Every human number attached to CJC-1295 comes from a trial of the other version. The no-DAC form, Mod GRF 1-29, has never been through a published human study. Its dosing, its IGF-1 response and its half-life are inferred, not measured.
There is a second story here that rarely gets told: the CJC-1295 development programme ended in 2006, and the reason it ended is not a footnote. This article is the evidence audit — what belongs to this molecule, what was borrowed from its sibling, and what was never measured at all. For per-injection volume, use the CJC-1295 and ipamorelin calculator alongside the reconstitution calculator, and see the growth hormone peptides category for the rest of the axis.
Has CJC-1295 without DAC ever been tested in humans?
No published human study of the no-DAC form exists. The two human trials routinely cited for CJC-1295 — Teichman 2006 and Ionescu and Frohman 2006, both in JCEM — used the DAC form, the long-acting variant carrying an albumin-binding linker. Every figure that travels with this compound belongs to that molecule: the 2- to 10-fold GH elevation, the 1.5- to 3-fold IGF-1 rise, the 5.8–8.1 day half-life. None of it was measured with the no-DAC molecule.
That is a strong claim, so it is worth being precise about what it does and does not mean.
It does not mean CJC-1295 without DAC has no effect. It is a GHRH receptor agonist, GHRH agonism is well characterised, and the mechanistic case that it raises GH in people is close to certain.
It means nobody has measured how much, for how long, at what dose, or with what safety profile in a human being, and published it. The compound sits on solid mechanistic ground and almost no empirical ground.
Where does the CJC-1295 human evidence actually come from?
The evidence comes from three papers, none of them about the no-DAC molecule. Campbell et al., "Enhanced stability and potency of novel growth hormone-releasing factor (GRF) analogues" (Peptides, 1994) established the tetrasubstituted GRF(1-29) framework that both CJC-1295 forms use. ConjuChem Biotechnologies in Montreal then added the albumin linker, published in Endocrinology, 2005, identifying CJC-1295 as a long-lasting GRF analogue — the DAC form. The human data followed, and all of it concerns that form.
Teichman et al. (JCEM, 2006) — two randomised, placebo-controlled ascending-dose studies in healthy adults aged 21–61. Single subcutaneous doses raised mean plasma GH 2- to 10-fold for six days or more and IGF-1 1.5- to 3-fold for 9–11 days. Half-life 5.8–8.1 days.
Ionescu and Frohman (JCEM, 2006) — showed that pulsatile GH secretion persists under continuous stimulation, with trough GH elevated 7.5-fold, mean GH up 46% and IGF-1 up 45%.
That second finding is genuinely important, and it is the strongest argument for the GHRH-analogue approach as a class: the compound augments the body's own GH pulses rather than flattening them into a continuous exogenous signal, which is what recombinant hGH does.
It is also the finding most often quoted as though it were a property of the vial people actually buy. It is not. It was measured under continuous stimulation from a molecule with a half-life of days.
Why did CJC-1295 development stop in 2006?
The Phase 2 programme was halted after a participant died. NCT00267527, a trial of CJC-1295 in HIV-associated visceral obesity, is recorded as terminated; it was stopped in July 2006 after a participant died of a myocardial infarction hours after receiving an eleventh weekly dose. The attending physician attributed the event to pre-existing asymptomatic coronary artery disease rather than the study drug.
That attribution may well be correct. The participant had undiagnosed heart disease, and single events in small trials rarely establish causation.
But ConjuChem ended the programme, and no sponsor has pursued registration since. Twenty years on, that remains the terminal point of CJC-1295's clinical development.
Anyone evaluating this compound should know that its trial history ends with a death and an abandoned programme, whatever the causal verdict. That is not the same as saying the compound killed someone. It is the reason there is no Phase 3, no label, and no long-term human safety dataset for either form.
What is the molecule, and what does the DAC addition change?
CJC-1295 without DAC is GHRH(1-29) carrying four substitutions — D-Ala2, Gln8, Ala15, Leu27 — and a C-terminal amide, CAS 863288-34-0, formula C₁₅₂H₂₅₂N₄₄O₄₂, molecular weight 3,367.9 g/mol, half-life about 30 minutes. The substitutions exist to resist enzymatic degradation, principally by DPP-IV, which clears native GHRH within minutes. The DAC form adds one thing: a thirtieth lysine bearing a maleimidopropionyl group that binds covalently to circulating albumin.
