CJC-1295 no DAC 10mg

What is CJC-1295 no DAC?

CJC-1295 no DAC, also known as Modified GRF (1-29) or Mod GRF 1-29, is a synthetic analog of growth hormone-releasing hormone (GHRH) consisting of 29 amino acids with an approximate molecular weight of 3,367 Daltons. It is derived from the first 29 amino acids of endogenous GHRH(1-44), which represents the minimally active fragment required for full receptor activation. What distinguishes CJC-1295 no DAC from native GHRH(1-29) — also known as Sermorelin — are four strategic amino acid substitutions designed to enhance metabolic stability and resistance to enzymatic degradation by dipeptidyl peptidase-IV (DPP-IV).

The key modifications include the substitution of alanine at position 2 with D-alanine, glutamine at position 8 with alanine, asparagine at position 15 with alanine, and methionine at position 27 with norleucine. These changes confer significantly improved resistance to DPP-IV cleavage, extending the functional half-life from approximately 5–7 minutes (native GHRH) to roughly 30 minutes. Unlike CJC-1295 with DAC, this version lacks the Drug Affinity Complex (DAC) — a maleimidopropionic acid moiety that enables covalent binding to serum albumin. The absence of DAC means CJC-1295 no DAC produces shorter, more physiological pulses of growth hormone (GH) release rather than sustained elevation, which is a critical distinction for researchers studying pulsatile GH dynamics (Jetté et al., 2005).

Mechanism of Action

CJC-1295 no DAC exerts its biological effects by binding to the growth hormone-releasing hormone receptor (GHRH-R), a class B G protein-coupled receptor (GPCR) expressed predominantly on somatotroph cells of the anterior pituitary gland. Upon binding, the peptide activates the Gsα subunit of the heterotrimeric G protein complex, which in turn stimulates adenylyl cyclase to increase intracellular cyclic adenosine monophosphate (cAMP) levels. This cAMP accumulation activates protein kinase A (PKA), triggering a phosphorylation cascade that culminates in the opening of voltage-gated calcium channels, calcium influx, and the exocytotic release of GH from secretory granules (Mayo et al., 2000).

Beyond acute GH secretion, GHRH-R activation through the cAMP/PKA pathway also promotes the phosphorylation of cAMP response element-binding protein (CREB), a transcription factor that drives GH gene expression and somatotroph cell proliferation. Research in GHRH knockout mouse models has demonstrated that administration of GHRH analogs increases pituitary GH mRNA content and somatotroph cell numbers, confirming a trophic role beyond simple secretagogue activity (Alba et al., 2006).

A key pharmacodynamic feature of CJC-1295 no DAC is its ability to stimulate pulsatile GH release that closely mimics the body's natural secretory pattern. Unlike the DAC version, which produces sustained GH elevation through continuous GHRH-R stimulation, Modified GRF 1-29 without DAC creates discrete pulses that preserve the normal oscillatory dynamics of GH secretion. Research has shown that even with continuous GHRH-R stimulation, pulse frequency and amplitude can be maintained, as somatostatin-mediated negative feedback continues to function, modulating GH release into distinct secretory episodes (Ionescu & Frohman, 2006).

The downstream effects of increased GH secretion include hepatic production of insulin-like growth factor 1 (IGF-1), which mediates many of GH's anabolic and metabolic effects. Studies have documented that GHRH analog administration results in sustained IGF-1 elevation, with increases of 1.5- to 3-fold above baseline persisting for days after a single dose of long-acting analogs (Teichman et al., 2006). The GH/IGF-1 axis activation also influences protein synthesis, lipolysis, glucose metabolism, and tissue repair pathways throughout the body.

