CJC-1295 Dosage: With DAC vs No DAC, the Human Trial Doses, Half-Life & Reconstitution

CJC-1295 at a glance

What it is

A synthetic analogue of GHRH(1-29), the shortest fully active fragment of growth-hormone-releasing hormone. Two forms are sold under one name: with DAC (Drug Affinity Complex) and without DAC, the latter being the same molecule marketed as Mod GRF 1-29 or CJC-1295 no-DAC.

What the DAC actually is

Not a coating or a carrier. CJC-1295 was identified as a tetra-substituted hGRF(1-29) carrying an N-epsilon-3-maleimidopropionamide derivative of lysine at the C-terminus (PMID 15817669). That maleimide reacts with the free thiol on cysteine-34 of circulating serum albumin, so the peptide becomes covalently attached to albumin in the bloodstream.

The dose with data behind it

DAC form — 30, 60 and 90 mcg/kg as single subcutaneous injections across two trials (PMID 16352683, PMID 17018654) — roughly 2,100, 4,200 and 6,300 mcg for a 70 kg adult. Reported community figures for the DAC form (~1,000-2,000 mcg per week) are below the smallest single dose either trial administered.

Human dose actually studied (no DAC)

None. No human efficacy or pharmacokinetic trial of the no-DAC peptide is indexed in PubMed. Every human number on this page belongs to the DAC form.

Plasma half-life

DAC form: 5.8-8.1 days (PMID 16352683). No-DAC form: no published human measurement — see below. This is a measurement in healthy adults, not an estimate — and it is a property of the albumin conjugate, not of the GHRH backbone.

The no-DAC '30 minutes'

Not a measurement of this peptide. It is inherited from GHRH(1-29) chemistry: unmodified GRF(1-29)NH2 is cleaved by dipeptidyl peptidase IV to the inactive fragment GRF(3-29)NH2, and the substitutions in the Mod GRF backbone are the ones designed to resist that cleavage (PMID 8583376). See the half-life section for what that does and does not license.

Mechanism

GHRH-receptor agonism at the pituitary somatotroph, raising GH and downstream IGF-1. Notably, pulsatility survives it: after a single injection, GH secretion increased with pulsatility preserved (PMID 17018654).

Registered trials

One study lists CJC-1295 as an intervention on ClinicalTrials.gov — NCT00267527, in HIV patients with visceral obesity — and its status is TERMINATED. There is no approved product in either form.

Regulatory status

Not FDA-approved in either form; prohibited in sport under the WADA list. Research and educational use only.

Reported ranges from research/community — examples, not recommendations.

What it is / mechanism

CJC-1295 acts at the growth-hormone-releasing hormone receptor on pituitary somatotrophs, the same receptor the endogenous hormone uses. Agonism there raises growth hormone output, and the sustained rise in GH drives hepatic IGF-1 production, which is the downstream marker both human trials tracked. Nothing about the mechanism is exotic; the whole engineering story is about how long the molecule survives to keep doing it. That story starts with a specific enzymatic vulnerability. Native GHRH(1-29) is cleaved rapidly in plasma by dipeptidyl peptidase IV, which removes the first two residues and leaves GRF(3-29)NH2 — a fragment reported as the major metabolite and as inactive (PMID 8583376). The same paper showed that a substituted analogue, [desNH2Tyr1, D-Ala2, Ala15]-GRF(1-29)NH2, was resistant to that plasma cleavage and dramatically more stable. The D-alanine at position 2 is the substitution that matters most: DPP-IV cleaves after the second residue, and a D-amino acid there is not a substrate it recognises. The tetra-substituted backbone shared by CJC-1295 and Mod GRF 1-29 exists for that reason. The DAC is a second, separate piece of engineering layered on top. In the paper that identified the compound, three maleimido derivatives of hGRF(1-29) were synthesised and bioconjugated to human serum albumin; the best of them, designated CJC-1295, was a tetra-substituted hGRF(1-29) with an N-epsilon-3-maleimidopropionamide derivative of lysine added at the C-terminus (PMID 15817669). Maleimides react selectively with free thiols, and the one free thiol available in circulation at any useful concentration is cysteine-34 of serum albumin. So the injected peptide finds albumin and forms a covalent bond with it. In rats, plasma levels persisted beyond 72 hours, and a western blot of plasma from an injected animal showed the CJC-1295 immunoreactive species sitting on the band corresponding to serum albumin, appearing after 15 minutes and remaining beyond 24 hours. That is the whole difference between the two products sold under this name. Both share a DPP-IV-resistant GHRH(1-29) backbone. Only one of them carries the chemistry that attaches it to a protein with a multi-week circulating lifetime. Treating them as the same compound at different strengths misdescribes what was built. One mechanistic result deserves its own line, because it is counter-intuitive and it was measured rather than assumed. A standing objection to any long-acting GHRH analogue is that continuous receptor stimulation should flatten the natural GH rhythm, and pulsatile GH secretion is considered important for many of the hormone's physiological effects. Ionescu and Frohman tested it directly: healthy men aged 20-40 were sampled every 20 minutes across an overnight 12-hour window, before and one week after a single injection of 60 or 90 mcg/kg. GH secretion was increased with pulsatility preserved (PMID 17018654). Whatever else is uncertain here, that specific worry was checked in humans and did not materialise at those doses.

Researched effects

The honest summary is that the human evidence for CJC-1295 is three Phase 1-scale pharmacology studies in healthy volunteers, all on the DAC form — no efficacy trial, no long-term study, and no completed clinical programme. The pharmacokinetic study (PMID 16352683) ran two randomised, placebo-controlled, double-blind ascending-dose trials of 28 and 49 days in healthy subjects aged 21-61. CJC-1295 or placebo was given subcutaneously as ascending single doses in the first trial and as two or three weekly or biweekly doses in the second. After a single injection, mean plasma GH rose 2- to 10-fold for six days or more, and mean plasma IGF-1 rose 1.5- to 3-fold for nine to eleven days. After multiple doses, mean IGF-1 remained above baseline for up to 28 days. The estimated half-life was 5.8-8.1 days. No serious adverse reactions were reported, and the authors singled out doses of 30 or 60 mcg/kg as safe and relatively well tolerated. The pulsatility study (PMID 17018654) is the second human dataset. Single injections of 60 or 90 mcg/kg, overnight 20-minute sampling before and one week after, GH increased with pulsatility preserved. A third study (PMID 19386527, 2009) looked for biomarkers rather than for an effect: it examined serum protein profile changes after GH/IGF-1 axis activation by CJC-1295 in normal adult subjects, motivated by the fact that the existing markers of GH activity — IGF-1, IGFBP-3 and collagen peptides — vary substantially across the population and are not reliably predictive of GH therapy's physiological effects or of GH abuse by athletes. It is worth knowing this study exists, and worth being clear about what it is: a biomarker-discovery study in which the compound is the tool, not the subject. Two things follow that the market rarely states together. First, both trials measured hormone concentrations in healthy volunteers — GH and IGF-1 levels, not body composition, not strength, not recovery, not sleep. An IGF-1 rise is a pharmacodynamic response, and reading it as a clinical outcome is an inference the trials did not make. Second, the development programme that generated these data did not continue to an approved product. The one registered study listing CJC-1295 as an intervention, NCT00267527 in HIV patients with visceral obesity, is recorded as terminated, and no CJC-1295 product has been approved in any jurisdiction. For the no-DAC form the evidence section is shorter, because it is empty. PubMed indexes no human efficacy or pharmacokinetic trial of the tetra-substituted peptide without the DAC. Every human figure quoted for CJC-1295 anywhere — the half-life, the GH multiples, the IGF-1 duration, the tolerability — was generated using the albumin-binding version. When those numbers appear on a page about the no-DAC product, they have been moved across a molecular boundary that the chemistry does not permit.

Dosage — reported ranges (overview)

The single most useful fact about CJC-1295 dosing is that the arriving question — what dose of the DAC form was actually studied — has a precise published answer, and it is far from the figure the market repeats. The published human doses are 30, 60 and 90 mcg/kg as single subcutaneous injections. Because they are per-kilogram, they only become comparable to a vial once bodyweight is fixed. For a 70 kg adult they work out to roughly 2,100 mcg at 30 mcg/kg, 4,200 mcg at 60 mcg/kg, and 6,300 mcg at 90 mcg/kg. For a 90 kg adult: about 2,700, 5,400 and 8,100 mcg. The pharmacokinetic trial described 30 and 60 mcg/kg as the doses that were safe and relatively well tolerated, and the multiple-dose arm gave two or three injections weekly or biweekly — not daily. Set that against what is commonly reported in community protocols for the DAC form, which is somewhere around 1,000-2,000 mcg per week. That is below the smallest single dose used in either trial. The two figures are not variations on a theme; they describe different exposure entirely, and a page that quotes the trial's half-life while quoting the community's dose has silently combined two incompatible sources. For the no-DAC form, the commonly reported figure is around 100 mcg per injection, one to three times daily, frequently described as a 'saturation dose' — the amount said to produce a maximal single GH pulse. This is a community heuristic. It is not derived from a published dose-response study of this peptide in humans, because no such study is indexed, and the saturation framing should be read as a rule of thumb rather than a measured ceiling. None of the above is a recommendation, a protocol, or a suggestion that any of these figures is appropriate for anyone. They are the published trial doses and the commonly reported community figures, stated so that the two are not confused with each other.

A printable protocol sheet with a reconstitution reference and an injection log comes with All-Access Lifetime.

Reconstitution — bac-water math

Reconstitution is arithmetic, and it is the same arithmetic for both forms. Concentration in mcg per mL equals the total mcg in the vial divided by the mL of bacteriostatic water added. On a U-100 insulin syringe, 100 units equals 1 mL, so one unit is 0.01 mL and the volume for a given amount is (mcg wanted / concentration) x 100 units. The table below uses a 5 mg (5,000 mcg) vial, the common presentation, with two reported no-DAC example amounts. Every row has been checked against the 100-unit ceiling of a 1 mL U-100 syringe: all of them draw comfortably within a single syringe. A vial of a different strength changes every number in the table, so the vial in hand — not the table — is the input that matters. Use the reconstitution calculator to run your own vial size and volume rather than adapting these rows by eye.

This is concentration math, not a dose recommendation.

Injection / administration basics

Both trials administered CJC-1295 subcutaneously, and subcutaneous injection with a U-100 insulin syringe is what community reports describe for both forms. Site rotation across the abdomen, flank and thigh is the usual reported practice. The timing difference between the forms is worth stating plainly because it follows from the chemistry rather than from preference. The no-DAC peptide is reported as short-acting and is therefore described as being given once to several times a day, often fasted or at bedtime — an attempt to place a brief GH pulse where the natural one would fall. The DAC form was studied as weekly or biweekly dosing, which is what a 5.8-8.1 day half-life implies. Applying a daily schedule to the DAC form ignores the only reason to use it. No route, dose, frequency or schedule is being recommended here. The trials' route is stated because it is the route under which every human number on this page was generated, and figures obtained one way do not automatically transfer to another.

Half-life & frequency rationale

This is the field where the two forms are most often merged, so it is worth separating them by source. The DAC form has a measured human half-life of 5.8-8.1 days (PMID 16352683), and the companion study describes the analogue as binding permanently to endogenous albumin after injection with a half-life of 8 days (PMID 17018654). These are real measurements in healthy adults. Critically, they are properties of the albumin conjugate. Albumin itself circulates for weeks, and a molecule covalently bonded to Cys34 inherits much of that persistence — which is precisely what the maleimide was put there to achieve. The no-DAC form is routinely quoted at about 30 minutes. That figure is not a published human measurement of this peptide, and no dedicated pharmacokinetic study of the no-DAC peptide in humans is indexed. What can be sourced is the chemistry underneath it: unmodified GRF(1-29)NH2 is cleaved by dipeptidyl peptidase IV to the inactive GRF(3-29)NH2 and is short-lived in plasma, while the substituted backbone resists that specific cleavage (PMID 8583376). So the no-DAC peptide should outlast native GHRH(1-29) — the substitutions do something — but 'longer than a few minutes' is a direction, not a number, and the widely repeated half-hour figure has the status of an estimate that has been quoted long enough to look like data. The practical reading: for the DAC form the half-life is one of the best-supported facts about the compound; for the no-DAC form it is one of the weakest, and the fact that both circulate under the same product name is the reason the distinction keeps collapsing.

Stacking — overview

The pairing discussed most often is a GHRH analogue with a growth-hormone secretagogue such as ipamorelin, on the rationale that the two act at different receptors — the GHRH receptor and the ghrelin/GHS receptor — and that community reports describe a larger combined GH response than either alone. That rationale is mechanistic and plausible; what does not exist is a human trial of the combination, so the pairing's popularity rests on reasoning and reports rather than on measurement. Where the DAC form is concerned there is a specific reason for caution that follows from the half-life rather than from any interaction: a compound with a 5.8-8.1 day half-life is still present when the next week's injections land, so 'stacking' it means adding to a standing concentration rather than to a cleared one. Combination figures reported for the short-acting no-DAC peptide do not carry over. Stacks are described here as reported practice for educational purposes. Nothing in this section is a protocol or a recommendation.

For how combinations are grouped by research context, the named blends, and why a pre-mixed blend vial cannot be calculated from its total milligrams, see the peptide stacks guide.

Storage & handling

• Lyophilised vials are typically stored refrigerated; the powder is the stable state and the reconstituted solution is not.
• After reconstitution with bacteriostatic water, storage is refrigerated. Bacteriostatic water contains 0.9% benzyl alcohol as a preservative, which is what makes multiple withdrawals from one vial possible; sterile water contains no preservative and does not.
• Protect from light and avoid repeated freeze-thaw cycles, which are a routine cause of peptide degradation independent of the compound.
• Label the vial with the date of reconstitution and the concentration in mcg/mL. The concentration is not recoverable from looking at the vial, and mixing up two vials reconstituted to different strengths is the most common source of a unit-math error.

Evidence File

CJC-1295 with DAC: The Human Record, Read Line by Line

The free guide lists the human studies for CJC-1295 with DAC. This file goes back to the source documents and reads them the way a reviewer would: who was enrolled, how many independent cohorts there really are, which sentences are measurements and which are background summaries repeating someone else, and what the one registered trial record does and does not contain once every field is opened. It also carries a US federal regulatory entry naming this compound that the free page does not mention, a published third-party evidence grade, and a list of endpoints that no published human study has ever measured.

• 3 publications, at most 2 independent human cohorts
• Half-life 5.8-8.1 days measured; the famous 8 days is a background line
• 1 registered trial: no results table, no linked publication, no stated reason
• FDA names CJC-1295 in its nominated-but-withdrawn category-2 table

Sourcing File

CJC-1295 with DAC: What a Certificate Has to Prove, and the Numbers That Prove It

Two different molecules are sold under the name CJC-1295, and on a certificate of analysis they are separated by one exactly known number. This file derives that number from the registered sequence, shows where two official databases disagree about this compound's own formula and which one to trust, identifies a mass value in a public record that looks like a protonated ion and is not, names the one US federal label document that does exist for this substance and what it actually is, works the salt and water arithmetic that decides how much peptide a labelled vial really holds, and reads a certificate line by line to say what each line establishes and what it leaves open.

• 279.122 Da is the entire difference between the DAC and no-DAC molecules
• PubChem ExactMass 3646.0188 is the 13C peak, not [M+H]+ at 3646.0228
• A 5 mg TFA-salt vial can hold about 4.0 mg of actual peptide
• This molecule has no sulfur, so a +16 Met-oxide impurity is impossible

Benefit & Outcome Review

CJC-1295 with DAC: Eleven Marketed Claims, Graded Against the Evidence That Exists

The claims made for this compound are not a matter of opinion, and neither is the evidence behind each one. This file takes eleven claims in circulation, names where each of them came from, and grades them one at a time with human, animal and laboratory evidence kept strictly apart. It states what would have to exist for any of the ungraded claims to move, using an approved compound in the same class and the same patient population as the yardstick. It also traces the most-quoted strength figure in the market back to the experiment it appears to have come from, and sets out what the published record says about how individual people responded.

• 11 marketed claims graded; 3 supported in humans, all as hormone readings
• Strength, sleep, skin and healing: never measured in any species
• The quoted strength result traces to a rat study of ipamorelin and a steroid
• No published study reports how many subjects responded, or by how much

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