Property | Value |
|---|---|
Sequence | GHRH(1-29) with D-Ala2, Gln8, Ala15, Leu27 substitutions and a C-terminal amide |
Length | 29 amino acids |
CAS | 863288-34-0 (PubChem CID 56841945) |
Formula / MW | C₁₅₂H₂₅₂N₄₄O₄₂ / 3,367.9 g/mol |
Half-life | ~30 minutes |
Also known as | Mod GRF 1-29, Modified GRF (1-29) |
That single addition extends half-life from about half an hour to roughly 5.8–8.1 days and mass from 3,367.9 to about 3,647 Da. Same backbone, radically different pharmacokinetics — and, as it turns out, radically different amounts of evidence.
One correction to our own page. The CJC-1295 without DAC compound page currently shows a molecular weight of 3,645.9, which is a DAC-form figure — roughly 280 daltons above this molecule's actual mass, and the same gap that separates the two products. The correct value for the no-DAC form is 3,367.9 g/mol. That page is being corrected, and until it is, use the value in the table above rather than the one on the page.
The closest related molecule with an approval history is sermorelin — native, unmodified GHRH(1-29), which sits 10 daltons below the no-DAC form at 3,357.9 and is the only member of this family FDA ever approved.
What is actually known about the no-DAC form?
Almost nothing specific, and the table below is mostly a column of unknowns. The half-life figure of ~30 minutes is the only quantitative property with broad agreement, and it is consistent with the absence of albumin binding rather than derived from a published human pharmacokinetic study. Everything downstream of that — the GH magnitude, the IGF-1 response over weeks, the body-composition effect, the optimal dose — has no measurement in people for this molecule.
Question | Status |
|---|---|
Does it raise GH in humans? | Mechanistically near-certain — it is a GHRH receptor agonist — but never measured in a published human study |
By how much? | Unknown. The 2–10× figure belongs to the DAC form |
IGF-1 response over weeks? | Unknown. No dose-response study exists |
Half-life | ~30 minutes, consistent with the absence of albumin binding |
Effect on body composition | No published human trial |
Safety | No dedicated human safety data for this form |
Optimal dose | No trial has established one |
For a GHRH analogue that does have a human trial record and an FDA approval, see tesamorelin — approved for HIV-associated visceral adiposity on the strength of Phase 3 data.
Claims versus evidence
Of the eight claims routinely made for CJC-1295 without DAC, not one is supported by a human study of this molecule. Two are supported by human studies of the DAC form — pulsatile GH release and the pulsatility-preservation finding. Three are inferences from GH physiology that were never tested. Two are community conventions with no dose-response data behind them. One, the half-life, is structurally plausible and lightly sourced. That distribution is the article in a single table.
Claim | Evidence | Verdict |
|---|---|---|
Raises GH in a pulsatile, physiological pattern | Demonstrated — for the DAC form | Wrong form, right principle |
Increases IGF-1 by a specific percentage | No no-DAC dose-response study exists | No source |
Half-life ~30 minutes | Consistent with structure; widely reported | Plausible, lightly sourced |
Preserves natural GH pulsatility | Demonstrated for the DAC form under continuous stimulation | Parent-form evidence |
Builds lean mass / reduces fat | No human body-composition trial | No data |
Improves deep sleep and collagen synthesis | Extrapolated from GH physiology, not tested | Inference |
Saturation dose around 100 mcg | Community convention; no dose-response data | Unverified |
Safer than the DAC form because it clears faster | Reasonable hypothesis; never tested comparatively | Untested |
Can pharmacies compound CJC-1295, and is it banned in sport?
No to the first, yes to the second. CJC-1295 is not approved for human use by the FDA, EMA or TGA. FDA placed it in 503A Category 2 in September 2023, then removed it in September 2024 after the nominators withdrew and referred it for advisory review. At the Pharmacy Compounding Advisory Committee meeting of December 4, 2024, FDA proposed that all five CJC-1295 substances not be included on the 503A bulks list, and the committee agreed.
The five are the free base, the acetate, the DAC free base, the DAC acetate and the DAC trifluoroacetate — every form on the market, including the one this article is about.
CJC-1295 was not on the July 2026 PCAC agenda, so that December 2024 outcome stands. Note that this is the opposite direction from BPC-157, KPV, TB-500 and MOTS-c, which the committee recommended in July 2026. CJC-1295 was reviewed earlier and rejected — a distinction worth keeping straight, because "peptides are being reconsidered by FDA" is true in general and false for this one.
Both forms are prohibited at all times on the 2026 WADA Prohibited List under S2.2.4, Growth Hormone Releasing Factors, which names GHRH analogues explicitly alongside CJC-1293, sermorelin and tesamorelin. See our FDA peptide regulation timeline.
