CJC-1295 No DAC
Research PeptideAlso known as: Modified GRF 1-29 · Mod GRF 1-29 · CJC-1295 without DAC · Tetrasubstituted GRF(1-29)
Preliminary Human
No published human efficacy trial tests Modified GRF 1-29 (CJC-1295 No DAC) alone. Every clinical study commonly cited for "CJC-1295" was conducted on the WITH-DAC variant — a structurally distinct, albumin-binding, ~6–8 day half-life compound — most notably the ConjuChem-sponsored Teichman 2006 Phase I/II (n=64) and the Phase II HIV lipodystrophy trial (NCT00267527, n=192) which was TERMINATED in July 2006 after a participant died of acute MI two hours post-injection. The no-DAC form's published evidence is mechanistic inference + extrapolation from sermorelin and the WITH-DAC trials; the preliminary_human tier reflects the extrapolated nature of the signal, not a direct human efficacy dataset.
Most "CJC-1295" clinical evidence online is actually for a different compound
Every published human clinical trial of a compound labeled "CJC-1295" — Teichman 2006 (n=64), Ionescu 2006 pulsatility, Sackmann-Sala 2009 proteomics, the terminated NCT00267527 Phase II (n=192) — studied the WITH-DAC variant: a 30-amino-acid peptide that covalently binds serum albumin and has a 6–8 day half-life. CJC-1295 No DAC (Modified GRF 1-29) is the 29-residue CORE of that compound WITHOUT the albumin-binding extension; its half-life is ~30 minutes. No published human efficacy or pharmacokinetic trial has tested Mod GRF 1-29 alone. Clinical claims about CJC-1295 No DAC — GH increases, IGF-1 elevation, body-composition effects — rest on extrapolation from the WITH-DAC literature and from sermorelin, not on direct evidence for this compound.
The only large CJC-1295 Phase II trial was terminated after a participant death
ConjuChem's Phase II trial of CJC-1295 WITH-DAC in HIV-associated visceral obesity (NCT00267527, n=192) was TERMINATED in July 2006 after a participant in Argentina died of acute myocardial infarction approximately 2 hours after their eleventh injection. The attending physician attributed the death to pre-existing coronary artery disease, not the drug, and no formal causality assessment was completed. ConjuChem halted development entirely and went out of business shortly thereafter. The trial's efficacy endpoints were never reported. This termination is routinely omitted from online content citing ConjuChem's Phase I GH and IGF-1 data as support for CJC-1295; any honest summary of the compound's clinical history should include both. The no-DAC variant has no equivalent trial history because it has never been tested in an adequately-powered human trial.
Research use only. Not approved for human consumption in any jurisdiction listed here unless the Regulatory Status table below explicitly states otherwise.
Evidence Tier
Preliminary Human
Human Studies
4
FDA Status
Not Nominated
WADA Status
Prohibited (S2)
Mol. Weight
3367.9 Da
Last Reviewed
Apr 21, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Preliminary Human3
- Increases GH secretion acutely after injection
- Increases IGF-1 levels
- Preserves "pulsatile" GH physiology vs long-acting analogs
Anecdotal3
- Improves body composition (reduces fat, increases lean mass)
- Improves sleep quality / deep sleep
- Accelerates recovery from injury / wound healing
Unsupported2
- Anti-aging / longevity effects
- Cognitive enhancement
Regulatory watch
FDA PCAC meetings scheduled July 23–24, 2026 — broader peptide compounding review under the HHS-Secretary-directed policy shift. CJC-1295 is among the peptides expected to be re-evaluated.
Outcome will determine whether CJC-1295 returns to any 503A compounding pathway or remains in the current "off Category 2, not on Category 1, PCAC-declined" limbo. Prior PCAC vote declined to recommend inclusion; whether that position holds under the new policy direction is the open question.
WADA 2027 Prohibited List annual review (publication typically late September / early October).
No reclassification of CJC-1295 is anticipated; GHRH-analog listing has been stable since 2017. Included as a routine watch item.
Expected 2026-10-01 · WADA
Vendors selling CJC-1295 No DAC
Found 10 vendors currently offering CJC-1295 No DAC in their catalog.
