Mod GRF 1-29

Modified GRF 1-29, "CJC-1295 without DAC", "CJC-1295 no DAC", tetrasubstituted GRF(1-29), [D-Ala2, Gln8, Ala15, Leu27]-GRF(1-29)-NH2

Growth hormone axis

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Summary

Class: Synthetic 29-amino-acid analogue of the active fragment of growth-hormone-releasing hormone (GHRH), with four amino acids swapped to resist breakdown
Mechanism: Acts on the GHRH receptor in the pituitary to trigger a pulse of growth hormone; the four substitutions slow enzymatic clearance so the pulse is larger and longer than with native GHRH
Routes studied: Subcutaneous (community); the related molecules sermorelin and CJC-1295 were studied subcutaneously and intravenously in humans
Dose range reported: No human trial of this exact molecule. Community: 100 µg subcutaneous, 1–3 times daily, almost always paired with a GHRP such as ipamorelin; "100/100" is the common shorthand. Sermorelin (GRF 1-29) was labelled at 30 µg/kg in children
Half-life: Not measured in humans. Estimated at roughly 30 minutes from its design and from GRF analogue data; native GRF 1-29 is ~10–20 minutes. Not to be confused with CJC-1295 with DAC (~6–8 days)
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate; community practice is use within ~4 weeks. GRF analogues are considered less stable in solution than GHRPs
Regulatory status: Not approved for any indication anywhere

Doses are as reported in studies or by the community — never recommendations.

1What it is

Growth-hormone-releasing hormone is a 44-amino-acid hypothalamic hormone, and its first 29 amino acids (GRF 1-29) carry the full activity. Sermorelin is simply GRF 1-29 and was once an approved medicine. The problem with GRF 1-29 is that it is destroyed in minutes by enzymes in the blood, chiefly dipeptidyl peptidase IV (DPP-IV), which clips off the first two amino acids.

Mod GRF 1-29 is GRF 1-29 with four changes designed to stop that: a D-alanine at position 2 (blocks DPP-IV), glutamine at position 8 (stops the asparagine there from spontaneously deamidating), alanine at position 15 (improves receptor binding and stability) and leucine at position 27 (replaces a methionine that oxidises). These substitutions were worked out in GRF structure–activity research in the late 1980s and 1990s and were later used by the company ConjuChem as the peptide backbone of CJC-1295. CJC-1295 proper adds a "drug affinity complex" (DAC) that bonds the peptide to albumin, extending the to about a week.

The community name "CJC-1295 without DAC" is therefore accurate but confusing: the two compounds share a sequence and differ enormously in how long they act. This page covers the short-acting molecule. The DAC version has its own page (CJC-1295).

2How it's thought to work

Mod GRF 1-29 binds the GHRH receptor on pituitary somatotroph cells, raising cyclic AMP and causing GH synthesis and release. Because it works on the GHRH receptor rather than the ghrelin receptor, it is additive, and in human studies of the parent molecules strongly synergistic, with GHRPs (GHRP-6, GHRP-2, ipamorelin) that act on the ghrelin receptor. The combination of a GHRH analogue plus a GHRP is the basis of almost all community protocols.

Its short duration is the point: it produces a GH pulse that is over within an hour or two, which is argued to preserve the natural pulsatile pattern rather than flattening it. Somatostatin tone still governs how big the pulse is, which is why timing relative to meals and sleep is discussed so much.

Modified GRF(1-29) at the GHRH receptor on the pituitary — the same receptor and the same pulsatile release as sermorelin, which is GRF(1-29) itself. The four substituted amino acids slow its breakdown; they do not change what it does.Schematic — not to scale

3What the research shows

Graded D (this molecule); A (parent molecules)

GH release

There are no published controlled human trials of mod GRF 1-29 as such. The claim that it releases GH rests on three things: (1) GRF 1-29 itself is an established GH releaser with decades of human data (sermorelin trials in children and adults, e.g. Thorner 1996); (2) the individual substitutions were each shown in receptor-binding and plasma-stability work to preserve or improve activity while slowing breakdown (Frohman 1989, J Clin Invest — DPP-IV degradation of GHRH; Campbell 1991, Peptides — GRF analogue structure–activity); (3) CJC-1295, which uses this exact sequence plus DAC, raised GH and IGF-1 in healthy adults (Teichman 2006, JCEM). None of these is a trial of the non-DAC molecule, and the difference means the CJC-1295 data in particular do not transfer directly. [1][2][3][6]

