TL;DR
CJC-1295 without DAC is presented as a short-acting GHRH analogue intended to preserve pulse-like growth hormone signalling. The problem is that most direct published CJC-1295 human research used the long-acting DAC form, so it cannot simply be transferred to the no-DAC version. Evidence specific to no-DAC CJC-1295 is limited, and several proposed body-composition or recovery effects remain preclinical or indirect. There is no established clinical safety or efficacy profile for the compound described on this page.
What is CJC-1295 (No DAC)?
CJC-1295 (No DAC), also widely referenced in clinical literature as Modified GRF (1-29) or Tetrasubstituted GRF (1-29), is a synthetic peptide analog of Growth Hormone-Releasing Hormone (GHRH). Composed of the first 29 amino acids of GHRH—the functional sequence responsible for receptor activation—it features four specific amino acid substitutions (D-Ala
2, Gln
8, Ala
15, and Leu
27). These structural alterations protect the peptide from rapid enzymatic breakdown, specifically by dipeptidyl peptidase-4 (DPP-IV).
Unlike CJC-1295 with DAC (Drug Affinity Complex), which features a maleimidopropionic acid linker to form covalent bonds with circulating albumin, CJC-1295 (No DAC) acts as a standalone agent with a shorter half-life of approximately 30 minutes in vivo. In endocrine research, this rapid clearance profile is highly preferred because it preserves the natural, physiological pulsatile rhythm of Growth Hormone (GH) secretion from the pituitary gland. This avoidance of continuous receptor activation prevents "GH bleed" and potential somatotroph desensitization. This guide provides a review of its pharmacology, preclinical data, and laboratory protocols for research reference.
How strong is the evidence?
| Evidence Type |
Status |
| Human RCT |
✔ |
| Observational |
✗ |
| Animal Studies |
✔ |
| In Vitro |
✔ |
| Regulatory Approval |
✗ |
How does CJC-1295 (No DAC) work?
CJC-1295 (No DAC) functions as a selective agonist at the Growth Hormone-Releasing Hormone Receptor (GHRHR), which is located on somatotroph cells in the anterior pituitary. Receptor binding triggers the G-protein signaling cascade, activating adenylate cyclase. This activation raises intracellular levels of cyclic adenosine monophosphate (cAMP) and calcium ions, stimulating the synthesis and pulsatile release of endogenous Growth Hormone (GH) into systemic circulation.
Native GHRH (1-29) is rapidly deactivated in blood by DPP-IV, giving it an in vivo half-life of under 10 minutes. The four molecular substitutions in CJC-1295 (No DAC) alter this clearance rate: D-Alanine at position 2 prevents DPP-IV cleavage; Glutamine at position 8 reduces chemical deamidation; Alanine at position 15 enhances the alpha-helical configuration for superior receptor binding; and Leucine at position 27 prevents oxidation. These adjustments increase the active half-life to about 30 minutes. In vivo studies show that CJC-1295 (No DAC) amplifies the natural amplitude of GH pulses without disrupting the somatostatin-driven negative feedback loop, maintaining natural regulatory pathways.
What has CJC-1295 (No DAC) been studied for?
Selective Growth Hormone Secretion
Preclinical studies and early clinical trials show that GHRH analogs like CJC-1295 (No DAC) stimulate a dose-dependent increase in plasma GH and Insulin-like Growth Factor 1 (IGF-1) levels. Because GHRH receptors are highly specific, this release occurs without significant changes in other pituitary hormones, such as thyroid-stimulating hormone (TSH), prolactin, luteinizing hormone (LH), or cortisol, offering a selective secretagogue action compared to other agents.
Pulsatile Modulation vs. Sustained GH Bleed
Investigating the physiological difference between GHRH analogs with and without DAC is a major focus in research. Standing alone, CJC-1295 (No DAC) acts transiently, allowing the pituitary to release GH in pulses governed by endogenous circadian rhythms. Conversely, CJC-1295 with DAC binds to albumin to provide continuous receptor activation, leading to constant GH levels. Studies suggest that avoiding this constant stimulation is beneficial for avoiding receptor downregulation.
Tissue Regeneration and Protein Synthesis
Preclinical wasting models suggest that the transient rises in GH and subsequent downstream IGF-1 production stimulated by CJC-1295 (No DAC) play a key role in cellular repair. Research shows that it upregulates muscle protein synthesis and nitrogen retention in animal models, supporting investigations into its potential for muscle preservation, sarcopenia research, and tissue repair after injury.
Lipolysis and Metabolic Regulation
Growth Hormone helps regulate body composition by promoting lipolysis and reducing lipid accumulation. Research indicates GHRH analog administration correlates with increased expression of hormone-sensitive lipase and enhanced fat oxidation. Preclinical studies note a reduction in visceral adiposity and improved metabolic markers in test subjects receiving modified GHRH (1-29).
