CJC-1295: the monograph

CJC-1295 is a long-acting synthetic analog of growth hormone-releasing hormone (GHRH). Injected subcutaneously, it signals the pituitary to release the body's own growth hormone, and a chemical anchor keeps it bound to serum albumin so a single dose keeps signaling for days instead of minutes.

Two facts make this compound unusual among research peptides, and this site leads with both. First, real randomized human trials exist: in healthy adults, single doses raised mean growth hormone 2- to 10-fold for 6 days or more and IGF-I 1.5- to 3-fold for 9 to 11 days. Second, a real FDA adverse-event record exists: FDA has identified serious adverse events associated with CJC-1295, including increased heart rate and systemic vasodilatory reaction. Most compounds in this market have neither the trials nor the warning. CJC-1295 has both, and honest reading requires holding them together.

This monograph covers what the trials measured and what they never measured, the confusion between CJC-1295 with DAC and without DAC that the market monetizes, the physiology of a week-long GH elevation, and where the evidence simply stops. Every numbered citation resolves to a primary source.

The name CJC-1295 is doing double duty in the marketplace, and the two things it names are pharmacologically different. CJC-1295 proper, the compound ConjuChem identified in 2005, is a tetrasubstituted form of GRF(1-29) with a lysine added at position 30 carrying a maleimidopropionamide linker, the Drug Affinity Complex (DAC). That linker bonds covalently to serum albumin after injection, which is what stretches its action from minutes to days.

What vendors sell as CJC-1295 without DAC, also called Mod GRF 1-29 or modified GRF(1-29), is the same tetrasubstituted 29-amino-acid backbone without the albumin anchor. The four substitutions harden the peptide against enzymatic degradation, but without DAC the molecule remains short-acting. The peer-reviewed record on this second compound is close to empty: a 2026 review found no controlled clinical studies have directly evaluated it in humans, with claims about it extrapolated from sermorelin and from non-academic sources.

FDA's substance registry records CJC-1295 as a 30-residue amidated peptide, sequence YaDAIFTQSYRKVLAQLSARKLLQDILSRK, where the lowercase a is D-alanine at position 2 and the final lysine carries the linker. PubChem lists it as CID 91971820: formula C165H269N47O46, molecular weight 3647.2 Da. When a product page does not say which form is in the vial, that ambiguity is not a detail; the two forms differ in half-life by roughly three orders of magnitude.

CJC-1295 has never been an FDA-approved drug in any form: a Drugs@FDA search for the active ingredient returns no records. It is also not a compound FDA has stayed silent about. FDA's compounding safety-risks page lists CJC-1295 by name, citing immunogenicity risk for certain routes, peptide-impurity and API-characterization complexities, identified serious adverse events, and limited available clinical data.

FDA also states the general rule that applies to every vial sold today: compounded drugs are not FDA-approved, and FDA does not verify their safety, effectiveness, or quality before marketing. For athletes there is a second regulator: the WADA 2026 Prohibited List names CJC-1295 explicitly among growth hormone releasing factors, prohibited at all times.

CJC-1295 was a real drug candidate with a real corporate sponsor. ConjuChem, the Montreal company whose chemists identified it, ran the healthy-adult trials published in 2006 and registered a multicenter, randomized, placebo-controlled phase 2 trial in HIV-associated visceral obesity beginning December 2005, the same indication tesamorelin later won approval for.

The registry tells the rest plainly: the phase 2 study is recorded as TERMINATED, no results were ever posted, and the record has not been updated since October 2006. As of this writing, ClinicalTrials.gov lists no other interventional study of CJC-1295, active or otherwise. Twenty years after its identification, the compound has no sponsor, no development program, and no approval anywhere; what remains is the gray market.

CJC-1295 is a GHRH-receptor agonist: it binds the same pituitary receptor as natural GHRH and triggers synthesis and release of the body's own growth hormone, which in turn drives IGF-I production in the liver. Downstream feedback (somatostatin, IGF-I) remains in place, which distinguishes the whole GHRH-analog class from injecting growth hormone itself.

Two chemical modifications explain its persistence. The tetrasubstitution: native GHRH is destroyed within minutes, its 2-3 bond cleaved by dipeptidylpeptidase IV (DPP-IV); a D-amino acid at position 2 blocks that cleavage, and CJC-1295 carries D-Ala2 plus three further substitutions (positions 8, 15, and 27 of the registry sequence) that harden it against proteolysis. The DAC: a maleimidopropionamide group on the added Lys30 bonds to the free thiol on Cys34 of serum albumin, so the peptide rides the bloodstream's most abundant protein, protected from clearance for days.

In the identification study, albumin-bound CJC-1295 stayed bioactive: conjugates resisted DPP-IV in vitro and still stimulated GH secretion from cultured pituitary cells, and in rats the albumin-bound species appeared within 15 minutes of injection and persisted beyond 24 hours.

The Teichman 2006 program remains the entire controlled human evidence base. Two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults aged 21 to 61 ran 28 and 49 days. Single subcutaneous doses raised mean plasma GH 2- to 10-fold for 6 days or more and mean IGF-I 1.5- to 3-fold for 9 to 11 days; repeated weekly or biweekly dosing held IGF-I above baseline for up to 28 days with evidence of accumulation.

