CJC-1295 Dosage: DAC vs No-DAC - Dosage Peptide

Search for “CJC-1295 dosage” and the answers you find will contradict each other violently: one page says 2 mg once a week, the next says 100 mcg every night. Both pages may be quoting their sources accurately — because “CJC-1295” is a name that has been attached to two chemically different molecules whose durations of action are not remotely comparable: one with a measured human half-life of 5.8–8.1 days, the other short-acting on a scale of minutes. This article answers the only research question that actually matters here: which molecule is in the vial, what does the published human literature document about its dosing, and where does the documented evidence stop and folklore begin?

Why does “CJC-1295 dosage” have two completely different answers?

The confusion is not the reader’s fault. It is a genuine naming collision that entered the field around 2009–2010 and never got cleaned up.

The original compound — the one that appears in peer-reviewed human trials, the one ConjuChem Inc. developed, the one the World Anti-Doping Agency names by number — is CJC-1295 with DAC. DAC stands for Drug Affinity Complex. It is a chemical appendage that makes the peptide bind covalently to circulating albumin, and it is the entire reason the molecule is interesting. Without the DAC, there is no long half-life, no sustained IGF-I elevation, and no weekly dosing.

The second compound is what the research-chemical market calls CJC-1295 no-DAC — the same modified 29–amino acid peptide backbone with the albumin-binding linker simply left off. This molecule already had a name before anyone called it CJC-1295: Modified GRF(1-29), usually written Mod GRF(1-29). It is not a slow-release version of anything. It is a short-acting secretagogue whose action is measured in minutes.

So when a forum post, a vendor page, or an AI summary says “CJC-1295 is dosed at X,” the statement is meaningless without the DAC qualifier. The two molecules are not interchangeable at any dose, on any schedule, for any purpose. They produce different endocrine profiles by design. Getting the distinction wrong is not a rounding error — it is the difference between a once-weekly compound and a nightly one.

The naming timeline, briefly

ConjuChem’s medicinal chemistry program screened several maleimido derivatives of human growth hormone-releasing factor, hGRF(1-29). The paper that named CJC-1295 — Jetté and colleagues in Endocrinology, 2005 — identifies CJC-1295 explicitly as the tetrasubstituted form of hGRF(1-29) carrying an added Nε-3-maleimidopropionamide derivative of lysine at the C-terminus[1]. Read that carefully: in the primary literature, the maleimide linker is part of the definition of CJC-1295. The compound the market calls “CJC-1295 without DAC” is, by the naming convention of the paper that coined the name, not CJC-1295 at all — it is the tetrasubstituted GRF(1-29) intermediate.

The date the collision began is actually documentable, which is more than most of this topic can say. FDA’s 2024 evaluation of these substances notes that CJC-1295 DAC was first described in 2005, and that a linker-free version first surfaces in the scientific literature in a 2010 report describing a preparation seized by Norwegian police and customs authorities in 2009 — a preparation whose mass spectrometric data matched the CJC-1295 sequence but which did not contain DAC. FDA states plainly that this “appears to be the first reference to CJC-1295 without DAC in the literature”[11]. In other words, the no-DAC molecule entered the record not as a published research compound but as a black-market product carrying a borrowed name.

That is the root of the mess. Someone took the recognisable number and applied it to the cheaper, simpler intermediate, appended “no DAC” as a disclaimer, and the internet did the rest. Sixteen years later, half the dosing advice online is describing one molecule using the other molecule’s name — and the collision is now baked into US regulatory text. When FDA evaluated these compounds in 2024, it had to enumerate five separate bulk drug substances across two distinct active moieties: “CJC-1295 (free base)” and “CJC-1295 acetate” for the no-DAC molecule, and “CJC-1295 DAC (free base),” “CJC-1295 DAC acetate” and “CJC-1295 DAC trifluoroacetate” for the DAC one[11]. When a regulator has to spell out which “CJC-1295” it means before it can evaluate anything, the name is no longer doing its job. Our companion explainer on what CJC-1295 DAC and no-DAC actually are as molecules walks through the chemistry in more detail.

What is the research context for CJC-1295?

To read the dosing literature honestly you need to know what problem CJC-1295 was built to solve, because the design constraints explain every number in this article.

Growth hormone-releasing hormone (GHRH) is a hypothalamic peptide that acts on the GHRH receptor on pituitary somatotrophs to trigger growth hormone (GH) synthesis and release. Its biologically active fragment is the first 29 amino acids, GRF(1-29) — the molecule marketed pharmaceutically as sermorelin. GRF(1-29) works, but it is almost useless as a drug for one reason: it is destroyed almost immediately in plasma. Dipeptidyl peptidase-IV (DPP-4) cleaves the N-terminal dipeptide within minutes, and renal clearance handles the rest. Jetté’s own rat data illustrate the scale of the problem: after subcutaneous injection, native GHRH(1-29) was detectable in plasma for only about one hour, whereas CJC-1295 DAC remained detectable beyond 72 hours[1]. That is why sermorelin-type agents were confined to diagnostic testing and daily paediatric dosing rather than sustained endocrine therapy.

Two engineering strategies were pursued against that problem, and they map exactly onto the two molecules in this article.

Strategy one: modify the peptide backbone

Four amino acid substitutions were introduced into the GRF(1-29) backbone. FDA’s evaluation states them precisely: positions 2, 8, 15 and 27 of GHRH(1-29), natively L-alanine, L-asparagine, L-glycine and L-methionine, were substituted to D-alanine, L-glutamine, L-alanine and L-leucine respectively[11]. Three of those four are stability jobs. One is not, and being precise about that matters, because almost every explainer online asserts otherwise.

D-Ala2 — the important one for stability. DPP-4 cleaves after position 2, and swapping the natural L-amino acid for its D-enantiomer makes that bond a poor substrate. FDA supports this point with the general finding that peptides carrying D-alanine in that position have been shown to be resistant to DPP-IV[11].

Gln8 — replaces an asparagine, per the authors, to overcome potential asparagine rearrangement or amide hydrolysis to aspartate, i.e. deamidation[11].

Leu27 — replaces the sole methionine, intended to prevent methionine oxidation[11].

Ala15 — not a degradation fix at all. Position 15 is a glycine in native GRF(1-29), twelve residues away from the only methionine, and neither Jetté nor FDA’s review ties it to any degradation liability[11]. Substituting a helix-favouring alanine at that position is a potency modification of a kind long documented in the GRF structure–activity literature — it raises GH-releasing potency in isolated pituitary cells, an assay that reflects receptor affinity rather than pharmacokinetics. It is bundled in with three stability modifications and then routinely described as though it were one of them.

So the tetrasubstituted core is three stability modifications plus one potency modification, bundled together and usually described as though all four were the same kind of fix. Together they produce the tetrasubstituted GRF(1-29) — the molecule sold as Mod GRF(1-29) or “CJC-1295 no-DAC.”

Here is a citation trap worth flagging, because it is the same failure this article exists to warn about. Jetté’s paper is frequently quoted for DPP-4 resistance of the tetrasubstituted peptide. What the paper actually says is: “All three human serum albumin conjugates showed enhanced in vitro stability against dipeptidylpeptidase-IV”[1]. That measurement was made on the DAC-bearing conjugates, not on the bare no-DAC intermediate. DPP-4 resistance for the no-DAC molecule follows from the chemistry of the D-Ala2 substitution, which is well established for peptides generally — it is not something that paper measured for that molecule. A DAC result quietly supporting a no-DAC claim is exactly how this whole topic went wrong.

Note also what backbone modification does and does not buy. It buys resistance to one protease. It does not stop renal filtration of a 3.4 kDa peptide. The result is a compound that survives longer than native GRF(1-29) — better, but still a pulse agent.

Strategy two: make the peptide too big to filter

The second strategy is the DAC. A maleimidopropionic acid group is attached via a lysine residue. Maleimide chemistry is thiol-selective: it reacts with free sulfhydryl groups. Circulating human serum albumin carries exactly one accessible free thiol, at cysteine-34. So when the peptide is injected subcutaneously, it finds albumin in the interstitium and plasma and forms a covalent bond to Cys34.