🇺🇸Ascension Peptides
USA
COA Coverage
9/16
56%
✓ HPLC✓ MS— Endo— Ster— Metals
Verified Peptides
COA Coverage
138/138
100%
✓ HPLC✓ MS✓ Endo✓ Ster— Metals
Peptide Partners
COA Coverage
29/35
83%
✓ HPLC— MS✓ Endo✓ Ster✓ Metals
🇪🇺Particle Peptides
Slovakia
COA Coverage
25/25
100%
✓ HPLC✓ MS✓ Endo✓ Ster✓ Metals
SwissChems
COA Coverage
23/52
44%
✓ HPLC✓ MS— Endo— Ster— Metals
🇺🇸Core Peptides
USA
COA Coverage
18/103
17%
✓ HPLC✓ MS— Endo— Ster— Metals
HYB Peptides
No verified COAs
COA Coverage
0/32
0%
— HPLC— MS— Endo— Ster— Metals
BioEdge Research Labs
No verified COAs
COA Coverage
0/20
0%
— HPLC— MS— Endo— Ster— Metals
Research Peptides Europe
No verified COAs
COA Coverage
0/36
0%
— HPLC— MS— Endo— Ster— Metals
Blue Sky Peptide
No verified COAs
COA Coverage
0/45
0%
— HPLC— MS— Endo— Ster— Metals
All CJC-1295 No DAC products
Every CJC-1295 No DAC product across 10 verified vendors — sorted by vendor trust tier, then by COA purity (quantified reports beat unquantified), then by most recent COA date.
| Vendor | Product | Size | COA Date | Purity | Lab | COA |
|---|---|---|---|---|---|---|
| Ascension Peptides Recommended | CJC-1295 no DAC (5MG) | 5mg | — | — | — | — |
| Verified Peptides Trusted | Mod-GRF(1-29) | 2mg | 2020-06-10 | 100.00% | — | View |
| Peptide Partners Trusted | CJC-1295 no DAC (10mg vials) | 10mg | 2026-02-27 | 99.92% | TrustPointe AnalyticsTier 2 — Functional | View |
| Particle Peptides Trusted | Mod GRF 1-29 (CJC-1295 no DAC) 5mg | 5mg | 2026-01-29 | 99.80% | LiquilabsTier 3 — Limited | View |
| Verified Peptides Trusted | CJC-1295 No DAC Peptide Purity | — | 2025-12-31 | — | Janoshik AnalyticalTier 1 — Established | View |
| Verified Peptides Trusted | CJC-1295 No DAC Peptide | 5mg | 2025-12-30 | — | Janoshik AnalyticalTier 1 — Established | View |
| SwissChems Unrated | CJC-1295 without DAC 2 mg | 2mg | 2026-03-22 | — | — | View |
| BioEdge Research Labs Unrated | CJC-1295 No Dac (10mg) | 10mg | — | — | — | — |
| Blue Sky Peptide Unrated | CJC-1295 NO-DAC 2mg (MOD GRF 1-29) | 2mg | — | — | — | — |
| Core Peptides Unrated | CJC-1295 NO DAC (Mod GRF 1-29) (5mg) | 5mg | — | — | — | — |
| HYB Peptides Unrated | CJC-1295 NO DAC 2 mg - 10 Vials | 2mg | — | — | — | — |
| Research Peptides Europe Unrated | CJC 1295 no DAC 5mg | 5mg | — | — | — | — |
About this peptide
Plain English
The body naturally produces a hormone called GHRH that tells the pituitary to release growth hormone. CJC-1295 No DAC is a lab-made version of the first 29 amino acids of that hormone, with four small structural changes that make it more resistant to the body's enzymes. Unlike the longer-lasting WITH-DAC variant (which binds to albumin and stays active for roughly a week), the no-DAC form has a half-life of about 30 minutes, producing a short pulse of growth hormone release rather than a prolonged elevation. It has never been approved as a medicine anywhere in the world and — importantly — nearly every piece of clinical evidence online referring to 'CJC-1295' is actually from trials of the WITH-DAC variant, a different compound.
