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Five Compounds, Five Very Different Evidence Bases
Regulatory status is not a proxy for mechanism, and mechanism is not a proxy for human proof. Here is where each of the five actually stands.
The short version
The five compounds on this desk are not interchangeable, and lumping them together as "research peptides" hides the most important differences between them: whether a regulator has approved them, and how much of the supporting evidence comes from people rather than animals. This page puts those two axes side by side so a reader can calibrate expectations before reading any single compound page in depth.
One is an approved medicine with outcome trials in tens of thousands of people. Two have exactly one controlled human trial each, and one of those trials missed its primary endpoint. One has real human dose-response data but no proven clinical-outcome benefit yet. One is well studied topically but almost entirely unstudied for any other route. None of the five should be read through the others' evidence base — that is the entire point of this comparison.
How the five compare
| Compound | Category | Regulatory status | Strongest human evidence | Key open question |
|---|---|---|---|---|
| BPC-157 | Gastric pentadecapeptide | Not FDA-approved; research chemical | One 2-person IV safety pilot [1] | Rodent-to-human translation is essentially untested [2] |
| Semaglutide | GLP-1 receptor agonist | FDA-approved (diabetes, weight, CV risk, MASH) | Multiple large RCTs, 1,900-17,600 participants [8][10][11] | Long-term regain after stopping [12] |
| Ipamorelin | Selective GH secretagogue | Not FDA-approved; research chemical | One Phase 2 RCT, n=114 — missed its endpoint [15] | No long-term human safety data exists [15][16] |
| NAD+ | Redox coenzyme / precursor supplement | Sold as supplement; NMN status contested | Multiple human dose-response RCTs [19][22] | Blood-level rise vs. clinical-outcome proof [18] |
| GHK-Cu | Copper-binding tripeptide | Legal topical cosmetic ingredient; systemic use unapproved | Controlled topical/hair trials [25][26] | Poor skin penetration; systemic use unstudied [23] |
Reading the evidence-maturity gradient
Line the five up by how much of their case rests on controlled human trials versus animal or cell work, and a clear gradient appears. Semaglutide anchors one end: it has been tested in tens of thousands of people across diabetes, obesity, cardiovascular and kidney outcomes, and its approvals reflect that record [8][9][10][11]. NAD+ precursors sit next: real, repeated human dose-response trials exist, but they consistently stop short of proving a hard clinical-outcome benefit, a gap a 2025 review states outright [18].
GHK-Cu occupies an unusual middle position — genuinely strong topical human evidence [25][26], but essentially no data at all once the question moves to systemic or injectable use [23]. BPC-157 and ipamorelin sit at the thin end together, though for different reasons: BPC-157's human record is three small pilot studies total [2], while ipamorelin's is a single Phase 2 trial that did not demonstrate the effect it was built to test [15]. Neither pattern should be read as proof of harm — only as proof that the confident claims sometimes made about either compound outrun what has actually been measured in people.
A note on regulatory status across borders
Regulatory status is jurisdiction-specific. The source corpus documents the US position more fully than the Canadian one. This comparison therefore reports FDA status where supplied and does not convert it into a Health Canada conclusion. The distinction matters. Scientific evidence can cross a border; approval and access rules do not. A current Canadian status requires a current Canadian regulatory source. None is invented here.