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CJC-1295 No DAC
Research PeptideAlso known as: Modified GRF 1-29 · Mod GRF 1-29 · CJC-1295 without DAC · Tetrasubstituted GRF(1-29)
Animal Only
The evidence for Modified GRF 1-29 (CJC-1295 No DAC) is limited to animal and in vitro studies, and critically, every study commonly cited for "CJC-1295" was conducted on the WITH-DAC variant, a structurally distinct, albumin-binding, ~6–8 day half-life compound. The only animal-model study in this record (Jette et al. 2006, GHRH-knockout mice) demonstrates GH/IGF-1 axis activation by the WITH-DAC compound in an extreme GH-deficiency model not representative of healthy physiology. The no-DAC form's evidence base is mechanistic inference and extrapolation from sermorelin and the WITH-DAC animal literature; no direct efficacy or pharmacokinetic data exists for Mod GRF 1-29 in any published study at this time.
Most "CJC-1295" evidence online is actually for a different compound
Every published study of a compound labeled "CJC-1295", Teichman 2006, Ionescu 2006 pulsatility, Sackmann-Sala 2009 proteomics, the terminated NCT00267527 study, studied the WITH-DAC variant: a 30-amino-acid peptide that covalently binds serum albumin and has a 6–8 day half-life. CJC-1295 No DAC (Modified GRF 1-29) is the 29-residue CORE of that compound WITHOUT the albumin-binding extension; its half-life is ~30 minutes. The evidence base for Mod GRF 1-29 is limited to animal and in vitro studies. Claims about CJC-1295 No DAC, GH increases, IGF-1 elevation, body-composition effects, rest on extrapolation from the WITH-DAC animal literature and from sermorelin, not on direct evidence for this compound.
The only large CJC-1295 study was terminated after a participant death
ConjuChem's NCT00267527 study of CJC-1295 WITH-DAC was TERMINATED in July 2006 after a participant died of acute myocardial infarction approximately 2 hours after their eleventh injection. The attending physician attributed the death to pre-existing coronary artery disease, not the drug, and no formal causality assessment was completed. ConjuChem halted development entirely and went out of business shortly thereafter. The study's efficacy endpoints were never reported. This termination is routinely omitted from online content citing ConjuChem's early GH and IGF-1 data as support for CJC-1295; any honest summary of the compound's research history should include both. The no-DAC variant has no equivalent research history because it has never been studied in an adequately-powered published trial.
For laboratory research use only. Not for human or animal consumption.
Evidence Tier
Animal Only
Mol. Weight
3367.9 Da
Last Reviewed
Apr 21, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Anecdotal3
- Improves body composition (reduces fat, increases lean mass)
- Improves sleep quality / deep sleep
- Accelerates recovery from injury / wound healing
Unsupported2
- Anti-aging / longevity effects
- Cognitive enhancement
About this peptide
Plain English
The body naturally produces a hormone called GHRH that tells the pituitary to release growth hormone. CJC-1295 No DAC is a lab-made version of the first 29 amino acids of that hormone, with four small structural changes that make it more resistant to the body's enzymes. Unlike the longer-lasting WITH-DAC variant (which binds to albumin and stays active for roughly a week), the no-DAC form has a half-life of about 30 minutes, producing a short pulse of growth hormone release rather than a prolonged elevation. Importantly, nearly every piece of published evidence online referring to 'CJC-1295' is actually from animal and in vitro studies of the WITH-DAC variant, a pharmacokinetically distinct compound.