Technical
Modified GRF(1-29) is a tetrasubstituted peptide analog of endogenous hGHRH that binds and activates the pituitary GHRH receptor (GHRH-R), a Gs-coupled GPCR signaling through cAMP-PKA and Gq/phospholipase-C-IP3-Ca²⁺ cascades to stimulate GH synthesis and exocytosis in anterior pituitary somatotrophs. The four substitutions — D-Ala² (DPP-IV resistance), Gln⁸ (deamidation prevention), Ala¹⁵ (conformational stability), Leu²⁷ (Met-oxidation prevention) — collectively extend plasma half-life from ~3–5 minutes for native hGHRH(1-29) to ~30 minutes for Mod GRF 1-29. This half-life remains far shorter than CJC-1295 WITH-DAC (~6–8 days), which additionally incorporates an Nε-maleimidopropionyl-Lys³⁰ extension that covalently binds serum albumin. Every published clinical trial of a compound marketed as "CJC-1295" studied the WITH-DAC variant; Mod GRF 1-29 alone has no published human PK/PD or efficacy data of its own. Claims about its effects rely on extrapolation from sermorelin, from the WITH-DAC trials, and from GHRH-axis physiology.
Mechanism of action
GHRH receptor agonism → pulsatile GH secretion
Modified GRF 1-29 binds GHRH-R on pituitary somatotrophs. Receptor activation elevates intracellular cAMP via Gαs and activates phospholipase C via Gαq, leading to PKA-mediated CREB phosphorylation and intracellular Ca²⁺ release. Both pathways converge on GH gene transcription and secretory granule exocytosis. Release occurs as a pulse because the peptide is cleared within ~30 minutes, avoiding the blunted receptor sensitivity associated with prolonged GHRH exposure. IMPORTANT: the direct human pharmacodynamic evidence supporting this mechanism was generated with CJC-1295 WITH-DAC and sermorelin — not Mod GRF 1-29 itself.
IGF-1 axis stimulation (GH → hepatic GHR → JAK2/STAT5b → IGF-1)
GH released in response to GHRH-R activation travels to the liver, where it activates GH receptors and stimulates IGF-1 synthesis. IGF-1 circulates and mediates many downstream anabolic effects (protein synthesis, lipolysis, glucose regulation). IGF-1 and GH also participate in long-loop negative feedback on both the hypothalamus (stimulating somatostatin release) and pituitary (reducing GHRH-R sensitivity). The magnitude and duration of IGF-1 elevation following Mod GRF 1-29 dosing specifically has not been characterised in published human literature.
Preservation of pulsatile GH profile (proposed advantage over long-acting analogs)
The short half-life of Mod GRF 1-29 (~30 min) means GHRH-R stimulation ceases rapidly, allowing somatostatin tone to re-assert and preserving the natural alternating suppression/release pattern of GH. The Ionescu & Frohman 2006 paper — often cited in support of this claim — is in fact a study of the WITH-DAC variant, demonstrating pulsatility is preserved even under sustained stimulation. Whether the no-DAC form produces more "physiological" GH profiles than long-acting variants is inferred mechanistically but not directly tested in any published comparative human trial.
GH-axis physiology is broadly conserved between rodents and humans, but magnitude, receptor density, and regulatory dynamics differ substantially. All three mechanisms above have supporting evidence from GHRH analog research conducted primarily with CJC-1295 WITH-DAC, sermorelin, or native hGHRH — not with Mod GRF 1-29 specifically. Evidence derived from the WITH-DAC variant cannot be cleanly extrapolated to the no-DAC version given the ~15-fold difference in half-life and distinct pharmacokinetic profile (no covalent albumin binding → short pulse rather than sustained elevation). The Teichman 2006, Ionescu 2006, and Sackmann-Sala 2009 studies were all conducted by ConjuChem employees or ConjuChem-linked investigators; no independent academic replication exists for either the WITH-DAC or the no-DAC form.
Key studies
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 (2006)
Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA · Journal of Clinical Endocrinology & Metabolism 91(3):799–805
- Participants
- 64 healthy adults aged 21–61 across two sub-studies (28-day and 49-day)
- Methodology
- Two randomized, placebo-controlled, double-blind, ascending-dose trials. Single and multiple (weekly / biweekly) doses of CJC-1295 WITH-DAC versus placebo.
- Result
- Single doses produced mean plasma GH increases of 2–10-fold for ≥6 days and IGF-1 increases of 1.5–3-fold for 9–11 days. Multiple doses further elevated IGF-1 up to 3-fold. Half-life 5.8–8.1 days.
