CJC-1295 (no DAC)
Also known as: Modified GRF (1-29), Mod GRF (1-29), Modified GRF 1-29, tetrasubstituted GRF(1-29), [D-Ala², Gln⁸, Ala¹⁵, Leu²⁷]-GRF(1-29)-NH₂, commonly marketed as “CJC-1295 no DAC” or “CJC-1295 without DAC”
3 notable studies · 3 references
TLDR
Modified GRF (1-29) is a tetrasubstituted 29-amino-acid analogue of sermorelin designed to retain GHRH-receptor activity while improving peptide stability, but despite its popularity under names such as Mod GRF and “CJC-1295 no DAC,” direct human evidence for the exact non-DAC molecule is extremely limited and evidence from sermorelin or albumin-binding CJC-1295 should not automatically be attributed to it.
Observations Reported in Research
- No peer-reviewed controlled human study of the exact non-DAC tetrasubstituted Modified GRF (1-29) has been identified
- Human evidence for sermorelin/GHRH(1-29) and for CJC-1295 with DAC concerns related but distinct molecules, not this exact peptide
These are brief summaries of what the referenced research examined or reported — not conclusions about safety or effectiveness, and not medical advice. See Notable Studies and Sources & References below for the full context and citations.
At a Glance
Classification: Synthetic tetrasubstituted GHRH(1-29) analogue; short-acting experimental GHRH analogue
CJC-1295 (no DAC) is a 29-amino-acid analogue of sermorelin/GHRH(1-29) containing four amino-acid substitutions. Relative to native GHRH(1-29), the commonly described sequence substitutes: Position 2: Ala → D-Ala Position 8: Asn → Gln Position 15: Gly → Ala Position 27: Met → Leu. The resulting peptide remains C-terminally amidated. These substitutions were intended to address liabilities of native GHRH(1-29), particularly enzymatic degradation and chemical instability. But here is the big Aminodex correction: The extensive human sermorelin literature does not belong to Modified GRF (1-29). And: The published human CJC-1295-with-DAC studies don't automatically belong to Modified GRF (1-29), either. The exact non-DAC modified peptide has remarkably little direct clinical literature despite being extremely common in today's research market.
What Is CJC-1295 (no DAC)?
Start with sermorelin: native GHRH(1-29)-NH₂ Then change four positions: Ala² → D-Ala² Asn⁸ → Gln⁸ Gly¹⁵ → Ala¹⁵ Met²⁷ → Leu²⁷ ↓ Modified GRF (1-29). The resulting peptide is generally described as: Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH₂. The most important modification is D-Ala², which is intended to make the N-terminal region more resistant to cleavage by DPP-IV. The other substitutions address additional stability liabilities, including Asn and Met.
What Are Researchers Studying?
GHRH-receptor signaling
Modified GRF was designed to preserve the biological activity of GHRH while improving stability. Therefore its expected target is the GHRH receptor on pituitary somatotrophs. However, the distinction between design rationale and direct exact-compound evidence matters. The published human literature demonstrating GHRH-receptor stimulation is enormous for native GHRH and sermorelin, but much thinner for this exact four-substitution peptide. Current evidence reviews note the lack of a substantial peer-reviewed human literature specifically for the non-DAC molecule.
Protease resistance
Native GHRH(1-29) is susceptible to rapid enzymatic degradation. The D-Ala² substitution is designed to increase resistance to DPP-IV-mediated cleavage. That is one of the principal reasons Modified GRF exists at all. But more protease-resistant than sermorelin does not mean long-acting like CJC-1295 with DAC. Those are completely different strategies.
Peptide stability
The substitutions at positions 8 and 27 replace residues susceptible to chemical degradation: Asn → Gln and Met → Leu. The resulting analogue was designed to retain GHRH-like activity while being chemically/metabolically more stable than the native sequence.
Growth-hormone secretion
The intended pharmacology is: Modified GRF → GHRH receptor → endogenous GH release. That is highly plausible from its structure and lineage. What Aminodex should not do is cite a sermorelin GH-response study and label it a Modified GRF study. Those subjects received a different molecule.
Combination with GHSR agonists
Modified GRF is frequently discussed in the research market alongside compounds such as Ipamorelin, GHRP-2, and GHRP-6. There is a sound physiological rationale because GHRH-receptor and ghrelin-receptor pathways can interact synergistically in stimulating GH release; direct human experiments demonstrate this principle with GHRH(1-29) and GHRP-2. But GHRH + GHRP-2 evidence is related-pathway evidence, not a direct trial of Modified GRF + Ipamorelin. That distinction is routinely lost online.