Technical
Modified GRF(1-29) is a tetrasubstituted peptide analog of endogenous hGHRH that binds and activates the pituitary GHRH receptor (GHRH-R), a Gs-coupled GPCR signaling through cAMP-PKA and Gq/phospholipase-C-IP3-Ca²⁺ cascades to stimulate GH synthesis and exocytosis in anterior pituitary somatotrophs. The four substitutions, D-Ala² (DPP-IV resistance), Gln⁸ (deamidation prevention), Ala¹⁵ (conformational stability), Leu²⁷ (Met-oxidation prevention), collectively extend plasma half-life from ~3–5 minutes for native hGHRH(1-29) to ~30 minutes for Mod GRF 1-29. This half-life remains far shorter than CJC-1295 WITH-DAC (~6–8 days), which additionally incorporates an Nε-maleimidopropionyl-Lys³⁰ extension that covalently binds serum albumin. Every published study of a compound marketed as "CJC-1295" studied the WITH-DAC variant; Mod GRF 1-29 alone has no published PK/PD or efficacy data of its own. Claims about its effects rely on extrapolation from sermorelin, from the WITH-DAC animal and in vitro literature, and from GHRH-axis physiology.
Mechanism of action
GHRH receptor agonism → pulsatile GH secretion
Modified GRF 1-29 binds GHRH-R on pituitary somatotrophs. Receptor activation elevates intracellular cAMP via Gαs and activates phospholipase C via Gαq, leading to PKA-mediated CREB phosphorylation and intracellular Ca²⁺ release. Both pathways converge on GH gene transcription and secretory granule exocytosis. Release occurs as a pulse because the peptide is cleared within ~30 minutes, avoiding the blunted receptor sensitivity associated with prolonged GHRH exposure. IMPORTANT: the pharmacodynamic evidence supporting this mechanism was generated in animal and in vitro studies using CJC-1295 WITH-DAC and sermorelin, not Mod GRF 1-29 itself.
IGF-1 axis stimulation (GH → hepatic GHR → JAK2/STAT5b → IGF-1)
GH released in response to GHRH-R activation travels to the liver, where it activates GH receptors and stimulates IGF-1 synthesis. IGF-1 circulates and mediates many downstream anabolic effects (protein synthesis, lipolysis, glucose regulation). IGF-1 and GH also participate in long-loop negative feedback on both the hypothalamus (stimulating somatostatin release) and pituitary (reducing GHRH-R sensitivity). The magnitude and duration of IGF-1 elevation following Mod GRF 1-29 administration specifically has not been characterised in any published literature.
Preservation of pulsatile GH profile (proposed advantage over long-acting analogs)
The short half-life of Mod GRF 1-29 (~30 min) means GHRH-R stimulation ceases rapidly, allowing somatostatin tone to re-assert and preserving the natural alternating suppression/release pattern of GH. The Ionescu & Frohman 2006 paper, often cited in support of this claim, is in fact a study of the WITH-DAC variant, demonstrating pulsatility is preserved even under sustained stimulation of that compound. Whether the no-DAC form produces more "physiological" GH profiles than long-acting variants is inferred mechanistically but has not been tested in any published comparative study.
GH-axis physiology is broadly conserved between rodents and humans, but magnitude, receptor density, and regulatory dynamics differ substantially. All three mechanisms above have supporting evidence from GHRH analog research conducted primarily in animal and in vitro studies using CJC-1295 WITH-DAC, sermorelin, or native hGHRH, not with Mod GRF 1-29 specifically. Evidence derived from the WITH-DAC variant cannot be cleanly extrapolated to the no-DAC version given the ~15-fold difference in half-life and distinct pharmacokinetic profile (no covalent albumin binding, short pulse rather than sustained elevation). The Teichman 2006, Ionescu 2006, and Sackmann-Sala 2009 studies were all conducted by ConjuChem employees or ConjuChem-linked investigators; no independent academic replication exists for either the WITH-DAC or the no-DAC form.
Key studies
Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse (2006)
Jette L, Leger R, Thibaudeau K, et al. · American Journal of Physiology, Endocrinology and Metabolism 291(5):E1090–E1094
- Participants
- GHRH-knockout mice
- Methodology
- Animal study; once-daily CJC-1295 WITH-DAC SC injection in GHRH-deficient mice.
- Result
- Normalized body weight and linear growth; sustained GH and IGF-1 elevation.