How is CJC-1295 without DAC dosed?
No human trial has validated any no-DAC dosing regimen. Community practice runs to 100–200 mcg daily subcutaneously, often split morning and evening, on the reasoning that a 30-minute half-life calls for frequent dosing to mimic natural GHRH pulses. The commonly cited "saturation dose" of around 100 mcg per injection has no published dose-response study behind it — nobody has measured where the response curve flattens in humans for this molecule.
That reasoning is coherent. It is not evidence, and the distinction matters more here than for most compounds, because there is no measured curve anywhere to fall back on.
Reconstitution arithmetic is the one part of this that is deterministic rather than inferred. Use the CJC-1295 and ipamorelin calculator for per-injection volume, and see how to calculate peptide doses if you are converting between vial strengths.
Does pairing it with ipamorelin do anything?
The receptor rationale is sound and the human evidence is absent. The standard combination pairs a GHRH analogue with a ghrelin-receptor agonist, most often ipamorelin, because GHRH-R and GHS-R1a are separate receptors on the same pituitary somatotrophs and stimulating both is expected to produce a larger GH release than either alone. No controlled human trial of the pairing has quantified that effect, so the specific synergy percentages circulating for it are unsourced.
Two receptors, one cell type, a plausible additive mechanism — that is real endocrinology, and it is why the combination is popular rather than arbitrary.
What does not follow is a number. Any figure you see for how much more GH the pair releases than either compound alone has no controlled human study behind it, for this GHRH form. See the CJC-1295 and ipamorelin stack guide and the blend compound page.
How do you tell the no-DAC form from the DAC form in a vial?
Mass spectrometry, and nothing else. The two forms differ by about 280 Da — roughly 3,368 Da for the no-DAC form against 3,647 Da for the DAC form — which is a gap any mass spectrometer resolves trivially and no HPLC purity figure addresses. It needs resolving, because the two are frequently mislabelled, sold under the unqualified name "CJC-1295", and are not interchangeable products: one is dosed daily, the other weekly.
Without DAC (Mod GRF 1-29) | With DAC | |
|---|---|---|
Half-life | ~30 minutes | 5.8–8.1 days |
Dosing | Daily or twice daily | Weekly |
Mass | ~3,368 Da | ~3,647 Da |
GH pattern | Short pulses, closer to physiological | Sustained elevation with pulses preserved |
Human data | None published | Phase 1–2; programme terminated 2006 |
Check | What it confirms | How | Red flag |
|---|---|---|---|
Mass spectrometry | Which form you have — ~3,368 Da (no DAC) vs ~3,647 Da (with DAC) | Batch-matched CoA with MS | Purity given with no identity test |
CAS on the label | Vendor knows which form it sells | 863288-34-0 for the no-DAC form | Vendor uses "CJC-1295" with no qualifier |
HPLC purity | Proportion of intended peptide | Third-party CoA, named lab | Vendor's own document only |
Net peptide content | Peptide versus salts and water | Net content or amino acid analysis | Purity quoted as if it were quantity |
Endotoxin (LAL) | No pyrogens in injectable material | LAL result | Not tested, not mentioned |
A caution on public databases: PubChem's records for CJC-1295 carry conflated synonyms, with both DAC and no-DAC names attached to the same structure. Verify against the mass and the structure rather than trusting a name in a synonym list.
The Purity Index records the no-DAC form at 99.53 (verified August 2026), above the platform composite of 99.50 and above the 99.23 recorded for CJC-1295 with DAC. CJC-1295 without DAC price data publishes shops in stock, median and lowest price per milligram with the vial size behind the lowest figure, and is the current source for cost comparisons — read within a single vial-size band, since fixed per-vial costs push the per-milligram figure down as fill size rises. Those figures exclude shipping, taxes and customs, coupon codes, bulk tiers, multi-vial kits and account-gated pricing.
Peptigrity tracks 530 shops and 11,852 independent lab tests across 118 peptides, with 1,283 community reviews (verified August 2026), weighting community reviews and independently verified purity equally in every trust score. Compare individual results in the lab test database, and see mass spectrometry for peptides, how to read peptide lab test results and why 10 mg isn't 10 mg. The full side-by-side is in CJC-1295 vs CJC-1295 with DAC, and the DAC form has its own article at CJC-1295 with DAC long-acting GHRH science.
What should you monitor if you use it anyway?
The community convention is IGF-1 measured against an age-adjusted reference range every six to eight weeks, and two things about that practice need saying. It is community-derived, not clinical guidance. And the reference range is strongly age-dependent, so a flat cutoff like "stop above 250 ng/mL" is not meaningful — that value can be entirely normal in a young adult and clearly elevated in someone in their sixties. Bloodwork needs interpreting against your own age band, ideally with a clinician.
