Mod-GRF (1-29).
Mod GRF 1-29 (commonly sold as "CJC-1295 without DAC") is a synthetic 29-amino-acid analog of growth hormone-releasing hormone (GHRH).
Mod GRF 1-29 (commonly sold as "CJC-1295 without DAC") is a synthetic 29-amino-acid analog of growth hormone-releasing hormone (GHRH). Mod-GRF (1-29) is research / preclinical, and PepCue grades its published evidence F tier (29/100). Also known as CJC-1295 no-DAC. This is a research reference, not medical or dosing advice.
What it is
Mod GRF 1-29 (commonly sold as "CJC-1295 without DAC") is a synthetic 29-amino-acid analog of growth hormone-releasing hormone (GHRH). It is the same tetra-substituted GHRH(1-29) peptide backbone used in CJC-1295, but it lacks the maleimido "Drug Affinity Complex" (DAC) linker that the long-acting form carries, so it behaves as a short-acting GHRH secretagogue. Its parent fragment, native GHRH(1-29) ("sermorelin"), retains essentially the full GH-releasing activity of the 44-residue hormone, and the four engineered substitutions are added to slow enzymatic breakdown.
How it works
Like endogenous GHRH, the peptide binds the GHRH receptor on anterior-pituitary somatotrophs, raising intracellular cAMP and triggering pulsatile synthesis and release of growth hormone, which in turn drives hepatic IGF-1 production. The four amino-acid substitutions relative to native GHRH(1-29), typically described as D-Ala at position 2, Gln8, Ala15, and Leu27, are intended to resist degradation, with the D-alanine substitution at position 2 specifically blocking cleavage by dipeptidyl peptidase-IV (DPP-IV), the main enzyme that rapidly inactivates GHRH. Because it has no albumin-binding DAC tether, it is cleared quickly and is described as producing brief, pulse-like GH stimulation rather than the sustained "GH bleed" seen with the DAC version. It is mechanistically a secretagogue: it prompts the pituitary's own GH, rather than supplying GH directly.
Mechanism pathways
Stimulating the pituitary's GHRH receptor to release the body's own growth hormone.
Growth-hormone-releasing hormone is made in the arcuate nucleus of the hypothalamus and travels through the hypophyseal portal circulation to the anterior pituitary, where it binds a class B G-protein-coupled receptor on somatotroph cells. Receptor activation raises intracellular cyclic AMP, which triggers both the synthesis of growth hormone and its release in pulses. Downstream, growth hormone acts on the liver and peripheral tissues to raise insulin-like growth factor 1, and IGF-1 in turn feeds back to restrain further growth hormone output. Somatostatin, released from a separate hypothalamic population, provides the opposing brake. The appeal of targeting this receptor rather than administering growth hormone directly is that the feedback architecture stays intact. Because release remains pulsatile and IGF-1 can still shut the system down, the pituitary sets a ceiling on how much growth hormone appears. Direct growth hormone administration bypasses that ceiling entirely. This is the central argument for the whole class, and it is a genuine pharmacological difference rather than a marketing distinction. All compounds in this group are analogs of the biologically active fragment of GHRH, which is the first twenty-nine amino acids. Native GHRH is cleaved almost immediately by dipeptidyl peptidase-4 at the amino terminus, so every analog is essentially a different answer to that vulnerability. Some substitute amino acids near the cleavage site. Some add a chemical group at the amino terminus that the enzyme cannot process. Some attach a linker that lets the molecule bind covalently to circulating albumin, stretching duration from minutes to days and turning discrete pulses into a sustained elevation, which is a meaningfully different physiological signal from a short pulse. One member of this group is an approved medicine for a specific indication, which means the receptor mechanism has been demonstrated in humans and not merely in animals. That approval does not extend to the rest of the group. Most of the compounds here have never been approved for any use anywhere, are sold as research chemicals of unverified identity and purity, and have human data limited to short studies showing that growth hormone rises after administration. Demonstrating that a hormone level moves is not the same as demonstrating that anything clinically meaningful follows from it, and for most of this class that second step has not been taken.
The evidence
The well-known human trials in this family, Teichman et al. (JCEM, 2006), Ionescu & Frohman (JCEM, 2006), and Sackmann-Sala et al. (Growth Horm IGF Res, 2009), all studied CJC-1295 WITH DAC, the long-acting albumin-binding version, not the no-DAC Mod GRF 1-29; Alba et al. (2006) used a GHRH-knockout mouse model. There is no robust, peer-reviewed human clinical trial of Mod GRF 1-29 (the no-DAC peptide) under that name establishing efficacy or safety, so claims about it are largely inferred from GHRH/sermorelin pharmacology and from the DAC-form data rather than directly tested. The unmodified parent peptide, sermorelin/GHRH(1-29), was an FDA-approved diagnostic and pediatric GH agent and is the best-characterized human reference point. Most published mentions of the no-DAC compound itself come from anti-doping analytical chemistry (e.g., Henninge et al., Drug Test Anal, 2010, identifying CJC-1295 in an illicit preparation), which characterize the molecule but not its clinical effects. Honest bottom line: the human-versus-preclinical gap is wide here, and the short-acting form is plausible by analogy but essentially unproven in controlled human studies.
