Four experimental alterations
Different interventions expose different pieces of biology. Putting them side by side makes their preparation details easier to see.
What the experiments altered
A league table of these substances would send me in the wrong direction. The useful comparison is between the experimental changes: a fragment, an attachment, consumption of a coenzyme and a molecule that engages several receptors. Their names cover very different kinds of intervention. NAD+ is a coenzyme rather than a peptide.
| Subject | Experimental alteration | Measured result |
|---|---|---|
| KPV | Alpha-MSH fragment; also tested in mice with impaired MC1R | Anti-inflammatory activity remained in those mice. |
| GHK-Cu | Copper bound to GHK; formulation affects tissue delivery | Copper entered and remained in removed human skin. |
| NAD+ | Genetic deletion of the consuming enzyme CD38 in mice | NAD+ and mitochondrial function were preserved. |
| Retatrutide | One molecule engages GIPR, GLP-1R and GCGR | Cell assays found unequal potency against native hormones. |
These comparisons explain why a small chemical or biological change deserves close attention. They do not compare treatment effectiveness for a shared illness.
Human outcomes alongside the mechanisms
The most extensive human efficacy findings here concern retatrutide. Phase 2 trials measured body weight in an obesity population, liver fat in a defined subgroup and blood sugar and weight in type 2 diabetes. Each population carries its own entry criteria and follow-up period.
NR and NMN trials measured blood NAD+, walking and quality-of-life outcomes and muscle insulin sensitivity. The human-ageing review concludes that clinical efficacy is limited and tissue-specific evidence sparse. Those human trials ask a different question from deleting CD38 in mice.
GHK-Cu has small topical studies described in the skin reviews. The controlled GHK-containing hair trial used another active ingredient. KPV's bowel findings remain in cells and animals.
I trust a preparation's description to explain more than a broad category such as “repair peptides.” Even a credible mechanism leaves the amount of useful human change to be measured.
When the preparation changes
KPV in a targeted particle and hydrogel system and KPV co-assembled with an immunosuppressant introduce different variables from the unprotected fragment. The preparation determines what exposure was tested and which ingredients could have contributed.
GHK and GHK-Cu differ in copper binding. Skin creams, removed-skin experiments and systemic administration face different delivery and safety questions. The topical formulation review makes that dependence unusually visible.
Likewise, oral NR and NMN trials supply evidence about their respective precursors, while direct NAD+ has a separate delivery question. Retatrutide's clinical-trial drug has specified controls that the name on another preparation cannot establish.
An unglamorous repetition with a fully described preparation would improve my confidence far more than a new umbrella claim. The separate pages follow KPV delivery, copper and skin, NAD+ consumption and retatrutide receptor activity in detail.