I saw this recently on X, has anyone tried these for sleep?
What Gemini Pro has to say:
The scientific evidence supporting the use of CJC-1295 and Ipamorelin for sleep improvement is primarily mechanistic and extrapolated from studies on their endogenous counterparts (Growth Hormone-Releasing Hormone and Ghrelin) or related secretagogues (like MK-677).
While clinical wellness protocols frequently prescribe this stack to enhance sleep quality—specifically Slow-Wave Sleep (SWS) and REM—direct Randomized Controlled Trials (RCTs) quantifying sleep architecture changes specifically for this combination in healthy adults are largely absent from the peer-reviewed literature.
The following analysis details the evidence for each compound based on its pharmacological class.
1. CJC-1295 (GHRH Analog)
Mechanism: GHRH Agonism Slow-Wave Sleep (SWS) Promotion
CJC-1295 is a long-acting analog of Growth Hormone-Releasing Hormone (GHRH). The strongest evidence for sleep improvement lies in the well-established neurobiology of endogenous GHRH, which acts as a sleep-promoting substance.
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GHRH and Slow-Wave Sleep: Extensive research demonstrates a causal link between GHRH and the regulation of Non-Rapid Eye Movement (NREM) sleep.
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Intravenous administration of GHRH in humans has been shown to robustly increase Slow-Wave Sleep (Stages 3 and 4), particularly when administered in the latter part of the night [1].
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Conversely, the administration of GHRH antagonists (which block GHRH receptors) significantly suppresses SWS and growth hormone secretion, suggesting GHRH is essential for normal sleep depth [2].
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Clinical Extrapolation: While CJC-1295 extends the half-life of GHRH via Drug Affinity Complex (DAC) or modified pharmacokinetics, it activates the same receptors. Therefore, the claim that CJC-1295 improves deep sleep is scientifically plausible based on the GHRH-SWS axis, even in the absence of a CJC-1295 specific polysomnography trial.
2. Ipamorelin (Selective GH Secretagogue)
Mechanism: Ghrelin Receptor (GHS-R1a) Agonism Potential REM/SWS Modulation
Ipamorelin is a selective agonist of the ghrelin receptor. The evidence for its impact on sleep is more complex and derived largely from data on Ghrelin and other secretagogues like MK-677 (Ibutamoren).
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Ghrelin and Sleep Architecture: Ghrelin is an endogenous sleep-promoting factor. Studies indicate that ghrelin administration in humans can increase SWS and enhance delta-wave activity [3].
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The “Class Effect” Evidence:
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MK-677 (Ibutamoren): A non-peptide ghrelin mimetic (functionally similar to Ipamorelin but orally active and longer-lasting) has demonstrated clear clinical efficacy in sleep. A double-blind, placebo-controlled trial found that MK-677 treatment increased REM sleep by and Stage IV sleep (deep sleep) by in young adults () [4].
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GHRP-2: Conversely, other peptides in this class (e.g., GHRP-2) have shown no significant effect on sleep architecture in some trials, despite raising GH levels [5].
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Ipamorelin Specifics: Ipamorelin is distinct because of its high selectivity for the GH release pathway with minimal impact on cortisol or ACTH (unlike GHRP-2 or GHRP-6). While this makes it “cleaner” for metabolic use, there is a knowledge gap regarding its specific independent effect on sleep stages compared to the broader, “dirtier” secretagogues like MK-677 which have stronger clinical sleep data.
3. The Synergistic “Stack” and Clinical Reality
In longevity and performance medicine, these two peptides are stacked to mimic physiological pulsatility: CJC-1295 provides the basal GHRH “tone” (supporting SWS), while Ipamorelin provides the pulse (supporting GH release).
| Compound |
Primary Sleep Target (Theoretical) |
Strength of Mechanistic Evidence |
Direct Clinical Trial Data |
| CJC-1295 |
Slow-Wave Sleep (Deep) |
High (via GHRH studies) |
Low (Extrapolated) |
| Ipamorelin |
REM & SWS |
Moderate (via Ghrelin studies) |
Very Low (Inferred from MK-677) |
Scholarly Debate & Nuance:
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Somatotropic Axis Directionality: There is an ongoing debate regarding directionality. While GHRH promotes sleep, excessive Growth Hormone (e.g., in acromegaly or high-dose exogenous administration) can actually disrupt sleep and exacerbate sleep apnea [6]. The goal of peptide therapy is restoration to youthful physiological levels, not supraphysiological excess.
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Cortisol Impact: One advantage of Ipamorelin over other GHRPs is the lack of cortisol stimulation. Since elevated cortisol is antagonistic to sleep (increasing wakefulness), Ipamorelin’s selectivity theoretically makes it a superior choice for bedtime administration compared to GHRP-6 or Hexarelin.
Summary of Findings
There is strong mechanistic evidence that the GHRH pathway (targeted by CJC-1295) regulates Deep Sleep (SWS), and moderate clinical evidence from related compounds (MK-677) that the ghrelin pathway (targeted by Ipamorelin) can improve REM and sleep quality. However, specific peer-reviewed RCTs validating the sleep architecture effects of the CJC-1295 + Ipamorelin stack remain a data gap. Current clinical confidence is based on the verified pharmacodynamics of their receptor targets rather than direct outcome studies.
References
[1] Evidence against a role for the growth hormone-releasing peptide axis in human slow-wave sleep regulation (Comparison of GHRH vs GHRP effects)
[2] Blockade of endogenous growth hormone-releasing hormone receptors dissociates nocturnal growth hormone secretion and slow-wave sleep
[3] Ghrelin promotes slow-wave sleep in humans
[4] Prolonged oral treatment with MK-677, a novel growth hormone secretagogue, improves sleep quality in man
[5] Ipamorelin, the first selective growth hormone secretagogue (Selectivity profile)
[6] Complex relationship between growth hormone and sleep in children: insights, discrepancies, and implications