Research Applications

Growth Hormone Deficiency Models

One of the most extensively studied applications of GHRH analogs is in growth hormone deficiency (GHD) research. In GHRH knockout (GHRHKO) mouse models — which exhibit severe GH deficiency, dwarfism, and reduced IGF-1 — daily administration of CJC-1295 normalized body weight, body length, and bone development. This effect was accompanied by increased pituitary GH mRNA and somatotroph proliferation, suggesting that the peptide not only stimulates GH release but also restores pituitary function (Alba et al., 2006). These findings have significant implications for research into isolated GHD and pituitary insufficiency, where GHRH-based approaches offer a more physiological alternative to direct GH replacement.

Age-Related GH Decline and Anti-Aging Research

The progressive decline in GH secretion with aging — termed "somatopause" — is associated with increased adiposity, decreased lean mass, reduced bone density, and impaired immune function. Research has demonstrated that GHRH(1-29) analogs can restore GH and IGF-1 levels in elderly subjects. In a landmark study, long-term administration of [Nle27]GHRH(1-29)-NH2 in age-advanced men and women increased mean 24-hour GH concentrations and IGF-1 levels while improving lean body mass and reducing adipose tissue (Khorram et al., 1997). These results position CJC-1295 no DAC as a valuable research tool for studying anti-aging peptide interventions that target the somatotropic axis.

Body Composition and Metabolic Research

Studies on GHRH analogs consistently report favorable changes in body composition. In GHRHKO mice treated with CJC-1295, relative lean mass was normalized and subcutaneous fat distribution was restored to levels comparable with heterozygous controls (Alba et al., 2006). In clinical research, CJC-1295 administration produced dose-dependent increases in GH — with 2- to 10-fold elevations persisting for 6 or more days — and IGF-1 increases of 1.5- to 3-fold sustained for 9–11 days (Teichman et al., 2006). For researchers studying peptides for weight loss and metabolic regulation, these GH-mediated effects on lipolysis and protein anabolism are of particular interest.

Synergistic GH Release with Secretagogues

A major area of research involves combining GHRH analogs like CJC-1295 no DAC with growth hormone secretagogues (GHS) that act through the ghrelin/GHS receptor (GHS-R1a). Ipamorelin, the first selective GH secretagogue, stimulates GH release without significantly affecting cortisol or prolactin (Raun et al., 1998). When GHRH and GHS-R agonists are co-administered, the result is a synergistic amplification of GH release that exceeds the sum of either agent alone. This synergy occurs because GHRH and GHS act through distinct receptor pathways — cAMP/PKA for GHRH-R and phospholipase C/IP3/protein kinase C for GHS-R — that converge on the somatotroph cell. The CJC-1295 + Ipamorelin Blend is one of the most researched peptide stack combinations in the field.

Serum Protein Biomarker Research

Proteomic studies using two-dimensional gel electrophoresis have identified serum protein changes following GHRH analog administration, including alterations in apolipoprotein A1, transthyretin, and albumin fragment levels. These findings suggest potential biomarkers for GH/IGF-1 axis activation and have implications for both diagnostic development and understanding the broader metabolic effects of GH stimulation (Sackmann-Sala et al., 2009).

Published Research Studies

The following key studies form the foundation of CJC-1295 and Modified GRF 1-29 research:

Jetté et al. (2005) — Published in Endocrinology, this seminal study identified CJC-1295 from a series of maleimido derivatives of hGRF(1-29). The researchers demonstrated that CJC-1295 showed a 4-fold increase in GH area under the curve over a 2-hour period compared to native hGRF(1-29) when administered subcutaneously to Sprague Dawley rats. Western blot analysis confirmed CJC-1295 bioconjugation to serum albumin in vivo, appearing within 15 minutes and persisting beyond 24 hours (PMID: 15817669).

Teichman et al. (2006) — In the Journal of Clinical Endocrinology & Metabolism, this randomized, placebo-controlled, double-blind study in healthy adults (ages 21–61) showed that a single CJC-1295 injection produced dose-dependent GH increases of 2- to 10-fold lasting 6+ days and IGF-1 increases of 1.5- to 3-fold persisting for 9–11 days. Multiple doses demonstrated a cumulative effect, with IGF-1 remaining above baseline for up to 28 days. The estimated half-life was 5.8–8.1 days. No serious adverse events were reported (PMID: 16352683).

