Compound Physician required WADA prohibited Part of CJC-1295 + Ipamorelin

CJC-1295

Long-acting GHRH analog — raises pulsatile growth-hormone release.

The story

CJC-1295 is one of the few gray-market peptides with a completely conventional origin: it was designed, patented, named and taken into human trials by a publicly traded pharmaceutical company, and the record of that work is in the peer-reviewed literature under the company's own byline.

The company was ConjuChem Inc. (later ConjuChem Biotechnologies), a Montreal biotech whose entire platform was one idea: attach a small reactive chemical handle to a therapeutic peptide so that, once injected, it forms a covalent bond with the free thiol on Cys34 of the patient's own serum albumin. Albumin circulates for roughly three weeks; a peptide bolted to it inherits that longevity. ConjuChem called the handle a Drug Affinity Complex — DAC. The problem it addressed here is that native GHRH(1-29) is cleaved within minutes, principally by dipeptidyl peptidase-IV, which is why the unmodified fragment (marketed as sermorelin) must be injected repeatedly and still produces only a brief pulse.

The founding paper is Jetté et al., published in Endocrinology in 2005 with a ConjuChem research-department affiliation on the first author. The group made three maleimido derivatives of hGRF(1-29), conjugated them to human serum albumin, and screened them; the best of the three — a tetrasubstituted hGRF(1-29) ([D-Ala2, Gln8, Ala15, Leu27]) carrying an added C-terminal lysine with an Nε-3-maleimidopropionamide group — produced a four-fold larger growth hormone response than plain hGRF(1-29) in rats and was still detectable in plasma beyond 72 hours. Western blot confirmed the peptide riding on the albumin band. That compound was designated CJC-1295 (DOI 10.1210/en.2004-1286).

Human work followed immediately and was reported by Teichman et al. in the Journal of Clinical Endocrinology & Metabolism in 2006: two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults, showing a half-life of 5.8–8.1 days and IGF-1 elevated for up to 28 days after multiple doses (DOI 10.1210/jc.2005-1536). Jean-Paul Castaigne, ConjuChem's chief executive, is a co-author. Later that year Ionescu and Frohman at the University of Illinois at Chicago published the pulsatility substudy that remains the most physiologically interesting human paper on the compound (DOI 10.1210/jc.2006-1702).

ConjuChem pursued two indications. One was somatotropin deficiency — adult and paediatric GH deficiency, the obvious market for a once-weekly GHRH analog. The other was HIV-associated visceral obesity, the same indication Theratechnologies was pursuing with its own GRF analog TH-9507, later approved as tesamorelin. ConjuChem's Phase 2 lipodystrophy study (NCT00267527, GH100-013) was registered as a multicentre, randomized, double-blind, placebo-controlled 12-week trial with a 6-week follow-up (NCT00267527 — registry record — self-asserted, unverified: the design is as ConjuChem filed it, and no publication, regulator document or independent account of the trial's conduct exists against which to check it).

It ended abruptly, and the way it ended is the fact the rest of this compound's public life sits on top of: a participant died during a 2006 trial; the sponsor halted development; publicly available records never established causality. On 17 July 2006 ConjuChem halted the study following the death of a participant at an Argentine site. The contemporaneous account by NAM aidsmap reports that the company disclosed little beyond the fact of the death and the site, that the cause of death and its relationship to the study drug were "currently being investigated," and that ConjuChem's president said any problem would be "quite specific to GRF." An unconfirmed report from a Canadian participant described a man who died a few hours after his eleventh injection. Theratechnologies' competing TH-9507 Phase 3 program continued after its own safety monitoring board reviewed the data (aidsmap, 2006-07). The AdisInsight development record logs the program as suspended on 14 July 2006 and discontinued on 21 March 2007 — both the lipodystrophy programme and the somatotropin-deficiency programme on the same day (AdisInsight). No results were ever posted to ClinicalTrials.gov, no cause of death was ever published, and no peer-reviewed paper on the trial exists. ConjuChem redirected the DAC platform to an exenatide conjugate, CJC-1134-PC, for type 2 diabetes; one of its Phase 2 trials was terminated in 2013 for a "business decision," and the company was later delisted from the TSX (NCT01514149 — registry record — self-asserted, unverified).