Honest read
Animal study only. GHRH knockout is an extreme model of GH deficiency in mice, not representative of normal physiology in any species. WITH-DAC compound, not no-DAC. This study is routinely over-cited in pro-CJC-1295 content as if it supported efficacy beyond this knockout model, it does not.
Research timeline
- 1982
Guillemin et al. isolate and sequence native hGHRH from pancreatic tumors causing acromegaly. The minimal biologically active fragment hGHRH(1-29)-NH2 (sermorelin) is identified.
- 1997
Chapman IM et al. publish a 16-week study of [Nle27]GHRH(1-29)-NH2 in 19 age-advanced subjects, showing sustained GH and IGF-1 stimulation in that cohort. NOT the same compound as Mod GRF 1-29 (differs at position 27) but frequently cited as support by extension.
- 2005
ConjuChem Biotechnologies (Canada) completes early-stage animal and in vitro characterization of CJC-1295 WITH-DAC; identifies the albumin-binding mechanism and 5.8–8.1 day half-life.
- 2006
Teichman SL et al. publish data on CJC-1295 WITH-DAC in JCEM reporting GH and IGF-1 stimulation. Sponsor-authored (5 of 6 authors ConjuChem employees).
- 2006
Jette, Leger, Thibaudeau et al. publish rat and GHRH-knockout mouse data on CJC-1295 WITH-DAC, routinely over-cited as if it supported efficacy beyond the animal models studied.
- 2006
ConjuChem TERMINATES the NCT00267527 trial after a participant dies of acute MI approximately 2 hours post-injection. Attending physician attributes death to pre-existing coronary artery disease. Development of CJC-1295 WITH-DAC is abandoned.
- 2006
Ionescu M & Frohman LA publish pulsatility study: GH secretory pulse frequency and magnitude preserved despite sustained CJC-1295 WITH-DAC exposure in that study. This is the paper most commonly (mis)cited online to support no-DAC "pulsatility" claims, but it used WITH-DAC.
- 2009
Sackmann-Sala et al. publish exploratory serum proteomics post-CJC-1295 WITH-DAC exposure in that study: decreased ApoA1 and transthyretin, increased beta-hemoglobin and albumin fragments. Hypothesis-generating, no control arm, not replicated.
- 2010
Henninge et al. publish LC-MS identification of CJC-1295 WITH-DAC in a seized injectable pharmaceutical, establishing forensic analytical methodology in a doping-enforcement context.
- 2013
Mod GRF 1-29 begins circulating in research-chemical markets as "CJC-1295 No DAC", the tetrasubstituted GHRH(1-29) core of CJC-1295 WITHOUT the DAC moiety. No published research program is ever initiated for this shorter-acting variant.
- 2017
CJC-1295 and GHRH analogs are added to an international anti-doping prohibited list under the peptide hormones and growth factor class, reflecting their GH-stimulating activity.
- 2024
An advisory committee reviews CJC-1295 for potential authorized-use listing; the nomination was withdrawn by nominators earlier in 2024, and the compound ends 2024 without a positive listing determination.
- 2026
CJC-1293 and CJC-1295 are explicitly named by name on the 2026 international anti-doping prohibited list under the GHRH analog class. Separately, policy discussions continue in multiple jurisdictions regarding authorized access to research peptides.
What we don't know
- Direct pharmacokinetics of Modified GRF 1-29 specifically. Published PK data describes CJC-1295 WITH-DAC. The no-DAC half-life (~30 min) is extrapolated from its DPP-IV resistance properties and structural comparison with sermorelin. No published PK study characterises Mod GRF 1-29 directly.
- Efficacy for any claimed indication. No completed, published study has tested Mod GRF 1-29 alone for any outcome, including GH secretion, body composition, recovery, aging, cognition, or sleep.
- Dose-response and optimal administration intervals. Conventions circulating online are practitioner extrapolations from sermorelin, not findings derived from Mod GRF 1-29 studies.