Honest read
This is the most-cited study for CJC-1295 anywhere online, and it studied the WITH-DAC variant — NOT Modified GRF 1-29. Five of six authors (Teichman, Neale, Lawrence, Gagnon, Castaigne) were ConjuChem employees developing the compound as a commercial drug. Direct sponsor COI. The only independent academic co-author is Frohman (UCSF). Small sample for a Phase II. Crucially, half-life is ~7 days here versus ~30 min for no-DAC; all extrapolation across those pharmacokinetic profiles is assumption-dependent. No independent replication. ConjuChem subsequently went out of business after the Phase II termination.
Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog (2006)
Ionescu M, Frohman LA · Journal of Clinical Endocrinology & Metabolism 91(12):4792–4797
- Participants
- Small human subsample (frequent-sampling protocol; exact n not reliably recovered from abstracts)
- Methodology
- Frequent GH sampling during CJC-1295 WITH-DAC treatment; deconvolution analysis of pulse frequency + amplitude.
- Result
- GH pulsatility was preserved. Basal (trough) GH increased 7.5-fold; mean GH increased 46%; IGF-1 increased 45%. Pulse frequency and magnitude were not significantly altered.
Honest read
This is the paper most often miscited to support the claim that CJC-1295 No DAC "preserves pulsatility." It studied WITH-DAC, not no-DAC, and documented the opposite scenario — that pulsatility persists DESPITE sustained stimulation from a long-acting agent. The no-DAC form almost certainly also preserves pulsatility (it clears too quickly to impose sustained occupancy), but that inference is not a finding of this study. The comparative claim — that no-DAC produces SUPERIOR pulsatile profiles versus with-DAC or other long-acting variants — has no published evidence.
Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women (1997)
Chapman IM, et al. · Journal of Clinical Endocrinology & Metabolism 82(5):1472–1479
- Participants
- 19 adults aged 55–71 (10 women, 9 men)
- Methodology
- Single-blind, randomized, placebo-controlled. 4-week placebo lead-in followed by 16 weeks of nightly self-injection of [Nle27]GHRH(1-29)-NH2 at 10 µg/kg.
- Result
- Significant increase in 12-hour integrated nocturnal GH (women p<0.01; men p<0.05). Elevated IGF-1 and IGFBP-3. Improved general well-being and libido in men. Transient hyperlipidemia was the only adverse effect.
Honest read
[Nle27]GHRH(1-29)-NH2 is a DIFFERENT analog from Mod GRF 1-29 — it differs at position 27 (norleucine vs leucine) and has different substitution pattern. Results are not directly transferable. Single-blind design, small sample, no body-composition outcomes, generalizable only to older adults, not replicated. Included here because it is often cited in GHRH(1-29)-family discussions.
Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse (2006)
Jette L, Leger R, Thibaudeau K, et al. · American Journal of Physiology — Endocrinology and Metabolism 291(5):E1090–E1094
- Participants
- GHRH-knockout mice
- Methodology
- Animal study; once-daily CJC-1295 WITH-DAC SC injection in GHRH-deficient mice.
- Result
- Normalized body weight and linear growth; sustained GH and IGF-1 elevation.
Honest read
Animal study only. GHRH knockout is an extreme model of GH deficiency not representative of healthy human aging or any common clinical indication. WITH-DAC compound, not no-DAC. This study is routinely over-cited in pro-CJC-1295 content as if it supported human efficacy — it does not.
Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects (2009)
Sackmann-Sala L, et al. · Growth Hormone & IGF Research 19(6):471–477
- Participants
- 11 healthy young adult men
- Methodology
- Before/after proteomic profiling (2D gel electrophoresis + mass spectrometry) of serum sampled before and one week after CJC-1295 WITH-DAC injection.
- Result
- Decreased apolipoprotein A1 and transthyretin isoforms; increased beta-hemoglobin and C-terminal albumin fragments following GH/IGF-1 elevation.
Honest read
Exploratory proteomics in 11 subjects; no control arm; findings are hypothesis-generating only. Reduced ApoA1 is notable given cardiovascular implications of chronic GH excess. Authors were affiliated with the ConjuChem research ecosystem. Not replicated. WITH-DAC, not no-DAC.
Prospective, randomized, multicenter Phase II trial of CJC-1295 for HIV-associated visceral obesity (NCT00267527) — TERMINATED (2006)
ConjuChem Biotechnologies (sponsor) · ClinicalTrials.gov registration NCT00267527
- Participants
- 192 HIV patients with visceral obesity enrolled across North and South American sites
- Methodology
- Multicenter, randomized, placebo-controlled, double-blind. Escalating and fixed-dose cohorts of CJC-1295 WITH-DAC SC.