The peptide is now a passenger on a 66 kDa carrier protein with a plasma half-life of about three weeks. It cannot be filtered by the glomerulus. It is sterically shielded from many proteases. Jetté and colleagues confirmed the mechanism directly: Western blot of plasma from a CJC-1295-injected rat showed CJC-1295 immunoreactivity on the albumin band, appearing after 15 minutes and still present beyond 24 hours[1]. That is not a slow-release formulation trick. It is a bioconjugation strategy.

One honest caveat, and it is FDA’s, not ours. Jetté concluded that albumin bioconjugation accounts for CJC-1295 DAC’s greater stability. FDA’s reviewers note that direct evidence for that specific causal attribution is lacking: demonstrating that the half-life of CJC-1295 DAC is longer than that of CJC-1295 without the DAC modification is the experiment that would be needed, and it has not been published. FDA adds that the backbone substitutions themselves could have contributed to the observed stability, so “it remains to be determined the extent to which these amino acid substitutions contribute to the stability of CJC-1295 DAC”[11]. The albumin binding is measured. The long half-life is measured. The claim that the former causes the latter is a well-supported hypothesis that nobody has closed with a head-to-head comparison — worth knowing, given that this is the central premise of every DAC-versus-no-DAC explainer, including this one.

What happened to the development programme

CJC-1295 with DAC progressed into human trials. The ClinicalTrials.gov registry documents a ConjuChem-sponsored study, NCT00267527 — a multicentre, randomised, placebo-controlled, double-blind Phase 2 study of CJC-1295 administered for 12 weeks in HIV-infected patients with HIV-associated visceral obesity, with a registry enrolment estimate of 120 and a start date of December 2005. Its registry status is TERMINATED, with a completion date of September 2006[2]. The registry number understates the real exposure: FDA’s 2024 review reports that 192 subjects were actually enrolled and randomised[11].

We are going to be very disciplined about what follows, because the internet is not — in both directions. One camp asserts CJC-1295 killed someone; the other waves the event away. Both talk past a public record that actually exists.

What is documented. Contemporaneous reporting from NAM/aidsmap documents that ConjuChem halted the lipodystrophy study on 17 July 2006 following the death of a study participant at a site in Argentina, describes the design — once-weekly injections with three-week dose escalation of 60, 90 and 120 mcg/kg in the low-dose arm and 60, 120 and 240 mcg/kg in the high-dose arm against placebo, then continuing for a further nine weeks — and states that at the time, the cause of death and its relationship to the study drug was being investigated[3]. Eighteen years later, FDA’s briefing document for its December 2024 advisory committee meeting put the same event into the regulatory record with more clinical detail. FDA states that “ConjuChem Biotechnology withdrew CJC-1295 DAC from clinical trials in 2006 after the death of a subject involved in a phase 2 trial,” and describes it: two hours after receiving an eleventh weekly dose, one subject complained of chest discomfort, an ECG confirmed an acute myocardial infarction, and the subject died approximately one hour later. The attending physician’s stated most likely explanation was that the patient had asymptomatic coronary artery disease with plaque rupture and occlusion — that is, pre-existing disease rather than study drug. FDA also records that “the study was terminated, and the data from that study has not been published,” and that no further information about the other subjects or their adverse events was available[11].

What does not exist. A formal, published adjudication of drug causality. An attending physician’s opinion recorded in a secondary account is not a causality determination, and FDA itself characterises the underlying reports as anecdotal. Nor does the trial dataset exist in the public literature: 192 randomised patients, twelve weeks of dosing, and not one published table.

The honest summary is therefore narrower than either camp claims. Development was discontinued in 2006 after a fatal myocardial infarction in a phase 2 trial. The treating physician attributed it to pre-existing coronary disease. No independent causality determination was ever published. The dataset remains unpublished twenty years later. And FDA’s own advisory committee, reviewing all of it in 2024, still treated the compound’s cardiac and vasodilatory history as an unresolved part of the safety picture. That is the whole of what can be said, and it is worth more than either the rumour or the dismissal.

What mechanisms have been studied?

Both molecules are agonists at the same receptor. The differences are entirely pharmacokinetic — but pharmacokinetics is exactly what determines the endocrine output, which is why this matters more than it sounds.

The GHRH receptor and the somatostatin brake

The GHRH receptor (GHRHR) is a class B G-protein-coupled receptor on pituitary somatotrophs. Agonist binding drives Gs–adenylate cyclase–cAMP–PKA signalling, which does two things: it triggers release of stored GH, and over longer exposures it increases GH gene transcription and somatotroph proliferation. That second effect is not theoretical — in GHRH-knockout mice, once-daily CJC-1295 increased total pituitary RNA and GH mRNA in a pattern the authors interpreted as somatotroph proliferation, confirmed by immunohistochemistry[4]. Hold on to that finding; it reappears later in this article wearing a much less flattering outfit.

Critically, GHRH is not the only input. Somatostatin (SRIF) tonically inhibits GH release, and the alternation between GHRH drive and somatostatin brake is what produces the characteristic pulsatile GH profile. A GHRH agonist does not override somatostatin. It pushes against it. This has a direct dosing consequence that most protocol pages miss entirely: a GHRH analogue can only release GH when the somatostatin brake is off. During a somatostatin trough, the same dose produces a big pulse; during a somatostatin peak, it produces very little. This is the actual mechanistic reason behind the “dose at night” convention for the short-acting molecule, and it is a mechanistic rationale, not a demonstrated outcome.

Why the two molecules produce different endocrine shapes

Give a short-acting GHRH analogue and you get a pulse: a sharp GH rise, peak within roughly 15–30 minutes, back toward baseline within one to two hours. The pituitary reloads. Endogenous rhythm is preserved because the drug is gone before the next natural pulse window.

Give the DAC version and you get something structurally different: continuous, low-grade GHRH receptor occupancy for days. The key human finding here is Ionescu and Frohman’s 2006 study, which sampled GH every 20 minutes over a 12-hour overnight window before and one week after a single 60 or 90 mcg/kg CJC-1295 injection in healthy men aged 20–40. The result is more nuanced than either camp of the internet claims: pulsatility was preserved. The frequency and magnitude of GH secretory pulses were unaltered. What changed was the floor — basal (trough) GH rose 7.5-fold (p<0.0001), driving a 46% increase in mean GH (p<0.01) and a 45% increase in IGF-I (p<0.001). Notably, there was no significant difference between the 60 and 90 mcg/kg doses, and the IGF-I increases did not correlate with any parameter of GH secretion[5].

That last sentence is worth sitting with. The single most-repeated claim about CJC-1295 with DAC — that it “destroys natural pulsatility” and creates a flat bleed — is not what the human pulsatility study found. Pulses persisted; the trough rose. The equally common counter-claim — that it is simply a superior sustained version of the same thing — ignores that the trough elevation is precisely the non-physiological part, and that a dose increase from 60 to 90 mcg/kg bought nothing measurable.

Why CJC-1295 is so often paired with a ghrelin mimetic

GHRH analogues and growth hormone secretagogues (GHS) such as ipamorelin, GHRP-2 and hexarelin act on different receptors — GHRHR versus the growth hormone secretagogue receptor GHS-R1a, the ghrelin receptor. The class-level observation, established in the GHS literature long before CJC-1295 existed, is that the effect of a GHS on GH release is synergistic with GHRH rather than merely additive, and that GHS remain only partially suppressed by inhibitory influences that nearly abolish the GHRH response.

The synergy is not symmetric, and there is an elegant human experiment that proves it. In patients with a homozygous inactivating mutation of the GHRH receptor, intravenous hexarelin produced a complete absence of GH response — plasma GH stayed under 1 ng/mL, a 50- to 100-fold deviation from the normal response — while prolactin, ACTH and cortisol responses to hexarelin were normal[6]. The interpretation: an intact GHRH signalling system is required for a GHS to release GH at all. A ghrelin mimetic is not an independent GH lever; it is an amplifier of GHRH tone. That is the mechanistic case for the pairing, and it is a genuinely good one — but as we discuss below, a good mechanistic case is not a validated dose.

