CJC-1295 (No DAC) + Ipamorelin
Clinical evidence
Human trials confirm this reliably raises growth hormone and IGF-1 for days at a time. What those trials measured is the hormone response; the downstream effect on muscle, strength and recovery is still an open question, and the pairing has been studied as two separate compounds rather than as a combination.
Two randomized, placebo-controlled, double-blind human trials (28 and 49 days) found single/multiple CJC-1295 doses produced dose-dependent GH increases (2–10x) lasting 6+ days and IGF-1 increases (1.5–3x) lasting up to 28 days after repeated dosing. Important caveat: these trials measured hormone levels, so muscle growth, strength and body composition remain untested endpoints; raising GH/IGF-1 is a different claim from a proven strength result. The combined CJC-1295+Ipamorelin stack that is commonly used has been studied as its two separate compounds. The combination's rationale (complementary GH-release pathways) is mechanistic reasoning drawn from those individual trials.
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Ipamorelin
Clinical evidence
Confirmed in human trials to raise growth hormone cleanly and briefly. The trials measured the hormone response; effects on muscle, sleep and recovery remain untested endpoints.
A randomized, double-blind, placebo-controlled human trial confirmed Ipamorelin sharply raises GH (peaking ~40 minutes post-dose, back to low levels by 6 hours) with a cleaner side-effect profile than older secretagogues like GHRP-6, leaving cortisol, prolactin and appetite largely unchanged. Trials to date have measured the hormone response itself, so body composition, sleep quality and recovery remain untested endpoints. It holds no FDA approval for any indication, and existing human data is small-scale and short-term.
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GHRP-6
Clinical evidence
Reliably raises growth hormone in human studies and is used as a diagnostic test for GH deficiency. Its anabolic and anti-aging applications remain unconfirmed after decades of research, and it holds no regulatory approval.
Human studies confirm GHRP-6 reliably stimulates GH release (used alongside GHRH as a validated diagnostic test for adult GH deficiency). Despite reproducible GH-stimulating effects, "the clinical use of GHRP as orally active growth-promoting agents and anabolic anti-aging drugs remains to be confirmed": early enthusiasm for it as a GH-replacement alternative was not borne out in further research. It holds no clinical approval, and the available human safety data is short-term.
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Tesamorelin
Clinical evidence
FDA-approved on strong trial data, specifically for visceral fat in HIV-associated lipodystrophy. That is a real, well-proven effect in a population quite different from general fitness use.
The first FDA-approved GHRH analog, approved specifically for reducing visceral fat in HIV-associated lipodystrophy. Two Phase III trials (816 participants, 543 on drug during the 26-week placebo-controlled period) found 15–17% reductions in visceral abdominal fat by CT scan vs. placebo, with the effect specific to visceral fat rather than subcutaneous fat, limb fat, or overall body weight. Caveat: FDA approval covers HIV-associated lipodystrophy only. General fitness and performance use sits outside what the approval and trials establish.
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IGF-1 LR3
Cell-level research supports the mechanism, and native IGF-1 has real human data in a medical context. Evidence for this specific long-acting analog, as it is actually used, remains preclinical.
Human muscle-cell models show IGF-1 LR3 activates the Akt/mTOR pathway (increasing protein synthesis and myotube hypertrophy), and native IGF-1 studies in HIV-associated muscle wasting show meaningful lean-mass preservation. Human clinical evidence specific to IGF-1 LR3, the long-acting analog sold as a research compound, remains preclinical. Most real-world use in bodybuilding and athletic communities extrapolates from studies of native IGF-1. It holds no FDA approval for human use.
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Follistatin (FST)
The single human trial used gene-therapy delivery in six muscular dystrophy patients, a different route and population from the injectable peptide. Muscle-mass evidence beyond that comes from mouse studies.
A proof-of-principle trial delivered follistatin via gene therapy (AAV1.CMV.FS344 injected directly into the quadriceps) to six Becker muscular dystrophy patients, measuring walking-distance improvement, with no abnormal safety findings across monitored organ systems. Two important caveats: the trial used gene-therapy delivery rather than the injectable peptide sold in this catalog, and it studied six patients with a specific muscular dystrophy rather than general muscle-building in healthy adults. Broader evidence (increased strength and muscle mass) comes from mouse studies.
Sources
This is a summary of published and preclinical research, not medical advice. Every entry describes what a study found, not what you should do. These compounds are supplied for laboratory research only.
