Questions this desk gets, answered without a sales pitch

Does this site sell peptides?

No. Nothing on this site is for sale, and no seller, pharmacy, clinic or laboratory is named or recommended anywhere on it, in any country. There is no catalogue, no basket, no referral and no affiliate arrangement. The site is a literature digest: it reads published research and regulatory records and writes them up with numbered citations.

Then why is it called Buy Canadian Peptides?

Because that is a phrase people actually type, and behind it sits a real and under-answered question about jurisdiction: why does the same molecule have a different legal status depending on which country is asked? That question deserves a proper answer, and this site gives one.

What it does not give is the transactional half. No route for obtaining a substance in one country while living in another is described here, and no border procedure is described either. That is a legal question with a country-specific answer, and a research digest is the wrong place to ask it. A gap between two countries' approval decisions is a fact about paperwork, not an invitation.

What does Health Canada say about these four compounds?

This desk does not state it, deliberately. The sources behind this site are clinical literature and the regulatory notes carried in the audited source material for each compound — which document United States positions and the World Anti-Doping Agency's list. There is no audited source here for the current position of Health Canada or of any other national regulator.

That is a real limit and it is better stated than papered over. Regulatory positions also change, sometimes several times in a few years, so a summary written once and left standing would be wrong before long. The general structure — that each national regulator decides on the applications filed with it, indication by indication, on its own timetable — is what this site can honestly describe, and it is what the rest of these pages describe.

If a compound is approved in one country, is it approved everywhere?

No, and the assumption causes more confusion than any other single idea in this subject. An approval is a decision on an application filed with one regulator, covering one indication, on one date. Tirzepatide illustrates it cleanly: first approved for type 2 diabetes in May 2022 ^[18], then later for chronic weight management, then later again for obstructive sleep apnoea. Each of those was a separate decision, and each country that maintains a register runs its own sequence.

So a statement like "it is approved for weight loss" is incomplete until it names a country and a date.

Is a compound that is not approved anywhere automatically unsafe?

No — and it is not automatically safe either. Both readings are common and both make the same mistake.

Non-approval can mean an application failed, or that no application was ever made, or that one is pending. From outside, those look identical. BPC-157 is the case in point: it is approved as a medicine in no country, but the dominant reason is that the large controlled human trials an approval requires have not been run. A 2025 review counted only three small human pilot studies and concluded the compound is best treated as investigational ^[2]. That is an empty file, not a negative verdict — and an empty file is also no evidence of safety.

What does BPC-157 do in the body?

In animals, it acts as a cytoprotective and repair-promoting peptide, and the effect most consistently linked to those results is angiogenesis — the growth of new blood vessels into damaged tissue. The best-characterised route is up-regulation and internalisation of the VEGFR2 receptor, with downstream Akt and nitric-oxide signalling ^[4]. Additional reported routes include the FAK-paxillin complex governing cell migration, sensitisation of the growth-hormone receptor in tendon fibroblasts, and modulation of nitric-oxide and several neurotransmitter systems.

What it does in a human body is genuinely not established. Human data amount to three small pilot studies as of 2025 reviews ^[2].

Is BPC-157 a growth hormone?

No. BPC-157 is a fifteen-amino-acid peptide derived from a partial sequence of a protein found in human gastric juice — a different molecule, a different size and a different origin from growth hormone.

The confusion has a real root. In cultured tendon cells, BPC-157 increased growth-hormone-receptor signalling, which is part of how it is thought to promote tissue repair. Making a receptor more responsive is not the same as being the hormone that binds it, and the distinction matters: the reported growth-signalling effect is exactly why one of the documented cautions concerns unknown long-term effects on tissue growth.

Does BPC-157 work immediately?

There is no controlled human evidence on how quickly it does anything, so the honest answer is that nobody knows. The pharmacology points away from a lasting single-administration effect: the formal characterisation found linear pharmacokinetics, a very short elimination half-life, modest intramuscular bioavailability and rapid breakdown into small fragments that enter ordinary amino-acid metabolism ^[3].

Community reports frequently describe improvement within the first one to three weeks, but that material is anecdotal, not clinical evidence, and improvement over weeks is also the natural course of many of the injuries people describe.

Does BPC-157 damage the liver?

No human study has been designed to answer that, so the question cannot be closed either way. The only directly relevant human data point is a first-in-human intravenous safety pilot in which BPC-157 at up to 20 mg was given to two healthy adults with no observed adverse events and no measurable changes in cardiac, hepatic, renal, thyroid or glucose biomarkers ^[1].

Two participants over a short window is not a liver-safety dataset. The broader position is that large-scale human safety data simply do not exist ^[2], which is itself the most important safety fact about this compound.

What is NAD+ supplementation used for?

In the published human research it is studied mainly for ageing-related endpoints, on the rationale that tissue NAD+ declines with age while the enzymes that consume it — sirtuins, PARPs and the ectoenzyme CD38 — keep competing for a shrinking pool ^[9].

The trials that exist mostly measure whether precursor supplementation raises the pool, and it does: whole-blood NAD+ rose by 22%, 51% and 142% across an ascending 100 to 1000 mg per day range of nicotinamide riboside over eight weeks ^[10], and oral NMN raised it dose-dependently over sixty days while improving walking distance and quality-of-life scores against placebo ^[7]. One trial found improved muscle insulin sensitivity after ten weeks of NMN in prediabetic postmenopausal women ^[8]. A 2025 review of the whole field nonetheless concluded that human efficacy remains limited ^[6].