Read the outcome list before reading anything into those numbers: the trials measured hormone concentrations and pharmacokinetics. Not body composition, not strength, not sleep, not recovery, not skin, not any clinical outcome. Within the trials no serious adverse reactions were reported, and tolerability was described as best at 30 or 60 mcg/kg. A small companion study in 11 healthy men documented serum protein shifts one week after a dose, proposed as possible biomarkers of GH and IGF-I action.

That is the complete list. Everything else written about CJC-1295's effects in humans traces to these hormone measurements, to extrapolation, or to anecdote.

Growth hormone is normally secreted in bursts, mostly at night, with near-zero troughs between them. The standard objection to long-acting GHRH analogs is that a continuous signal should flatten that rhythm into a featureless bleed. This is one of the few questions about CJC-1295 with a direct experimental answer.

Ionescu and Frohman sampled healthy men every 20 minutes overnight, before and one week after a single 60 or 90 mcg/kg dose. The pulses survived: frequency and magnitude of GH secretory bursts were unaltered. What changed was the floor between pulses, and it changed dramatically: trough GH rose 7.5-fold, lifting mean GH 46% and IGF-I 45%. Continuous stimulation did not erase pulsatility; it raised the baseline the pulses ride on.

So the honest summary is neither the marketing version (fully physiologic) nor the forum version (destroys your pulses). The rhythm persists over a raised floor. Whether a chronically raised floor is benign is a different question with no answer: sustained IGF-I elevation is flagged in the 2026 review as a biologically plausible cancer-risk amplifier, the mouse data show somatotroph proliferation under daily dosing, and the longest trial of any GHRH analog in aging adults saw IGF-I fade back toward baseline by week 16, a durability question CJC-1295's 49-day trials were too short to answer.

In rats, CJC-1295 outperformed unmodified GRF(1-29) with a 4-fold higher GH area-under-curve over 2 hours and remained detectable in plasma beyond 72 hours. In GHRH-knockout mice, 2 mcg daily for 5 weeks normalized body weight and length; the same dose every 48 or 72 hours worked less well. These are mice with no GHRH of their own, a model of deficiency, not of healthy adults seeking enhancement.

The knockout study also reported increased pituitary GH mRNA and somatotroph proliferation confirmed by immunohistochemistry. In a deficiency model that reads as restoration; in a healthy person stimulating the same axis for months, glandular proliferation under sustained trophic signaling is exactly the kind of finding that belongs in the risk column until long-term data exist. None do.

CJC-1295 has no efficacy trials, so the nearest honest calibration comes from its axis. Growth hormone itself, tested in pooled randomized trials in the healthy elderly, produced about 2.1 kg less fat and 2.1 kg more lean mass, no significant weight change, and significantly more edema, joint pain, carpal tunnel syndrome, and gynecomastia; the reviewers concluded GH cannot be recommended as an antiaging therapy. That is the ceiling scenario: direct hormone, known exposure, measured outcomes.

The GHRH-analog class specifically: the longest trial in aging adults, 16 weeks of a nightly short-acting analog, saw IGF-I rise and then drift back toward baseline by trial end, small body-composition changes (lean mass in men only, thicker skin), unchanged sleep quality, and transient hyperlipidemia. Anyone extrapolating a body transformation from CJC-1295's hormone curves is claiming more than the class has ever delivered under measurement.

There is no approved label and therefore no established human dose. In the randomized trials, tolerability was described as best at 30 or 60 mcg/kg subcutaneously, given as single doses or two to three times weekly or biweekly; the pulsatility study used single doses of 60 or 90 mcg/kg. Those are study parameters recorded for education, not recommendations.

The gray market runs on different numbers: a 2026 peer-reviewed review documents forum protocols of 1 to 2 mg per week of the DAC form and 100 to 200 mcg once or twice daily of the no-DAC form. We report that mismatch because it is itself a finding: self-administered dosing has detached from the studied range, on products whose identity and purity nobody verifies.

No label exists, so no contraindication list was ever written for CJC-1295 itself; what follows is class reasoning, stated as such. The approved GHRH analog, tesamorelin, is contraindicated in active malignancy, disruption of the pituitary axis, pregnancy, and hypersensitivity, and the 2026 review's IGF-1 caution names prior malignancy, strong family history, and premalignant conditions as reasons for heightened concern with any sustained GH-axis stimulation.

Anyone with a cancer history, an endocrine condition, cardiovascular disease (remember what FDA's adverse-event line says: increased heart rate, systemic vasodilatory reaction), or who is pregnant, breastfeeding, or an athlete subject to anti-doping rules has, in our reading of the sources, categorical reasons to stay away. For everyone else the honest statement is different but not softer: nobody has studied whether long-term use is safe in you either.