The evidence, in brief
Modified GRF 1-29 (CJC-1295 without DAC) is a DPP-IV-resistant GHRH(1-29) fragment with a short half-life and pulsatile GH-releasing action. Evidence is largely preclinical; rigorous controlled human data for the no-DAC form are lacking. A research analogue, not approved.
- Once-daily CJC-1295 normalizes growth in the GHRH-knockout mouseAm J Physiol Endocrinol Metab, 2006 (PMID 16822960)
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #043
Mostly preclinical or mechanistic; little human data.
A plausible biological rationale, but little data behind it.
Claim receipts
Popular claims about Mod-GRF (1-29), checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
Those trials tested the long-acting DAC version; the no-DAC peptide was not the molecule studied.
GHRH-receptor pharmacology is well understood, but this specific peptide has no controlled human trial of its own.
Body-composition outcomes have never been measured for this peptide in controlled human studies.
The pulsatility argument is mechanistic; no human comparison of the two forms on safety exists.
Safety profile
Documented safety data specific to Mod GRF 1-29 are minimal because controlled human trials of the no-DAC peptide are lacking; what is known is extrapolated from GHRH analogs broadly. In studies of related GHRH analogs and sermorelin, injection-site reactions (redness, swelling), flushing, and headache are the most commonly reported effects, and any sustained elevation of the GH/IGF-1 axis carries theoretical concerns including fluid retention, joint discomfort, insulin resistance/altered glucose handling, and uncertainty about long-term proliferative risk because IGF-1 is mitogenic. A major real-world hazard is that material sold under this name is research-grade and unregulated, so purity, identity, sterility, and contamination are not assured; anti-doping case reports document the compound appearing in mislabeled or "unknown" pharmaceutical preparations. Interactions with somatostatin tone, other secretagogues, and underlying endocrine or oncologic conditions are not well characterized, and long-term human safety is simply unknown.
Compound notes
- Mod GRF 1-29 is the same compound as CJC-1295 “no-DAC”: a short-acting GHRH analog (the GRF 1-29 fragment with stabilizing modifications).
- It binds pituitary GHRH receptors to drive a brief, pulsatile growth-hormone release; half-life is short (~30 minutes).
Same receptor, opposite kinetics: Mod GRF 1-29 is pulsatile and short-acting; the DAC version is albumin-bound and sustained over days.
- Not FDA-approved; research-only.
- Long-term human safety is not established.
Regulatory status
Mod GRF 1-29 / CJC-1295 without DAC is not approved by the FDA or any major regulator for any indication and is an investigational/research-use-only compound; its unmodified parent, sermorelin, was previously FDA-approved but has been commercially discontinued. As a GHRH analog it falls under the World Anti-Doping Agency (WADA) Prohibited List class S2 (peptide hormones / growth factors and related substances) and is banned in sport at all times.
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01"Without DAC" is the defining feature: it omits the albumin-binding Drug Affinity Complex of CJC-1295, making it short-acting (reported plasma half-life on the order of ~30 minutes) rather than lasting days.
- 02It is a secretagogue that stimulates the pituitary's own pulsatile GH release via the GHRH receptor, not exogenous growth hormone.
- 03The four engineered substitutions (notably D-Ala at position 2) are designed to resist DPP-IV and other proteolytic degradation that rapidly inactivates native GHRH.
- 04Its peptide backbone is identical to CJC-1295's; the only structural difference from the long-acting drug is the missing DAC linker.
- 05The frequently cited CJC-1295 human trials (Teichman 2006, Ionescu 2006) tested the DAC form, not this no-DAC peptide.
- 06It is not FDA-approved and is prohibited in sport by WADA as a GHRH analog.
Mod-GRF (1-29): research formats
Choose the format you are researching to see route-specific notes.
Mod-GRF 1-29 and CJC-1295 no-DAC are the same compound, so the same format applies.
Mod-GRF (1-29) is the IUPAC-correct name for what vendors often sell as CJC-1295 no-DAC. Sold as a 2 mg lyophilized vial; 2.0 mL BAC water reconstitution gives 1,000 mcg/mL.
Sources
Every factual claim above resolves to a real, published source.
- Prolonged stimulation of GH and IGF-I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults (note: studied the DAC form)J Clin Endocrinol Metab, 2006; Teichman SL et al.; PMID 16352683
- Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analogJ Clin Endocrinol Metab, 2006; Ionescu M, Frohman LA; PMID 17018654
- Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparationDrug Test Anal, 2010; Henninge J et al.; PMID 21204297
- Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjectsGrowth Horm IGF Res, 2009; Sackmann-Sala L et al.; PMID 19386527
Cite this page
PepCue. “Mod-GRF (1-29): the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/mod-grf-1-29.
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