The elderly cohort
The Epithalamin follow-up in older people
This is the human survival paper I want to get right, down to the names of the preparations.
The observational follow-up
The 6-8 year follow-up of 266 elderly people examined Epithalamin, alone and combined with thymalin. Reduced mortality was associated with treatment compared with untreated controls. The study was observational, without randomization or a placebo control.
Epithalamin alone was associated with a 1.6-1.8-fold decrease in mortality. A combined thymalin-plus-Epithalamin group was associated with a 4.1-fold decrease. Figures of that size have obvious appeal. The causal interpretation still needs support beyond the observed association.
Without random assignment, the question of how treated and untreated people came to differ remains consequential. This is an inference about the study design, rather than a claim that a particular hidden difference explains the result. The association deserves investigation with a design better able to distinguish treatment effects from other differences between groups.

Epithalamin in the human paper
The mortality paper names Epithalamin. The review of Epitalon describes the AEDG tetrapeptide, while the mouse lifespan experiment specifically names Epitalon. My objection to merging their survival claims is straightforward: the preparation named in a study has to stay attached to its result.
I value this follow-up even with those limitations. Observing people over time is a meaningful undertaking, and the reported association is substantial. But a study of a named preparation does not silently become a trial of a differently named peptide, or establish what that peptide would do for a particular person.
The combined group introduces a further attribution problem. Its mortality finding concerns thymalin plus Epithalamin. Assigning the whole association to either component would go beyond what that comparison can establish.
The pineal-cell connection
A more contained experiment added Epithalon to rat pinealocyte cultures, cells from the pineal gland. It stimulated AANAT and pCREB synthesis and increased melatonin in the culture medium. Combined with norepinephrine, it potentiated expression of AANAT and pCREB.
I appreciate having an exact cellular output to discuss: a preparation, a cellular setting and a melatonin measurement. It gives the pineal research a mechanism to investigate. Connecting it to human survival would require further evidence; the culture result itself measured melatonin-related changes in rat cells.
A direct Epitalon survival trial with an appropriate comparison group would address a different question from either this culture experiment or the Epithalamin observational cohort. That comparison merits the same care devoted to harms as to any extension of life.