- Result
- Primary endpoint NEVER REPORTED — trial terminated July 17, 2006 following the death of a participant in Argentina (acute MI ~2 hours post-injection #11).
Honest read
The attending physician assessed the death as likely due to acute MI from pre-existing coronary artery disease, not drug-related. However, ConjuChem halted development entirely and dissolved shortly thereafter. The absence of a formal causality finding is not the same as established safety — no formal follow-up investigation was conducted and the compound (CJC-1295 WITH-DAC, not no-DAC) has no Phase III data. This termination is routinely omitted from online CJC-1295 content; anyone citing ConjuChem's Phase I / II GH and IGF-1 data in support of CJC-1295 should also cite this termination.
Research timeline
- 1982
Guillemin et al. isolate and sequence native hGHRH from pancreatic tumors causing acromegaly. The minimal biologically active fragment hGHRH(1-29)-NH2 (sermorelin) is identified.
- 1997
Chapman IM et al. publish a 16-week nightly trial of [Nle27]GHRH(1-29)-NH2 in 19 age-advanced adults, showing sustained GH and IGF-1 stimulation. NOT the same compound as Mod GRF 1-29 (differs at position 27) but frequently cited as support by extension.
- 2005
ConjuChem Biotechnologies (Canada) completes Phase I of CJC-1295 WITH-DAC in healthy adults; identifies the albumin-binding mechanism and 5.8–8.1 day half-life.
- 2006
Teichman SL et al. publish Phase I/II data (n=64) for CJC-1295 WITH-DAC in JCEM: 2–10× GH increase, 1.5–3× IGF-1 increase. Sponsor-authored (5 of 6 authors ConjuChem employees).
- 2006
Jette, Leger, Thibaudeau et al. publish rat + GHRH-knockout mouse data on CJC-1295 WITH-DAC — routinely over-cited as if it supported human efficacy.
- 2006
ConjuChem TERMINATES the Phase II HIV lipodystrophy trial (NCT00267527, n=192) after a participant in Argentina dies of acute MI ~2 hours post-injection #11. Attending physician attributes death to pre-existing coronary artery disease. Development of CJC-1295 WITH-DAC as a therapeutic is abandoned.
- 2006
Ionescu M & Frohman LA publish pulsatility study in JCEM: GH secretory pulse frequency and magnitude preserved despite sustained CJC-1295 WITH-DAC elevation; basal GH increased 7.5-fold. This is the paper most commonly (mis)cited online to support no-DAC "pulsatility" claims — but it used WITH-DAC.
- 2009
Sackmann-Sala et al. publish exploratory serum proteomics in 11 healthy men post-CJC-1295 WITH-DAC: decreased ApoA1 and transthyretin, increased beta-hemoglobin and albumin fragments. Hypothesis-generating, no control arm, not replicated.
- 2010
Henninge et al. publish LC-MS identification of CJC-1295 WITH-DAC in a seized injectable pharmaceutical — establishing forensic analytical methodology in a doping-enforcement context.
- 2013
Mod GRF 1-29 begins circulating in research-chemical markets as "CJC-1295 No DAC" — the tetrasubstituted GHRH(1-29) core of CJC-1295 WITHOUT the DAC moiety. No clinical trial program is ever initiated for this shorter-acting variant.
- 2017
WADA includes CJC-1295 and GHRH analogs on the Prohibited List under S2 (Peptide Hormones, Growth Factors, and Related Substances).
- 2024
FDA Pharmacy Compounding Advisory Committee reviews CJC-1295; the nomination for 503A inclusion was withdrawn by nominators earlier in 2024, and the committee declines to recommend it for the positive 503A list. CJC-1295 ends 2024 off Category 2 but NOT on Category 1 — effectively in limbo for compounding purposes.
- 2026
WADA 2026 Prohibited List enters force (January 1, 2026). CJC-1293 and CJC-1295 are explicitly named under S2 (GHRH analogues). Separately, the US HHS Secretary signals intent to move ~14 peptides back to compounding-permissible status; FDA convenes an advisory panel April 15, 2026 and schedules further PCAC meetings July 23–24, 2026.
