Every human number attached to CJC-1295 without DAC comes from a trial of the other version: FDA's 2024 review of the literature found three published human studies of CJC-1295, and all three gave healthy volunteers the long-acting DAC form. CJC-1295 without DAC is a synthetic 29-amino-acid analogue of growth hormone-releasing hormone (GHRH, also called growth hormone-releasing factor, GRF), the signal that tells the pituitary gland to release growth hormone (GH); it has a molecular weight of 3,367.9 daltons (Da), and, as of September 2026, no regulator anywhere has approved it for any use. The DAC form adds a drug affinity complex (DAC), a linker that binds the molecule to albumin in the blood so that it acts for days rather than minutes.
The no-DAC form, Mod GRF 1-29, has never been through a published human study as of September 2026. Its dosing, its IGF-1 response and its half-life are inferred, not measured. IGF-1, insulin-like growth factor 1, is the hormone the liver releases in response to growth hormone.
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. What vials sold as this form actually contain is a separate, measurable question, and the certificates on file are listed on the CJC-1295 without DAC lab tests page. The rest of the growth-hormone axis, from sermorelin to ipamorelin, is grouped with the other growth hormone peptides on Peptigrity's category page.
The short version
CJC-1295 without DAC, also sold as Mod GRF 1-29, is a lab-made version of the hormone that tells the pituitary gland to release growth hormone, with four changes that make it more stable and more potent.
No human study of this form has been published; all three human studies of CJC-1295 gave healthy volunteers the long-acting DAC form, and the only patient trial stopped in 2006 after a participant died.
Shops list it at a median $7.00 per milligram before shipping, taxes and customs (verified September 2026), and injection-site reactions were the most common side effect in the DAC-form trials.
A purity percentage cannot tell the two forms apart; a mass-spectrometry result, the lab test that weighs the molecule, can, at about 3,368 Da for this form against about 3,647 Da for the DAC form.
US pharmacies cannot compound it: it has no route under FDA's compounding rules, and FDA's advisory committee voted in December 2024 against adding any CJC-1295 form to the list that would create one; the World Anti-Doping Agency prohibits it at all times (both as of September 2026).
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 the Journal of Clinical Endocrinology & Metabolism (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.
FDA's own literature search reached the same result. The FDA Briefing Document Pharmacy Compounding Advisory Committee (PCAC) Meeting December 4, 2024 found three studies in which CJC-1295 was given to humans — the two above and Sackmann-Sala et al. 2009 — and all three gave the DAC form to healthy subjects; it also records that no clinical safety information on CJC-1295 (free base), FDA's name for the no-DAC molecule, was submitted by the nominators or found by the agency.
Where does the CJC-1295 human evidence actually come from?
The evidence comes from two preclinical papers and three published human studies, none of them about the no-DAC molecule. A 1994 paper in Peptides set out why GRF analogues need replacements at positions 2, 8, 15 and 27, the positions all four CJC-1295 substitutions occupy, and tested its analogues in rat pituitary cells and in pigs. ConjuChem Biotechnologies in Montreal then added the albumin linker and, in rats, identified CJC-1295 as a long-lasting GRF analogue — the DAC form. The human data followed, and all of it concerns that form.
The 1994 paper is "Enhanced stability and potency of novel growth hormone-releasing factor (GRF) analogues derived from rodent and human GRF sequences" (Campbell et al.), whose analogues were eleven to thirteen times more potent than native GRF when injected into pigs. The ConjuChem rat study 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 et al., Endocrinology, 2005), in which the conjugate bound albumin and was still circulating in rat plasma beyond 72 hours.
"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 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.
"Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog" (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.
