What do the evidence levels A, B, C, D mean?
Healthy Mango's evidence tiers describe how much human clinical evidence supports a compound. A = strong human RCTs; B = moderate human trials; C = early human data; D = preclinical only.
Last reviewed 2026-07-13
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Every compound page carries an evidence tier (A through D) that summarises how much human clinical evidence supports the compound. This is not a judgment of whether the compound 'works' — it is a description of what evidence exists in humans at what quality level.
Level A — Strong Human Evidence: multiple large randomised controlled trials in humans, and where applicable, approval by major regulatory agencies. Semaglutide, tirzepatide, thymosin alpha-1, tesamorelin, bremelanotide, and afamelanotide sit at this tier because they have well-conducted phase-3 human trials and either approval or extensive off-label human use.
Level B — Moderate Human Evidence: human trials exist but are limited in size, duration, or replication, or the compound is approved for related but not identical indications. Retatrutide (phase-3 in progress) and SS-31 (Barth syndrome approved, broader claims not) sit here.
Level C — Early Human Evidence: small-scale human studies, observational data, or off-label case reports only. Kisspeptin, Selank, and Semax with their smaller human trial bases sit here.
Level D — Preclinical Evidence: data are from animal models, cell studies, or anecdotal community reports. BPC-157, TB-500, MOTS-c, and many other research-supply peptides with rich preclinical literature but thin human evidence sit at this tier.
The tiers are honest signals, not judgments. A compound at level D may have important biology and real user experience but not enough controlled human evidence to make definitive clinical claims.
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What is a phase-3 trial and why does it matter?
Phase-3 trials are the large (often 1000–5000 participant), randomised, controlled, blinded trials that establish efficacy and safety for regulatory approval. They are the highest evidence tier in clinical medicine.
Why doesn't strong preclinical evidence guarantee a human clinical effect?
Mouse and human biology are similar but not identical, and rodent injury models differ from human clinical contexts in important ways. Preclinical strength predicts human effect in some biology (receptor pharmacology) and not others (tissue repair, cognition).
Why do some peptides become approved medicines while others don't?
Approval depends on biology plus patent protectability plus indication clarity plus market size — not simply on whether a compound works. Naturally-occurring sequences with broad, diffuse effects are often the least investible even when their biology is interesting.