Ionescu & Frohman (2006) — Also published in the Journal of Clinical Endocrinology & Metabolism, this study assessed GH pulsatility using 20-minute blood sampling over a 12-hour overnight period in healthy men before and 1 week after CJC-1295 injection. GH pulsatility was preserved, with unaltered pulse frequency and magnitude. However, basal (trough) GH levels increased 7.5-fold, contributing to a 46% overall increase in mean GH levels and a 45% increase in IGF-1 (PMID: 17018654).

Alba et al. (2006) — In the American Journal of Physiology – Endocrinology and Metabolism, the researchers demonstrated that once-daily CJC-1295 (2 μg) administration in GHRH knockout mice completely normalized body weight, body length, femur and tibia length, and lean body mass. The peptide also increased pituitary GH mRNA and stimulated somatotroph proliferation, confirming both secretagogue and trophic activity (PMID: 16822960).

Sackmann-Sala et al. (2009) — Published in Growth Hormone & IGF Research, this proteomic study in 11 healthy young adult men identified five serum protein changes following CJC-1295 injection, including alterations in apolipoprotein A1 and transthyretin isoforms. A linear correlation was found between specific protein fragments and IGF-1 levels, suggesting novel biomarkers for GH/IGF-1 axis activation (PMID: 19386527).

Dosage Protocols in Research

Note: The following information is provided for research purposes only and does not constitute medical advice.

In published animal studies, CJC-1295 has been administered at doses ranging from 2 μg per injection (in mouse models) to weight-based dosing of 30–90 μg/kg in larger animal and translational research models. The Teichman et al. (2006) study utilized ascending single subcutaneous doses in the first trial and multiple weekly or biweekly doses in the second trial, with dosages of 30 and 60 μg/kg showing optimal efficacy-to-safety ratios (Teichman et al., 2006). Ionescu and Frohman (2006) used doses of 60 and 90 μg/kg administered as a single subcutaneous injection (Ionescu & Frohman, 2006).

For Modified GRF 1-29 (CJC-1295 no DAC) specifically, the shorter half-life (~30 minutes) compared to the DAC version (~6–8 days) means it is typically studied using more frequent dosing intervals. In research protocols, it is often administered 1–3 times daily to maximize pulsatile GH release, frequently in combination with GH secretagogues such as Ipamorelin or GHRP-2. For detailed comparisons of GHRH peptide protocols, see our Growth Hormone Releasing Peptides Guide.

Reconstitution: For research use, CJC-1295 no DAC is typically reconstituted with bacteriostatic water (BAC water). Researchers should add the diluent slowly along the inner wall of the vial and gently swirl — never shake — to avoid peptide degradation. Refer to our How to Reconstitute Peptides guide for detailed instructions.

Storage and Handling

Proper storage is critical to maintaining the integrity and bioactivity of CJC-1295 no DAC. In its lyophilized (freeze-dried) form, the peptide should be stored at -20°C for long-term storage or at 2–8°C (refrigerator temperature) for shorter durations. Lyophilized CJC-1295 no DAC is stable for up to 24 months when stored at -20°C in a sealed vial away from light and moisture.

Once reconstituted, the solution should be refrigerated at 2–8°C and used within 3–4 weeks for optimal potency. Avoid repeated freeze-thaw cycles, as these can denature the peptide and reduce its biological activity. Reconstituted peptide solutions should be protected from direct light and stored in the original amber vial or wrapped in foil. All handling should follow sterile technique — use alcohol swabs on the vial stopper before each withdrawal and employ sterile syringes and needles. For comprehensive storage guidance, consult our How to Store Research Peptides guide.