Ipamorelin is the usual partner for a specific reason. Raun and colleagues characterised it as “the first selective growth hormone secretagogue”: it released GH from rat pituitary cells with potency and efficacy similar to GHRP-6, but — unlike GHRP-6 and GHRP-2, both of which raised ACTH and cortisol — ipamorelin did not release ACTH or cortisol at levels significantly different from GHRH stimulation, even at doses more than 200-fold above its ED50 for GH release[7]. That selectivity is why it displaced the older GHRPs in research pairings.

CJC-1295 DAC vs no-DAC: the side-by-side comparison

This is the table the whole article exists to produce. Every figure in the “documented research protocol” rows reflects what our protocol pages document, not a recommendation; every half-life and endocrine-profile figure is sourced.

Also called

CJC-1295, DAC:GRF, CJC-1295 DAC

Mod GRF(1-29), Modified GRF 1-29, tetrasubstituted GRF(1-29)

Structure

Tetrasubstituted hGRF(1-29) + Nε-3-maleimidopropionamide lysine at C-terminus[1]

Tetrasubstituted hGRF(1-29), no linker

Substitutions

D-Ala2, Gln8, Ala15, Leu27

D-Ala2, Gln8, Ala15, Leu27 (identical)

Binds albumin?

Yes — covalently, at Cys34

No

Half-life

5.8–8.1 days (estimated, human)[8]

Short — minutes. Commonly quoted as ~30 min; not established by any published human PK study we or FDA could locate

GH profile produced

Sustained elevation: trough GH ↑7.5-fold, mean GH ↑46%, pulsatility preserved[5]

Discrete pulse, peak ~15–30 min, back toward baseline within 1–2 h

IGF-I duration after one dose

1.5–3× baseline for 9–11 days; up to 28 days above baseline after multiple doses[8]

No comparable published multi-day IGF-I data

Accumulates with repeat dosing?

Yes — cumulative effect documented[8]

No meaningful accumulation

Documented protocol frequency

Twice weekly

Once daily (commonly before bed)

Documented per-injection range

300–1,000 mcg

100–300 mcg

Documented weekly total

~0.6–2 mg/week

~0.7–2.1 mg/week

Typical reconstitution (5 mg vial)

2.0 mL → 2.5 mg/mL (2,500 mcg/mL)

3.0 mL → ~1.67 mg/mL (~1,670 mcg/mL)

1 unit on a U-100 syringe

25 mcg

~16.7 mcg

Human data exists?

Ascending-dose studies in 63 healthy adults across three papers; the one registered Phase 2 in patients was terminated with no published data[2][11]

No human studies of any kind identified

Regulatory status

Neither is approved for human therapeutic use anywhere. Both are prohibited in sport at all times under WADA S2.

Notice the trap hidden in the weekly-total row. The two molecules land at roughly the same milligrams per week — around 1–2 mg. That coincidence is why the naming collision persists undetected: someone reading “2 mg per week” can apply it to the wrong molecule and the total will look plausible. It is the distribution across the week that differs completely, and distribution is the whole pharmacology. Two 1,000 mcg DAC injections per week and seven 300 mcg no-DAC injections per week are approximately 2 mg either way, and they are not remotely the same intervention.

What doses does the human literature actually document?

Here is where we depart sharply from most pages on this keyword, because the honest answer is uncomfortable.

The anchor study: Teichman et al., 2006

The only substantial controlled dose-ranging human dataset on CJC-1295 is Teichman and colleagues, Journal of Clinical Endocrinology & Metabolism, March 2006 — one of three human studies in total, and the only one designed around dose. Design: two randomised, placebo-controlled, double-blind ascending-dose trials of 28 and 49 days, in healthy subjects aged 21–61, at two investigational sites. The first study gave one of four ascending single subcutaneous doses; the second gave two or three weekly or biweekly doses[8].

What it found, in the authors’ own terms:

After a single injection, dose-dependent increases in mean plasma GH of 2- to 10-fold for 6 days or more.

Mean plasma IGF-I increased 1.5- to 3-fold for 9–11 days.

Estimated half-life of CJC-1295: 5.8–8.1 days.

After multiple doses, mean IGF-I remained above baseline for up to 28 days, with evidence of a cumulative effect.

No serious adverse reactions were reported. Administration was “safe and relatively well tolerated, particularly at doses of 30 or 60 mcg/kg.”

That is the evidentiary bedrock of every CJC-1295 dosing claim in existence. Note what it is: a pharmacokinetic and pharmacodynamic study in healthy volunteers, 28–49 days long, with surrogate endocrine endpoints. It is not an efficacy study. It measured hormones, not outcomes.

One word in that design description is doing more work than it can bear, and we are going to flag it rather than resolve it. The multiple-dose study administered “two or three weekly or biweekly doses.” “Biweekly” means both twice weekly and every two weeks, and the abstract does not disambiguate it. Given a 5.8–8.1 day half-life and a study designed around that half-life, the plain reading is every two weeks — but we are not going to resolve an ambiguity by guessing, in an article whose entire thesis is that frequency ambiguity is the problem. What can be said without guessing: no published trial administered CJC-1295 twice within a single week.

The arithmetic nobody performs

Now do something the protocol pages never do — convert the trial’s weight-based doses into absolute micrograms and compare them to what the research community actually uses. This requires no cross-species extrapolation whatsoever; these were human doses in humans.

Teichman 2006, best-tolerated doses[8]

30–60 mcg/kg

2,100–4,200 mcg

Weekly, or the paper’s ambiguous “biweekly”

Ionescu & Frohman 2006[5]

60 or 90 mcg/kg

4,200–6,300 mcg

Single dose

ConjuChem Phase 2 (terminated)[3]

60→120 mcg/kg escalating; 60→240 mcg/kg escalating

4,200–16,800 mcg

Once weekly × 12 weeks

Full published human range across all three studies[11]

30–250 mcg/kg

2,100–17,500 mcg

Up to four SC injections; 73% received one

Documented research protocols (this site’s DAC pages)

300–1,000 mcg fixed

300–1,000 mcg (≈4.3–14.3 mcg/kg)

The gap is roughly 2- to 14-fold, and it points downward: the doses circulating in research protocols are substantially lower per injection than the doses the only real human PK trial singled out as well tolerated. (Run it yourself: 2,100 ÷ 1,000 = 2.1 at the narrow end; 4,200 ÷ 300 = 14 at the wide end.) This is the single most useful and least-reported fact about CJC-1295 dosing, and it cuts in two directions at once.

On one hand, it is reassuring in the trivial sense: the community converged on doses below the studied range, not above it. On the other hand, it means that the community protocol is not the trial protocol. You cannot cite Teichman to justify 500 mcg twice weekly and then also cite Teichman’s 9–11 day IGF-I elevation as the expected effect — those are different doses. The 300–1,000 mcg twice-weekly convention has no published human PK or PD characterisation at all. It is an empirical folk convention that happens to fall in a conservative region relative to the studied doses. That is the accurate description, and it is much weaker than “clinically studied.”

There is also a mechanistic argument buried in Ionescu & Frohman that deserves attention: 90 mcg/kg produced no significant additional response over 60 mcg/kg[5]. The GHRH receptor is saturable and somatostatin still applies the brake. Beyond some point, more CJC-1295 stops buying more GH and buys only more of the receptor-occupancy duration and whatever risk attaches to it. This is a reasonable inference from the published data, not a demonstrated dose-response ceiling for the sub-milligram range.

What about the no-DAC molecule?