The route into fitness culture is documented forensically rather than journalistically. In 2009 Norwegian police and customs submitted an unknown pharmaceutical preparation for analysis; LC-HRMS/MS identified a 29-amino-acid C-terminally amidated peptide consistent with "a peptide currently marketed under the name CJC-1295," and the authors noted there was "reason to believe that it is being used within the bodybuilding community" (DOI 10.1002/dta.233). That paper is effectively the compound's birth certificate as a doping agent — and it also contains the first published trace of the identity problem, because the peptide the Norwegians actually found was the 29-residue form, not the DAC conjugate. A decade later, Danish customs seizures analysed by the same laboratory group turned up glycine-extended analogues of GHRP-2, GHRP-6, ipamorelin and modified GRF(1-29) (DOI 10.1002/dta.2489). By 2026 CJC-1295 was appearing by name in mainstream sports-medicine reviews as one of the handful of peptides clinicians should expect patients to arrive already using (DOI 10.1177/03635465261464420; DOI 10.3389/fendo.2026.1822475).

  1. 2005 Jetté et al. (ConjuChem) identify CJC-1295 as the best of three maleimido hGRF(1-29) derivatives; plasma presence beyond 72 h in rats
  2. 2005-12 ConjuChem registers NCT00267527, Phase 2, CJC-1295 in HIV-associated visceral obesity, 12 weeks, placebo-controlled, registered with an enrolment of 120 (a registry field; journalism reports 192)
  3. 2006-03 Teichman et al. publish the pivotal human PK/PD trials in JCEM: half-life 5.8–8.1 days, IGF-1 elevated up to 28 days
  4. 2006-07-14/17 Phase 2 lipodystrophy trial suspended after a participant death at an Argentine site; cause and relationship to drug "under investigation"
  5. 2006-12 Ionescu & Frohman show GH pulsatility is preserved but trough GH rises 7.5-fold after a single injection
  6. 2007-03-21 Both CJC-1295 programmes — lipodystrophy and somatotropin deficiency — recorded as discontinued
  7. 2009–2010 CJC-1295 identified by LC-HRMS/MS in a seized preparation submitted by Norwegian police and customs; flagged as a WADA S2 substance in bodybuilding use
  8. 2010s ConjuChem redirects DAC platform to CJC-1134-PC (exenatide conjugate) for type 2 diabetes; a Phase 2 terminated 2013 for "business decision"; company delisted from TSX
  9. 2018 Danish customs seizures found to contain glycine-extended modified GRF(1-29) alongside GHRP-2, GHRP-6 and ipamorelin analogues
  10. 2021-04-15 USADA announces a four-year sanction for a US cyclist whose ten-substance non-analytical violation included CJC-1295
  11. 2026-04-22 FDA bulks page, as last modified, lists CJC-1295 under "nominated but withdrawn," citing serious adverse events including increased heart rate and systemic vasodilatory reaction
  12. 2026-07-23/24 FDA Pharmacy Compounding Advisory Committee reviews seven peptides for the 503A bulks list. CJC-1295 is not among them

What it does

A long-acting GHRH analog with mechanistic and small-study human data, no standardized longevity protocol, and unresolved legal status. Considered only under physician supervision, and only where regulation permits.

A long-acting growth-hormone-releasing-hormone analog. It raises pulsatile growth-hormone release, which in turn raises IGF-1.

  • growth hormone (pulsatile release)
  • IGF-1

What the evidence shows

Every human datum ever recorded under the name CJC-1295 describes a different molecule from the one most people buy: all of it is CJC-1295 *with* DAC, the albumin-binding ConjuChem conjugate, and it amounts to one pharmacokinetic/pharmacodynamic study in healthy men plus a companion pulsatility substudy, both from 2006, both measuring hormone concentrations and pharmacokinetic parameters — between them the only human endpoints this compound has ever had — and nothing a person would notice. None of it transfers to the 'no-DAC' product sold under the same name, which is modified GRF(1-29), a molecule with a duration of action three orders of magnitude shorter and no controlled human study of any kind. The one trial that would have measured a clinical endpoint — a phase 2 efficacy trial in HIV-associated visceral obesity — never reported: a participant died during it in 2006; the sponsor halted development; publicly available records never established causality. What remains is a sponsor-authored dataset sharing an author across both published papers, unreplicated in twenty years, which establishes that the albumin trick raises GH and IGF-1 and establishes nothing about lean mass, fat mass, strength, sleep, recovery or safety in anyone who is not a healthy volunteer. The single biggest limitation is not the thinness of the record but its misattribution to the wrong product.