Set side by side, the record behind both forms is short, and none of it used the no-DAC molecule (RCT means randomised controlled trial):
Study | Type | n | Key finding | Limitation |
|---|---|---|---|---|
Campbell et al., 1994 | In vitro (rat pituitary cells) and animal (pigs) | Not a human study | Analogues substituted at positions 2, 8, 15 and 27 resisted breakdown and were 11–13 times more potent than native GRF in pigs | GRF(1-32) analogues, not CJC-1295 in either form |
Jetté et al., 2005 | Animal (rats) | Not a human study | The DAC conjugate bound albumin and was still in plasma beyond 72 hours | DAC form only |
Teichman et al., 2006 | Human RCT, two placebo-controlled trials | 42 and 24, per FDA's summary | GH up 2–10-fold for 6+ days and IGF-1 up 1.5–3-fold for 9–11 days after one dose; half-life 5.8–8.1 days | DAC form; healthy adults; one to three doses |
Ionescu and Frohman, 2006 | Human, before-and-after | Healthy men; n not given in the abstract | GH pulses preserved; trough GH up 7.5-fold, mean GH up 46%, IGF-1 up 45% | DAC form; one dose; one week |
Sackmann-Sala et al., 2009 | Human, before-and-after | 11 men from the Ionescu and Frohman study, per FDA | Serum protein profile changed after one dose | DAC form; adverse events not discussed |
NCT00267527 (ConjuChem, Phase 2) | Human RCT, terminated | 120 listed on the registry | Stopped in July 2006 after a participant died; no results published | DAC form; HIV-associated visceral obesity |
Any study of the no-DAC form | None | 0 | None published | No human data of any kind |
Why did CJC-1295 development stop in 2006?
The Phase 2 programme was halted after a participant died. The trial record, "A Study to Evaluate CJC 1295 in HIV Patients With Visceral Obesity" (NCT00267527), lists the study as terminated; it tested the DAC form in HIV-associated visceral obesity, meaning excess fat around the abdominal organs, and was stopped in July 2006 after a participant died of a myocardial infarction, a heart attack, hours after receiving an eleventh weekly dose. The attending physician's most likely explanation was asymptomatic coronary artery disease, with a ruptured plaque blocking an artery.
Those details come from anecdotal reports that FDA summarised in the FDA Briefing Document Pharmacy Compounding Advisory Committee (PCAC) Meeting December 4, 2024, which gives the regimen as weekly injections escalated over three weeks and continued for nine more, and records that the trial's data were never published.
That attribution may well be correct. 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 registry number 446036-97-1, formula C₁₅₂H₂₅₂N₄₄O₄₂, molecular weight 3,367.9 g/mol, half-life about 30 minutes. The substitutions make the peptide more stable and more potent: D-Ala2 guards the site where DPP-IV, the blood enzyme that clears native GHRH within minutes, cuts the molecule; Gln8 and Leu27 block chemical rearrangement and oxidation; and Ala15 strengthens receptor binding. 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 | 446036-97-1; PubChem also lists 863288-34-0, which FDA's December 2024 review calls a deleted CAS number |
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 used to show 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 page now carries the correct 3,367.9 g/mol (verified September 2026), and a no-DAC listing anywhere else that still prints 3,645.9 or about 3,647 is showing a DAC-form mass.
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 GRF(1-29) peptide FDA has ever approved, as Geref, since discontinued.
What is actually known about the no-DAC form?
Almost nothing specific is known about CJC-1295 without DAC, 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, as of September 2026. CJC-1295 is not approved for human use by the FDA, the European Medicines Agency (EMA) or Australia's Therapeutic Goods Administration (TGA), and it is not on the 503A bulks list, the route that lets pharmacies compound a substance neither in a USP monograph nor part of an approved drug. At the Pharmacy Compounding Advisory Committee meeting of December 4, 2024, FDA proposed that all five CJC-1295 substances not be included on that list, and the committee agreed.
FDA had placed CJC-1295 in 503A Category 2, its list of substances that may present significant safety risks in compounding, in September 2023, then removed it in September 2024 after the nominators withdrew their nominations, and evaluated it for the committee on its own initiative. The Final Summary Minutes of the Pharmacy Compounding Advisory Committee Meeting December 4, 2024 record a separate vote on each substance, because one member declined a single group vote: 0 in favour and 13 against for the free base, 1–12 for the acetate, and 0–13 for each of the three DAC substances.
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, which FDA's documents call CJC-1295 (free base). With no approved product and no compounding route, what reaches buyers is research-labelled material from the grey market for peptides, where nobody upstream answers for a batch.