What we don't know
- Direct human pharmacokinetics of Modified GRF 1-29 specifically. Published PK data describes CJC-1295 WITH-DAC. The no-DAC half-life (~30 min) is extrapolated from its DPP-IV resistance properties and structural comparison with sermorelin. No published PK study in humans characterises Mod GRF 1-29.
- Human efficacy for any claimed indication. No completed, published RCT has tested Mod GRF 1-29 alone in humans for any outcome — not GH secretion, body composition, recovery, aging, cognition, or sleep.
- Optimal dosing frequency, dose-response, and inter-injection timing. The "100–200 µg SC two or three times per day" conventions circulating online are practitioner extrapolations from sermorelin, not evidence-based dosing derived from clinical trials.
- Long-term safety. No chronic toxicology study in humans exists. Theoretical concerns include insulin resistance from sustained IGF-1 elevation, potential cancer promotion in subclinical malignancy, and GH-axis downregulation with very frequent dosing.
- Drug interactions. No formal interaction studies exist. Theoretical interactions with insulin (counter-regulatory glucose effects), glucocorticoids (GH-axis suppression), sex steroids (IGF-1 regulation), and somatostatin analogs (pharmacological antagonism) are unstudied.
- Immunogenicity. The tetrasubstituted sequence is immunologically non-native; anti-peptide antibody formation is theoretically possible with repeated use, but no clinical data exists.
- Cancer risk. Elevated IGF-1 is epidemiologically associated with increased risk of breast, colorectal, and prostate cancers. Whether GHRH-analog-induced IGF-1 elevation confers similar risk specifically for Mod GRF 1-29 users is unknown.
- Whether degradation products (deamidated Gln8, racemized D-Ala2) retain partial GHRH-R agonism or act as partial antagonists. Undefined.
- Non-injectable bioavailability. Mod GRF 1-29 is a 29-residue peptide with no known oral or transmucosal bioavailability. Any non-injectable formulations marketed as containing it are not validated.
Regulatory status
| Jurisdiction | Status | Details | Last Verified | Source |
|---|---|---|---|---|
| United States (FDA) | Not Nominated | No FDA approval for any indication. CJC-1295 was previously on Category 2 of the 503A Bulk Drug Substances Interim List; the nomination was WITHDRAWN by nominators in 2024, resulting in removal from Category 2. The FDA Pharmacy Compounding Advisory Committee (PCAC) subsequently reviewed CJC-1295 in 2024 and voted against recommending it for inclusion on the positive 503A list. Current state: not on Category 1, not on Category 2, no active nomination — effectively "not nominated" for the purposes of 503A compounding. FDA has scheduled further PCAC meetings for July 23–24, 2026 under the HHS-Secretary-directed broader peptide compounding review; a formal rule change has not been published. | 2026-04-21 | |
| Canada (Health Canada) | Not Authorized | No marketing authorization for CJC-1295 or Modified GRF 1-29 in any form. No Drug Identification Number (DIN). Not listed as an authorized natural health product. Importation for personal use is technically prohibited under the Food and Drugs Act. Note: ConjuChem Biotechnologies, the original developer of CJC-1295 WITH-DAC, was a Canadian company — the compound has Canadian research origins but no Canadian regulatory approval. | 2026-04-21 | |
| United Kingdom (MHRA) | Not Authorized | No MHRA marketing authorization. Unlicensed supply for human use is unlawful under the Human Medicines Regulations 2012. Research use is permissible under applicable exemptions when sold explicitly for non-human research purposes. Prohibited in sport per UK Anti-Doping adoption of the WADA Prohibited List. | 2026-04-21 | |
| European Union (EMA) | Not Authorized | No EMA central marketing authorization. No CHMP opinion on record. Not on the EU Union Register of medicinal products. Individual EU member states may have national licensing pathways for unlicensed medicines; status may vary by member state. | 2026-04-21 | |
| Australia (TGA) | Prescription Only | Schedule 4 (Prescription Only Medicine) under the Poisons Standard for the GHRH/GHS class. Not listed on the Australian Register of Therapeutic Goods (ARTG). Possession without a valid prescription is a criminal offence. Available via compounding pharmacy with a prescription under the extemporaneous compounding exemption. The TGA has issued active safety alerts about unapproved injectable peptide products. | 2026-04-21 | |
| WADA | Prohibited (S2) | Explicitly named in the 2026 WADA Prohibited List under category S2 (Peptide Hormones, Growth Factors and Related Substances — GHRH and analogues subsection). CJC-1293 and CJC-1295 are both named. Prohibited at all times (in-competition and out-of-competition) with no TUE pathway. Testing laboratories have LC-HRMS/MS detection methodology for GHRH analogs in plasma. | 2026-04-21 |
Safety profile
Reported side effects
- Injection-site reactions (transient redness, swelling) — most common AE in WITH-DAC Phase I/II
- Headache
- Flushing / facial warmth (dose-related; may be more acute with the shorter-acting no-DAC form because the GH pulse is sharper)
- Nausea (generally mild)
- IMPORTANT — there are NO published safety data for Modified GRF 1-29 (the no-DAC form) in humans. All reported side-effect data above is from the WITH-DAC variant, and acute effects (flushing, nausea) may be relatively MORE prominent immediately post-injection with the short-acting no-DAC form because the GH pulse is sharper.
