GH AXIS & LONGEVITY / FAQ
Questions From the Literature
Direct, citation-anchored answers to the questions readers most often bring to these four research compounds.
What is ipamorelin?
Ipamorelin is a synthetic pentapeptide (5 amino acids) designed as a selective agonist of the ghrelin / growth hormone secretagogue receptor, GHS-R1a. Activating that receptor on pituitary cells triggers a pulse of growth hormone release. Its defining characteristic is selectivity: unlike earlier GH-releasing peptides, it does not meaningfully raise ACTH, cortisol, or prolactin at doses that produce robust GH stimulation [1][4]. It has never been approved as a drug anywhere and is classified as a research chemical.
What does ipamorelin do for you?
In preclinical studies, ipamorelin raises growth hormone and was studied for postoperative ileus and bone growth in rats [5]. The only published human efficacy trial — a Phase 2 RCT in 114 surgical patients — did not demonstrate a statistically significant clinical benefit for its target endpoint [3]. Research-use community reports describe sleep improvement and faster recovery as commonly perceived effects, but these are anecdotal, unverified, and not from controlled human trials. This site cannot report what ipamorelin 'does for you' beyond what the cited literature shows.
What is ipamorelin peptide?
Ipamorelin is a synthetic peptide with the sequence Aib-His-D-2-Nal-D-Phe-Lys-NH2. The non-standard amino acids at positions 1 (alpha-aminoisobutyric acid), 3 (D-2-naphthylalanine), and 4 (D-phenylalanine) confer protease resistance and receptor selectivity. It is not a natural peptide extracted from the body; it was synthesized in the laboratory. It is classified and sold as a research chemical [4].
What are the risks of ipamorelin?
The published risk profile is defined more by gaps than by documented harms. Long-term human safety data do not exist — the only human data are a 7-day perioperative IV trial [3] and an acute IV PK study [4]. At the receptor-class level, a 28-day study of a related GHS-R1a agonist found myocardial degeneration in rats [2]. Mechanistic concerns include GH-driven IGF-1 elevation (tumor promotion risk), direct pancreatic beta-cell action in subjects with insulin dysregulation, and fluid retention via the GH axis. Research-grade material from unregulated suppliers carries unverified purity. Ipamorelin is banned in sport under WADA S2.
What is CJC-1295?
CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH), built on the first 29 residues of human GHRH with four amino-acid substitutions that resist enzymatic breakdown. The DAC (Drug Affinity Complex) variant adds an albumin-binding chemical arm that extends the plasma half-life to approximately 5.8 to 8.1 days; the no-DAC form (Modified GRF 1-29) lacks this arm and is short-acting. It is a research chemical, never approved by any regulatory body [9].
What does CJC-1295 do?
CJC-1295 binds the GHRH receptor on pituitary cells and drives sustained GH and IGF-1 elevation. In healthy adults, single subcutaneous doses of 30-60 µg/kg raised mean plasma GH 2- to 10-fold for 6 or more days and IGF-1 by 1.5- to 3-fold for 9-11 days, while preserving the pulsatile pattern of GH secretion [9][10]. What it does in terms of clinical health outcomes in healthy people over the long term is not established — there are no large, controlled human outcome trials.
Is CJC-1295 safe?
The short-term PK studies in healthy adults did not report serious adverse events [9][10], but those studies were not designed or powered to evaluate safety. The development program was discontinued before Phase 3. The FDA's 2024 Pharmacy Compounding Advisory Committee cited immunogenicity and other safety concerns [6]. Sustained IGF-1 elevation carries a mechanism-based theoretical cancer risk. The compound is not approved, and its long-term safety in humans is genuinely unknown. Caution is warranted.
How much CJC-1295 should I take?
This site does not provide dosing recommendations for any compound. Doses reported in the human PK studies (30-90 µg/kg subcutaneously in research participants) are described as they appeared in those studies — not as recommendations for self-administration [9][10]. CJC-1295 is a research chemical with no approved dose, no approved indication, and no established safety profile for self-directed research use. Nothing on this page constitutes medical advice.
What is NAD supplement used for?