We searched for controlled human trials of Mod GRF(1-29) / CJC-1295 no-DAC as a distinct entity. We did not find any, and neither did FDA: its 2024 literature review identified three human studies, all of CJC-1295 DAC, and it states that it identified no pharmacokinetic studies whatsoever of CJC-1295 free base or CJC-1295 acetate — the two no-DAC substances — nor any genotoxicity data for them[11]. There is no published human pharmacokinetic study establishing its half-life, no published dose-ranging study, no published efficacy trial. The ~30-minute half-life figure that appears on essentially every vendor page and every AI-generated summary is, as far as we can trace it, a repeated assertion rather than a citation to a measurement.

What can be said honestly: the molecule is a GRF(1-29) analogue with a DPP-4-resistant substitution and no albumin anchor; native GRF(1-29) has a plasma half-life measured in minutes; the substitutions plausibly extend that somewhat but cannot alter renal clearance of a small peptide. A short half-life on the order of tens of minutes is therefore chemically reasonable. It is not documented. The distinction matters, because the entire justification for daily-and-sometimes-multiple-daily dosing rests on that number.

CJC-1295 DAC: what do documented research protocols reference?

With the evidence properly framed, here are the figures our protocol pages document, presented as documentation of what the research literature and research protocols reference — not as instruction.

The reference protocol on our CJC-1295 DAC 5 mg vial dosage protocol page documents 300–1,000 mcg per injection, administered twice weekly, over an 8–12 week course. That works out to approximately 0.6–2 mg per week. The twice-weekly cadence is pharmacologically coherent given a 5.8–8.1 day half-life: dosing every 3–4 days means the second dose lands while roughly half the first is still conjugated to albumin, producing the smoothed steady-state the molecule was designed for. It is also worth noting that once-weekly at the same per-injection amount is equally defensible on half-life grounds, and that the twice-weekly convention is a community choice rather than a trial finding — no published trial administered this compound twice in a single week[8].

CJC-1295 DAC 5 mg vial: the reconstitution math

Concentration is a division problem, and it is the only calculation that matters:

Concentration = total mass in vial ÷ volume of diluent added

For a 5 mg vial with 2.0 mL of bacteriostatic water:

5 mg ÷ 2.0 mL = 2.5 mg/mL

2.5 mg/mL × 1,000 = 2,500 mcg/mL

A U-100 insulin syringe is graduated so that 100 units = 1.0 mL, therefore 1 unit = 0.01 mL

2,500 mcg/mL × 0.01 mL = 25 mcg per unit

Every dose is then dose ÷ 25:

300 mcg

0.12 mL

12 units

16 full doses

600 mcg

~8 weeks

400 mcg

0.16 mL

16 units

12 full doses

800 mcg

~6 weeks

500 mcg

0.20 mL

20 units

10 doses

1,000 mcg (1 mg)

5 weeks

750 mcg

0.30 mL

30 units

6 full doses

1,500 mcg

~3 weeks

1,000 mcg

0.40 mL

40 units

5 doses

2,000 mcg (2 mg)

2.5 weeks

Sanity-check the extremes. At 500 mcg twice weekly the vial delivers exactly 10 doses = 5 weeks, so an 8–12 week documented course consumes roughly two to two-and-a-half 5 mg vials. At 1,000 mcg twice weekly the same vial is gone in 2.5 weeks and a 12-week course would consume nearly five vials. The 2.0 mL of diluent fits comfortably in a standard 3 mL lyophilisation vial with room to spare — the actual vial capacity should be confirmed before any diluent volume is chosen rather than assumed.

CJC-1295 DAC 2 mg vial: a different concentration entirely

This is where the arithmetic goes wrong most often. The 2 mg DAC vial protocol documents the same 300–1,000 mcg twice-weekly range — but reconstituted with the same 2.0 mL, it is a completely different concentration:

2 mg ÷ 2.0 mL = 1 mg/mL = 1,000 mcg/mL

1,000 mcg/mL × 0.01 mL = 10 mcg per unit

That is 2.5× more dilute than the 5 mg vial at the same fill volume. Same drug, same dose, two-and-a-half times the units on the syringe:

30 units on the 5 mg vial = 750 mcg (2.5× intended)

50 units

50 units on the 5 mg vial = 1,250 mcg (2.5× intended)

100 units (a full syringe)

100 units on the 5 mg vial = 2,500 mcg (2.5× intended)

The failure mode is obvious once it is laid out. Carry a unit count from a 2 mg vial across to a 5 mg vial reconstituted at the same 2.0 mL, and the same 50 units now corresponds to 1,250 mcg rather than 500 — a 2.5-fold error introduced by nothing but a change of vial. Units are not a dose. Units are a volume. The dose only exists once the concentration is known, and the concentration only exists once both the vial mass and the diluent volume are known. The concentration must therefore be recomputed for every vial mass and diluent volume; a unit count is not portable between them. Our peptide dosage calculator performs the same division for any vial-size and diluent-volume combination.

Note also that 1,000 mcg from a 2 mg vial at 1 mg/mL requires a full 1.0 mL U-100 syringe — half the vial in one injection, and a large subcutaneous bolus volume. That practical constraint is a reason the 5 mg vial is generally the one referenced at the upper end of the documented range.

CJC-1295 no-DAC (Mod GRF 1-29): what do documented protocols reference?

Our CJC-1295 no-DAC 5 mg vial dosage protocol page documents 100–300 mcg per injection, once daily — commonly before bed — over an 8–12 week course. Read that against the previous section: this is a documented convention for a molecule with zero published human data of any kind. The reconstitution documented is 3.0 mL, which produces a deliberately different concentration from the DAC vial:

5 mg ÷ 3.0 mL = 1.667 mg/mL ≈ 1,670 mcg/mL

1,670 mcg/mL × 0.01 mL = ~16.7 mcg per unit

100 mcg

0.06 mL

6 units

700 mcg

50 days — far beyond the stability window

150 mcg

0.09 mL

9 units

1,050 mcg

~33 days

200 mcg

1,400 mcg

25 days

250 mcg

0.15 mL

15 units

1,750 mcg

20 days

0.18 mL

18 units

2,100 mcg (2.1 mg)

~16 days

The right-hand column is the one that catches people out and it deserves its own section.

The stability problem the no-DAC molecule has worst

Documented storage handling for these vials: lyophilised material refrigerated; once reconstituted, refrigerate and use within roughly 1–2 weeks, or freeze at ≤ −20 °C for longer-term storage.

Now look at the table again. At the low end of the documented range — 100 mcg daily — a reconstituted 5 mg vial theoretically contains 50 days of material. The stability window is 1–2 weeks. Those two facts are irreconcilable, and the arithmetic is unambiguous: a 5 mg no-DAC vial reconstituted all at once cannot be consumed at 100 mcg/day within its stability window. Depending on whether the window is taken as one week or two, 700–1,400 mcg of the 5,000 mcg is used — meaning roughly 72–86% of the vial sits past the documented window before it is used.

This is a real, practical, structural feature that almost no dosing page addresses. The DAC molecule has a milder version of the same problem, not an exemption from it: at 500–1,000 mcg twice weekly a 5 mg vial is consumed in 2.5–5 weeks, but at the 300–400 mcg low end of its documented range the same vial takes 6–8 weeks — also far outside a 1–2 week reconstituted window. So the constraint applies to both molecules; it simply bites hardest on the daily one at the bottom of its range. Three consequences follow from the division: a smaller vial size, partial reconstitution with the remainder frozen, or consumption at the upper end of the documented range where the vial empties in ~16 days. That is a description of what the arithmetic implies, not a menu. Our peptide reconstitution guide covers the mechanics, including why bacteriostatic water rather than sterile water is what makes multi-dose use of a reconstituted vial coherent in the first place.

FDA’s own review adds a dimension to the storage question that research-chemical pages rarely raise. Peptides such as CJC-1295 “can be extremely sensitive to product formulation, process, and environmental conditions (e.g., pH, heat (temperature), concentration, in-process related impurities, excipients), which may lead to the aggregation and degradation of peptides,” with consequent loss of biological activity — and detecting the resulting aggregates may require specific analytical methods such as size exclusion chromatography or field flow fractionation[11]. The practical implication is uncomfortable but honest: a 1–2 week window is a handling convention, not a measured stability specification for any particular vial, and degradation is not something that can be seen in a clear solution.

