CJC-1295 without DAC

The four substitutions (D-Ala at position 2, Gln at 8, Ala at 15 and Leu at 27) protect against dipeptidyl peptidase-4 cleavage, trypsin digestion and asparagine deamidation, raising potency and shelf stability well above native sermorelin while keeping the short duration of action. Acting at the GHRH receptor it increases cyclic AMP in somatotrophs and drives synthesis and release of GH, but it cannot overcome somatostatin tone on its own. That is why it is paired with a GHRP: the GHRP suppresses somatostatin and opens the gate while the GHRH analogue determines how much GH comes through it. The naming is a persistent source of confusion, since the actual ConjuChem compound called CJC-1295 was the DAC version and this fragment is more accurately called Mod GRF 1-29.

Targets: GHRH receptor (GHRHR), Adenylate cyclase / cAMP in somatotrophs, IGF-1 axis

• · 100 mcg is the widely used saturation dose - roughly 1 mcg/kg - and going higher does not enlarge the pulse much. Combined in the same syringe with 200 to 300 mcg ipamorelin.
• · The lowest-effort version. One injection per night, paired with a GHRP.

Work out your exact syringe units →

• commonFlushing and warmth after injection— GHRH analogues are directly vasoactive; it passes in minutes.
• commonInjection-site redness, itching or a small lump— Rotate sites.
• uncommonWater retention— Much less than the DAC version because exposure is pulsatile.
• uncommonHead rush or lightheadedness
• uncommonJoint aching— More likely if stacked at high doses with a GHRP for months.
• rareReduced insulin sensitivity— Pulsatile dosing largely avoids this compared with continuous GHRH exposure.

• Active malignancy.
• Active proliferative diabetic retinopathy.
• Known pituitary adenoma.
• Pregnancy and breastfeeding.

• synergyipamorelin — The canonical pairing. GHRH sets pulse amplitude, the GHRP removes somatostatin brake; the combined pulse is larger than the sum.
• synergyghrp-2 — Stronger GH output than with ipamorelin but with prolactin and cortisol drift.
• conflictsomatropin — IGF-1 feedback from exogenous GH suppresses the pituitary, leaving little for a GHRH analogue to release.
• redundantcjc-1295-dac — Same receptor and near-identical backbone; running both is pointless.

• · IGF-1 at baseline and at 8 to 12 weeks.
• · Fasting glucose if the stack runs longer than three months.
• · Objective markers matter more than feel: body composition, sleep tracking, recovery between sessions.

Not approved for human use in any jurisdiction; sold as a research chemical. Prohibited in sport under WADA S2.

• Published GHRH(1-29) human pharmacology underpinning the analogue design (review)
• Teichman et al. 2006 JCEM, which characterised the same peptide backbone in its DAC form (trial)

The parent sequence here was verified directly against the human GHRH precursor (UniProt P01286), whose mature peptide begins YADAIFTNSYRKVLGQLSARKLLQDIMSR and continues to residue 44. Apply the four documented substitutions at positions 2, 8, 15 and 27 and you get the molecule above. Mechanistically it is a straightforward GHRH-receptor agonist: Gs coupling, adenylate cyclase, cAMP, protein kinase A, CREB phosphorylation, followed by both immediate GH exocytosis and upregulated GH1 transcription. That transcriptional arm is why GHRH analogues replenish the somatotroph rather than exhausting it, and why receptor desensitisation is not the practical problem it is with GHS-R1a agonists. What a GHRH analogue cannot do alone is overcome somatostatin. Somatostatin acts through Gi to lower cAMP - it is directly antagonistic to the exact second messenger this drug is trying to raise - so if you inject during a period of high somatostatin tone the pulse is blunted regardless of dose. Hypothalamic somatostatin output oscillates roughly every three hours and is not something you can time. This is the precise reason the GHRP pairing works: the GHRP suppresses somatostatin, taking the Gi brake off, and the GHRH analogue then gets the full cAMP response it is capable of. The synergy is not additive because you are removing an inhibitor and adding a stimulator to the same second messenger, and that is multiplicative. The 100 mcg saturation figure - roughly 1 mcg/kg - reflects GHRH receptor occupancy, not the size of the granule pool, which is why exceeding it does very little.

Solution stability is the real-world failure mode, and it is underappreciated. This peptide degrades in bacteriostatic water noticeably faster than ipamorelin does, so a vial that has been reconstituted for five weeks at the back of a fridge door - the warmest part - can be substantially dead while looking perfectly clear. If a stack stops working after a month, suspect the GHRH component first. The second failure is the naming. 'CJC-1295' with no qualifier is ambiguous, and people who read about the DAC version's six-day half-life and then buy a no-DAC vial dose it weekly, getting one thirty-minute pulse per week and no result. Third is eating. A GHRH analogue is more sensitive to the fed state than a GHRP is, because free fatty acids suppress somatotroph responsiveness through a somatostatin-mediated route; injecting after a meal wastes the dose. Fourth is chasing dose. At 100 mcg you are already at the top of the GHRH-receptor dose-response curve; 300 mcg gets you a slightly wider flush and the same pulse.

• GHRH receptor (GHRHR), pituitary somatotroph — Higher potency than native GHRH(1-29) as a consequence of the Ala15 substitution and protease resistance; no published Kd for this exact analogue

  Gs coupling, cAMP rise, PKA/CREB activation. Immediate GH release plus increased GH synthesis, so pulse amplitude rather than pulse frequency is what changes.