Overall evidence strength: Low certainty

  • Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne J-P, Frohman LA (2006) — the pivotal human PK/PD study (2006) Randomized controlled trial

    one injection raised average growth hormone two- to ten-fold for six days or more and IGF-1 one-and-a-half to three-fold for nine to eleven days, with the drug itself persisting about a week — which establishes that the albumin trick works, and establishes nothing about muscle, fat, sleep, recovery or how anyone felt. No serious adverse reactions were reported, and the authors identify the two lower of the four ascending levels as the better-tolerated ones — the administered quantities are withheld throughout this file under the batch-1 trigger. Read that tolerability finding against what it covers: healthy volunteers, 28 and 49 days. The longer trial, in a patient population, ended in a participant's death.

    Source PMID 16352683

  • Ionescu M, Frohman LA (2006) — GH pulsatility under continuous GHRH stimulation (2006)

    a week after one injection the men's GH pulses were still coming at the same rate and size — but the floor between pulses had risen seven-and-a-half-fold, which is where essentially all of the extra GH exposure and the 45% IGF-1 rise came from. The IGF-1 increase did not correlate with any measure of GH secretion, so what drives it is not actually understood.

    Source PMID 17018654

  • Sackmann-Sala L et al. (2009) — serum proteomic response (2009)

    five serum protein spots moved after a single injection — apolipoprotein A1 and transthyretin isoforms down, beta-haemoglobin and albumin fragments up — a hint that GH-axis activation leaves a wider fingerprint than IGF-1 alone, and nowhere near a validated test.

    Source PMID 19386527

  • NCT00267527 (2005–2006) — the terminated Phase 2

    this is the only registered study of CJC-1295 whose endpoints were clinical rather than hormonal — and it was stopped in July 2006 after a participant died, with no results published and no cause of death made public. What it would have shown is unknown and unknowable from the record.

    Source

  • Alba M et al. (2006) — growth rescue in GHRH-knockout mice (2006) Preclinical / mechanistic

    mice genetically unable to make GHRH grew to normal weight and length on once-daily CJC-1295 and only partially caught up on less frequent dosing, with proliferation of pituitary GH-producing cells — a clean demonstration that the molecule does what a GHRH analog should, in an animal with no GHRH at all, which is a very different situation from a healthy adult who has plenty.

    Source PMID 16822960

  • Evidence syntheses (2026) (2026) Review / meta-analysis

    Three independent 2026 reviews cover CJC-1295 as a gray-market agent and agree on the shape of the evidence. An endocrinology narrative review grades CJC-1295-DAC tier B (phase I/II human studies not addressing performance or body-composition endpoints) and CJC-1295 without DAC tier D (no peer-reviewed human studies at all) (DOI 10.3389/fendo.2026.1822475). A PRISMA-guided AJSM scoping review of six gray-market peptides including CJC-1295 found 67% of identified publications used preclinical animal models, human studies "limited to a handful" (DOI 10.1177/03635465261464420). A JBJS Reviews structured narrative review found GLP-1 receptor agonists the only peptide class in its scope with reproducible randomized evidence (DOI 10.2106/JBJS.RVW.26.00027).

    Source

Common misconceptions

“CJC-1295 is one peptide, and the human research applies to what I'm buying.”