- Long-term toxicology. No chronic toxicology study exists for this compound. Theoretical concerns include insulin resistance from sustained IGF-1 elevation, potential cancer promotion in subclinical malignancy, and GH-axis downregulation with very frequent administration.
- Compound interactions. No formal interaction studies exist. Theoretical interactions with insulin, glucocorticoids, sex steroids, and somatostatin analogs are unstudied.
- Immunogenicity. The tetrasubstituted sequence is immunologically non-native; anti-peptide antibody formation is theoretically possible with repeated exposure, but no data exists.
- Cancer risk. Elevated IGF-1 is epidemiologically associated with increased risk of breast, colorectal, and prostate cancers. Whether GHRH-analog-induced IGF-1 elevation confers similar risk from Mod GRF 1-29 exposure is unknown.
- Whether degradation products (deamidated Gln8, racemized D-Ala2) retain partial GHRH-R agonism or act as partial antagonists. Undefined.
- Non-injectable bioavailability. Mod GRF 1-29 is a 29-residue peptide with no known oral or transmucosal bioavailability. Any non-injectable formulations marketed as containing it are not validated.
Stability & handling
- Lyophilized shelf life
- ~24–36 months properly stored (manufacturer / vendor data; no independently validated peer-reviewed stability study specific to Mod GRF 1-29 identified)
- Lyophilized storage
- Freeze at −20°C (long-term) or 2–8°C (short-term, up to months); sealed, desiccated, protected from light. Do not open cold vials until equilibrated to room temperature, moisture condensation is the primary degradation risk.
- Reconstitution diluents
- Bacteriostatic water for injection (benzyl alcohol preserved), standard for multi-dose research vials, Sterile water for injection (single-use only), Dilute acetic acid (0.1–1%), occasionally used for poorly soluble lots
- Reconstituted (refrigerated)
- Up to ~30 days at 2–8°C (general peptide guideline; no Mod-GRF-1-29-specific analytical stability validation)
- Reconstituted (room temp)
- Degradation begins above 8°C; use within hours if not refrigerated. CJC-1295 WITH-DAC retained ~68% potency at 25°C/24h in one vendor stability report, a useful analog but not a direct Mod GRF 1-29 measurement.
- OK to refreeze
- No
- Light sensitive
- Yes, protect from light
Critical stability failure modes specific to this compound: (1) D-Ala at position 2 can racemize back toward L-Ala under heat / long storage, which restores DPP-IV susceptibility and collapses the ~30-min half-life back toward sermorelin's ~3–5 min, standard reverse-phase HPLC does NOT detect this, only chiral HPLC or amino acid analysis after hydrolysis does. (2) Gln at position 8 can deamidate to glutamate under near-neutral pH or elevated temperature, producing a +1 Da mass shift detectable by mass spec but often co-eluting on HPLC. (3) DAC contamination, the WITH-DAC variant differs by ~279 Da and can co-elute on standard HPLC; only mass spec can confirm absence of WITH-DAC in a product sold as "no-DAC." (4) Standard lyophilization uses TFA counterions from preparative HPLC, acetate salt form is preferable for injection but requires ion exchange; COAs should report counterion identity and net peptide content distinct from chromatographic purity %.
Frequently asked questions
Is CJC-1295 No DAC the same as CJC-1295 (with DAC)?
No. "CJC-1295" in published literature (Teichman 2006, Ionescu 2006, Sackmann-Sala 2009, the terminated NCT00267527) refers to the WITH-DAC variant, a 30-amino-acid peptide that covalently binds albumin and has a half-life of 6–8 days. CJC-1295 No DAC (Modified GRF 1-29) is the first 29 amino acids of that compound without the albumin-binding extension; its half-life is approximately 30 minutes. They act through the same GHRH receptor but have completely different pharmacokinetic profiles. Nearly all evidence cited online for "CJC-1295 No DAC" was actually generated on the WITH-DAC form.
What's the difference between CJC-1295 No DAC and sermorelin?