Theoretical concerns
Cardiovascular event in the terminated ConjuChem Phase II (2006)
A participant in the NCT00267527 Phase II lipodystrophy trial (CJC-1295 WITH-DAC, n=192) died of acute MI ~2 hours after injection #11. The attending physician attributed the event to pre-existing coronary artery disease, but no formal causality assessment was ever completed. ConjuChem abandoned the compound entirely and went out of business shortly thereafter. The doses used in that trial (60–240 µg/kg/week) were substantially higher than the 100–200 µg/injection conventions used in research/clinical settings today, and the DAC variant produces sustained supraphysiologic IGF-1 elevation that the no-DAC form does not. But the absence of a formal drug-attribution finding is not the same as established safety.
Severity: documented
Cancer growth promotion via chronic IGF-1 elevation
Elevated IGF-1 is epidemiologically associated with increased risk of breast, prostate, and colorectal cancers. The Sackmann-Sala 2009 proteomics paper (WITH-DAC) also showed reduced ApoA1 — a cardiovascular-relevant finding in chronic GH excess. Individuals with subclinical malignancy taking GHRH analogs are a theoretical at-risk population.
Severity: theoretical
Insulin resistance from chronic GH-axis stimulation
GH has counter-insulin effects; chronic GH elevation can impair insulin sensitivity (the acromegaly model). Individuals with pre-diabetes or metabolic syndrome may be at heightened risk. No human data characterises this for Mod GRF 1-29 specifically.
Severity: theoretical
Fluid retention / mild edema
GH promotes sodium and water retention; mild edema is a known GH-excess effect. Not quantified for Mod GRF 1-29 specifically.
Severity: possible
Class-level risks of unapproved injectable peptides
Unapproved compounded / imported peptides have been associated at the class level with anaphylaxis, systemic inflammatory response, infection, and local tissue damage per multiple regulatory advisories. Mod GRF 1-29 is captured under these class-level risks.
Severity: possible
Contraindications
- Active malignancy or history of hormone-sensitive cancers (IGF-1 proliferation concern; theoretical, mechanism-based)
- Diabetic retinopathy or uncontrolled diabetes (GH counter-regulatory effects)
- Acromegaly, gigantism, or active pituitary tumors
- Pregnancy and breastfeeding (no safety data in any species)
- Known hypersensitivity to GHRH or any component of a given compounded preparation
Interactions
- No formal drug-interaction studies in humans have been conducted.
- Glucocorticoids suppress the GH axis and may blunt response to Mod GRF 1-29
- Sex steroids (estrogen, testosterone) modulate IGF-1; interaction with GHRH-analog effects is unstudied
- Insulin and oral antidiabetics — GH-mediated insulin resistance may require dose adjustment
- Somatostatin analogs (octreotide, lanreotide) are pharmacological antagonists; combination is expected to blunt or abolish the GH response
Dosing observed in the literature
No published clinical trial establishes a dose for CJC-1295 No DAC (Modified GRF 1-29) specifically. The "100–200 µg per injection, two or three times daily" convention circulating online is practitioner extrapolation from sermorelin dosing and the mechanistic assumption that no-DAC behaves like a short-acting version of the WITH-DAC form. It is not derived from published human pharmacokinetic or dose-response data for this compound. CJC-1295 / Mod GRF 1-29 is not approved for human use in any jurisdiction documented in this profile. Content is for research reference only and is not medical advice.
| Route | