Independent · Evidence-graded · Non-commercialFile 01

The label is a claim. Learn to read the proof.

Research peptides are sold on confident numbers and bold promises, with almost nothing to back them up. This is where you learn how the chemistry is actually verified, what the evidence really shows, and how to recognize a supply chain built to obscure accountability — so any decision you make is an informed one.

Fig. 1 — HPLC trace · UV 214nm
Vendor claim on the label 99.4% pure
DECLARED · 99.4% IMPURITY A IMPURITY B
ReadingThree peaks resolved. One disclosed. Tap a peak to inspect it, or reveal the two the headline number left out.
How to read it: purity is the area under the main peak — but the trace shows everything else in the vial too. Open the toolkit →

No products. No vendor links. No affiliate pitches. The independence is the point.

Start here

Four instruments. One job: replace trust with verification.

Each answers a different question you should be able to answer before you ever rely on a vial.

Interactive

The buyer-literacy toolkit

A live reconstitution & dose calculator, an interactive COA checker, a vendor red-flag scorecard, and a guide to what each lab test can and can't tell you.

Open the toolkit → Library

The science library

Plain-language compound pages graded on a four-tier evidence scale, separating what's been proven in humans from what's only shown in mice — or only claimed.

Browse compounds → Tracker

The regulatory tracker

What's actually changing in the law — compounding, GLP-1 enforcement, cosmetics rules — with a plain note on what each shift means for you.

Check the tracker → Stance

About & independence policy

Who runs this, how compounds are graded, and the explicit promise that keeps it honest: no vendor money, ever, and no links telling you where to buy.

Read the policy →
The object of study
Plate I — the anatomy of a claimSchematic

What arrives is a sealed glass vial and a printed number. Everything else — identity, purity, endotoxin, metals, the actual milligrams inside — is a claim until an instrument says otherwise.

This site is a manual for turning that claim back into evidence: read the trace, verify the certificate, and recognize when a seller is structured so no one can be held to account.

Note: illustration is schematic, not a real product. Nothing here is sold or linked.
What this is — and isn't

A literacy resource, not a storefront.

This is

Education and harm reduction. The aim is to make you a sharper, safer, harder-to-fool reader of certificates, claims, and sellers — and to grade the science honestly, including admitting how thin the human evidence is for most of these compounds.

This is not

A place to buy anything, a list of "trusted vendors," or a source of dosing protocols or medical advice. No affiliate links to grey-market sellers, because pointing you toward a purchase is exactly the conflict of interest this site stands apart from.

The one line worth repeating

A high purity number is not a safety certificate. Purity, identity, and contamination are measured on entirely different instruments — and "99% pure" can still mean unsafe to inject. The toolkit's test guide shows exactly why.

Science LibraryFile 02

Graded honestly — including how little we know.

Most "research peptides" are sold as if the science is settled. It usually isn't. Every compound here carries an evidence tier so you can see, at a glance, whether a claim rests on human trials, animal studies, or hope.

How to read the grades

The four-tier evidence scale

The tier reflects the strength of evidence in humans, not how interesting the molecule is. Plenty of Tier C compounds are fascinating — the tier just tells you not to mistake a mouse study for a settled fact.

Strongest human evidenceWeakest
TIER A

Approved drug, robust human RCTs. Large randomized trials, regulatory approval, well-characterized benefits and risks.

TIER B

Some human data, limited or lower quality. Real human studies exist but are small, short, or mixed. Promising, not proven.

TIER C

Preclinical only. Animal or in-vitro studies, no rigorous human trials. Where the majority of marketed research peptides actually sit.

TIER D

Theoretical or anecdotal. Mechanistic speculation or forum reports. No meaningful direct evidence either way.

Compounds

The library

Each card shows a schematic of the peptide's residue chain. Open a page for the full workup.

TIER C

BPC-157

A gastric-protein fragment with striking results in rodent healing models — and almost no rigorous human data behind the "heals everything" marketing.

Read the page → TIER B · TOPICAL

GHK-Cu

A copper-peptide complex with genuinely decent topical/cosmetic evidence — and far weaker support for the injectable, systemic claims.

Read the page → TIER A

Semaglutide

The honest counterexample: large trials, FDA approval, real efficacy. Featured to show this site is pro-evidence, not anti-peptide.

Read the page → TIER B

Retatrutide

A triple-receptor agonist with the largest weight loss yet recorded in a trial — and no approval, no approved source, and unfinished phase 3.

Read the page → TIER C

Ipamorelin

A pentapeptide that really does raise growth hormone — attached to body-composition claims that human trials never tested.

Read the page → TIER C

TB-500

A synthetic fragment of thymosin beta-4, sold on human trial data that belongs to a different molecule entirely.

Read the page → TIER B

CJC-1295

Real human trial data on raising growth hormone — and a 2006 patient death that halted the one efficacy trial ever attempted.

Read the page → TIER C

Epitalon

A four-residue pineal peptide with genuine rodent lifespan data — from almost exclusively one lab, never independently replicated.

Read the page →
Not peptides

Sold alongside, not related

These show up in the same storefronts and the same IV clinics as the peptides above — sometimes in the same visit — but they are not peptides, so there's no residue-chain diagram. Same evidence-tier standard, different chemistry.

TIER B ORAL · TIER C IV

NAD+

Real trial evidence for raising it with a pill — and a popular IV version that can't actually enter a cell the way its marketing implies.

Read the page →
← Science library

BPC-157

TIER C · PRECLINICAL ONLY

A 15-amino-acid peptide derived from a protein found in gastric juice. Remarkable in animal healing studies; essentially untested in rigorous human trials, despite marketing that implies otherwise.

Fig. — residue chain (schematic)15 aa · hover a residue
Hover any residue to read its amino acid. Highlighted beads mark the terminal residues.
CERTIFICATE OF ANALYSIS № ITV-001 HPLC · UV 214nm PURITY99.4% IDENTITY ENDOTOXINnot listed SPECIMEN
Plate II — the certificate and the vial it claims to describe. A headline purity figure, two undisclosed peaks, and no endotoxin line — the gap this page reads back into evidence. Schematic.
Class
Synthetic peptide fragment
Evidence tier
C — animal / in-vitro
Human trial data
Minimal to none
Regulatory status
Not FDA approved

What it is

BPC-157 — "Body Protection Compound 157" — is a synthetic chain of 15 amino acids, corresponding to a partial sequence of a protein isolated from human gastric juice. A notable property is its stability in stomach acid. Despite the "body protection" name, it is a laboratory peptide, not an approved therapeutic.

How it's proposed to work

The proposed mechanisms come almost entirely from animal and cell models. The most cited is promotion of angiogenesis — new blood-vessel formation — alongside effects on growth-factor signaling and the nitric oxide system. Plausible and interesting, but "proposed mechanism in rodents" is very different from "demonstrated effect in people."3

State of the evidence

In rodent models, BPC-157 shows consistent, often impressive results across tendon, ligament, muscle, bone, and gastrointestinal injury. The preclinical literature is genuinely substantial.124

In humans, there is essentially no rigorous clinical-trial evidence of efficacy — no large randomized controlled trials establishing that it heals injuries or repairs the gut. What circulates instead is anecdote and extrapolation from animal work. That gap is the single most important fact on this page.1

Animal results don't transfer automatically

A large fraction of compounds that work beautifully in mice fail in humans. Strong rodent data is a reason to run human trials — not a substitute for them. BPC-157 is a textbook case of a reputation resting on a bridge that hasn't been built.

Studied in humans vs. animals

  • Animals (extensive): tendon-to-bone healing, ligament and muscle repair, fracture models, gastric ulcer and IBD models.
  • Humans (minimal): no robust efficacy RCTs; safety over meaningful timeframes is not well characterized.

Risks & open unknowns

  • Long-term safety is unknown in humans. Absence of reported harm in short anecdotal use is not evidence of safety.
  • The angiogenesis question cuts both ways — a compound that grows new blood vessels raises a reasonable, unresolved question about processes you would not want fed.
  • Grey-market quality is its own hazard — no approved source means variable purity, potency, and contamination, confounding both safety and what a "dose" delivers.