Safety Profile in Research

Published clinical research on GHRH analogs, including the CJC-1295 family, has generally demonstrated a favorable safety profile. In the Teichman et al. (2006) dose-escalation study, no serious adverse reactions were reported across all dosing groups. The most commonly observed side effects in research subjects included mild, transient injection site reactions (redness, swelling, or discomfort), facial flushing, and headache. These effects were typically dose-dependent and resolved without intervention (Teichman et al., 2006).

As a GHRH analog that works through the natural GHRH receptor, CJC-1295 no DAC inherently preserves the body's regulatory feedback mechanisms. Somatostatin continues to modulate GH release, preventing the supraphysiological GH levels that can occur with direct GH administration. Research by Ionescu and Frohman (2006) confirmed that GH pulse frequency and amplitude remained within normal physiological ranges even during continuous GHRH-R stimulation (Ionescu & Frohman, 2006).

Potential considerations noted in the research literature include transient effects on glucose metabolism — since GH promotes insulin resistance — and mild water retention. Long-term safety data specifically for CJC-1295 no DAC remains limited in the peer-reviewed literature, and further research is necessary. For a broader overview of peptide safety in research settings, see our Research Peptide Safety Guide.

Related Peptides

CJC-1295 no DAC belongs to the GHRH analog class of peptides. CJC-1295 with DAC shares the same core sequence but includes the Drug Affinity Complex, extending its half-life to 6–8 days and producing sustained rather than pulsatile GH elevation — for a detailed analysis, see our CJC-1295 DAC vs. No DAC Comparison. Sermorelin is the unmodified GHRH(1-29) fragment with a shorter half-life and lower DPP-IV resistance, compared in our Sermorelin vs. Ipamorelin Comparison.

On the secretagogue side, Ipamorelin is the most selective GHS-R agonist and is frequently paired with CJC-1295 no DAC for synergistic effects. Other GH secretagogues include GHRP-2, GHRP-6, and Hexarelin, each with distinct receptor selectivity and side-effect profiles. Tesamorelin is another related GHRH analog studied in research settings. For oral GHS-R research, MK-677 (Ibutamoren) offers a non-peptide approach to GH axis stimulation.

Frequently Asked Questions

What is CJC-1295 no DAC used for in research?

CJC-1295 no DAC (Modified GRF 1-29) is used in research to study growth hormone-releasing hormone (GHRH) receptor activation, pulsatile GH secretion dynamics, the GH/IGF-1 axis, and its downstream effects on body composition, metabolism, tissue repair, and aging. It is also a key component in combination studies with GH secretagogues like Ipamorelin.

What is the difference between CJC-1295 with DAC and CJC-1295 no DAC?

The primary difference is half-life and release pattern. CJC-1295 with DAC includes a Drug Affinity Complex that binds to albumin, extending the half-life to approximately 6–8 days and producing sustained GH elevation. CJC-1295 no DAC (Mod GRF 1-29) has a half-life of approximately 30 minutes and produces shorter, pulsatile GH release that more closely mimics the body's natural secretory pattern. For a comprehensive analysis, see our CJC-1295 DAC vs. No DAC Comparison.

How does CJC-1295 no DAC differ from Sermorelin?

Both are GHRH(1-29) fragments, but CJC-1295 no DAC contains four amino acid substitutions (positions 2, 8, 15, and 27) that confer resistance to DPP-IV enzymatic degradation. This gives Modified GRF 1-29 a half-life of approximately 30 minutes compared to Sermorelin's 5–7 minutes, making it significantly more potent on a per-dose basis in research settings.

Why is CJC-1295 no DAC often combined with Ipamorelin?

CJC-1295 no DAC (GHRH analog) and Ipamorelin (GHS-R agonist) act through two distinct receptor signaling pathways — cAMP/PKA and PLC/PKC, respectively — on pituitary somatotrophs. Research indicates that co-administration produces a synergistic amplification of GH release that significantly exceeds the sum of either peptide administered alone. Ipamorelin's selectivity for GH release without affecting cortisol or prolactin makes it an ideal research companion.