Both are 29-amino-acid GHRH analogs that activate the GHRH receptor and stimulate pulsatile GH release. Sermorelin IS native hGHRH(1-29)-NH2; Modified GRF 1-29 adds four substitutions (D-Ala2, Gln8, Ala15, Leu27) that extend half-life from ~3–5 minutes to ~30 minutes and reduce enzymatic degradation. Sermorelin has a longer track record in the published literature than Mod GRF 1-29. The two compounds are pharmacokinetically distinct despite sharing the same receptor target.
Why do people stack CJC-1295 No DAC with ipamorelin?
The two peptides act through different receptors: Mod GRF 1-29 activates the GHRH receptor (the pituitary "go" signal), while ipamorelin activates the GHS-R ghrelin receptor (a separate "go" signal that also suppresses somatostatin, the counter-regulatory "stop" signal). In animal studies and extrapolation from GH-axis physiology, combining a GHRH-R agonist with a GHS-R agonist can produce supra-additive GH release. No published study has tested this specific combination. The amplification figures cited online are receptor-pharmacology extrapolations, not published experimental results.
Has anyone died from CJC-1295?
A participant in ConjuChem's NCT00267527 study of CJC-1295 WITH-DAC died of acute MI approximately 2 hours after the eleventh injection in 2006. The attending physician attributed the death to pre-existing coronary artery disease, not to the drug. ConjuChem halted the study as a precaution and subsequently abandoned the compound entirely. No formal causal assessment was completed. The no-DAC variant has no similar research history, as it has never been studied in an adequately-powered published trial.
What's the real half-life of CJC-1295 No DAC?
Approximately 30 minutes. Native hGHRH(1-29) has a plasma half-life of ~3–5 minutes due to rapid DPP-IV cleavage; the D-Ala2 substitution blocks that cleavage, extending half-life to roughly 30 minutes. IMPORTANT: this figure is not from a published PK study of Modified GRF 1-29, it is a mechanistic inference based on the compound's DPP-IV resistance and structural similarity to sermorelin. No direct PK data for Mod GRF 1-29 has been published.
Will CJC-1295 No DAC show up on a drug test?
Yes, if the test panel covers GHRH analogs. CJC-1295 is explicitly named on international anti-doping prohibited lists and LC-HRMS/MS detection methodology exists for it. The no-DAC form's short half-life means the detection window is substantially shorter than for the WITH-DAC form, but detection remains possible. This is a research-use-only compound, not for human or animal consumption.
Is the evidence for "preserving pulsatile GH secretion" real?
The Ionescu & Frohman 2006 paper commonly cited for this claim is a study of CJC-1295 WITH-DAC, demonstrating that GH pulsatility is preserved even under sustained WITH-DAC stimulation in that experiment. The no-DAC form almost certainly also preserves pulsatility (it clears too quickly to impose sustained receptor occupancy), so the claim is mechanistically coherent. What is NOT demonstrated is that pulsatile profiles produced by Mod GRF 1-29 are superior to the elevated-but-pulsatile profiles produced by WITH-DAC. That comparative claim has no evidentiary basis.
What should I look for on a CJC-1295 No DAC COA?
Four things, separately reported: (1) MASS SPEC CONFIRMATION that the compound is no-DAC, not WITH-DAC, the two differ by ~279 Da and can co-elute on standard HPLC; a COA showing only HPLC purity cannot confirm the absence of WITH-DAC contamination. (2) CHIRAL CONFIRMATION of D-Ala at position 2, reverse-phase HPLC does not detect D→L racemization, which silently collapses the half-life back to sermorelin's ~3–5 min; chiral HPLC or amino-acid analysis after hydrolysis is required. (3) NET PEPTIDE CONTENT distinct from HPLC chromatographic purity, TFA and acetate counterions plus residual water contribute to stated vial mass; COAs should report peptide content as a percentage of gross weight. (4) ENDOTOXIN (LAL) testing per USP <85> because the product is injectable. A COA showing only "≥98% purity by HPLC" without these four items has not characterized what's actually in the vial.
Last researched: Apr 21, 2026
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