CJC-1295

What it is

CJC-1295 is a synthetic 29-amino acid peptide designed to mimic and extend the activity of endogenous growth hormone-releasing hormone (GHRH), the hypothalamic signal that instructs the pituitary to release growth hormone. Native GHRH has a half-life of only a few minutes because it is rapidly cleaved by the enzyme dipeptidyl peptidase IV (DPP-IV). CJC-1295 was engineered with a drug affinity complex (DAC) modification that allows it to bind reversibly to serum albumin, the most abundant protein in blood, extending its effective half-life to approximately 6 to 8 days in humans. [1]

The compound is sometimes called CJC-1295 with DAC to distinguish it from modified GRF(1-29), a related GHRH analog with a similar amino acid sequence but no albumin-binding modification and a much shorter half-life. The two are sold under similar names and are frequently confused in non-scientific sources. CJC-1295 is not approved by the FDA for any indication and is sold outside approved pharmaceutical channels as a research compound.

What researchers study it for

• Sustained GH and IGF-1 elevation The landmark human trial by Teichman et al. enrolled healthy adults aged 21 to 61 and found that a single subcutaneous injection of CJC-1295 produced dose-dependent increases in serum GH lasting 6 days and IGF-1 elevations lasting 9 to 11 days, with cumulative effects observed after multiple doses. [2] A follow-up analysis of serum protein profiles in healthy subjects confirmed activation of the GH/IGF-1 axis with measurable downstream biomarker changes. [5]
• GH pulsatility and sleep architecture One concern with continuous GHRH stimulation is that it might suppress the natural pulsatile pattern of GH release that occurs predominantly during slow-wave sleep. A human clinical study by Ionescu and Frohman found that CJC-1295 increased trough and mean GH secretion while preserving the physiological pulsatile pattern, suggesting the pituitary retains its normal signaling rhythm even under sustained GHRH stimulation. [4]
• Body composition and growth normalization In GHRH knockout mice, once-daily administration of CJC-1295 normalized body weight and linear growth, reversing the dwarfism phenotype characteristic of severe GH deficiency in that model. [3] Researchers have studied whether analogous effects on lean mass and adipose tissue apply in GH-deficient human populations, though robust clinical trials in that population have not been published.
• Age-related GH decline GH and IGF-1 secretion decline progressively with age, a process sometimes called somatopause. Because CJC-1295 stimulates the pituitary through the endogenous GHRH pathway rather than introducing exogenous GH directly, researchers have explored whether it might offer a more physiological approach to studying the effects of partial GH axis restoration in aging models. [2]
• Metabolic signaling downstream of IGF-1 IGF-1 plays a broad role in glucose metabolism, protein synthesis, and lipid handling. The serum protein profiling study found that CJC-1295-induced IGF-1 elevation was accompanied by changes in multiple circulating proteins, including those involved in metabolic and inflammatory signaling pathways, though the clinical significance of these changes in healthy adults remains unclear. [5]

Research context

The human evidence base for CJC-1295 is narrow but substantive for its primary endpoint: GH and IGF-1 elevation. The Teichman et al. 2006 JCEM trial remains the primary human RCT, enrolling 65 participants across multiple dose cohorts and establishing the pharmacokinetic profile that defines the compound. [2] The Ionescu and Frohman 2006 study provides the key finding that GH pulsatility is preserved, which distinguishes CJC-1295 from continuous GH infusion protocols in terms of physiological signaling. [4]

Neither study was powered to evaluate clinical outcomes like body composition, bone density, or metabolic markers over time. The animal research in GHRH knockout mice provides mechanistic grounding for what prolonged GHRH agonism can achieve in a deficient state, but those models do not translate directly to healthy or normally aging humans. [3] There are no published RCTs examining CJC-1295 in people with GH deficiency, in postmenopausal populations, or in studies longer than a few weeks. Researchers interested in GH axis modulation should treat the existing literature as early-stage pharmacokinetic evidence rather than a confirmed efficacy profile.

Typical research parameters

References

1. [1] Jetté L, Léger R, Thibaudeau K, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052–8. PubMed ↗
2. [2] Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. Journal of Clinical Endocrinology and Metabolism. 2006;91. PubMed ↗
3. [3] Alba M, Fintini D, Salvatori R, et al. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. American Journal of Physiology: Endocrinology and Metabolism. 2006;291(6):E1290–4. PubMed ↗
4. [4] Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. Journal of Clinical Endocrinology and Metabolism. 2006;91. PubMed ↗
5. [5] Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Hormone and IGF Research. 2009;19(6):471–7. PubMed ↗

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