How Does It Work?
The expected mechanism is: Modified GRF (1-29) ↓ GHRH receptor activation ↓ pituitary somatotroph signaling ↓ endogenous GH release ↓ downstream GH/IGF-1 signaling. The substitutions modify the peptide's stability rather than creating an entirely new intended receptor target. But Modified GRF does not contain the defining albumin-binding feature of published CJC-1295 with DAC. Therefore it should not inherit CJC-1295's prolonged albumin-associated pharmacokinetics.
What Does the Research Show?
Human research
Exact Modified GRF (1-29): VERY LOW / no substantial direct human clinical literature identified. This is the surprising part. Human research exists for Sermorelin / GHRH(1-29) and separately for CJC-1295 with DAC. But current evidence reviews find essentially no peer-reviewed human clinical program specifically for the exact non-DAC tetrasubstituted peptide sold as Modified GRF (1-29). Direct human evidence: VERY LOW / NOT ESTABLISHED, rather than borrowing from its relatives.
Animal research
Related GHRH-analogue biology exists, but the exact-compound evidence base is much thinner than its market popularity suggests. Studies should only count as DIRECT when the exact tetrasubstituted non-DAC peptide can be verified.
In-vitro research
Mechanistic expectations are strongly supported by GHRH biology and analogue development. Aminodex should distinguish class/mechanism evidence from exact-compound experimental evidence.
Notable Studies
No peer-reviewed controlled human study of the exact non-DAC tetrasubstituted Modified GRF (1-29) meeting Aminodex’s direct-evidence criteria was identified.
humanNo peer-reviewed controlled human study of the exact non-DAC tetrasubstituted Modified GRF (1-29) meeting Aminodex’s direct-evidence criteria was identified. No exact-compound human clinical study currently qualifies.
Limitations: Direct human evidence for the exact non-DAC peptide is VERY LOW / NOT ESTABLISHED. Human evidence for sermorelin/GHRH(1-29) and for CJC-1295 with DAC must not be attributed to this molecule.
Related-compound evidence — Sermorelin
humanHuman GHRH(1-29) studies establish that the parent 29-residue sequence can stimulate GH release and increase growth velocity in selected GH-deficient children. Evidence identity: RELATED MOLECULE, not exact Modified GRF (1-29).
Limitations: Sermorelin / GHRH(1-29) is a different molecule (no D-Ala², Gln⁸, Ala¹⁵, Leu²⁷ substitutions). These subjects did not receive Modified GRF (1-29).
View publication →Related-compound evidence — CJC-1295 with DAC
humanPublished CJC-1295 incorporates an albumin-binding modification absent from Modified GRF (1-29). Its human pharmacokinetic findings therefore should not simply be assigned to the non-DAC peptide. Evidence identity: RELATED MOLECULE / DIFFERENT PHARMACOKINETIC CONSTRUCT.
Limitations: Modified GRF (1-29) does not contain the defining albumin-binding feature of published CJC-1295 with DAC and should not inherit CJC-1295’s prolonged albumin-associated pharmacokinetics.
What We Still Don't Know
• Exact human pharmacokinetics • Exact human half-life • Human bioavailability • Human dose-response • Human GH-response magnitude • Human IGF-1 response • Long-term safety • Long-term endocrine effects • Clinical efficacy • Body-composition effects • Sleep effects • Recovery effects • Healthy-adult benefits • Whether combinations with GHSR agonists produce clinically meaningful advantages • Whether research-market products labeled “CJC-1295 no DAC” actually contain the canonical Modified GRF sequence.
Related Compounds
Recent publications
Latest titles from PubMed, not reviewed by Aminodex. Not an endorsement. See all on PubMed ↗
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Sources & References
- Prakash A, Goa KL. Sermorelin clinical review — useful parent-compound evidence for GHRH(1-29), not direct Modified GRF evidence.
- Human GHRH(1-29)/GHRP-2 endocrine challenge study — related pathway evidence rather than exact Modified GRF evidence.
- Current evidence/identity review of Modified GRF (1-29), including the four substitutions and lack of compound-specific human clinical data. Source label in packet: Origen Collective (no direct URL given).
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