What is the downside of taking NAD+?

The audited source material behind this site carries no formal safety-caution set for NAD+ and no register of community-reported effects, so what follows is a list of open disputes rather than documented harms.

Oral NAD+ itself is poorly taken up by cells intact, and some researchers argue plain NAD+ capsules are largely ineffective. Intravenous NAD+ therapy is marketed well ahead of its evidence; infused NAD+ clears rapidly from plasma, and infusions can cause chest or abdominal discomfort, flushing and nausea if run too quickly. Compounded injectable NAD+ carries a contamination risk — the FDA has issued a Class I recall of one compounded NAD+ injection for elevated bacterial endotoxin. A theoretical oncology concern exists, since NAD+ supports proliferating cells and its roles in cancer are dual and context-dependent. And supplement-grade product purity varies, with third-party testing not guaranteed.

Is it safe to take NAD+ every day?

This desk does not advise on personal use, and the question as asked is a clinical one. What the trials recorded can be stated precisely.

Oral NMN at 300 to 900 mg per day for sixty days was reported without safety issues at any level tested in a multicentre double-blind randomised trial ^[7]. Nicotinamide riboside across a 100 to 1000 mg per day range for eight weeks produced no flushing and no significant difference in adverse events from placebo at any level ^[10]. Those are observations in selected participants over defined, fairly short periods, under trial supervision. They are not a general finding about daily use over years, and no trial cited here was built to produce one.

Does NAD+ cause weight gain?

Nothing in the literature behind this site addresses it. The human trials cited here measured blood NAD+ levels ^{[10] [7]}, muscle insulin sensitivity ^[8], and walking distance and quality-of-life scores ^[7] — not body weight as an endpoint.

An absence of evidence is not a result in either direction, and the honest answer is that the question has not been asked in the trials on this desk.

What is semaglutide, and what is it used for?

Semaglutide is a 31-amino-acid engineered analogue of the gut hormone GLP-1, built to resist the enzyme that destroys the natural hormone and to bind reversibly to serum albumin, which is what makes a once-weekly schedule workable. It is marketed under several trade names, including Ozempic, Wegovy and Rybelsus.

It is FDA-approved across several indications and two formulations — a once-weekly subcutaneous injection and a once-daily oral tablet — covering type 2 diabetes, chronic weight management, reduction of major adverse cardiovascular events in adults with established cardiovascular disease and overweight or obesity, and, in 2025, metabolic dysfunction-associated steatohepatitis. The evidence behind those includes a 17,604-participant cardiovascular outcome trial ^[13] and a 3,533-participant kidney outcome trial ^[12].

How does semaglutide work for weight loss?

Mostly through the brain rather than the stomach. Rodent work traced semaglutide to the brainstem, area postrema, hypothalamic arcuate nucleus and parabrachial nucleus, where it reduced food intake and modified food preference without decreasing energy expenditure ^[16]. In the arcuate nucleus it activates the appetite-suppressing POMC and CART neurons and inhibits the appetite-driving NPY and AgRP neurons. Slowed gastric emptying contributes, but the central appetite effect dominates.

The magnitude in trials is substantial: a mean body-weight change of -14.9% from baseline to week 68 with once-weekly semaglutide 2.4 mg, against -2.4% with placebo ^[14].

What is tirzepatide, and how does it work?

Tirzepatide is a synthetic peptide that activates two incretin receptors at once — the glucose-dependent insulinotropic polypeptide receptor and the glucagon-like peptide-1 receptor. Most of the class before it engaged only the second. It was FDA-approved in May 2022 for type 2 diabetes ^[18], with later approvals covering chronic weight management and moderate-to-severe obstructive sleep apnoea in adults with obesity.

Activating both arms potentiates glucose-dependent insulin secretion, restrains glucagon, slows gastric emptying and reduces appetite. In a 72-week phase 3 trial in 2,539 adults with obesity, mean weight change was -15.0%, -19.5% and -20.9% across three ascending amounts against -3.1% with placebo ^[20]; in a 72-week open-label head-to-head trial in 751 adults, it produced -20.2% against -13.7% with semaglutide ^[11].

Are any of these prohibited in sport?

One of the four. BPC-157 is prohibited at all times by the World Anti-Doping Agency under its category for non-approved substances — a category named for exactly that absence of approval, which is why a compound nobody has approved becomes automatically prohibited for a tested athlete in every signatory country at once.

NAD+ and its precursors NMN, NR and nicotinamide are not prohibited. Neither semaglutide nor tirzepatide is specifically prohibited, though both are prescription medicines and athletes are expected to verify current status independently, since the list is revised.

Why does this site cite numbers in brackets?

Every quantitative claim on this site — a percentage, a participant count, a hazard ratio, a duration — carries a bracketed number pointing to a fixed entry on the references page. The list is numbered once and never renumbered, and no study appears in the text that is missing from the list.

Where a documented caution has no citable source behind it in the audited material, it appears here without a bracket rather than with a borrowed one. That is deliberate: an unbracketed caution is a signal that the claim is real but that this desk cannot point at the paper.