Why “before bed” — and why that is a rationale, not a finding

The bedtime convention for the short-acting molecule comes directly from the somatostatin mechanism described earlier. Endogenous GH secretion is heavily weighted toward the first hours of slow-wave sleep, when somatostatin tone is lowest. A pulse agent administered into that window is pushing on a door that is already opening. Administered mid-afternoon against high somatostatin tone, the same dose would be expected to do less.

That is a coherent mechanistic argument. It is not supported by a published human study of Mod GRF(1-29) timing, because no human study of Mod GRF(1-29) of any kind exists. Label it correctly: a physiologically-motivated convention, not an evidence-based schedule.

The CJC-1295 + ipamorelin question, including the 10 mg blend

This is the most-searched practical question on the topic, so it gets a direct answer: there is no controlled human trial establishing a dose for the CJC-1295 + ipamorelin combination. Not for the DAC version, not for the no-DAC version, not for the blend. The mechanistic rationale is strong and well-grounded — two complementary receptors, ipamorelin’s selectivity for GH over ACTH/cortisol[7], and the GHRH-receptor dependence that makes the pairing logical rather than redundant[6]. But a strong mechanistic rationale is a hypothesis. It is the reason to run the trial, not a substitute for having run it.

Anything describing an “optimal” CJC-1295/ipamorelin ratio is describing a convention, and the conventions in this field are inherited from bodybuilding forums rather than derived from data. We are not aware of a controlled study — or of any published source — that establishes a ratio. Where a number has no trial behind it, the honest label is “community convention,” and that label applies to every CJC-1295/ipamorelin ratio in circulation.

Separate vials vs pre-mixed blends

The two research configurations documented on this site differ in a way that follows directly from everything above.

Separate vials. Our CJC-1295 DAC 5 mg + ipamorelin 5 mg stack protocol keeps the compounds in separate vials. This is the only configuration that is pharmacologically coherent when the DAC molecule is involved, and the reason is arithmetic: the DAC molecule is dosed twice weekly and ipamorelin is dosed daily (see our ipamorelin dosage protocol guide for its documented figures). A twice-weekly compound and a daily compound cannot share a vial and a single schedule without one of them being wrong by a factor of three or four.

Pre-mixed blends. A CJC-1295 + ipamorelin blend vial exists precisely because the no-DAC molecule and ipamorelin share a dosing frequency — both are short-acting, both are dosed daily. That shared cadence is what makes a fixed-ratio blend chemically sensible. This is the answer to the common query about “CJC-1295 ipamorelin 10 mg blend dosage per day”: a blend of that description is a no-DAC blend by structural necessity, and it is dosed daily. If a product is advertised as a “CJC-1295 + ipamorelin blend” with a weekly schedule, or as a DAC blend with a daily schedule, one of the two claims is wrong.

The pairing is not purely a research-chemical phenomenon, and the regulatory record is oddly specific about it: FDA’s 2024 review notes that a US outsourcing facility reported compounding a multiple-ingredient injection powder containing CJC-1295 at 6 mg/mL and ipamorelin at 15 mg/mL in 2019 and 2020 — which form of CJC-1295 was not stated — and that no outsourcing facility has reported compounding any CJC-1295-containing product since 2020[11]. Note that even in a compounded product, nobody recorded which molecule was in the vial. The naming collision reaches all the way into the federal reporting system.

The constraint of a blend is inflexibility: a 10 mg blend vial fixes the ratio of the two peptides permanently at whatever the manufacturer chose. The total drawn can be changed; the ratio cannot. Given that no trial has established what the ratio should be, that permanence encodes a manufacturer’s guess rather than a finding.

What is the current evidence level for CJC-1295?

Precision here is the whole point, so we will tier it explicitly rather than gesture at it.

CJC-1295 DAC binds albumin covalently at Cys34

Established (animal)

Confirmed by Western blot on the albumin band in rat plasma[1]

CJC-1295 DAC has a multi-day human half-life

Measured in humans

5.8–8.1 d estimated in healthy adults[8]

The DAC is the cause of that extended half-life

Proposed — not demonstrated

FDA notes direct comparative evidence is lacking; a DAC vs no-DAC half-life comparison has never been published[11]

CJC-1295 DAC raises GH and IGF-I in healthy adults

Randomised, placebo-controlled ascending-dose studies in healthy volunteers (phase 1-type design; surrogate endpoints only)

Two ascending-dose RCTs, 28 and 49 days[8]; overnight pulsatility study[5]

CJC-1295 DAC normalises growth in GHRH-deficient animals

Preclinical / animal only

GHRH-knockout mouse, once-daily dosing[4]

CJC-1295 DAC improves any clinical outcome in humans

Not established

The only Phase 2 outcome trial was terminated; FDA confirms its data were never published[2][11]

CJC-1295 DAC induces DNA damage in pituitary tissue

In-vitro and rodent only

Comet assay and γH2AX in mouse pituitary, in vitro and in vivo[9]

CJC-1295 no-DAC half-life is ~30 minutes

Unverified assertion

No published human PK study; FDA identified no PK study of either no-DAC substance at all[11]

CJC-1295 no-DAC does anything in humans at 100–300 mcg daily

No human studies of the no-DAC molecule identified, by us or by FDA[11]

CJC-1295 + ipamorelin at any ratio

Mechanistic hypothesis only

GHRH-receptor dependence of the GHS response is established[6]; this combination has no controlled human trial

The 300–1,000 mcg twice-weekly convention

Folk convention

~2–14× below studied doses; no published PK/PD characterisation at this range

The comparison that puts it in perspective

It is instructive to hold CJC-1295 next to a GHRH analogue that did finish the job. Tesamorelin — a different GRF analogue — is FDA-approved (2010, marketed as Egrifta) for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. Note the precision of that indication: one population, one endpoint, not “anti-aging.” And note what it took to get there — 410 patients randomised (273 tesamorelin, 137 placebo) for an initial 26 weeks, then a 26-week extension phase into which 315 patients were re-randomised, showing visceral adipose tissue reduction sustained at −18% over 52 weeks of treatment (p<0.001 versus baseline), plus the honest finding that VAT reaccumulated on discontinuation and the effects did not last beyond the duration of treatment[10].

That is what an evidence base looks like for a GHRH analogue: hundreds of randomised patients, a year of treatment, a hard endpoint, a regulator’s review, and an honest negative finding about durability. CJC-1295’s entire human record is 63 healthy volunteers across three papers, none longer than 49 days, none measuring an outcome, plus one terminated patient trial whose data were never published. Anyone presenting CJC-1295 as a validated intervention is asking you to treat those two things as equivalent. They are not in the same category.

The regulatory position, stated precisely

CJC-1295 — in either form — is not approved by the FDA, EMA, or any comparable regulator for any indication, in any country. It is not a medicine. It is a research chemical. There is no approved label, no approved dose, and no approved route. Every number in this article is either a trial-documented figure or a documented research-protocol convention. None of it is a prescription.

The US compounding history is more interesting than a simple “banned,” so precision matters. CJC-1295 was nominated for inclusion on the section 503A bulk drug substances list and was placed in Category 2 of FDA’s interim policy — the bucket for substances FDA identified as presenting potential significant safety risks. The nominations were later withdrawn by the nominators. Withdrawal did not end the review, and this is the detail that gets reported backwards: FDA states that after the nominations were withdrawn it evaluated the substances “at its discretion” and carried them forward “on its own initiative”[11]. CJC-1295 today appears on FDA’s public list of bulk drug substances nominated but withdrawn — previously in Category 2 — and FDA’s stated safety rationale is still published there verbatim: compounded drugs containing CJC-1295 “may pose risk for immunogenicity for certain routes of administration” and may have complexities regarding peptide-related impurities and API characterisation; FDA “has identified serious adverse events associated with CJC-1295 including increased heart rate and systemic vasodilatory reaction”; and “available clinical data are limited”[12].