Regulatory status

Not approved by the FDA for any use, and the subject of shifting compounding policy — see the regulatory tracker for the current position, including the 2026 advisory-committee review.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Heals tendons and injuries fast"Strong in rodents; no rigorous human efficacy data.Unproven in humans
"Fixes leaky gut / heals the gut"Promising in animal GI models; not shown in human trials.Unproven in humans
"Totally safe, no side effects"Long-term human safety is not established.Not supported
"Pharmaceutical-grade from vendors"No approved pharmaceutical source exists; quality varies.Misleading

Verify this yourself

Don't take this page on faith either — that's the whole ethic here. Search the compound on PubMed and notice the rigorous studies are overwhelmingly animal and in-vitro. When you see a human claim, look for the randomized controlled trial behind it. The absence of one is the answer.

Sources

  1. Gwyer D, Wragg NM, Wilson SL. Gastric pentadecapeptide body protection compound BPC 157 and its role in accelerating musculoskeletal soft tissue healing. Cell Tissue Res. 2019;377(2):153–159. doi:10.1007/s00441-019-03016-8Review
  2. Seiwerth S, et al. Stable gastric pentadecapeptide BPC 157 and wound healing. Front Pharmacol. 2021;12:627533. doi:10.3389/fphar.2021.627533Review
  3. Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JS. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol. 2011;110(3):774–780. doi:10.1152/japplphysiol.00945.2010Animal / in-vitro
  4. Staresinic M, et al. Stable gastric pentadecapeptide BPC 157 and striated, smooth, and heart muscle. Biomedicines. 2022;10(12):3221. doi:10.3390/biomedicines10123221Review

Records located via PubMed. Evidence searched August 2026. Note that a large share of the BPC-157 literature comes from a small number of research groups — a limitation the 2019 review states directly.

← Science library

GHK-Cu

TIER B TOPICAL · TIER C INJECTABLE

Copper tripeptide-1 — a naturally occurring peptide-copper complex. One of the better-supported peptides in skincare, and one of the more overreached when sold as an injectable.

Fig. — residue chain (schematic)Gly-His-Lys + Cu²⁺
Hover any residue to read its amino acid. The diamond marks the bound copper ion (Cu²⁺).
Class
Copper-peptide complex (GHK + Cu²⁺)
Evidence tier
B topical / C injectable
Human data
Topical: moderate · Systemic: weak
Regulatory status
Legal cosmetic ingredient

What it is

GHK-Cu is the tripeptide glycyl-L-histidyl-L-lysine bound to a copper ion. It occurs naturally in human plasma, saliva, and urine, and its concentration declines with age — the basis of much of the "youth molecule" framing. In cosmetics it appears as copper tripeptide-1.

How it's proposed to work

It's thought to act as a copper-delivery vehicle and a signaling molecule, with effects on gene expression, stimulation of collagen, elastin and glycosaminoglycan synthesis, antioxidant activity, and wound healing. Unlike many peptides here, a meaningful share of this work exists in human skin, not just rodents.14

State of the evidence

Topically, the evidence is among the most credible in the peptide space: support for improvements in the appearance of skin firmness and fine lines, and a role in wound healing — hence Tier B.23

Systemically / injected, the picture is much thinner. Broad anti-aging or organ-level "regeneration" claims for injectable GHK-Cu aren't backed by rigorous human trials, dropping injectable use to Tier C. Notably, the legal, defensible product — a topical — sits exactly where the evidence is strongest.4

Studied in humans vs. animals

  • Humans (topical): skin appearance, firmness, fine lines, wound-healing support.
  • In-vitro / animal: collagen and matrix-protein synthesis, antioxidant effects.
  • Humans (systemic): limited rigorous efficacy data for broad claims.

Risks & open unknowns

  • Topical use is generally well tolerated; mild irritation is the usual risk.
  • Copper load matters — essential in trace amounts, toxic in excess; the margin for repeated systemic dosing isn't well characterized.
  • Formulation is finicky — pH-sensitive, can discolor, interacts with some actives and preservatives.

Regulatory status

As a cosmetic ingredient, copper tripeptide-1 is used legally in topicals under cosmetic rules rather than drug approval, and has generally been treated more favorably than peptides like BPC-157 — see the tracker. The key legal line is claims: cosmetic appearance claims are fine; therapeutic claims convert it to an unapproved drug.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Improves appearance of fine lines & firmness" (topical)Reasonable human and cosmetic-use support.Best-supported
"Supports wound healing" (topical)Some supporting evidence.Plausible
"Injected, it regenerates the whole body"Not established by rigorous human trials.Overreach
"Reverses aging because levels drop with age"The decline is real; the reversal is an inference, not a proven outcome.Inference, not proof

Verify this yourself

The strongest GHK-Cu studies are topical and dermatological. When a seller pushes injectable systemic benefits, look for the human trial — and notice you're usually handed a skin study or an in-vitro result instead. The mismatch between evidence type and claim is the tell.

Sources

  1. Pickart L. The human tri-peptide GHK and tissue remodeling. J Biomater Sci Polym Ed. 2008;19(8):969–988. doi:10.1163/156856208784909435Review · author COI
  2. Miller TR, Wagner JD, Baack BR, Eisbach KJ. Effects of topical copper tripeptide complex on CO2 laser-resurfaced skin. Arch Facial Plast Surg. 2006;8(4):252–259. doi:10.1001/archfaci.8.4.252Randomised controlled trial
  3. Buffoni F, Pino R, Dal Pozzo A. Effect of tripeptide-copper complexes on the process of skin wound healing and on cultured fibroblasts. Arch Int Pharmacodyn Ther. 1995;330(3):345–360. PMID 8836453.Animal / in-vitro
  4. Ogórek K, Nowak K, Wadych E, Ruzik L, Timerbaev AR, Matczuk M. Are we ready to measure skin permeation of modern antiaging GHK-Cu tripeptide encapsulated in liposomes? Molecules. 2025;30(1):136. doi:10.3390/molecules30010136Review

Records located via PubMed. Evidence searched August 2026. Two caveats a careful reader should weigh: the controlled trial found no objective improvement in wrinkles or skin quality after laser resurfacing — only patient-reported satisfaction was higher; and the most widely cited GHK-Cu reviews are authored by the founder of a company selling GHK-Cu skincare, a conflict of interest worth knowing when the same papers are quoted back at you in marketing.

← Science library

Semaglutide

TIER A · APPROVED, ROBUST RCTs

A GLP-1 receptor agonist with large randomized trials and FDA approval. Featured on purpose: it shows what real evidence looks like — and that this site is pro-evidence, not anti-peptide.

Fig. — residue chain (schematic)GLP-1 analog + fatty-acid tail
Hover a residue to read its amino acid. The ochre chain is the engineered fatty-acid tail that extends half-life.
Class
GLP-1 receptor agonist
Evidence tier
A — large human RCTs
Human data
Extensive, high quality
Regulatory status
FDA approved

What it is

Semaglutide is an engineered, long-acting analog of the human hormone GLP-1, and the active ingredient in several FDA-approved products for type 2 diabetes and chronic weight management. A real, approved pharmaceutical — the opposite end of the spectrum from the research-only compounds elsewhere here.

How it works

It activates the GLP-1 receptor: glucose-dependent insulin secretion, glucagon suppression, slowed gastric emptying, and reduced appetite via central pathways. Crucially, these mechanisms are established in humans, not inferred from animals.

State of the evidence

This is what Tier A means — large, multi-year randomized controlled trials across glycemic control, weight loss, and cardiovascular outcomes, showing meaningful, reproducible effects, with a major outcomes trial demonstrating reduced cardiovascular risk in a defined population. Benefits and harms are both well characterized — exactly what's missing for the research peptides.12

Why a regulated drug is on this site

Including semaglutide isn't an endorsement to source it casually — it's a calibration point. When you can see what a genuine evidence base looks like, the thinness behind a Tier C peptide's marketing becomes obvious by contrast. The point is the standard, not a side.

Risks & known side effects

  • Gastrointestinal effects — nausea, vomiting, diarrhea — are common, especially during dose escalation.
  • Less common but serious: pancreatitis, gallbladder problems.
  • A boxed warning reflects rodent thyroid C-cell tumors; contraindicated with personal/family history of medullary thyroid carcinoma or MEN-2.
  • These are knowable precisely because it was studied properly — "well-evidenced" means risks understood, not risk-free.

Regulatory status & the grey-market caveat

FDA approved. During recent shortages, compounded versions proliferated; with shortages resolved, the rules on compounding copies tightened — see the tracker. The literacy point: a compounded or grey-market version carries the same sourcing, purity, dosing, and contamination risks as any research-chemical product. The evidence behind the molecule does not vouch for the vial in front of you.

Claims vs. what the data supports

ClaimWhat the evidence actually showsVerdict
"Produces significant weight loss"Supported by large randomized weight-management trials.Well supported
"Improves blood sugar in type 2 diabetes"Core, well-established effect.Well supported
"Has cardiovascular benefit"Demonstrated in a major outcomes trial for a defined population.Supported in that group
"Grey-market/compounded vials are equivalent & safe"Same quality and dosing risks as any unregulated source.Not supported

This page is not a prescribing guide

Semaglutide is a prescription medication with real contraindications and an escalation protocol that belongs in a clinical relationship. This page explains the evidence; it does not tell you how to use it. Evidence literacy, not dosing instruction — the line this whole site holds.

Sources

  1. Wilding JPH, et al. Once-weekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384(11):989–1002. doi:10.1056/NEJMoa2032183Randomised controlled trial
  2. Lincoff AM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med. 2023;389(24):2221–2232. doi:10.1056/NEJMoa2307563Randomised controlled trial

Records located via PubMed. Evidence searched August 2026. These are the trials that earn the Tier A grade: 1,961 randomised participants over 68 weeks, and a separate cardiovascular-outcome trial. Note what that scale buys — an effect size measured against placebo, not a testimonial.

Regulatory TrackerFile 03

What's changing — and what it means for you.

Peptide rules are moving fast and unevenly. This tracks the shifts that matter, in plain language, with a clear note on the practical implication. Every entry shows when it was last checked, because a tracker without dates is just an opinion.

Last reviewed: September 2026

Status key: In effect Pending In flux Closed / barred

Loading tracker…

How this tracker is kept honest

Once a month: re-check the FDA compounding pages and the PCAC docket, scan two or three law-firm regulatory trackers, update any row that changed, and move the "last reviewed" date. Entries that go stale without a fresh date should be trusted less — including these. Nothing here is legal advice.

Get the tracker digest

An email when something in the regulatory tracker actually changes — a committee vote, an FDA action, an enforcement pattern worth knowing. No fixed schedule, because manufactured urgency is how the rest of this industry talks to you.

Your address is stored only to send this digest, is never sold or shared, and every email carries a one-click unsubscribe. Nothing else about you is collected. Reading the site still contacts no outside company — see the privacy notice.

About & IndependenceFile 04

The value here is that nothing is for sale.

Most peptide information online is downstream of someone trying to sell you peptides. This isn't. The entire point is to be the resource with no stake in your purchase — so the guidance can be honest, even when honesty is bad for a sale.

Why this exists

The gap this fills

Go looking for straight answers about research peptides and you mostly find vendor marketing dressed as education, or forum folklore. Both share a blind spot — no incentive to tell you when the evidence is thin, when a certificate is meaningless, or when a seller is structured to be unreachable.

This occupies the missing third position: genuine due diligence — reading certificates critically, grading the science honestly, tracking the law — with no product to move at the end. The skills are forensic, not promotional: tracing corporate structures, interrogating what a lab test does and doesn't prove, and separating human evidence from a mouse study.

The promise

Independence policy

The part that matters most, stated plainly and kept public. If any of these stops being true, this page changes first.

1

No vendor money

No peptide seller pays for coverage, placement, ratings, or favorable treatment — directly or indirectly. No vendor can buy its way onto or up this site.

2

No "where to buy"

No links, codes, or recommendations pointing you toward purchasing research compounds. Telling you where to buy is precisely the conflict this site refuses. The toolkit teaches you to evaluate, never to acquire.

3

No dosing or medical advice

Evidence and harm-reduction literacy, not a protocol manual and not medical advice. "What the data shows" is education; "here's your dose" is practicing medicine, and that line is not crossed.

4

Honest grading, including against interest

Compounds are graded on the evidence even when the honest grade is unflattering. "There's barely any human data" is a finding this site will state out loud.

5

Full disclosure if anything changes

If legitimate, non-conflicting support is ever added — say, a sponsor from a licensed testing lab or a reader membership — it will be disclosed openly, and never include grey-market sellers.

Fit

Who this is for — and not for

For

Anyone who wants to be harder to mislead — to read a COA critically, calibrate a marketing claim against real evidence, and recognize a supply chain built to dodge accountability.

Not for

Anyone looking for a vendor recommendation, a dosing protocol, or encouragement to use an unapproved compound. This site won't provide those, by design.

A note on scope and honesty

An independent educational project, not a medical or legal authority. It can be wrong and can fall behind. Treat it as a sharp starting lens, verify what matters to you, and bring real decisions to a licensed professional.

MethodologyFile 06

How this site decides what it claims.

A grade is only worth what the method behind it is worth. This page states who writes the site, what is searched, how evidence tiers are assigned, where the limits are, and how to get something corrected.

Who writes this

This site is written and maintained by Alexander Ayala, a Health Science undergraduate at the University of South Florida, a Florida-licensed Certified Nursing Assistant, and a Patient Care Technician working in hospital medical-surgical care.

What that background is good for: reading clinical literature, taking evidence quality seriously, and a working familiarity with how care and documentation actually function. It is a healthcare background, not a laboratory or legal one.

What that background is not

No medical degree, no pharmacy licence, no formal training in analytical chemistry, and no legal qualification. This site nonetheless makes claims about chromatography, endotoxin testing and federal compounding rules. That gap is exactly why every substantive claim on the compound pages now carries a citation to a primary source: you are not being asked to trust the author's authority, because the author does not claim any. Check the sources.

No external peer review. Nothing here is reviewed by an independent expert before publication. Treat it as a well-sourced starting point for your own reading, not as a settled reference.

Independence and affiliation

This is a personal, independent project. It is not affiliated with, endorsed by, funded by, or representative of the University of South Florida, AdventHealth, or any employer, school, laboratory or vendor. Nothing here is written on behalf of any organisation, and no organisation reviews it.

No vendor money, no affiliate links, no purchase recommendations — the financial position is stated in full on the independence policy.

What gets searched

Compound pages are built from primary literature located through PubMed and ClinicalTrials.gov, plus the relevant regulatory record — Federal Register notices, FDA guidance and advisory-committee materials, and published enforcement actions.

Every cited DOI is checked against the DOI registry to confirm it resolves to the exact title, journal and year listed. A reference that cannot be resolved does not get published.

How evidence tiers are assigned

The tier answers one narrow question: how strong is the evidence in humans? It is not a measure of how promising, interesting or popular a compound is.

TierWhat it requiresWhat it does not mean
ARegulatory approval plus large, multi-year randomised controlled trials with published outcomes.That any given vial contains the approved product.
BReal human studies exist, but are small, short, mixed, or not yet through phase 3.Proven. Promising and unfinished are different things.
CAnimal or in-vitro work only, with no rigorous human efficacy trials.That the compound does nothing — only that humans have not been tested.
DMechanistic speculation, anecdote or forum report, with no meaningful direct evidence either way.Disproven. Absence of evidence is the finding.

Where evidence differs by route of administration, the tier is split rather than averaged — GHK-Cu is graded separately for topical and injectable use, because the underlying evidence genuinely differs.

Grading against interest, on purpose

Semaglutide is Tier A. It is included precisely because a site that only ever graded compounds poorly would be an anti-peptide site wearing evidence as a costume. The scale has to be able to return a high grade or it is not a scale.

Known limits

  • Single author, no peer review. Errors are likelier than in a reviewed publication.
  • Literature searches are point-in-time. Each compound page states the month its evidence was last searched. A page without a recent date should be trusted less — including these.
  • Citation counts are uneven by design. A short reference list often reflects a thin literature rather than a shallow search. Where that is true, the page says so.
  • Regulatory content moves faster than the site. The regulatory tracker carries its own review date; nothing here is legal advice.
  • Conflicts of interest in the sources themselves are flagged where identified — for example, where the most-cited reviews of a compound are authored by someone selling it.

Corrections

If something here is wrong, it should be fixed and the fix should be visible. Report errors to corrections@in-the-vial.com.

Factual corrections are made promptly, and material changes are noted with the date on the affected page. The full edit history of this site is public in its source repository, so any change can be inspected rather than taken on trust.

The standard this site asks of sellers

Show your evidence, state your limits, date your claims, and make it possible to check you. This page exists so the same standard can be applied here.

← Science library

Retatrutide

TIER B · REAL TRIALS, NOT APPROVED

An investigational triple-receptor agonist that produced the largest weight loss yet reported for a drug of its class. It is also, for now, an unapproved compound with no legitimate consumer source.

Fig. — residue chain (schematic)39 aa · N-terminal fragment shown
Hover a residue to read its amino acid. Only the N-terminal fragment is drawn; the ochre chain is the fatty-acid tail that extends half-life.
Class
GIP / GLP-1 / glucagon triple agonist
Evidence tier
B — published human RCTs
Human data
Phase 2 complete; phase 3 ongoing
Regulatory status
Investigational — not approved

What it is

Retatrutide is a synthetic peptide roughly 39 amino acids long, carrying an engineered fatty-acid side chain that slows clearance and allows weekly dosing. It is an Eli Lilly investigational drug, also known by its development code LY3437943.

Where semaglutide activates one receptor and tirzepatide two, retatrutide activates three: the GLP-1 receptor, the GIP receptor, and — the genuinely novel part — the glucagon receptor, which is thought to raise energy expenditure rather than only suppress appetite.

How it works

The GLP-1 and GIP arms do what they do in the approved drugs: enhance glucose-dependent insulin secretion, slow gastric emptying, and reduce appetite through receptors in the brain. Adding glucagon-receptor agonism is counterintuitive, since glucagon raises blood sugar, but at these doses the dominant effect appears to be increased energy expenditure and hepatic fat mobilisation, with the incretin arms offsetting the glycaemic downside.

State of the evidence

This is the part that separates retatrutide from most compounds catalogued here: the human data are real, randomised, placebo-controlled, and published in a major peer-reviewed journal.

A phase 2 trial reported mean weight reductions around 24% at 48 weeks at the highest dose — the largest figure yet published for an incretin-class drug, and approaching what bariatric surgery achieves. Phase 3 trials are underway and had not reported final results as of this review.1

Strong trial evidence is not the same as an approved product

Everything above describes a pharmaceutical-grade compound administered under trial conditions with known purity and dose. None of it describes a vial bought online. The evidence supports the molecule; it says nothing about what a grey-market seller shipped you.

Studied in humans vs. animals

  • Humans (substantial): phase 2 randomised controlled trials in obesity and type 2 diabetes, with phase 3 in progress.
  • Animals (foundational): the receptor pharmacology and early dose-finding work that preceded human dosing.
  • Not established in humans: long-term safety beyond trial duration, effects after discontinuation, and use in people who would not have met trial eligibility criteria.

Risks & open unknowns

  • Gastrointestinal effects are common — nausea, vomiting and diarrhoea were the most frequent adverse events, and were dose-related.
  • Heart rate increased modestly in trials; the long-term cardiovascular meaning of that is not yet settled.
  • Long-term safety is genuinely unknown. Phase 3 exists precisely because phase 2 cannot answer it.
  • Muscle loss is a real concern with rapid weight reduction and is not fully characterised here.
  • No approved source exists. Anything sold to a consumer today is unapproved and of unverified identity, purity and concentration.

Regulatory status

Not approved by the FDA or any comparable regulator for any indication. It is an investigational drug in active trials, which means the only lawful human administration is inside one of those trials. Selling it for human use is the introduction of an unapproved new drug into commerce — see the regulatory tracker for how enforcement in this space is moving.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"The most effective weight-loss compound available"Trial results are genuinely the strongest published in its class.Supported in trials
"Clinically proven, so it's safe"Phase 2 measured 48 weeks. Long-term safety is what phase 3 is still testing.Overstated
"Pharmaceutical grade from a research supplier"No approved manufacturer sells to consumers. The phrase describes nothing verifiable.Misleading
"Same as Ozempic but stronger"Different molecule, three receptors instead of one, and unlike semaglutide it is not approved.Not supported

Verify this yourself

Don't take this page on faith either — that's the whole ethic here. Search the compound on PubMed and ClinicalTrials.gov, read the phase 2 publication rather than a summary of it, and check whether any phase 3 result has since reported.

Sources

  1. Jastreboff AM, Kaplan LM, Frías JP, et al. Triple-hormone-receptor agonist retatrutide for obesity — a phase 2 trial. N Engl J Med. 2023;389(6):514–526. doi:10.1056/NEJMoa2301972Phase 2 randomised controlled trial

Records located via PubMed. Evidence searched August 2026. One trial, phase 2, 48 weeks — genuinely strong for its stage and still not an approval. Phase 3 is where long-term safety gets answered, and it had not reported at the time of this review.

← Science library

Ipamorelin

TIER C · LIMITED HUMAN DATA

A five-residue growth-hormone secretagogue. The pharmacology is real and reasonably clean; the body-composition and anti-ageing claims built on top of it were never the thing that got tested.

Fig. — residue chain (schematic)5 aa · 3 non-standard residues
Hover any residue to read it. Three of these five are not standard amino acids — a deliberate design choice that resists breakdown in the body.
Class
Growth-hormone secretagogue (ghrelin-receptor agonist)
Evidence tier
C — limited human data
Human data
Small early trials, none for the marketed uses
Regulatory status
Not approved anywhere

What it is

Ipamorelin is a pentapeptide — a chain of just five residues — developed in the 1990s as a selective growth-hormone secretagogue. Three of its five residues are non-standard, including two in the mirror-image D-configuration, which is why the body's enzymes struggle to break it down.

It was originally investigated by a pharmaceutical developer for post-operative ileus, the sluggish return of bowel function after abdominal surgery. That programme did not succeed, and ipamorelin has never been approved for anything, anywhere.

How it works

It binds the ghrelin receptor in the pituitary and hypothalamus, triggering a pulse of growth hormone release. Its selling point among earlier compounds in its class is selectivity: it raises growth hormone with comparatively little effect on cortisol and prolactin, which the older secretagogues raised alongside.1

That selectivity is a genuine and reproducible pharmacological finding. It is also the point where the evidence and the marketing part company.1

Raising growth hormone is a mechanism, not an outcome

That ipamorelin increases growth hormone is well established. That increasing growth hormone this way produces more muscle, less fat, better sleep or slower ageing in healthy adults is a separate claim — and it is the claim that has not been demonstrated in controlled human trials. A measurable change in a blood marker is not the same as a benefit you would notice or want.23

Studied in humans vs. animals

  • Humans (limited): early-phase work establishing that it raises growth hormone, plus a discontinued clinical programme in post-operative ileus.
  • Animals (extensive): growth-hormone release, bone and body-composition models.
  • Not studied in humans: the marketed uses — muscle gain, fat loss, recovery, sleep quality and anti-ageing — in healthy adults, over any meaningful duration.

Risks & open unknowns

  • Long-term safety is unknown. No trial has followed healthy people using it for extended periods.
  • Growth hormone has real downside potential at sustained elevation, including insulin resistance, fluid retention and joint pain.
  • The cancer question is unresolved. Growth hormone and IGF-1 signalling influence cell proliferation, and no study has been large or long enough to characterise that risk here.
  • Non-standard residues complicate verification. Ordinary purity testing may not distinguish the correct D-configuration residues from cheaper L-forms, so identity testing matters more than usual — see the buyer toolkit.

Regulatory status

Not approved by the FDA or any comparable regulator, and not an approved compounding ingredient. It sits in the same unapproved category as most compounds catalogued here — see the regulatory tracker. It is also a banned substance in competitive sport under anti-doping rules.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Raises growth hormone naturally"It does raise growth hormone. "Naturally" is marketing language for an injected synthetic peptide.Half true
"Builds muscle and burns fat"Not demonstrated in controlled human trials in healthy adults.Not supported
"Safer than other secretagogues"More selective, yes — but selectivity is not the same as established long-term safety.Overstated
"Anti-ageing"No human trial has tested any ageing outcome.Not supported

Verify this yourself

Don't take this page on faith either — that's the whole ethic here. Search the compound on PubMed, note how few human trials exist and what they actually measured, and check whether any of them tested the outcome being sold to you.

Sources

  1. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552–561. doi:10.1530/eje.0.1390552Animal / early pharmacology
  2. Andersen NB, Malmlöf K, Johansen PB, et al. The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced decrease in bone formation. Growth Horm IGF Res. 2001;11(5):266–272. doi:10.1054/ghir.2001.0239Animal study
  3. Aagaard NK, Grøfte T, Greisen J, et al. Growth hormone and growth hormone secretagogue effects on nitrogen balance and urea synthesis. Growth Horm IGF Res. 2009;19(5):426–431. doi:10.1016/j.ghir.2009.01.001Human, short-term metabolic

Records located via PubMed. Evidence searched August 2026. Worth noticing what these sources are and are not: the foundational work is animal pharmacology, and the human record is small and short-term metabolic. A total PubMed record of roughly a dozen papers is itself the finding — none of them tested muscle gain, fat loss, recovery or ageing in healthy adults, which is what the compound is sold for.

← Science library

TB-500

TIER C · PRECLINICAL ONLY

A synthetic fragment of thymosin beta-4, sold on human wound-healing trial data — that belongs to a different, full-length molecule, tested by a different route, for a different condition.

Fig. — residue chain (schematic)Ac-LKKTETQ · 7 aa fragment
Hover any residue to read its amino acid. This short fragment is the actin-binding region of a much longer, 43-residue parent protein.
Class
Synthetic actin-binding fragment of thymosin β4
Evidence tier
C — preclinical only, for this fragment
Human data
None for TB-500 itself
Regulatory status
Not approved; recommended (non-binding) for 503A list

What it is

TB-500 is a synthetic heptapeptide, Ac-LKKTETQ (molecular weight ≈889 Da), corresponding to the N-acetylated actin-binding region — residues 17–23 — of thymosin β4 (Tβ4), a 43-amino-acid protein present in nearly every human cell. TB-500 is not thymosin β4 itself. It is a small fragment chosen for ease of synthesis, not because it was shown to reproduce everything the full-length protein does.

How it's proposed to work

Full-length Tβ4 binds actin monomers and is implicated in cell migration, blood-vessel formation, and wound repair. The reasoning behind TB-500 is that this isolated fragment retains the actin-binding activity thought to drive some of those effects. That reasoning rests on Tβ4 pharmacology — it has not itself been demonstrated for the isolated fragment outside in-vitro work and small rodent models.

The TB-500-vs-Tβ4 gap

Direct evidence for TB-500 is limited to in-vitro and animal work. The only published human data on this general family of molecules belongs to full-length recombinant Tβ4 — a chemically distinct, larger protein — dosed intravenously in a phase I safety trial, and to a separate topical gel formulation tested in two phase 2 wound-healing trials. Neither tested TB-500. Neither tested the injection routes marketed online. "Thymosin beta-4 was studied in humans" is a true sentence routinely stretched to cover a product it was never shown to apply to.12

Studied in humans vs. animals

  • Humans (different molecule): a phase I intravenous safety trial of full-length recombinant Tβ4 in healthy volunteers, and two phase 2 trials of a topical Tβ4 gel in venous stasis and pressure ulcers — real human data, for compounds and routes that are not TB-500.
  • Animals (TB-500 itself): a rat Achilles-tendon repair model found improved biomechanical strength and histological healing scores at four weeks.3
  • Not studied in humans at all: TB-500, injected, for any of the tendon, muscle or joint-recovery claims it is marketed for.

Risks & open unknowns

  • Long-term safety of TB-500 specifically is unknown. No human trial of any kind has used this molecule.
  • Tβ4 overexpression is independently linked to increased tumor-cell migration and metastasis in colon, breast and lung cancer models in mechanistic research.4 This doesn't prove TB-500 causes cancer — it is a real, unresolved mechanistic concern that marketing uniformly omits.
  • Grey-market vials carry the same identity and purity-verification problems as any unregulated peptide — see the buyer toolkit.
  • Banned in competitive sport under anti-doping rules, and a known designer drug in horse racing.

Regulatory status

Not approved by the FDA or any comparable regulator. In July 2026, an FDA advisory committee recommended TB-500 for the 503A Bulks List alongside BPC-157, KPV, MOTS-c, Epitalon and Semax — an 8–6 vote with one abstention, non-binding, over the objections of FDA's own career scientists. Separately, in April 2026, TB-500 was removed from FDA's "Category 2" flagged-safety-risk compounding list along with BPC-157 and CJC-1295, but not moved to the permitted Category 1 — a genuine grey zone, not a green light. See the regulatory tracker.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Backed by human thymosin beta-4 trials"Those trials tested a different molecule, a different route, for a different condition.Misleading
"Speeds tendon, ligament and muscle recovery"One rat tendon study exists. No human recovery trial of any kind.Not supported
"Same science as the FDA-studied drug"Same parent protein's binding domain, a different compound entirely.Overreach
"Natural, since it's a body-protein fragment"Derived from a protein your cells make, yes — that says nothing about an injected, unregulated synthetic version.Half true

Verify this yourself

When a seller cites "thymosin beta-4 research," check whether the cited study actually used TB-500, the full-length protein, or a different derivative — and whether it tested injection or a topical gel. The three are not interchangeable, and the gap between them is exactly where the marketing lives.

Sources

  1. Wang X, Liu L, Qi L, et al. A first-in-human, randomized, double-blind, single- and multiple-dose, phase I study of recombinant human thymosin β4 in healthy Chinese volunteers. J Cell Mol Med. 2021;25(17):8222–8228. doi:10.1111/jcmm.16693Phase I trial · different molecule
  2. Treadwell T, Kleinman HK, Crockford D, Hardy MA, Guarnera GT, Goldstein AL. The regenerative peptide thymosin β4 accelerates the rate of dermal healing in preclinical animal models and in patients. Ann N Y Acad Sci. 2012;1270:37–44. doi:10.1111/j.1749-6632.2012.06717.xPhase 2 review · different molecule
  3. Biçer O, Adanir O, Güleryüz Y, et al. Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: a histopathological and biomechanical study. Jt Dis Relat Surg. 2026;37(3):822–837. doi:10.52312/jdrs.2026.2951Animal study · direct TB-500 data
  4. Tang MC, Chan LC, Yeh YC, et al. Thymosin beta 4 induces colon cancer cell migration and clinical metastasis via enhancing ILK/IQGAP1/Rac1 signal transduction pathway. Cancer Lett. 2011;308(2):162–171. doi:10.1016/j.canlet.2011.05.001Mechanistic / in-vitro & animal

Records located via PubMed. Evidence searched September 2026. The most telling thing about these sources is what they don't show: of the four references behind this molecule's reputation, only one — the rat tendon study — actually tested TB-500 itself, rather than the larger, differently-dosed protein it's named after.

← Science library

CJC-1295

TIER B · SERIOUS SAFETY SIGNAL

A long-acting growth-hormone-releasing-hormone analog with genuine published human trials behind it — and a halted 2006 trial, after a participant's death, that most sellers never mention.

Fig. — residue chain (schematic)N-terminal fragment shown · DAC tail
Hover a residue to read its amino acid. Only the N-terminal fragment of the 30-residue analog is drawn; the ochre chain is the DAC tag that binds albumin and extends half-life.
Class
GHRH analog, DAC (albumin-binding) format
Evidence tier
B — published human PK/safety RCTs
Human data
Two small trials; a larger efficacy trial was halted
Regulatory status
Not approved; WADA-prohibited

What it is

CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH), built on the 29-residue GRF(1-29)/sermorelin backbone with four stabilizing substitutions (D-Ala2, Gln8, Ala15, Leu27) and, in the version actually studied, a C-terminal maleimidopropionyl-lysine tag — the "Drug Affinity Complex" (DAC) — that binds reversibly to circulating albumin and extends its half-life to roughly 5.8–8.1 days, versus a few minutes for unmodified GHRH.

Two products share the name. "CJC-1295 with DAC" is the long-acting, albumin-binding version — the one tested in the human trials below. "CJC-1295 without DAC", commonly sold as Mod GRF 1-29, is a different pharmacokinetic entity with a half-life of minutes, and was not the drug used in these trials. A listing that just says "CJC-1295" without specifying which is not telling you which drug you'd be getting.

How it works

It binds the GHRH receptor on the pituitary, stimulating pulsatile growth-hormone release and downstream IGF-1 production — without materially changing the frequency or shape of the body's natural GH pulses. It raises the trough level between pulses, rather than the rhythm itself.

State of the evidence

Genuinely published, randomized, placebo-controlled human data exist here — a real rarity in this catalog. Two ascending-dose trials in healthy adults established the pharmacokinetics, short-term safety, and GH/IGF-1 response of CJC-1295 with DAC, with no serious drug-related adverse events reported.12

What these trials did not test

They measured hormone levels, not outcomes. No published trial has tested CJC-1295 for muscle gain, fat loss, recovery, sleep, or longevity — the uses it's actually marketed for. Raising GH and IGF-1 is a real, demonstrated pharmacodynamic effect; by itself, it is not evidence for any benefit built on top of it.

Studied in humans vs. animals

  • Humans (small, published): two ascending-dose, placebo-controlled trials (2005–2006) establishing pharmacokinetics and short-term safety of CJC-1295 with DAC in healthy adults.
  • Humans (larger, unpublished): a phase 2 trial in people with HIV-associated lipodystrophy (NCT00267527, n=192) was halted in July 2006 after a participant died of a myocardial infarction roughly three hours after a dose. Investigators attributed the death to pre-existing coronary artery disease rather than the drug, but the trial was stopped and no efficacy results were ever published.
  • Animals: growth and GH/IGF-1 stimulation across several species, preceding the human work.
  • Not studied: any use beyond a few weeks, any of the muscle, fat, recovery or longevity claims, and CJC-1295 without DAC specifically.

Risks & open unknowns

  • The 2006 trial halt is the central safety fact most sellers omit. A causal link to the drug was never established, but the one trial built to test real-world efficacy never produced a result, because it was stopped after a death.
  • Chronic GH/IGF-1 elevation carries recognized risks: insulin resistance, fluid retention, joint pain, and a theoretical mitogenic (cancer-promoting) concern not ruled out over long-term use.
  • No modern phase 2 or 3 trial of CJC-1295 with DAC has been registered since 2006.
  • CJC-1295 without DAC — the form most commonly sold under the name — has its own shorter-half-life pharmacology that these trials never evaluated at all.

Regulatory status

Not approved anywhere, and a WADA-prohibited substance. No FDA approval pathway exists, and unlike BPC-157, TB-500, KPV, MOTS-c, Epitalon and Semax, it has not been part of the FDA's 503A Bulks List committee review — see the regulatory tracker.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Clinically studied and proven safe"Two short trials in healthy adults found no serious drug-related events; a larger efficacy trial in a patient population was halted after a death.Incomplete picture
"Raises growth hormone and IGF-1"Directly demonstrated, repeatedly, in published trials.Supported
"Builds muscle, burns fat, reverses aging"Never tested as an outcome in any published human trial.Not supported
"Same compound in every CJC-1295 product"With-DAC and without-DAC are pharmacologically different drugs; most listings don't specify which.Misleading as sold

Verify this yourself

Ask whether a product is with or without DAC, and whether the seller can produce testing distinguishing them. Then look up NCT00267527 yourself — it is the one human efficacy trial of this molecule ever attempted at scale, and the one almost nobody selling it will mention.

Sources

  1. Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799–805. doi:10.1210/jc.2005-1536Randomised controlled trial
  2. Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792–4797. doi:10.1210/jc.2006-1702Clinical trial
  3. ClinicalTrials.gov. Safety and efficacy study of CJC-1295 in HIV-infected subjects with excess abdominal fat (lipodystrophy). NCT00267527.Trial registry · terminated 2006
  4. Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, Ruchała M. The emerging landscape of performance-enhancing peptides modulating the GH-IGF1 axis. Front Endocrinol (Lausanne). 2026;17:1822475. doi:10.3389/fendo.2026.1822475Review

Records located via PubMed and ClinicalTrials.gov. Evidence searched September 2026. The 2006 trial halt (NCT00267527) is documented in the registry and in contemporaneous trade-press coverage; the investigators' attribution of the death to pre-existing coronary disease, not the study drug, is also reported there — readers should weigh that attribution themselves rather than take either reading on faith.

← Science library

Epitalon

TIER C · SINGLE-LAB EVIDENCE

A four-amino-acid pineal peptide with genuine rodent lifespan-extension data — and a human evidence base that consists almost entirely of one research group's own, unreplicated reports.

Fig. — residue chain (schematic)Ala-Glu-Asp-Gly
Hover any residue to read its amino acid. All four are standard amino acids — one of the simplest chains in this library.
Class
Synthetic tetrapeptide, modeled on a pineal tissue extract
Evidence tier
C — animal data only
Human data
Same-lab reports only, no controlled design described
Regulatory status
Not approved; outside current FDA review

What it is

Epitalon (also spelled Epithalon) is a synthetic tetrapeptide, Ala-Glu-Asp-Gly (AEDG), designed to reproduce the activity of Epithalamin, a bovine pineal-gland tissue extract developed earlier by the same St. Petersburg research group that went on to design Epitalon itself.

How it's proposed to work

Proposed mechanisms include restoring age-related decline in pineal melatonin secretion, tissue-specific effects on gene expression the developing group calls "peptide bioregulation," antioxidant activity, and — the claim repeated most in marketing — telomerase activation. A 2025 independent pharmaceutical-chemistry review found laboratory support for several of these mechanisms, while stating plainly that it "remains uncertain whether these are the sole mechanisms of action."1

A single-source evidence base

Nearly every primary study of Epitalon — animal and human alike — originates from one research group, published overwhelmingly in that group's own house journal. That concentration doesn't by itself make the findings wrong, but a result never independently replicated by an unaffiliated lab carries less weight than one that has been — and the group that discovered the compound is the same one reporting its "geroprotector" and lifespan effects.

Studied in humans vs. animals

  • Animals (most of the real evidence): lifespan extension in mice and fruit flies, restored circadian melatonin rhythm and improved glucose/insulin handling in aged rhesus monkeys, reduced chemically induced colon-tumor incidence in rats, and antioxidant-enzyme effects in fruit flies.234
  • Humans: reports describe giving Epitalon or Epithalamin to "elderly people" and observing melatonin-rhythm normalization, but the available record gives no sample size, randomization, blinding, or control arm — clinical observation from the developing lab, not a controlled trial.5
  • Not demonstrated anywhere, in any species: that telomerase activation translates into a measurable lifespan or disease-outcome benefit, or that the specific dosing protocols sold online match any regimen actually studied.

Risks & open unknowns

  • No independent, blinded, controlled human trial exists for any outcome claimed.
  • Telomerase activation is a double-edged finding. It's mechanistically plausible per cited in-vitro work, but telomerase reactivation is also a hallmark of many cancers — a tension marketing rarely addresses.
  • Replication can't be cross-checked. Because almost all data comes from one lab's own publications, dosing and adverse-event reporting can't be verified against independent sources the way better-studied compounds here can.
  • Grey-market vials carry the same identity and purity-verification problems as any unregulated peptide — see the buyer toolkit.

Regulatory status

Not reviewed by the FDA's Pharmacy Compounding Advisory Committee alongside BPC-157, TB-500, KPV, MOTS-c and Semax in July 2026, and not listed in either FDA compounding category. It simply sits outside the current U.S. regulatory conversation — neither flagged nor endorsed. See the regulatory tracker.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Activates telomerase"Supported by laboratory/mechanistic studies cited in independent reviews.Mechanistically supported
"Clinically proven geroprotector in humans"The only "clinical" human reports come from the compound's own developing lab, with no described controls.Unverified
"Extends lifespan"Demonstrated in mice and fruit flies; not demonstrated in any human study of any design.Animal-only
"Safe because it's natural, from the body"It's a synthetic lab compound modeled on a tissue extract — "natural" describes the inspiration, not the injected product.Misleading framing

Verify this yourself

Before trusting an Epitalon lifespan or anti-ageing claim, check who ran the study. If the answer is the same institute every time, that isn't confirmation — it's the opposite of it. Independent replication is what to look for, and this site could not find it.

Sources

  1. Araj SK, Brzezik J, Mądra-Gackowska K, Szeleszczuk Ł. Overview of Epitalon — highly bioactive pineal tetrapeptide with promising properties. Int J Mol Sci. 2025;26(6):2691. doi:10.3390/ijms26062691Independent review
  2. Anisimov VN, Khavinson VKh, Zavarzina NYu, et al. Effect of pineal peptide on parameters of the biological age and life span in mice. Ross Fiziol Zh Im I M Sechenova. 2001;87(1):125–136. PMID 11227856.Animal · same lab
  3. Anisimov VN, Khavinson VKh, Popovich IG, Zabezhinski MA. Inhibitory effect of peptide Epitalon on colon carcinogenesis induced by 1,2-dimethylhydrazine in rats. Cancer Lett. 2002;183(1):1–8. doi:10.1016/s0304-3835(02)00090-3Animal · same lab
  4. Goncharova ND, Vengerin AA, Khavinson VKh, Lapin BA. Pineal peptides restore the age-related disturbances in hormonal functions of the pineal gland and the pancreas. Exp Gerontol. 2005;40(1–2):51–57. doi:10.1016/j.exger.2004.10.004Primate · same lab
  5. Korkushko OV, Lapin BA, Goncharova ND, et al. Normalizing effect of the pineal gland peptides on the daily melatonin rhythm in old monkeys and elderly people. Adv Gerontol. 2007;20(1):74–85. PMID 17969590.Human report · same lab

Records located via PubMed. Evidence searched September 2026. Four of the five sources above share at least one author with the original development group, and the exception (Araj et al., 2025) is a secondary review of that same primary literature, not independent new data. The one reference involving people at all names no sample size, randomization, or control group.

← Science library

NAD+

TIER B ORAL · TIER C IV

A coenzyme every cell makes, not a peptide — grouped here because it's sold in the same clinics, often in the same visit, as the compounds above. Real trial evidence backs the pill form; the popular IV version rests on a mechanism its own researchers say doesn't work the way it's marketed.

Class
Dinucleotide coenzyme (NAD+) and its precursors (NMN, NR) — not a peptide
Evidence tier
B precursor (oral) · C direct IV
Human data
Multiple oral RCTs; IV data limited to small retrospective comparisons
Regulatory status
NMN relisted as lawful supplement (Dec 2025); IV infusion unregulated compounding

What it is

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme every human cell makes and uses constantly, central to the redox reactions that extract energy from food and to DNA-repair and sirtuin signaling pathways. Blood and tissue NAD+ levels decline with age — a genuine, repeatedly measured finding, and the basis of most of the marketing built on top of it.

It is grouped in this library because of where it's sold, not what it is: wellness clinics and online sellers routinely offer NAD+ injections or IV drips in the same catalog — sometimes the same visit — as BPC-157 or CJC-1295. Chemically it has nothing in common with a peptide — it's a dinucleotide, not a chain of amino acids — so it gets no residue-chain diagram here, but it gets the same evidence standard.

How it's proposed to work

Two different products are sold under this one name, and they're proposed to work differently. Oral NAD+ precursors — nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) — are absorbed intact by cells and converted into NAD+ through the body's own salvage pathway, raising intracellular NAD+ over hours to weeks. Direct IV "NAD+" is marketed as delivering the finished coenzyme straight into cells, bypassing digestion entirely. That isn't how the chemistry works — see below.

A mechanism problem the industry's own research flags

NAD+ itself cannot cross an intact cell membrane. At the concentrations used in IV infusions, extracellular NAD+ is hydrolyzed before it ever reaches the inside of a cell, breaking down into NMN and then NR — which are what actually get imported, through dedicated transporters. A retrospective comparison of IV NAD+ against IV NR in the same clinic found the NAD+ infusions took nearly three times as long to administer and caused significantly more adverse effects — gastrointestinal symptoms, a faster heart rate, chest pressure — to deliver, in the end, the same precursor molecule NR provides directly, at a fraction of the cost and the infusion time.1

State of the evidence

Oral precursor supplementation has real human trial support. Multiple double-blind, placebo-controlled trials of NMN (250–2000 mg/day, 2–12 weeks) reliably and significantly raise blood NAD+ and its metabolites — that part is well established. Measured health outcomes are more modest: one trial found maintained walking speed and improved sleep quality, another found a longer six-minute walking distance and a slower rise in a "biological age" score, and a third found improved aerobic capacity in trained runners. Two separate meta-analyses, though, found no significant effect on body weight, fasting glucose, HbA1c or lipid profile.2345

Direct IV NAD+ has far less behind it: the only comparative human data located is the small retrospective study above (14 participants total), and the oldest, most-repeated claim about it — that it treats addiction withdrawal — traces mainly to a single retrospective case series from 1961, not a controlled trial.6

An honest Tier D

The addiction/detox claim specifically earns a lower grade than the rest of this page. It isn't just under-tested like most compounds here — the primary evidence behind it is a 104-patient retrospective report from 1961, repeatedly cited by modern reviews because nothing more rigorous has replaced it. Mechanistic speculation stacked on a six-decade-old anecdote is what Tier D looks like.

Studied in humans vs. animals

  • Humans (oral precursor, substantial): multiple double-blind RCTs, 2021–2026, in middle-aged and older adults and in athletes, measuring blood NAD+, walking speed, sleep, arterial stiffness and aerobic capacity.
  • Humans (direct IV, minimal): one small retrospective tolerability comparison and a 1961 retrospective case series on withdrawal; no randomized controlled trial of IV NAD+ against placebo was located.
  • Not demonstrated in any design: that either form slows aging, improves cognition, or treats addiction the way an approved therapy would need to show.

Risks & open unknowns

  • Direct IV NAD+ caused more adverse effects than IV NR in the one comparative study available — gastrointestinal symptoms, tachycardia, chest pressure — while taking substantially longer to infuse.
  • Unregulated compounding means unverified dose and purity, the same risk every grey-market peptide on this site carries — see the buyer toolkit.
  • Long-term safety of high-dose chronic supplementation is unknown; studied oral doses (250–2000 mg/day) run far above ordinary dietary intake.
  • Chronic NAD+/NMN elevation and cancer risk has not been ruled out — NAD+ metabolism intersects pathways (sirtuins, PARPs) implicated in both aging and tumor biology, and no long-term human cancer-outcome data exist.