No drug-interaction studies exist for CJC-1295; this is a checked absence, not a clean bill. Reasoning from the axis: raising GH and IGF-I moves glucose metabolism (the peptide-class reviews flag insulin resistance and dysglycemia), so diabetes and glucose-lowering medication deserve particular respect. Real-world use patterns compound the problem: the 2026 review documents frequent co-use with anabolic steroids, thyroid hormone, stimulants, and other agents, with overlapping cardiovascular and metabolic risks that make attribution of any symptom unreliable.

The one interaction with a regulator attached: sport. CJC-1295 is named on the WADA 2026 Prohibited List and is detectable; anti-doping laboratories have published confirmation methods since 2010, beginning with a seized-vial identification.

Within the two randomized trials, no serious adverse reactions were reported and the compound was described as relatively well tolerated, particularly at 30 or 60 mcg/kg; the abstract does not enumerate the non-serious events. That in-trial record is the reason gray-market marketing calls the compound safe.

The post-trial record is why that word does not hold: FDA's page lists identified serious adverse events, increased heart rate and systemic vasodilatory reaction, and 2026 reviews add the peptide-class pattern of fluid retention, musculoskeletal symptoms, injection-site reactions, and endocrine-metabolic disturbances. Small screened trials and an unscreened market generate different safety records; both are real.

Zero data. No pregnancy or lactation study of CJC-1295 exists in any species we could locate, no label ever existed to carry a pregnancy section, and the approved drug in the same class, tesamorelin, is contraindicated in pregnancy. An unapproved albumin-bound GH-axis stimulant with a multi-day half-life and an FDA adverse-event record has no defensible use case in pregnancy or breastfeeding.

There is no FDA-reviewed storage guidance, because there is no FDA-reviewed product; vendor storage claims inherit the same evidence vacuum as everything else they print. What can be said from the pharmacology: the DAC linker's maleimide chemistry is reactive by design (its job is to find a thiol), lyophilized research peptides in general are sold for reconstitution with bacteriostatic water, and none of the sources this site accepts has published stability data for either form of this specific compound. We flag the gap rather than filling it with supplier folklore.

Subcutaneous injection in every human study: single ascending doses and two- to three-times weekly or biweekly schedules in the randomized trials, and single doses in the pulsatility study. Because the DAC form binds albumin and lasts days, trial schedules were weekly-scale, not the multiple-daily-injection pattern forums apply to the no-DAC form.

With DAC, the human numbers are unusually solid for this market: estimated half-life 5.8 to 8.1 days, GH elevation lasting 6 or more days and IGF-I elevation 9 to 11 days after one dose, and accumulation across repeated weekly dosing. The mechanism is covalent albumin binding demonstrated in the identification study.

Without DAC, no published human pharmacokinetics exist under the compound's own name; the 2026 review records it as essentially uncharacterized in humans. The closest measured anchor is single-substitution data: D-Ala2 alone stretched GRF(1-29)'s half-life from 4.3 to 6.7 minutes in men. The 30-minute figures circulating on vendor pages are not traceable to any trial we can cite. Minutes versus days is the honest comparison, and it is why the two forms cannot be dosed interchangeably.

CJC-1295 reaches users through channels no regulator inspects. The forensic literature documents the consequence concretely: in 2009 the Norwegian doping-control laboratory identified a police-seized unknown preparation as a 29-residue amidated peptide consistent with material marketed as CJC-1295. Note the residue count: FDA's registry sequence for CJC-1295 proper runs 30 residues, the last being the DAC-linker lysine. A vial labeled with one name, and a market that rarely says which form it means, is the product landscape in a single anecdote.

The 2026 reviews say the general version: gray-market peptides are frequently mislabeled or contaminated, quality concerns are the rule, and rigorous human safety data are scarce with potential for serious harm. FDA's compounding rule applies to the licensed end of the spectrum: even properly compounded drugs are not FDA-approved and get no premarket review. Qualitative research on user forums documents that users themselves voice concerns about dosing estimation and long-term consequences.

Stated as checked absences, with the checks in the claims ledger: no efficacy trial of CJC-1295 for body composition, strength, sleep, recovery, skin, or longevity has ever been completed; the one phase 2 that tried (visceral fat in HIV) was terminated without posted results, and the registry lists nothing else. No trial has exceeded 49 days of dosing. Long-term safety of a chronically raised GH/IGF-I floor is unmeasured, with sustained IGF-1 elevation flagged as a plausible cancer-risk amplifier. The no-DAC form has no controlled human data at all. Enrollment sizes for the 2006 trials are not stated in the openly accessible abstracts, so we do not state them. And FDA itself closes its entry with the same admission: available clinical data are limited.

Sermorelin is the short-acting original this molecule descends from, once FDA-approved as Geref and formally determined not to have been withdrawn for safety reasons; tesamorelin is the GHRH analog that finished the journey CJC-1295 abandoned, carrying a current FDA approval for HIV-associated lipodystrophy; ipamorelin is the ghrelin-receptor secretagogue most often stacked with this compound, on anecdotal rationale a 2026 review finds unsupported by controlled evidence. Full comparisons below; our sister sites sermorelinco.com and ipamorelinco.com cover the siblings in monograph depth.