degradation products. It says nothing about how much is in the vial. Content is the absolute mass determination, the figure that governs any quantitative solution, and the one most often omitted. A vial can be 99% pure and underfilled, or correctly filled and 90% pure. You need both, from the same lot, with the lot matching the label. Full walkthrough: how to read a peptide COA.

Measured content here exceeds the nominal fill by about 21%, which is ordinary in lyophilised fills and is not a defect — but a calculation assuming exactly 5.00 mg will be wrong by that margin, which is more than enough to move a dose–response curve.

One point nobody in this category raises. The salt form matters and is not stated on an HPLC report. Synthetic peptides are commonly isolated as acetate or trifluoroacetate salts, and total vial mass is not peptide mass. Quantitative content determination measures the peptide, which is the right quantity — but if you are reconciling a gravimetric weight against a content figure, the counter-ion accounts for part of the difference. We do not print a salt form for this lot because it was not assayed, and we will not state one we have not measured.

Every citation below was checked against a MEDLINE-derived record or a publisher page. Design and size are stated because they determine what each result can support.

1. Lau J, Bloch P, Schäffer L, et al. Discovery of the Once-Weekly Glucagon-Like Peptide-1 (GLP-1) Analogue Semaglutide. J Med Chem. 2015;58(18):7370–7380. PMID 26308095. — The discovery paper. In vitro and animal. Source for the Aib⁸/Arg³⁴ substitutions, Lys²⁶ derivatisation, GLP-1R affinity 0.38 ± 0.06 nM and the 46.1 h mini-pig intravenous half-life.

2. Marso SP, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834–1844. PMID 27633186. — SUSTAIN-6. Randomised, double-blind, placebo-controlled cardiovascular safety trial in type 2 diabetes; the first outcome evidence for the molecule.

3. Wilding JPH, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989–1002. PMID 33567185. — STEP 1. Randomised, double-blind, placebo-controlled, n = 1,961, 68 weeks, measuring mean body-weight change against placebo.

4. Davies M, Færch L, Jeppesen OK, et al. Semaglutide 2·4 mg once a week in adults with overweight or obesity, and type 2 diabetes (STEP 2). Lancet. 2021;397(10278):971–984. PMID 33667417. — Randomised, double-blind, double-dummy, placebo-controlled phase 3. The type 2 diabetes population, where weight effects are consistently smaller than in STEP 1.

5. Rubino D, et al. Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance: The STEP 4 Randomized Clinical Trial. JAMA. 2021;325(14):1414–1425. PMID 33755728. — Randomised withdrawal design after a 20-week run-in; the continuation-versus-withdrawal comparison.

6. Wilding JPH, Batterham RL, Davies M, et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Diabetes Obes Metab. 2022. doi:10.1111/dom.14725. PMID 35441470. — The citable source on discontinuation. n = 327 followed to week 120, measuring weight regained off treatment; cardiometabolic variables reverted towards baseline. We could not confirm the final volume and page range against a primary record and therefore give the DOI and PMID instead.

7. He L, et al. Association of Glucagon-Like Peptide-1 Receptor Agonist Use With Risk of Gallbladder and Biliary Diseases: A Systematic Review and Meta-analysis of Randomized Clinical Trials. JAMA Intern Med. 2022. PMID 35344001. — 76 randomised trials, 103,371 participants. Overall RR 1.37 (1.23–1.52), with the dose, duration and indication gradients given above. Volume and page range not independently confirmed; year and PMID are.

8. Sodhi M, Rezaeianzadeh R, Kezouh A, Etminan M. Risk of Gastrointestinal Adverse Events Associated With Glucagon-Like Peptide-1 Receptor Agonists for Weight Loss. JAMA. 2023. PMID 37796527. — Retrospective claims-database cohort, not randomised. 613 semaglutide users. Pancreatitis aHR 9.09 (95% CI 1.25–66). Cited here for the width of its intervals as much as for its point estimates.

9. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. N Engl J Med. 2023;389(24):2221–2232. PMID 37952131. — SELECT. Randomised, double-blind, placebo-controlled, n = 17,604, mean follow-up 40 months, measuring a primary MACE composite against placebo. Discontinuation for adverse events 16.6% versus 8.2%.