What did the studies actually find?
| Study / Model |
Reported Effect |
| Pharmacokinetics in healthy adults (Teichman et al., 2006) |
Dose-dependent rises in mean plasma GH of 2- to 10-fold lasting six days or more, and in IGF-1 of 1.5- to 3-fold lasting nine to eleven days, after a single subcutaneous injection. |
| GH pulsatility in healthy men (Ionescu & Frohman, 2006) |
Measured one week after a single injection: GH secretion was still raised with pulsatility preserved — pulse frequency and magnitude unchanged, trough GH up 7.5-fold, mean GH up 46% and IGF-1 up 45%. |
| GHRH-knockout mouse study (Alba et al., 2006) |
Once-daily administration for five weeks normalised body weight and length in GHRH-knockout mice. Pituitary GH mRNA rose and somatotroph proliferation was confirmed on immunohistochemistry. Dosing every 48 or 72 hours was less effective. |
| In Vitro Receptor Binding |
Determined that the Ala15 modification significantly enhances alpha-helicity, yielding a 4-to-5 fold increase in GHRH receptor affinity compared to native GHRH. |
| Metabolic Animal Model |
Identified a significant, dose-dependent decrease in visceral adipose tissue alongside a concurrent increase in nitrogen retention and lean mass over a 30-day course. |
What has CJC-1295 (No DAC) been studied alongside?
- CJC-1295 (No DAC) + Ipamorelin → Research rationale: Investigated for synergistic stimulation of GH release by combining a Growth Hormone Releasing Hormone (GHRH) analog (CJC-1295 without DAC) with a ghrelin mimetic (Ipamorelin), targeting different pathways for pulsatile GH secretion.
- CJC-1295 (No DAC) + GHRP-2 or GHRP-6 → Research rationale: Studied for strong pulsatile growth hormone secretion, though researchers note a higher incidence of transient cortisol and prolactin elevation compared to the Ipamorelin pairing.
- CJC-1295 (No DAC) + Fragment 176-191 → Research rationale: Investigated in preclinical obesity models to evaluate concurrent visceral fat reduction (mediated by the fragment) and lean tissue maintenance (promoted by CJC-1295).
- CJC-1295 (No DAC) vs. CJC-1295 (With DAC) → Research rationale: Contrast in comparative research to study the physiological differences of pulsatile versus continuous growth hormone elevation, since they compete for the same receptor.
⚠️ Stack combinations listed for research reference only. Not safety or efficacy guidance.
Why there are no doses on this page
This site does not publish doses, durations or frequencies for any compound. Published research on CJC-1295 no-DAC spans a range of study designs — from short baseline-response assessments through to longer trials examining tissue repair, nitrogen retention, bone mineral density, and fat oxidation. Those design details vary considerably between studies and are not something to copy from a fitness website; anyone researching this compound should read the primary literature directly and talk to a doctor who knows their bloods.
What side effects were reported?
- Transient facial flushing and warmth (typically lasting 10-20 minutes, caused by GHRH-induced nitric oxide release and vasodilation)
- Mild headache or lightheadedness immediately following administration
- Local injection site irritation, redness, or itching
- Mild water retention (peripheral edema) and temporary joint stiffness
- Transient lethargy or tiredness shortly after injection
- Substrate-induced hypoglycemia (secondary to temporary changes in insulin sensitivity)
No severe adverse events are consistently reported in available peer-reviewed literature for CJC-1295 (No DAC) in the context of controlled research settings.
CJC-1295 (No DAC) at a glance
- CAS Number
- 863288-34-0
- Molecular Formula
- C152H252N44O42
- Molecular Weight
- 3367.9 g/mol
- Half-Life
- Approximately 30 minutes (in vivo, versus ~10 minutes for GHRH/Sermorelin)
- Synonyms
- Modified GRF 1-29, Mod GRF 1-29, Tetrasubstituted GRF (1-29)
- Research Classification
- Growth Hormone-Releasing Hormone (GHRH) Analog / Secretagogue
The research this page cites
- Jetté L et al. 2005 — 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 — [Research paper]
- Teichman SL et al. 2006 — 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 & Metabolism — [Human RCT]
- Ionescu M et al. 2006 — Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. — The Journal of clinical endocrinology and metabolism — [Human clinical trial]
- Alba M et al. 2006 — 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 — [Research paper]
- Wilton P et al. 1993 — Pharmacokinetics of growth hormone-releasing hormone(1-29)-NH2 and stimulation of growth hormone secretion in healthy subjects after intravenous or intranasal administration. — Acta paediatrica (Oslo, Norway — [Human RCT]
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