• Somatostatin receptor tone (opposed, not bound) — Not applicable - this is an antagonistic input, not a target

  Somatostatin signals through Gi and lowers the same cAMP this drug raises. Unopposed, it caps the achievable pulse. This is why a GHRP co-injection changes the result so much.

• Hepatic IGF-1 production (indirect) — Not applicable

  Modest IGF-1 elevation with daily pulsatile dosing - far less than the DAC version, because total GH exposure across 24 hours is much smaller.

• Soule et al., comparison of GHRH(1-29)NH2 and [D-Ala2]-GHRH(1-29)NH2 pharmacokinetics in normal men 1 · 1994

  The D-Ala2 substitution increased half-life and decreased metabolic clearance rate relative to native GHRH(1-29)NH2 in healthy men. This is the closest thing to direct human evidence for the design of Mod GRF 1-29, and it covers only one of the four substitutions.

GH begins climbing within about ten minutes of a subcutaneous injection and peaks at 15 to 30 minutes, returning to baseline within roughly ninety minutes to two hours. Flushing and facial warmth, if they occur, are immediate and gone in twenty minutes. The first subjective change is almost always sleep - deeper, sometimes with more vivid dreams - within the first week to ten days of nightly dosing. Improved recovery between sessions and reduced joint stiffness show at two to four weeks. IGF-1 moves modestly and slowly, and week 8 is the earliest sensible measurement. There is nothing to wash out: 24 hours after the last injection this compound is pharmacologically gone.

This compound is not really meant to be run alone, and running it alone is the most common way people conclude it does nothing. Its job is to set pulse amplitude; a GHRP's job is to open the gate. Paired with 200 to 300 mcg ipamorelin in the same syringe at 100 mcg, it produces the largest GH pulse per dollar available in this class. Paired with GHRP-2 the pulse is bigger still and you accept prolactin and cortisol drift; with GHRP-6 you accept hunger; with hexarelin you get the biggest pulse of all and two weeks before tachyphylaxis. Mixing in one syringe is chemically fine - both are lyophilised peptides in bacteriostatic water and there is no documented incompatibility - though it means both degrade at the rate of the less stable component, which is this one. Do not stack with the DAC version: same receptor, same backbone, and the DAC's continuous signal makes the pulsatile one irrelevant. Do not stack with tesamorelin for the same reason. Stacking with exogenous GH is self-defeating.

Against sermorelin: same receptor, same effect, but sermorelin has a ten-minute half-life against this one's thirty, is FDA-approved history rather than research chemical, and is available through compounding pharmacies with actual quality control. If you can get sermorelin legitimately, the case for the grey-market fragment weakens considerably - the protease resistance is a real advantage but not a transformative one when both are gone within the hour. Against CJC-1295 with DAC: covered at length elsewhere, but the short version is that they share a backbone and nothing else practically important. Against tesamorelin: tesamorelin is the evidence-backed member of this receptor family, with a documented visceral-fat effect and an FDA approval, at roughly ten times the dose and a comparable half-life. If your goal is visceral fat specifically, the fragment is a poor substitute for the drug that was actually tested. Against a GHRP alone: they are complements, not competitors - the question is not which but whether you are running both.

$20–$55/month. Approximate grey-market pricing. A 5 mg vial typically runs 25 to 45 USD and at 100 mcg per pulse a single nightly protocol uses about 3 mg a month, so one vial covers roughly six weeks. Three pulses daily triples that. It is the cheapest component of the standard stack. Prices are observed and approximate.

• ?The commonly quoted 30-minute half-life for the tetrasubstituted fragment has no primary human pharmacokinetic source that this session could resolve. It is inferred from the D-Ala2 work plus the general behaviour of protease-resistant GHRH analogues.
• ?No published human trial exists of this exact molecule - no PK, no dose-response, no efficacy. Everything practical about it is GHRH-class pharmacology plus consistent user reporting.
• ?The 100 mcg saturation dose is a widely repeated figure whose primary source was not located. It is consistent with roughly 1 mcg/kg GHRH dosing used in diagnostic testing.
• ?The molecular weight of 3367.9 given in the Core record was not independently confirmed and is not resolvable from PubChem under an unambiguous name.
• ?Whether the Ala15 substitution actually increases potency in humans, as opposed to in receptor assays, is not established.
• ?The claim that this fragment is meaningfully less stable in solution than other peptides is consistent with the design rationale and with user reports, but no formal stability study was located.

• Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men Soule S, King JA, Millar RP, Journal of Clinical Endocrinology and Metabolism, 1994 · PMID 7962295

  The only human pharmacokinetic evidence directly bearing on why this molecule is designed the way it is.

• 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 Jetté L, Léger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, Pham K, Bridon DP, Endocrinology, 2005 · PMID 15817669

  Documents the tetrasubstituted GRF(1-29) backbone that this compound is, and shows what happens when you attach a DAC to it. Useful for understanding exactly what the naming confusion is about.

• 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 Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA, Journal of Clinical Endocrinology and Metabolism, 2006 · PMID 16352683

  Further reading. This characterised the same peptide backbone in its DAC form, not the bare fragment people inject nightly, and is routinely misquoted as evidence for this compound.

• UniProtKB P01286, somatoliberin (human growth hormone-releasing hormone precursor) UniProt Knowledgebase

  Primary sequence reference. The mature GHRH sequence YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL was retrieved directly and is the parent from which the tetrasubstituted analogue is derived.