Two pharmacologically different molecules are sold under this one name. CJC-1295 with DAC is the ConjuChem compound. It carries a C-terminal lysine bearing a maleimidopropionamide group that covalently binds Cys34 of serum albumin after injection. Its measured half-life in humans is 5.8–8.1 days; a single injection raises GH for six days or more and IGF-1 for nine to eleven (DOI 10.1210/jc.2005-1536; DOI 10.1210/en.2004-1286). "CJC-1295 no-DAC" is not CJC-1295 at all. It is modified GRF(1-29) — the same four amino-acid substitutions, but without the lysine-DAC extension, so it never binds albumin. Its duration of action is measured in minutes to a couple of hours. A 2026 narrative review in Frontiers in Endocrinology states the position plainly: "CJC-1295 without DAC" remains "essentially uncharacterised in the peer-reviewed human literature," with "no controlled clinical studies… directly evaluated this compound in humans," and assertions about it derived "largely from extrapolation from related compounds (primarily GHRH(1–29), known as sermorelin)… as well as from non-academic sources." The review's evidence-tiering assigns CJC-1295-DAC to tier B and CJC-1295 without DAC to tier D — no peer-reviewed human studies at all (DOI 10.3389/fendo.2026.1822475). The confusion runs through reference works, the literature and the forensic record alike — the compound's own chemistry entry notes that modified GRF(1-29) is "marketed as CJC-1295 without DAC" and is distinct "despite frequent scientific literature confusion" (Wikipedia — tertiary source, cited only for nomenclature and for the fact that the confusion is documented). The 2009 Norwegian seizure analysed by Henninge et al. contained a 29-amino-acid C-terminally amidated peptide — the no-DAC form — yet was published under the heading "Identification of CJC-1295" (DOI 10.1002/dta.233); Danish customs material analysed in 2018 was catalogued as "modified GRF (1-29)" (DOI 10.1002/dta.2489). What that means for anything a buyer reads: every human number attached to the name CJC-1295 — the 5.8–8.1 day half-life, the 2- to 10-fold GH rise, the 28-day IGF-1 elevation, the tolerability finding at the levels those trials used — comes from studies of the DAC compound. Applied to a no-DAC vial they are simply the wrong numbers, describing a different molecule with a half-life roughly three orders of magnitude shorter. A comparison of the two forms that cites human data on one side and none on the other is not a comparison of two options; it is a category error.

“The no-DAC version is better because it preserves natural GH pulsatility.”

The pulsatility question has been measured exactly once, in the DAC form, and the result does not support either side's slogan. Ionescu and Frohman sampled GH every 20 minutes overnight before and one week after a single CJC-1295 injection. Pulse frequency and magnitude were unaltered. What changed was the floor: basal (trough) GH rose 7.5-fold (P < 0.0001), driving a 46% rise in mean GH and a 45% rise in IGF-1. The authors' own conclusion is that CJC-1295 "increased trough and mean GH secretion and IGF-I production with preserved GH pulsatility" (DOI 10.1210/jc.2006-1702). So the marketing claim that DAC "flattens" pulsatility is not what the one study found; and the counter-claim that the paper vindicates DAC as physiological is also more than the paper says, because a seven-fold higher inter-pulse baseline is not a normal GH profile either. Whether the no-DAC form produces a more physiological pattern in humans has never been measured — there is no human pulsatility study of modified GRF(1-29) at all (DOI 10.3389/fendo.2026.1822475).

“CJC-1295 is proven to build muscle and cut fat.”

No human study of CJC-1295 has ever measured lean mass, fat mass, strength, or physical performance. The two published human trials measured hormone concentrations and pharmacokinetics (DOI 10.1210/jc.2005-1536; DOI 10.1210/jc.2006-1702). The only trial with a body-composition indication — the Phase 2 in HIV-associated visceral obesity — was terminated and never published (NCT00267527 — registry record — self-asserted, unverified). The 2026 Frontiers in Endocrinology review places CJC-1295-DAC in the tier of compounds with "phase I/II human studies that do not address performance- or body-composition endpoints" and states there is "no peer-reviewed support for clinically meaningful effects on body composition or performance outcomes" for the no-DAC form (DOI 10.3389/fendo.2026.1822475). The 2026 AJSM scoping review found that 67% of the publications it identified across six gray-market peptides used preclinical animal models (DOI 10.1177/03635465261464420).

“The trials found no serious adverse reactions, so it's safe.”