FDA’s Pharmacy Compounding Advisory Committee took up all five CJC-1295-related substances at its meeting on 4 December 2024, and voted separately on each. The transcript records the tallies against recommending that FDA place them on the 503A Bulks List: 0 yes / 13 no on four of the five substances, and 1 yes / 12 no on the remaining one[13]. The nuance that gets lost elsewhere: removal from Category 2 is not permission. It lifts a designation; it does not place a substance on the authorised bulks list. And the committee outcome went firmly against inclusion. The practical position for CJC-1295 in the United States is therefore that it is neither approved as a drug nor recommended for 503A compounding. This landscape has been actively moving, so anyone tracking it should check FDA’s current listings rather than rely on any article, including this one.

Anti-doping

CJC-1295 is explicitly named on the WADA Prohibited List. The 2026 List names it at S2.2.4: “growth hormone-releasing hormone (GHRH) and its analogues (e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin).” Ipamorelin, capromorelin, ibutamoren (MK-677), anamorelin, hexarelin (examorelin) and GHRP-2 (pralmorelin) are named in the same section. S2 substances are prohibited at all times — in and out of competition — and the List states verbatim that “all prohibited substances in this class are non-Specified Substances,” which carries the stricter sanctioning consequences[14].

Two points that matter practically. First, S2.2.4 reads “including, but not limited to,” and covers GHRH analogues as a class — so there is no carve-out for the no-DAC form. A GRF(1-29) analogue is a GHRH analogue whether or not it carries a linker.

Second, on detection, be precise about what is and is not known, because this is a topic where confident claims outrun evidence in both directions. CJC-1295 has been identified by liquid chromatography–high-resolution tandem mass spectrometry in a seized pharmaceutical preparation submitted by Norwegian police and customs authorities in 2009 — the same report, discussed above, that first documented the no-DAC molecule[11]. Validated liquid chromatography–mass spectrometry methods covering GHRH analogues, including both CJC-1295 and CJC-1295 with DAC, have since been published in the anti-doping literature, with characterisation of their in vitro metabolites. What has not been demonstrated is real-world detection: the same method literature notes that although there is evidence of use based on admissions and intelligence, GHRH analogues do not appear to have been found in anti-doping samples by WADA-accredited laboratories, attributed to their low concentration in urine and limited knowledge of their metabolism. The honest statement is therefore neither “undetectable” nor “solved”: validated methods exist, and whether they have produced findings in practice is a separate question the published record does not answer in the affirmative. Nothing about that is a reason to assume safety, and prohibition does not depend on detectability.

What safety signals appear in the literature?

This section describes what the published literature reports. It is not safety advice, and nothing here should be read as suggesting human use.

What the CJC-1295 trials reported

Teichman reported no serious adverse reactions, and described administration as safe and relatively well tolerated, particularly at 30 or 60 mcg/kg[8]. That single quoted phrase is the most-recycled sentence on this entire topic, and it is routinely presented as though the studies found nothing at all. Read the underlying adverse event tables, which FDA reproduced in 2024, and “well tolerated” turns out to be a relative statement rather than a clean one[11]:

In study 1, adverse events were reported in 33 of 35 (94%) subjects on drug versus two of seven (29%) on placebo.

Injection site reactions (irritation, erythema, induration, pain, itching) in approximately 70% of subjects on drug and rarely on placebo — more severe and/or prolonged after higher doses.

Headache in 63% on drug versus 14% on placebo.

Diarrhoea in 43%, in the drug group only; transient loose stools or diarrhoea reached 45% and 100% incidence in the 125 and 250 mcg/kg groups respectively.

Transient urticarial rash at the injection site in almost 30% — the one adverse event that was not dose-related.

Systemic vasodilatory reactions — flushing, warmth and transient hypotension — in 30%, drug group only.

In study 2, injection site reactions occurred in every subject who received drug. Flushing occurred only in actively treated subjects, within 30 minutes of injection, and was dose-dependent: 40% after low-dose and 100% after high-dose injections. One subject had transient involuntary leg muscle contractions and some loss of coordination after a second 30 mcg/kg injection; two had transient dizziness and hypotension after a first 30 mcg/kg injection, which resolved spontaneously and did not recur.

Crucially: “all AEs (with the exception of transient urticarial rashes) were more common at higher doses (125 or 250 mcg/kg)” — which is precisely why the authors singled out 30 and 60 mcg/kg as the better-tolerated doses. The phrase that gets quoted approvingly is inseparable from the dose-response that produced it.

On the reassuring side, and it belongs here too: the authors reported no consistent changes in blood or urine laboratory values — including glucose levels and liver function studies — or in electrocardiographic findings in either study[11].

So the correct reading is not “no signal.” It is a high rate of dose-related, mostly local and vasomotor events, with no serious adverse reactions, in studies 28 and 49 days long in healthy volunteers, powered for pharmacokinetics and not for detecting uncommon serious events. Across the whole published human programme, 63 healthy adults received CJC-1295 DAC at 30–250 mcg/kg, 87% of them men, and 73% of them received a single injection[11]. No serious adverse reactions in 63 healthy people, most of whom were dosed once, is weak evidence of absence.

Preclinical genotoxicity — the signal most dosing pages have never heard of

Ben-Shlomo and colleagues reported in the Journal of Clinical Investigation in 2020 that cAMP stimulation of pituitary cells — including with a long-acting GHRH analogue — increases GH production and concomitantly induces DNA damage in the tissue it acts on. In mouse primary pituitary cultures, stimulation increased GH and produced DNA damage measured by H2AX phosphorylation and a comet assay; octreotide, which inhibits cAMP and GH, reversed the DNA damage induction; and in vivo, long-acting GHRH treatment also induced pituitary DNA damage in mice. Their conclusion was that the same cAMP signalling that induces somatotroph proliferation and GH secretion may concomitantly induce DNA damage, potentially linking hormone hypersecretion to genome instability[9].

FDA’s 2024 evaluation identifies the analogue in that work as CJC-1295 DAC and supplies the parameters. In vitro, 16-hour incubation of mouse primary pituitary cultures with CJC-1295 DAC produced a concentration-dependent increase in GH in the medium, and at 10 ng/mL caused DNA damage on comet assay together with increased γH2AX expression, a marker of the double-strand-break response. In vivo, eight weeks of CJC-1295 DAC in four-month-old mice (10 mcg/kg subcutaneously, three times weekly) significantly increased the relative weight of the anterior pituitary gland, induced pituitary DNA damage, and significantly increased pituitary γH2AX expression. FDA’s conclusion is that these signals “demonstrate the genotoxic potential of CJC-1295 DAC-related substances … in mammalian somatotrophs,” and it notes that it identified no studies assessing the genotoxic potential of the two no-DAC substances at all[11].

State the tier precisely, because this is exactly the kind of finding that gets inflated in both directions. This is in-vitro and rodent. It is not evidence that CJC-1295 causes tumours in humans, and no such evidence exists in either direction. But note two things. First, it is a mechanism-adjacent finding in the target organ, and it is the direct counterpart to the very same somatotroph proliferation that the GHRH-knockout mouse study reported as a benefit[4] — the same biology, read as a feature in one paper and as a hazard signal in the other. Second, the in-vivo dose was 10 mcg/kg three times weekly, which is not an absurd multiple of anything: it is in the same order of magnitude as the mcg/kg equivalents of the protocol figures discussed above. That does not make it a human finding. It does mean it cannot be dismissed as a mega-dose artefact.

What the toxicology package does and does not contain

FDA’s review is also useful for what it could not find, and this is worth stating plainly because “no data” is itself a finding. FDA identified no acute toxicity studies and no repeat-dose toxicity studies of any of the five named CJC-1295 substances. The three repeat-dose studies it did identify were of an unspecified form of CJC-1295 DAC and are published as conference abstracts only — not as full papers. Only a single developmental toxicity study exists, also an abstract. In those abstract-only animal studies: rats given CJC-1295 DAC intravenously every other day for 14 days showed reduced red blood cell counts, haemoglobin and haematocrit at all doses, increased liver weight at all doses, and minimal injection site haemorrhage, inflammation and necrosis at all doses. Beagle dogs given daily subcutaneous injections showed dose- and pH-dependent injection site irritation at all doses, including microscopic evidence of “inflammation, hemorrhage, and minimal to mild necrosis”[11].

Be honest about how to read that: the doses in those studies were milligrams per kilogram, which is orders of magnitude above anything referenced in research protocols, and dose-limiting toxicology is designed to find effects. The relevant point is not the injection site necrosis in dogs. The relevant point is that this — three abstracts and one developmental abstract — is the entire toxicology package for a compound that people are injecting.

Class-level concerns for GH secretagogues

Because CJC-1295 works by raising GH and IGF-I, the concerns discussed in the literature for that entire class apply mechanistically, regardless of which secretagogue produced the elevation. FDA made the same inference in 2024, reasoning that because these compounds act by increasing endogenous GH, one may expect a safety profile similar to that of approved human GH formulations[11]. Treat that carefully in both directions: it is an inference from mechanism, not an observation about CJC-1295.

Insulin sensitivity. GH is a counter-regulatory hormone; it antagonises insulin action. That is textbook endocrinology and it is why the concern is raised for every GH-axis intervention. What must be stated precisely is that it was not observed in the CJC-1295 studies: the authors reported no consistent changes in glucose levels in either study[11] — in 63 healthy adults, most dosed once, over 28 to 49 days. That is not a design capable of detecting metabolic drift, so the correct label is “not measured adequately,” not “shown to be absent.”

The mechanistic point specific to CJC-1295 with DAC is worth drawing out anyway, because it is rarely raised. Ionescu & Frohman showed that what the DAC molecule primarily elevates is trough GH — 7.5-fold[5]. Physiological GH signalling is pulsatile with deep troughs, and the troughs are plausibly where insulin sensitivity is restored between pulses. A compound whose defining action is raising the floor rather than the peaks is, mechanistically, doing the thing most likely to matter metabolically. That is a hypothesis generated by the data, not a demonstrated harm — but it is a coherent one, and it follows directly from the single best human study of the compound.

Fluid retention. GH promotes sodium and water retention via renal tubular effects, and oedema, arthralgia and carpal-tunnel-type symptoms are the classic dose-limiting effects of recombinant GH therapy. Be precise about what transfers: those effects are documented for exogenous GH, not for CJC-1295. Neither CJC-1295 human study reported them; the adverse events actually reported were local, vasomotor, headache and gastrointestinal, as listed above. The class concern is mechanistic — a compound whose entire purpose is raising GH is operating on the axis those effects come from — not an observed CJC-1295 finding.

IGF-I and occult malignancy — stated carefully. IGF-I is mitogenic and anti-apoptotic. A systematic review and meta-regression of 21 studies (26 datasets, 3,609 cases, 7,137 controls) found that high circulating IGF-I was associated with increased risk of prostate cancer (OR 1.49, 95% CI 1.14–1.95, comparing 75th with 25th percentile) and premenopausal breast cancer (OR 1.65, 1.26–2.08)[15]. Read that with the authors’ own caveats: these are observational associations with endogenous IGF-I, the associations are described by the authors themselves as modest and varying by site, and no study has shown that pharmacologically raising IGF-I with a secretagogue causes cancer. The concern discussed in the literature is narrower and more specific: sustained IGF-I elevation is theoretically undesirable in the presence of an undetected existing malignancy, because IGF-I is a growth factor for tissue that is already there. That is the accurate statement of the concern. It is not a claim that CJC-1295 causes cancer, and this article makes no such claim.

Immunogenicity. A chemically modified peptide covalently bolted to a self-protein is a plausible antigen, and FDA names immunogenicity as one of its stated concerns for compounded CJC-1295[12]. Anti-drug antibodies could in principle neutralise the compound or, less benignly, cross-react. A six-month cynomolgus monkey study of two DAC-modified peptides concluded that they produced no evidence of immunogenic or immunotoxic effects — but FDA notes that the data description is vague, that the absence of neutralising antibodies appears to apply only to the other compound in that study, and that no assessment of plasma GH or IGF-1 was provided for the CJC-1295 DAC-treated monkeys to demonstrate that pharmacological activity even persisted through the dosing period[11]. That is not resolution. That is an abstract that does not answer the question.

What are the limitations of the evidence?

Everything above should be read through these constraints. This is not boilerplate — each of these materially changes what you can conclude.

1. The human evidence base is three small papers, and only two of them are about dosing

FDA’s own 2024 literature review identified exactly three studies in which CJC-1295 DAC was given to humans: Teichman et al. 2006, Ionescu and Frohman 2006, and Sackmann-Sala et al. 2009 — the last a serum-proteomics study in 11 healthy young men sampled one week after a single injection, which contributes nothing on dose. Across all three, 63 healthy adults (87% men) received CJC-1295 DAC at 30–250 mcg/kg, and 73% received a single injection. Every subject was healthy. FDA states plainly: “No studies were found in which any form of CJC-1295 was administered to subjects with a disease or condition”[11]. That is the whole thing. Twenty years have passed without replication. A field this loud resting on a base this thin should give anyone pause.

2. Surrogate endpoints are not outcomes

Every human CJC-1295 finding is an endocrine measurement: GH went up, IGF-I went up. That is not the same as anything happening to a person. The tesamorelin literature is the cautionary comparison — it took 410 randomised patients and 26-week extension phases totalling 52 weeks of treatment to establish an effect on an actual endpoint, and even then the effect vanished on discontinuation[10].

3. The doses in the literature are not the doses in circulation

As shown above, documented research protocols reference roughly 2–14× less per injection than the trials studied. Trial findings therefore do not transfer to protocol doses, in either direction — not the efficacy, and not the tolerability. The dose-related adverse events reported by Teichman clustered at 125 and 250 mcg/kg, which is 8,750–17,500 mcg for a 70 kg adult — nowhere near the range in circulation. That is a reason not to import the tolerability finding either.

4. Healthy volunteers are not the population using it

Teichman studied healthy adults aged 21–61. The terminated Phase 2 population was HIV-associated visceral obesity, with diabetes explicitly excluded per the registry record[2], and its data were never published. Neither maps onto the population actually interested in GH secretagogues, which skews older, more metabolically heterogeneous, and frequently using other compounds simultaneously — a combination on which zero data exists.

5. The no-DAC molecule is essentially undocumented

Its half-life, its dose-response, its duration of action, its accumulation behaviour, its genotoxicity, its long-term profile: none of it is established. FDA searched for the same things and found nothing for either no-DAC substance[11]. Everything about it is inference from the chemistry — and, as noted above, even the premise that the DAC is what makes the difference has never been closed with a head-to-head comparison.

6. Combinations have no data at all

Not CJC-1295 + ipamorelin. Not any of the blends. The mechanistic case for pairing a GHRH analogue with a GHS is real and rests on solid receptor pharmacology[6], and that is the strongest statement available. Anyone who tells you a ratio is telling you a convention.

7. Research-chemical material is not pharmaceutical material

Everything above assumes the vial contains what the label says at the mass the label says. That assumption is doing enormous work in every dose calculation in this article. Content, purity, endotoxin, residual solvents, correct isomers at four substituted positions, and correct DAC conjugation are not verified by any regulator for research-chemical material. FDA’s own evaluation dwells on exactly this: peptides can be extremely sensitive to formulation, process and environmental conditions; aggregation and degradation may follow with loss of biological activity; and multiple specific analytical methods may be needed to detect the resulting impurities, meaning peptides may require more testing than small molecules rather than less[11]. A calculation of 20 units = 500 mcg is only true if the vial holds 5 mg of the right molecule. That is an assumption, not a measurement.