What is the purity of CJC-1295 no DAC from Iron Peak Peptides?

All CJC-1295 no DAC from Iron Peak Peptides undergoes rigorous third-party testing with high-performance liquid chromatography (HPLC) and mass spectrometry (MS) verification. Each batch ships with a quality assurance documentation documenting purity of ≥99%, amino acid composition, and peptide content.

How should CJC-1295 no DAC be reconstituted?

CJC-1295 no DAC should be reconstituted with bacteriostatic water by slowly adding the diluent along the inner vial wall and gently swirling until fully dissolved. Never shake the vial, as this can denature the peptide. Detailed step-by-step instructions are available in our How to Reconstitute Peptides guide.

Is CJC-1295 no DAC the same as Modified GRF 1-29?

Yes. CJC-1295 no DAC, Modified GRF (1-29), and Mod GRF 1-29 are different names for the same peptide — a tetrasubstituted analog of GHRH(1-29) without the Drug Affinity Complex. The "no DAC" designation specifically differentiates it from CJC-1295 with DAC, which includes the albumin-binding maleimidopropionic acid moiety.

Why Buy CJC-1295 no DAC from Iron Peak Peptides?

Iron Peak Peptides is committed to supplying the highest-quality research peptides available. Every batch of CJC-1295 no DAC 10mg undergoes comprehensive third-party analytical testing, including HPLC purity analysis and mass spectrometry identity confirmation, ensuring ≥99% purity and accurate molecular weight verification. Each order ships with a detailed quality assurance documentation that researchers can review for full quality assurance documentation.

Our CJC-1295 no DAC is manufactured under strict quality control protocols using Good Manufacturing Practice (GMP)-grade raw materials. We provide 10mg vials — among the most generous quantities available — to support extended research protocols and reduce the cost per experiment. With fast shipping, dedicated customer support from a knowledgeable team, and a satisfaction guarantee, Iron Peak Peptides is the trusted source for researchers studying GHRH receptor biology, pulsatile GH release, and GH/IGF-1 axis modulation. Browse our full selection of growth hormone releasing peptides to find the right tools for your research.

References

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):3052-3058. PubMed
2. Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Bhatt R. 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. J Clin Endocrinol Metab. 2006;91(3):799-805. PubMed
3. Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-4797. PubMed
4. Alba M, Fintini D, Sagazio A, et al. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290-E1294. PubMed
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 Horm IGF Res. 2009;19(6):471-477. PubMed
6. Mayo KE, Miller TL, DeAlmeida V, et al. Regulation of the pituitary somatotroph cell by GHRH and its receptor. Recent Prog Horm Res. 2000;55:237-266. PubMed
7. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. PubMed
8. Khorram O, Laughlin GA, Yen SS. Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women. J Clin Endocrinol Metab. 1997;82(5):1472-1479. PubMed
9. Corpas E, Harman SM, Piñeyro MA, Roberson R, Blackman MR. Continuous subcutaneous infusions of growth hormone (GH) releasing hormone 1-44 for 14 days increase GH and insulin-like growth factor-I levels in old men. J Clin Endocrinol Metab. 1993;76(1):134-138. PubMed
10. Alba M, Schally AV, Salvatori R. Partial reversibility of growth hormone (GH) deficiency in the GH-releasing hormone (GHRH) knockout mouse by postnatal treatment with a GHRH analog. Endocrinology. 2005;146(3):1506-1513. PubMed
11. Clemmons DR. Long-acting forms of growth hormone-releasing hormone and growth hormone: effects in normal volunteers and adults with growth hormone deficiency. Horm Res. 2007;68(Suppl 5):178-181. PubMed
12. Mayo KE. Growth hormone-releasing hormone: synthesis and signaling. Recent Prog Horm Res. 1995;50:35-73. PubMed