Both halves of that sentence are true and they do not combine into safety, because the sentence leaves out how the development programme actually ended: a participant died during a 2006 trial; the sponsor halted development; publicly available records never established causality. That is the reason this is a misconception rather than a fact. Teichman et al. reported no serious adverse reactions — in healthy volunteers, over study periods of 28 and 49 days, at a handful of ascending levels (DOI 10.1210/jc.2005-1536). The longer trial in a patient population was halted in July 2006 after a participant died, and the cause of death and its relationship to the study drug were, at the time of the only contemporaneous report, "currently being investigated." No finding was ever published (aidsmap, 2006-07). Both programmes were discontinued the following March (AdisInsight). Separately, FDA's bulk drug substances page states that the agency "has identified serious adverse events associated with CJC-1295 including increased heart rate and systemic vasodilatory reaction," and that "available clinical data are limited" (FDA). ⚠️ Unverified and marked as such. The claim circulating online that the death was cardiac and was attributed by the attending physician to pre-existing coronary artery disease appears in tertiary encyclopedic sources without a citable primary document. We could not verify it against a company release, a regulatory filing, an autopsy report, or any peer-reviewed source. It is not established that the death was drug-related; it is equally not established that it was not. Both the confident "a man died from CJC-1295" and the confident "it was just his pre-existing heart disease" go beyond the record.

“It's safer than injecting growth hormone because it works through your own pituitary.”

The mechanistic premise is real — GHRH analogs act on the pituitary GHRH receptor and the axis retains somatostatin feedback, which is why this class was pursued as an alternative to exogenous GH and why the one approved compound in it (tesamorelin) exists (DOI 10.3389/fendo.2026.1822475). But "safer than GH" is a comparative claim, and no head-to-head human comparison has been done on any endpoint. What is documented is that the DAC form produces GH exposure that is continuous rather than intermittent — trough GH up 7.5-fold a week after one injection, IGF-1 above baseline for up to 28 days after multiple doses (DOI 10.1210/jc.2006-1702; DOI 10.1210/jc.2005-1536). Sustained IGF-1 elevation is the pharmacology this class shares with GH, and the cautions attached to it — dysglycaemia, fluid retention, arthralgia and myalgia — are documented class effects.

“What's in the vial is CJC-1295.”

Every published forensic analysis of seized material in this class has found something other than a clean labelled product. The 2009 Norwegian seizure sold as CJC-1295 contained the 29-residue no-DAC peptide (DOI 10.1002/dta.233). Danish customs seizures analysed in 2018 contained glycine-extended analogues of GHRP-2, GHRP-6, ipamorelin and modified GRF(1-29) — an extra N-terminal amino acid on each, significant enough that the authors concluded doping-control assays had to be updated for it (DOI 10.1002/dta.2489). ECRI and ISMP reported gray-market peptide purity of 5%–75% with arsenic and lead above toxicity thresholds; that describes the peptide market generally and we do not attribute it to CJC-1295 (ECRI/ISMP). ---

Who it's for, who should skip

Only under direct physician supervision, and only where regulation permits. Status is gray_zone — removed from Category 2 in April 2026 but not moved to Category 1, with no lawful channel currently. Not for anyone with active or recent cancer, or who is pregnant.

Skip it if

  • active or recent cancer — GH-axis agents are contraindicated in active or recent malignancy — growth signaling can accelerate tumor growth. hard block
  • pregnancy — Contraindicated in pregnancy. hard block

Running it

No dosing protocol is published for this compound — there is no lawful supervised channel for the use this guide covers. What follows is monitoring, expectations, and safety framing only.

Form
injectable

What to expect

  • Days 1–11 after a single dose — Mean plasma GH up 2- to 10-fold for ≥6 days; mean plasma IGF-1 up 1.5- to 3-fold for 9–11 days, dose-dependently (Confidence: Trial-documented (randomized, placebo-controlled, double-blind) — DOI 10.1210/jc.2005-1536)
  • One week after a single dose — GH pulse frequency and amplitude unchanged; trough GH 7.5-fold higher; mean GH +46%; IGF-1 +45% (Confidence: Trial-documented (healthy men only, small n) — DOI 10.1210/jc.2006-1702)
  • Repeat dosing to 4 weeks — Cumulative effect; mean IGF-1 above baseline up to 28 days after multiple doses (Confidence: Trial-documented — DOI 10.1210/jc.2005-1536)
  • 12 weeks — The only 12-week trial was terminated after a participant death; nothing reported (Confidence: No data — NCT00267527, registry record — self-asserted, unverified, cited only for the record's own terminated status and absence of results; aidsmap)
  • Post-cessation — Never studied. The 5.8–8.1 day half-life implies exposure persists for days after a last dose; no study followed anyone to a return-to-baseline endpoint or looked for rebound (Confidence: Inference, not documented)
  • Long-term — No human exposure beyond 49 days exists in the published record (Confidence: No data)
  • "CJC-1295 no-DAC" at any timepoint — No controlled human study exists (Confidence: No data — DOI 10.3389/fendo.2026.1822475)
  • Sleep, recovery, body composition, strength — Never measured in a human study of this compound (Confidence: Anecdotal, low confidence — mainstream consumer peptide explainer, cited as evidence of what is claimed)

Response signs

Likely working

  • A measured rise in serum IGF-1 — Trial-documented — the only objectively verifiable sign the compound is doing anything · DOI 10.1210/jc.2005-1536 Trial-documented
  • Improved sleep quality; faster recovery; changes in lean or fat mass — Anecdotal, low confidence — the dominant claims in circulation, never measured in any CJC-1295 study · consumer peptide explainer — what is claimed; DOI 10.3389/fendo.2026.1822475 Anecdotal

Adverse — seek review

  • Palpitations, resting tachycardia, unexplained rise in heart rate — Regulator-reported adverse event, compound-specific — FDA names increased heart rate among serious adverse events identified for CJC-1295 · FDA
  • Flushing, warmth, light-headedness, or a blood-pressure drop after a dose — Regulator-reported adverse event, compound-specific — "systemic vasodilatory reaction" · FDA
  • New swelling in hands, ankles or face; wrist/hand numbness or night pain — Inference from class pharmacology — fluid-retention syndromes documented across GH-axis peptides; not documented for CJC-1295 · DOI 10.3389/fendo.2026.1822475 Inference
  • Rising fasting glucose, new thirst or polyuria — Inference from class pharmacology — dysglycaemia is a class effect; never measured in a CJC-1295 human study · DOI 10.3389/fendo.2026.1822475 Inference
  • New joint or muscle pain after starting — Inference from class pharmacology · DOI 10.3389/fendo.2026.1822475 Inference
  • Injection-site reaction, particularly spreading, warm, or persisting — Inference — class effect, plus FDA's immunogenicity concern for compounded product by certain routes · FDA Inference

Common / neutral

  • No perceptible acute effect — Consistent with the pharmacology — with the DAC form exposure builds over days and peaks nowhere in particular; there is no acute felt signature to read · Inference from trial-documented PK (DOI 10.1210/jc.2005-1536) Trial-documented
  • Feeling "nothing" from a no-DAC product — Uninterpretable: with a half-life in minutes and no human data, absence of effect distinguishes neither an inert vial from an active one nor a correct product from a mislabelled one · No data (DOI 10.3389/fendo.2026.1822475) No data

Getting it right

  • Monitoring: IGF-1 with a pre-exposure baseline is the only interpretable efficacy-adjacent measurement — it is the marker the trials moved, and a value with nothing to compare it to says very little (DOI 10.1210/jc.2005-1536). mitigate side effect
  • Monitoring: Timing the draw is unsolved for the DAC form. IGF-1 stayed above baseline up to 28 days after multiple doses, so one value cannot separate response from accumulation, and no published sampling schedule exists. mitigate side effect
  • Monitoring: Glycaemic markers are the class watch-list — not because CJC-1295 has been shown to move them (no human study measured them) but because dysglycaemia is the documented class effect of sustained GH–IGF-1 activation (DOI 10.3389/fendo.2026.1822475). mitigate side effect
  • Monitoring: Heart rate and blood pressure are the compound-specific ones, on the strength of FDA's identified adverse events (FDA). mitigate side effect
  • Monitoring: There is no observed-safety window to extrapolate from. The longest published human exposure is 49 days in healthy volunteers; the one 12-week trial was terminated (NCT00267527 — registry record — self-asserted, unverified). mitigate side effect
  • General safety: Identity is the first-order risk, more than for most compounds in this batch, because the ambiguity is built into the product name: a vial labelled CJC-1295 may contain the DAC conjugate, modified GRF(1-29), or a glycine-extended analogue of either (DOI 10.1002/dta.233; DOI 10.1002/dta.2489). A seller's certificate of analysis is not independent verification. mitigate side effect
  • General safety: A long half-life removes the ability to stop quickly. With the DAC form an adverse reaction cannot be reversed by skipping the next dose; exposure persists for days, which follows directly from the measured 5.8–8.1 day half-life (DOI 10.1210/jc.2005-1536). mitigate side effect
  • General safety: Stacked use makes attribution impossible — no combination containing CJC-1295 has been studied against its components. mitigate side effect
  • General safety: Athletes and service members face strict liability — CJC-1295 is named in WADA S2.2.4 and prohibited at all times. mitigate side effect
  • The physician conversation: Which compound is actually in the vial — with DAC or without? ("I don't know" is an answer, and it changes what the human literature can be asked to say.) mitigate side effect
  • The physician conversation: What is the baseline IGF-1, and when was it drawn relative to the last dose? mitigate side effect
  • The physician conversation: What would count as it working, by when, and what happens if that date passes? mitigate side effect
  • The physician conversation: What else is being taken — ghrelin-receptor agonists, anabolic steroids, thyroid hormone, insulin, anything from a non-pharmacy source? Polypharmacy is the norm here and confounds every symptom (DOI 10.3389/fendo.2026.1822475). mitigate side effect
  • The physician conversation: Is there personal or family history of diabetes, cardiovascular disease, or cancer? mitigate side effect
  • The physician conversation: Is there any competitive-sport, collegiate, or military testing obligation? (.) mitigate side effect

Measuring it

Retest IGF-1 — Baseline, then on a clinician-set schedule — no guideline sets an IGF-1 interval for this agent, and the rhGH cadence is not borrowed..

  • IGF-1 baseline
  • IGF-1 on cycle
  • Fasting glucose baseline
  • Fasting glucose on cycle
  • HbA1c baseline
  • HbA1c quarterly

How biomarkers respond

  • Fasting glucose May deteriorate — The canonical watch markers for anything that sustains GH and IGF-1 elevation. Dysglycaemia is documented as an adverse-effect pattern across GH–IGF-1-axis performance peptides — Inference from class pharmacology — not measured in any published CJC-1295 human study. Note that the terminated Phase 2's registered eligibility criteria excluded diabetics at entry, so even that trial would not have addressed it (DOI 10.3389/fendo.2026.1822475; NCT00267527 — registry record — self-asserted, unverified) Inference
  • Cortisol May deteriorate — Included here to rule them out: elevation of these is largely a feature of the older ghrelin-mimetic GHRPs (GHRP-2, GHRP-6, hexarelin), not of GHRH analogs. They become relevant only if a ghrelin-receptor agonist is in the stack — Trial-documented for the GHRP class; not expected and not documented for CJC-1295 (DOI 10.3389/fendo.2026.1822475) Trial-documented

Safety

  • injection-site reactions
  • water retention

Interactions

  • Ipamorelin — Named beneficial pair — the GHRH-analog + ghrelin-mimetic combination produces a stronger, still-pulsatile GH release than either alone. synergistic

Stacking & alternatives

  • Complements Ipamorelin — Ghrelin-receptor agonist; the canonical stack partner. FDA lists it in 503B category 2 since 2023-09-29 and cites a published study identifying serious adverse events including death with IV administration for gastric motility (FDA)
  • Alternative to MK-677 (Ibutamoren) — Same downstream endpoint without injection. FDA places it in 503A and 503B category 2, citing a randomized trial in hip-fracture recovery "terminated early due to a potential safety signal of congestive heart failure" (FDA)

Access & cost

Legally unsettled. Access, where it exists at all, runs through a physician — not a consumer purchase. See the status note above.