Stop if joint pain or swelling appears, if headaches or vision changes occur without another explanation, or if IGF-1 stays persistently elevated.
Anyone with a history of cancer, diabetes or impaired glucose tolerance should not be self-experimenting with the GH axis at all. GH elevation reduces insulin sensitivity, and the IGF-1 axis is implicated in tumour growth — two mechanisms that turn a theoretical risk into a specific one for those groups.
The trial that would settle this
The missing study is unusually simple to specify: a randomised, placebo-controlled trial of the no-DAC molecule itself, dosed subcutaneously the way people dose it, with GH and IGF-1 measured across a dose range and body composition as a secondary endpoint. Every property this compound is sold on — magnitude, duration, saturation point, body-composition effect — currently comes from the DAC form or from GH physiology. One dose-ranging study in humans would replace all of it with measurement.
Element | Requirement | Why |
|---|---|---|
Molecule | The no-DAC form itself | Every published human result used the DAC form |
Design | Randomised, placebo-controlled | The compound has no controlled human data of its own |
Dosing | A dose range spanning 100–200 mcg | The "saturation dose" has no dose-response study behind it |
Primary endpoint | GH and IGF-1 across weeks | The 2–10× and 1.5–3× figures belong to the sibling |
Secondary endpoint | DEXA body composition | No human body-composition trial exists for either form outside HIV |
Comparator arm | The DAC form, and ipamorelin co-administration | Both comparisons are asserted constantly and tested never |
Frequently Asked Questions
Is there any human trial of CJC-1295 without DAC?
No. The published human data — Teichman 2006 and Ionescu 2006, both in JCEM — used the DAC form. The no-DAC molecule has never been through a published human study, so its magnitude, duration and safety in people are inferred rather than measured.
What's the actual difference between the two forms?
One addition: a thirtieth lysine carrying a maleimidopropionyl group that binds covalently to albumin. That extends the half-life from about 30 minutes to nearly a week and adds about 280 Da of mass. The backbone is otherwise identical.
Is CJC-1295 legal to compound now?
No. FDA proposed in December 2024 that all five CJC-1295 substances — free base, acetate, DAC free base, DAC acetate and DAC trifluoroacetate — not be included on the 503A bulks list, and the advisory committee agreed. It was not revisited in July 2026.
Why did development stop?
The Phase 2 trial in HIV-associated visceral obesity was halted in July 2006 after a participant died of a myocardial infarction hours after an eleventh weekly dose. The death was attributed to pre-existing coronary disease, but the programme ended and no sponsor has restarted it in twenty years.
How do I know which form is in my vial?
Mass spectrometry: roughly 3,368 Da is the no-DAC form, roughly 3,647 Da is the DAC form. Vendors frequently sell both under the unqualified name "CJC-1295," and an HPLC purity figure cannot tell them apart.
Does it work better with ipamorelin?
The receptor rationale is sound — GHRH-R and GHS-R1a are two different receptors on the same pituitary cells. No controlled human trial has quantified the combination, so specific synergy figures are unsourced.
Where CJC-1295 without DAC sits
CJC-1295 without DAC is a well-designed molecule on a well-understood pathway, with a development history that ended two decades ago and a human evidence base belonging to its sibling. That is not a reason to dismiss it. GHRH agonism is real pharmacology, and the pulsatility finding is a genuinely good argument for the approach — arguably the best argument any GH secretagogue has.
It is a reason to be precise about what is known. Nearly everything specific said about this compound in humans is either borrowed from the DAC form or extrapolated from GH physiology. The molecule itself has never been measured.
The practical consequence is narrower than "avoid it" and wider than "it's fine". If you buy it, you are buying a molecule whose identity you can verify to the dalton and whose effects you cannot verify at all. Those two facts should carry different weights in the decision, and usually do not.
Browse the growth hormone peptides category, or our complete peptide guide with 118 compounds (verified August 2026). For per-injection volume, use the CJC-1295 and ipamorelin calculator alongside the reconstitution calculator. Compare shops through independent lab tests and community-verified shop reviews.
This article is for educational and informational purposes only and does not constitute medical advice. Peptides discussed may be investigational compounds not approved by the FDA (or equivalent regulators in your jurisdiction) for human use. Always consult a qualified healthcare provider before using any peptide or research compound. Peptigrity is an independent review platform and does not sell, endorse, or recommend specific products or vendors.