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, in and out of competition, under S2.2.4, Growth Hormone Releasing Factors, of the World Anti-Doping Agency's 2026 list, The Prohibited List, which names CJC-1295 explicitly among the GHRH analogues, alongside CJC-1293, sermorelin and tesamorelin. The wider FDA sequence for peptides in 2025 and 2026 is laid out in FDA Peptide Regulation 2025-2026, step by step.
How is CJC-1295 without DAC dosed?
CJC-1295 without DAC has no established human dose: no human trial has tested any no-DAC dosing regimen. Community-reported protocols run to 100–200 mcg a day by subcutaneous injection (under the skin), 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.
The only doses ever given to people in a published study were of the DAC form, and none of them transfers to a molecule whose half-life is measured in minutes rather than days:
Form | Route | Dose (as stated by the source) | Frequency | Duration | Evidence level | Source |
|---|---|---|---|---|---|---|
Without DAC | Subcutaneous | No established human dose; community protocols report 100–200 mcg a day, often split in two | Daily | Not reported | Community-reported | None; no trial has tested any dose |
Without DAC | Subcutaneous | "Saturation dose" of about 100 mcg per injection | Per injection | Not reported | Community-reported | None; no dose-response study exists |
With DAC | Subcutaneous | One dose at one of four ascending levels, up to 250 mcg/kg | Once | 28-day study | Human RCT, healthy adults | Teichman et al., 2006, study 1 (n = 42) |
With DAC | Subcutaneous | Two or three doses of up to 60 mcg/kg | Weekly or 14 days apart | 49-day study | Human RCT, healthy adults | Teichman et al., 2006, study 2 (n = 24) |
With DAC | Subcutaneous | One dose of 60 or 90 mcg/kg | Once | One week | Human, before-and-after, healthy men | Ionescu and Frohman, 2006 |
Reconstitution arithmetic is the one part of this that is deterministic rather than inferred. The Peptide Reconstitution Calculator converts a vial's milligrams and the volume of diluent added into a concentration and syringe units; the arithmetic is exact, and no dose it is applied to has been tested in people.
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. Vials that combine the two have their own compound page, CJC-1295 + Ipamorelin blend, with the lab results filed for them.
How do you tell the no-DAC form from the DAC form in a vial?
Mass spectrometry, and nothing else, tells CJC-1295 without DAC from the DAC form. 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 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 (community-reported) | Weekly or every two weeks in the trials |
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 |
A certificate of analysis (CoA), the lab report that comes with a batch, settles the question only if it carries a mass-spectrometry (MS) result; a purity result from HPLC (high-performance liquid chromatography) is not an identity test:
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 |
High-resolution mass spectrometry | Not sermorelin, which is 10 Da lighter | Elemental composition on the CoA, not one rounded mass | A 10-dalton gap treated as within tolerance |
CAS on the label | Vendor knows which form it sells | 446036-97-1 for the no-DAC form; 863288-34-0 is a deleted number | 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 record for the no-DAC molecule, C152H252N44O42 | CID 56841945, carries conflated synonyms, with DAC-form names attached to the no-DAC structure. FDA's December 2024 review found the same problem in its own substance registry, whose Unique Ingredient Identifier (UNII) entry for the no-DAC free base shows the DAC 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 99.54 across 223 single-vial results (verified September 2026), above the platform composite of 99.51 and above the 99.23 recorded for CJC-1295 with DAC. Peptigrity holds 296 lab certificates for the no-DAC form from 156 shops and 23 labs, 223 of them for single vials; the single-vial results show a median HPLC purity of 99.62% and a median measured content of 107% of the label, 5 of the 222 with a content figure measured below 90% of it, and only 34 of the 223 report endotoxin, the bacterial toxin that causes fever when injected (verified September 2026). They are certificates shops chose to publish, verified for authenticity before listing, a selection bias Peptigrity states openly.
The CJC-1295 without DAC price comparison shows 42 shops in stock at a median $7.00 per milligram, from $2.50 on a 10mg vial, excluding shipping, taxes and customs (verified September 2026), 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: the median is $7.70 for 5mg vials and $6.00 for 10mg. Those figures also exclude coupon codes, bulk tiers, multi-vial kits and account-gated pricing.