Regulatory status

NMN's status has reversed twice. In November 2022 the FDA excluded it from the dietary-supplement definition, ruling it was first studied as an investigational drug. On September 29, 2025 the FDA reversed that determination, and on December 2, 2025 reinstated NMN's New Dietary Ingredient status — it is a lawful supplement ingredient again, subject to the standard 75-day NDI notification. Direct IV NAD+ infusion is a different regulatory question entirely: it's typically offered as a compounded injectable at wellness clinics, outside FDA review for any of the indications it's marketed for — the same unregulated position as the peptides elsewhere in this library. See the regulatory tracker.

Marketing claims vs. what the data supports

Common claimWhat the evidence actually showsVerdict
"Raises blood NAD+ levels" (oral)Demonstrated repeatedly in randomised trials.Supported
"IV NAD+ delivers the coenzyme directly into your cells"Contradicted by the same hydrolysis research the industry itself cites.Mechanism doesn't hold
"Treats addiction and withdrawal"Rests on a 1961 case series; no randomised trial exists.Tier D, not supported
"Slows or reverses aging"The age-related decline is real; reversal in humans isn't demonstrated.Inference, not proof

Verify this yourself

Ask an NAD+ seller which product you're actually getting — a capsule of NMN or NR, or an infusion — and whether they can show you a trial that tested that exact form for the benefit they're describing. For the IV version, also ask how it crosses into a cell; the honest research on this says it mostly doesn't, not the way the brochure implies.

Sources

  1. Reyna K, Heinzen G, Patel N, Ritter M, Siojo A, Legere H, Pojednic R. Intravenous infusion of nicotinamide adenine dinucleotide (NAD+) versus nicotinamide riboside (NR): a retrospective tolerability pilot study in a real-world setting. Front Aging. 2026;7:1652582. doi:10.3389/fragi.2026.1652582Retrospective · direct IV data
  2. Yi L, Maier AB, Tao R, et al. The efficacy and safety of β-nicotinamide mononucleotide (NMN) supplementation in healthy middle-aged adults. Geroscience. 2023;45(1):29–43. doi:10.1007/s11357-022-00705-1Randomised controlled trial
  3. Morifuji M, Higashi S, Ebihara S, Nagata M. Ingestion of β-nicotinamide mononucleotide increased blood NAD levels, maintained walking speed, and improved sleep quality in older adults. Geroscience. 2024;46(5):4671–4688. doi:10.1007/s11357-024-01204-1Randomised controlled trial
  4. Liao B, Zhao Y, Wang D, Zhang X, Hao X, Hu M. Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners. J Int Soc Sports Nutr. 2021;18(1):54. doi:10.1186/s12970-021-00442-4Randomised controlled trial
  5. Chen F, Zhou D, Kong AP, Yim NT, Dai S, Chen YN, Hui LL. Effects of nicotinamide mononucleotide on glucose and lipid metabolism in adults. Curr Diab Rep. 2024;25(1):4. doi:10.1007/s11892-024-01557-zMeta-analysis
  6. Braidy N, Villalva MD, van Eeden S. Sobriety and satiety: is NAD+ the answer? Antioxidants. 2020;9(5):425. doi:10.3390/antiox9050425Review · addiction claim origin

Records located via PubMed. Evidence searched October 2026. The oral-precursor trials above are genuine, randomised and published — more human evidence than most compounds in this library have. The gap that matters is between that evidence and the specific product sold as "NAD+ IV therapy," which is neither the same molecule's direct effect nor backed by comparable trials.

Buyer Literacy & Harm ReductionFile 05

Know what's actually in the vial.

A vendor's number on a label is a claim, not a fact. These four tools teach you to read the chemistry, verify the paperwork, and spot the structures built to mislead you.

Reconstitution & dose calculator

Enter what's on the vial and what you added. The readout shows concentration, the volume per dose, and where it lands on a standard U-100 insulin syringe.

mg
mL
mcg
Live readoutU-100 syringe
8.0
units on a U-100 syringe · 0.08 mL draw
5,000
mcg / mL
50
mcg / unit

Why the math can still betray you

This calculator assumes the label is true. If a vendor's real fill is off by ±20% — common where quality control is loose — your actual delivered dose shifts by that much, no matter how precisely you draw. The arithmetic is only as good as the label claim, which is exactly why the next three tabs exist.

Read a Certificate of Analysis

Tick what a COA actually contains. A real one is independent, verifiable, batch-specific, and complete. Items marked CRITICAL carry the most weight.

—
0 of 12 checks0%

Independence & verification

Traceability

Analytical completeness

Injectable safety — if it will be injected

Vendor red-flag scorecard

Tick everything that's true about a seller. These are the structural and behavioral tells that a supply chain is built to obscure accountability rather than prove quality.

Clear
0 flags raisedLow risk

What each test actually tells you

Purity, identity, and safety are answered by completely different instruments. A single high number on one assay says nothing about the others.

Assay
What it answers
What it can't tell you
HPLC
purity
How much of the sample is the target compound vs. impurities.
Nothing about identity, endotoxin, metals, or sterility.
LC-MS/MS
identity
Whether it's actually the molecule it claims to be.
The amount of any contaminants present.
LAL / rFC
endotoxin
Bacterial pyrogen load — fever-causing residue from gram-negative bacteria.
Chemical purity or whether live microbes are present.
ICP-MS
heavy metals
Mercury, lead, arsenic, cadmium from reagents or equipment.
Anything about the peptide's identity or potency.
Sterility
USP <71>
Whether anything grows at all. Pass/fail — no growth is permitted.
Endotoxin — dead bacteria leave it behind even when sterile.
TAMC / TYMC
microbial count
How many bacteria, yeast or mould are present, counted against a limit.
Sterility. A product can meet a count limit and still not be sterile.
GC-MS
residual solvents
Leftover manufacturing solvents in the finished product.
Identity, potency, or biological contamination.
99% pure does not mean safe to inject.

A compound can be 99% the correct molecule and still carry endotoxin or heavy metals far above any acceptable limit — because purity, identity, and safety are measured on different instruments. A complete picture needs HPLC and mass spec and, for anything injected, endotoxin and heavy-metal screening.

CorrectionsFile 07

What this site got wrong.

This site asks you to distrust claims that arrive without a record. It would be incoherent not to keep one of its own. Every substantive error found in a published claim is listed here, with what it said, what is actually true, and how long the wrong version was live.

What counts as a correction

A factual error in something the site asserted: a regulatory status, a date, a description of what an agency did, or a claim about evidence. Typos, styling and broken links are fixed without ceremony and are not listed.

The log begins 24 September 2026, when the first substantive errors were found. Earlier changes exist in the public commit history but were not recorded in this format at the time, and are not reconstructed here rather than risk describing them inaccurately.

24 September 2026 — two regulatory tracker entries

Both were found by a scheduled review on 1 September and verified against the Federal Register before correction. Both had been wrong on the live site for roughly six weeks.

Corporate Transparency Act — said a final rule was still pending. The entry read that a March 2025 interim rule applied and that the final rule was pending. FinCEN published its final rule on 14 August 2026, effective the same day. The entry was corrected and its status moved from In flux to In effect. A trailing clause about the law being upheld on appeal was removed rather than carried forward, because it was not re-verified.

503B exclusion — described an action the FDA is not taking. The entry said an FDA proposal would permanently remove semaglutide, tirzepatide and liraglutide from the 503B Bulks List. Those substances are not on that list. The FDA proposed not to include them, which is a decision about admission, not removal. The notice date was also wrong, 1 May 2026 rather than 30 April, and the status still read Comment period after comments closed on 30 July 2026.

The second error is the one worth dwelling on. Saying a regulator is removing something it never listed is exactly the kind of unearned claim this site exists to teach readers to catch. It was published here for six weeks.

How errors get found

A scheduled review checks every tracker lane against primary sources each month and reports what changed. It cannot edit anything; a human verifies each finding and makes the change. That review found both errors above. It also means the review is only as useful as the reading of it, and the September report sat unread for three weeks while the site stayed wrong.

Report an error

If something here is wrong, say so: corrections@in-the-vial.com. Corrections are made whether or not they are flattering, and they are logged here either way.

← Methodology