No lawful channel to price. As of 2026-08-28 there is no lawful US route to obtain CJC-1295 for human use — it is not approved, and it sits in the "nominated but withdrawn" table of FDA's bulk drug substances page rather than on any list permitting compounding (FDA). There is no legitimate brand, pharmacy or telehealth price to report. A gray market nonetheless exists and is documented in the peer-reviewed record rather than only in journalism: 2026 reviews describe a "parallel 'gray market' of unapproved compounds… operating largely outside of regulatory oversight" for peptides including CJC-1295 (DOI 10.1007/s40279-026-02437-0), and its physical reality is documented by customs and police seizures in Norway and Denmark (DOI 10.1002/dta.233; DOI 10.1002/dta.2489). No INTERNAL subsection is included for this compound: no journalist-reported price figures specific to CJC-1295 were located, and the only priced comparator with a lawful channel is tesamorelin, whose pricing belongs in that compound's dossier. ---

Questions

Does CJC-1295 actually work?
It reliably does the pharmacological thing it was designed to do — raise GH and IGF-1, dose-dependently, for days after one injection, in randomized placebo-controlled trials (DOI 10.1210/jc.2005-1536). Whether that produces anything a person would notice has never been tested in a human being; the one trial designed to answer a body-composition question was terminated in 2006 and never reported (NCT00267527 — registry record — self-asserted, unverified).
What's the difference between CJC-1295 with DAC and CJC-1295 "no-DAC"?
They are different molecules. The DAC version binds your albumin and lasts about a week (half-life 5.8–8.1 days); the no-DAC version is modified GRF(1-29), does not bind albumin, and clears in minutes to hours. All human research is on the DAC version; the no-DAC version has no peer-reviewed human studies at all (DOI 10.3389/fendo.2026.1822475). See — the single most consequential thing to understand about this compound.
Is there an oral or nasal form that works?
No human study of CJC-1295 has used any route except subcutaneous injection. The entire mechanism depends on the albumin-conjugating group reaching the bloodstream intact and finding Cys34 on albumin (DOI 10.1210/en.2004-1286), and FDA's stated concern for compounded CJC-1295 is immunogenicity for certain routes of administration (FDA). Treat oral or nasal "CJC-1295" as unevidenced.
Does it raise IGF-1, and is that good?
It does — 1.5- to 3-fold after a single dose, above baseline up to 28 days after multiple doses (DOI 10.1210/jc.2005-1536). Whether sustained IGF-1 elevation is desirable is a question this compound's literature does not answer. In the one study that looked, the IGF-1 rise did not correlate with any parameter of GH secretion (DOI 10.1210/jc.2006-1702). See.
Did someone die in a CJC-1295 trial?
Yes — and the honest one-sentence version is that a participant died during a 2006 trial; the sponsor halted development; publicly available records never established causality. In more detail: a participant in ConjuChem's Phase 2 trial in HIV-associated visceral obesity died at an Argentine site, and the company halted the trial on 17 July 2006. Cause of death and its relationship to the drug were under investigation; no result was ever published, and both programmes were discontinued in March 2007 (aidsmap; AdisInsight). Anyone stating confidently that the death was, or was not, caused by the drug is going beyond the public record. See.
What are the side effects?
Not established for real-world use — and the trial record reads more reassuringly than it is, because a participant died during a 2006 trial; the sponsor halted development; publicly available records never established causality. Healthy-volunteer trials reported no serious adverse reactions, over 28 and 49 days, in people who were not ill (DOI 10.1210/jc.2005-1536). FDA states it has identified serious adverse events including increased heart rate and systemic vasodilatory reaction (FDA). At class level the documented pattern spans dysglycaemia, fluid retention, arthralgia/myalgia and injection-site reactions (DOI 10.3389/fendo.2026.1822475).
Will it show up on a drug test?
Yes, and it is prohibited by name under WADA S2.2.4, at all times (2026 Prohibited List). Validated immunoaffinity LC-HRMS methods detect GHRH analogues including CJC-1295 at picogram-per-millilitre levels (DOI 10.1016/j.ymeth.2011.08.009). See.
Is what I'd buy actually CJC-1295?
Frequently not. Seized preparations sold under the name have contained the no-DAC peptide rather than the DAC conjugate (DOI 10.1002/dta.233) and, later, glycine-extended analogues rather than the peptide itself (DOI 10.1002/dta.2489). Gray-market peptide purity has been measured market-wide at 5%–75% (ECRI/ISMP). ---

Last reviewed 27 August 2026. Regulatory status verified 27 August 2026.