8. Regulatory status moves

The 503A landscape has changed repeatedly in recent years and continues to. Verify current status against FDA’s own listings rather than any secondary source, including this one.

Frequently Asked Questions

What is the difference between CJC-1295 with DAC and without DAC?

DAC is a maleimide linker that covalently binds the peptide to albumin at cysteine-34. With DAC, the estimated human half-life is 5.8–8.1 days, producing sustained GH and IGF-I elevation and weekly-to-twice-weekly dosing. Without DAC, the same peptide backbone has a short half-life measured in minutes and produces a discrete GH pulse, hence daily dosing. They are different molecules with different schedules and are not interchangeable at any dose.

How much CJC-1295 per week do research protocols document?

For the DAC form, documented protocols reference 300–1,000 mcg per injection twice weekly — roughly 0.6–2 mg per week — over an 8–12 week course. For the no-DAC form, 100–300 mcg once daily works out to roughly 0.7–2.1 mg per week. The weekly totals are similar; the distribution is completely different. Neither figure is a validated human dose, and both are well below the doses used in published trials.

Is Mod GRF(1-29) the same as CJC-1295 no-DAC?

Yes — they are the same molecule under two names: the tetrasubstituted GRF(1-29) peptide (D-Ala2, Gln8, Ala15, Leu27) without the albumin-binding linker. “Mod GRF(1-29)” is arguably the more accurate name, since the paper that coined “CJC-1295” defined it as including the maleimidopropionamide group. This naming collision is the direct cause of most contradictory dosing information online, and FDA had to enumerate five separate substances across two active moieties to work around it.

What doses were actually used in the CJC-1295 human trials?

Teichman et al. (2006) used ascending single subcutaneous doses and two or three weekly or biweekly multiple doses, describing 30 and 60 mcg/kg as safe and relatively well tolerated. For a 70 kg adult that is roughly 2,100–4,200 mcg per injection. Ionescu and Frohman used 60 or 90 mcg/kg. Across the three published human studies the full range was 30–250 mcg/kg in 63 healthy adults. All are substantially higher per injection than the 300–1,000 mcg figures that circulate in research protocols.

How is a CJC-1295 5 mg vial reconstituted, and how many units is 500 mcg?

For DAC, documented protocols use 2.0 mL of bacteriostatic water: 5 mg ÷ 2.0 mL = 2.5 mg/mL = 2,500 mcg/mL. On a U-100 syringe, 1 unit = 0.01 mL = 25 mcg, so 500 mcg = 20 units and 1,000 mcg = 40 units. For no-DAC, 3.0 mL gives ~1.67 mg/mL, so 1 unit ≈ 16.7 mcg and 100 mcg ≈ 6 units. The concentration is specific to each vial mass and diluent volume, and must be recomputed for each.

Why do the 2 mg and 5 mg DAC vials need different unit counts for the same dose?

Because units measure volume, not drug. A 2 mg vial with 2.0 mL gives 1 mg/mL (10 mcg per unit); a 5 mg vial with the same 2.0 mL gives 2.5 mg/mL (25 mcg per unit) — 2.5× more concentrated. So 500 mcg is 50 units from the 2 mg vial but only 20 units from the 5 mg vial. Carrying a unit count across vial sizes produces a 2.5-fold error.

Is there a validated dose for CJC-1295 with ipamorelin?

No. No controlled human trial has established a dose or ratio for this combination, for either CJC-1295 form or for any pre-mixed blend. The mechanistic rationale is legitimate — GHRH analogues and ghrelin-receptor secretagogues act on different receptors, and a GHS cannot release GH at all without intact GHRH signalling — but mechanism is a hypothesis, not a dose. Ratios found in blends reflect manufacturer choices, not trial data.

Why is a CJC-1295 + ipamorelin 10 mg blend dosed daily rather than weekly?

Because a blend of that description must contain the no-DAC form. A fixed-ratio blend only makes sense when both components share a dosing frequency, and no-DAC and ipamorelin are both short-acting daily compounds. The DAC form is dosed twice weekly, so it cannot share a vial with a daily compound without mis-dosing one of them. A product advertised as a DAC blend on a daily schedule is internally inconsistent.

Is CJC-1295 approved or legal?

CJC-1295 is not approved by FDA, EMA or any comparable regulator for any indication, in either form. FDA states that ConjuChem withdrew it from clinical trials in 2006 after the death of a subject in a phase 2 trial, and it never reached Phase 3. FDA’s Pharmacy Compounding Advisory Committee considered all five CJC-1295-related substances on 4 December 2024 and voted against recommending any of them for the 503A Bulks List. It is also explicitly named on the WADA Prohibited List at S2.2.4 and is prohibited in sport at all times.

References

Jetté L, Léger R, Thibaudeau K, et al. 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. Endocrinology. 2005;146(7):3052-8. doi:10.1210/en.2004-1286

ConjuChem. A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Phase 2 Study to Evaluate the Efficacy and Safety of CJC 1295 Administered for 12 Weeks in HIV Infected Patients With HIV Associated Visceral Obesity. ClinicalTrials.gov identifier NCT00267527. Status: Terminated.

Bernard EJ. Lipodystrophy study halted after patient death. NAM aidsmap, 31 July 2006.

Alba M, Fintini D, Sagazio A, et al. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290-4. doi:10.1152/ajpendo.00201.2006

Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-7. doi:10.1210/jc.2006-1702

Maheshwari HG, Rahim A, Shalet SM, Baumann G. Selective lack of growth hormone (GH) response to the GH-releasing peptide hexarelin in patients with GH-releasing hormone receptor deficiency. J Clin Endocrinol Metab. 1999;84(3):956-9. doi:10.1210/jcem.84.3.5523

Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-61. doi:10.1530/eje.0.1390552

Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. 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. 2006;91(3):799-805. doi:10.1210/jc.2005-1536

Ben-Shlomo A, Deng N, Ding E, et al. DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas. J Clin Invest. 2020;130(11):5738-5755. doi:10.1172/JCI138540

Falutz J, Allas S, Mamputu JC, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. AIDS. 2008;22(14):1719-28. doi:10.1097/QAD.0b013e32830a5058

U.S. Food and Drug Administration. FDA Briefing Document — Pharmacy Compounding Advisory Committee Meeting, 4 December 2024: CJC-1295-Related Bulk Drug Substances (CJC-1295 (free base), CJC-1295 acetate, CJC-1295 DAC (free base), CJC-1295 DAC acetate, and CJC-1295 DAC trifluoroacetate).

U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks — Category 2 of the bulk substances nominated under sections 503A or 503B, including the list of substances nominated but withdrawn.

U.S. Food and Drug Administration. Pharmacy Compounding Advisory Committee Meeting, 4 December 2024 — Topic 1: CJC-1295-Related Bulk Drug Substances (official meeting transcript, including the recorded votes).

World Anti-Doping Agency. The Prohibited List 2026 (effective 1 January 2026) — Section S2.2.4: Growth hormone releasing factors.

Renehan AG, Zwahlen M, Minder C, O’Dwyer ST, Shalet SM, Egger M. Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis. Lancet. 2004;363(9418):1346-53. doi:10.1016/S0140-6736(04)16044-3

Research use only. CJC-1295, in both its DAC and no-DAC forms, is an investigational compound that is not approved for human therapeutic use by the FDA, EMA, or any comparable regulatory authority, for any indication, in any jurisdiction. Its clinical development was discontinued in 2006 and never resumed. This article is an educational summary of published research and of the figures documented on research protocol reference pages. It is not medical advice, it is not a dosing recommendation, and nothing in it should be interpreted as suggesting or endorsing human administration. All doses described are reported as what the cited literature or referenced research protocols document — never as instruction. dosagepeptide.com is an independent reference library and does not sell peptides. Both compounds are prohibited in sport at all times under the WADA Prohibited List. Anyone with questions about growth hormone, IGF-I, or endocrine health should consult a qualified, licensed physician.