GH Axis & Secretagogues.
The largest bench here: CJC-1295 with and without DAC, GHRP-2 and GHRP-6, ipamorelin, sermorelin, tesamorelin, IGF-1 LR3, PEG MGF, gonadorelin, somatropin and HCG. It is also the most easily confused corner of the market, so every page names the exact molecule — DAC or no DAC included — rather than a family name.
Worth reading first
PerformanceGHRP-2 and GHRP-6: the two hexapeptides, and what the human studies actually measured
Both are synthetic hexapeptides that release growth hormone, and the two papers here separate them sharply. In normal men, intravenous GHRP-6 raised GH, ACTH and cortisol and increased stage 2 sleep without changing slow-wave sleep. In hypercortisolism, GHRP-6 and GHRH respond differently: endogenous hypercortisolism blunted both pathways, exogenous hypercortisolism blunted GHRH but left the GHRP-6 pathway apparently preserved. Neither paper measures lean mass, strength or any outcome beyond hormones and sleep EEG.
PerformanceSomatropin: the randomised GH-replacement endpoints, read carefully
The best randomised body-composition dataset in growth hormone is the REAL 1 trial, and it is easy to misread: it tested somapacitan, a once-weekly albumin-binding derivative, against placebo and against daily GH — not somatropin against placebo. The primary endpoint was truncal fat percentage, reduced by 1.53 percentage points against placebo at 34 weeks. The one-step-upstream GH-axis trial, GHRH in 31 men with HIV lipodystrophy, moved lean mass by 0.9 kg.
PerformanceMGF and PEG-MGF: the satellite-cell mechanism, and the absence of a human trial
MGF is the exercise-inducible splice variant of the IGF-I gene, and the C-terminal peptide it produces is a different molecule from systemic IGF-I. The mechanism is well described: it activates muscle satellite cells, its expression declines in ageing and fails in dystrophic muscle. The record cited here contains no human administration of PEG-MGF, and this page does not imply one.