Graded A (for GRF 1-29 or GHRH combined with GHRP-6/GHRP-2)

Synergy with GHRPs

Human studies in the 1990s showed that co-administering GHRH with GHRP-6 or GHRP-2 produced GH peaks far larger than either alone (Bowers 1990, JCEM). Community protocols assume the same holds for mod GRF 1-29 plus ipamorelin. Plausible, not demonstrated. [5]

Body composition, sleep, recovery, anti-ageing

No human data for this molecule. Sermorelin and tesamorelin (the GHRH analogues that were actually studied) showed modest IGF-1 increases and, for tesamorelin, visceral fat reduction in HIV lipodystrophy; whether equivalent dosing of mod GRF 1-29 does the same is unknown.

4Reported side effects and interactions

Literature-reported

none specific to this molecule. GHRH analogues in trials cause flushing, injection-site reactions, headache and transient dizziness; tesamorelin trials also recorded joint pain, oedema and raised glucose.

Community-reported

a brief flush or warmth and a "head rush" within minutes of injection are the most common; injection-site redness; occasional headache, sleepiness after evening doses, water retention and tingling in the hands with sustained use.

Theoretical. anything that raises GH and IGF-1 carries the class concerns — reduced insulin sensitivity, fluid retention, and caution in anyone with an active malignancy. GRF analogues can in principle provoke antibody formation; sermorelin trials reported low-titre antibodies without clinical effect.

Interactions. additive with all GH . Somatostatin, high blood glucose, high free fatty acids and glucocorticoids blunt the GH response to GHRH; this is physiology rather than a drug interaction but explains the "inject fasted" convention. Glucose-lowering medicines may need monitoring if IGF-1 rises.

Markers researchers commonly monitor

Based on GH-axis physiology; nothing is specific to this molecule:

Marker	Why it's watched
IGF-1	the integrated readout of GH exposure. For a short-acting GHRH analogue a modest rise is expected; a large rise suggests over-exposure.
Fasting glucose, fasting insulin, HbA1c	GH lowers insulin sensitivity; the key safety markers for any GH-axis compound.
Lipid panel	GH shifts lipids, direction varies.
TSH / free T4	GH increases T4-to-T3 conversion and can lower free T4.
Morning cortisol and prolactin	GHRH analogues should not move these; a baseline shows whether the paired GHRP does.
Blood pressure and body weight (same time each morning)	picks up fluid retention early.
IGFBP-3	sometimes requested alongside IGF-1 to interpret it; optional.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Usually supplied as 2 mg or 5 mg vials. with , swirl gently, do not shake. GRF analogues are reported to degrade faster in solution than GHRPs, so smaller reconstituted volumes used within a few weeks are the community norm. Frequently drawn into the same syringe as ipamorelin; the calculator supports a two-peptide mix.

Open in calculator, pre-loaded →

6Commonly studied alongside

Ipamorelin (the standard pairing), GHRP-2, GHRP-6, hexarelin. CJC-1295 (the DAC version — same sequence, long-acting; see that page). Sermorelin and tesamorelin as the closest studied relatives.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. CJC-1295 appears in Category 2 of the FDA's 2023 bulk drug substances list; whether that entry is read to include the non-DAC molecule varies †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved; GHRH analogues fall under prescription-only scheduling †
South Africa	Not registered
Sport	Prohibited by WADA (S2 — GHRH and its analogues are named; CJC-1295 and sermorelin are listed as examples)

8Open questions

Actual human pharmacokinetics of mod GRF 1-29 — nobody has published them.
Whether repeated doses at community levels change IGF-1 or body composition.
Whether the synergy shown for GHRH + GHRP-6 holds for mod GRF 1-29 + ipamorelin.
Antibody formation with long-term use.

9References

1Frohman LA, Downs TR, Heimer EP, Felix AM (1989). Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma. J Clin Invest. PubMed · DOI
2Campbell RM et al. (1991). GRF analogs and fragments: correlation between receptor binding, activity and structure. Peptides. PubMed · DOI
3Teichman 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. J Clin Endocrinol Metab. PubMed · DOI
4Jetté L et al. (2005). Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats. Endocrinology. PubMed · DOI
5Bowers CY et al. (1990). Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. J Clin Endocrinol Metab. PubMed · DOI
6Thorner MO et al. (1996). Once daily subcutaneous growth hormone-releasing hormone therapy accelerates growth in growth hormone-deficient children during the first year of therapy. J Clin Endocrinol Metab. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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11Page history

26 Oct 2026Profile published — awaiting medical review

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