Peptigrity lists 720 shops and 13,190 published lab certificates across 118 peptides, with 870 community reviews (verified September 2026), and its Trust Score weights community reviews and lab purity at 50% each, scaled by how much data sits behind each, as How Peptigrity actually works sets out (last updated 14 September 2026). How a mass result verifies identity is covered in Mass Spectrometry for Peptides, including molecular-weight matching. The 280 daltons between the two forms are the whole identity question, and CJC-1295 vs CJC-1295 with DAC walks through which mass a certificate of analysis must show. The long-acting form has its own compound guide, CJC-1295 with DAC, with its lab record and regulatory status.
What side effects have been recorded, and in which studies?
No side-effect data have been published for CJC-1295 without DAC itself, so every recorded adverse event belongs to the DAC form. In the first Teichman trial, adverse events occurred in 33 of 35 volunteers given the DAC form and in 2 of 7 on placebo: injection-site reactions in about 70%, headache in 63% against 14% on placebo, diarrhoea in 43%, and flushing, warmth and transient low blood pressure in 30%, most often at the higher doses of 125 and 250 mcg/kg.
Those frequencies are FDA's summary of the trial in the FDA Briefing Document Pharmacy Compounding Advisory Committee (PCAC) Meeting December 4, 2024, which also records transient hive-like rashes in about 30%, the one reaction not concentrated at the higher doses, and lists a dose-dependent rise in heart rate after a single dose in the Ionescu and Frohman study. FDA's reviewers noted that no serious adverse events were reported in these small, short studies of healthy adults, and that some of the effects warrant further study in people at risk of falls or with heart disease.
The two FDA documents grade the same reactions differently. The agency's compounding-risk page, Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks, still lists CJC-1295 among the nominations withdrawn by their nominators, current as of 22 April 2026, and states that "FDA has identified serious adverse events associated with CJC-1295 including increased heart rate and systemic vasodilatory reaction." Whether the shorter-acting form causes fewer of these reactions has never been tested.
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.
Stop and seek care: swelling of the face or throat, difficulty breathing or hives after an injection are signs of a serious allergic reaction; spreading redness, warmth or pus at an injection site with fever is an infection; severe or persistent abdominal pain with vomiting on a GLP-1 drug can be pancreatitis; confusion, sweating or shaking on an IGF-1 or insulin-adjacent compound can be hypoglycaemia. Call your local emergency number (911 in the US, 112 in the EU, 999 in the UK, 000 in Australia) or go to an emergency department, and bring the vial and its label. Research-use vials are not approved products in any jurisdiction, even where a prescription product of the same molecule exists; no article on this site replaces a clinician who knows your history.
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, and a 2009 analysis of a subset of the 2006 volunteers — 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.
Can US pharmacies compound CJC-1295 now?
No, as of September 2026. 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 attending physician's most likely explanation was 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.
When should you talk to a clinician before using CJC-1295 without DAC?
Before any use. With a history of cancer, diabetes or impaired glucose tolerance, the GH axis is not one to self-experiment with at all, because GH elevation reduces insulin sensitivity and the IGF-1 axis is implicated in tumour growth; heart disease is a reason to ask first as well, since FDA's reviewers flagged heart-rate and blood-pressure effects in the DAC-form studies. An unexplained reaction after an injection is a reason to stop and get checked.
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.
The check this article can hand you works on any vial: a batch-matched mass-spectrometry result near 3,368 Da, not a purity percentage. A vial that arrived without one can still be sent to a lab, and how to test your peptides covers what each test measures and what it costs. Shops that list the compound, with their reviews and lab records, are compared in the peptide shops directory.
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; research peptides are sold for laboratory use and are not manufactured, tested or labelled to pharmaceutical standards. Peptigrity does not recommend doses: every dose figure above is an approved-label value, a published-trial value or a community report, and is labelled as such — a community report is not a recommendation. Self-injection carries risks of infection, allergic reaction and dosing error; signs of a serious allergic reaction, an injection-site infection with fever, severe abdominal pain, or confusion and sweating on an IGF-1 or insulin-adjacent compound are medical emergencies — call your local emergency number. 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.