NAD+ and its precursors NMN and nicotinamide riboside are studied as strategies to maintain cellular energy metabolism and the activity of sirtuin and PARP enzymes that consume NAD+ during DNA repair and stress response — functions that decline with age as NAD+ tissue levels fall [14][16]. In human trials, NMN raised blood NAD+, improved walking distance and quality-of-life scores [12], and in a separate study improved muscle insulin sensitivity in prediabetic women [13]. These are research findings in defined populations, not therapeutic claims.
What is the downside of taking NAD+?
Several honest caveats apply. Oral NAD+ capsules may be largely ineffective because NAD+ is poorly absorbed intact — the precursors NMN and nicotinamide riboside are the pharmacologically rational oral approach. IV NAD+ wellness infusions can cause chest tightness, abdominal cramping, flushing, and nausea if infused too rapidly, and compounded injectable NAD+ has been subject to a Class I FDA recall for bacterial endotoxin contamination. A theoretical concern exists that NAD+ supplementation could fuel existing tumors (NAD+ supports proliferating cells). The regulatory status of NMN as a dietary supplement is contested by the FDA [11].
Is it safe to take NAD daily?
Clinical trial evidence supports short-to-medium-term tolerability of NMN and nicotinamide riboside at studied doses. In the NR dose-escalation trial, 8 weeks of 100-1000 mg/day was well-tolerated with no significant adverse event differences from placebo at any dose [15]. In the multicenter NMN RCT, 60 days at up to 900 mg/day was safe with no reported safety issues [12]. Long-term (years) safety data are not available for either precursor. As with any supplement regimen, consultation with a clinician is appropriate for people with medical conditions or taking other medications.
Does NAD cause weight gain?
Neither NAD+ precursor supplementation studies reviewed on this desk nor the foundational mechanistic literature associates NAD+ supplementation with weight gain. In the NMN muscle insulin sensitivity trial, no significant change in body composition was observed [13]. In the NR dose-escalation trial, LDL cholesterol and 1-carbon metabolism were unaffected [15]. NAD+ pathway activation through sirtuins and AMPK is associated in preclinical models with improved metabolic function — the opposite of a mechanism that would predict weight gain [14]. This is an absence of evidence, not a positive safety finding.
What does the MOTS-c peptide do?
In preclinical research, exogenous MOTS-c activates AMPK via folate-cycle inhibition, modulates glucose uptake in skeletal muscle, and under metabolic stress travels from the mitochondrion to the nucleus to regulate antioxidant gene expression via NRF2 [22]. In aged mice, MOTS-c improved treadmill performance, grip strength, and gait [21]. A 2024 study identified casein kinase 2 as a direct molecular binding target [18]. In humans, circulating MOTS-c (endogenous) correlated with cardiovascular and mortality outcomes in a hemodialysis cohort [19] — an observational finding, not an interventional one. No controlled human trials of exogenous MOTS-c exist.
What are the negative side effects of MOTS-c?
Because no controlled human trials of exogenous MOTS-c have been published, there is no human safety dataset to report from [20]. The compound is classified as a research chemical of unverified purity from commercial suppliers. Known risk factors specific to MOTS-c biology include genotype interactions: a mitochondrial DNA variant (m.1382A>C) is associated with a pro-diabetogenic effect, and exercise-induced MOTS-c responses differ by ancestry — effects are not uniform across all people [20]. Rodent doses studied (0.5-15 mg/kg/day) cannot be extrapolated to humans without bridging safety data that do not exist.
Is MOTS-c legal to buy?
In most jurisdictions, MOTS-c can be purchased from research chemical suppliers for laboratory research purposes. It is not an approved drug or regulated medicine, so possession for personal research is generally not prohibited by statute in many countries — but regulatory frameworks vary. In sport, the picture is unambiguous: MOTS-c is prohibited at all times by WADA and anti-doping bodies such as USADA under peptide hormone and metabolic modulator categories. Athletes subject to testing face sanctions for use regardless of the source [20].
How often do you inject MOTS-c?
This site does not provide dosing or injection-frequency guidance for any compound. Dosing regimens reported in published mouse studies — for example, subcutaneous injections in aged mice — are described as they appeared in those studies and are not translatable to humans without validated pharmacokinetic and dose-finding data that do not exist [21]. Any dosing discussion for MOTS-c in humans rests on extrapolation from animal data, not on characterized human evidence. This is not medical advice.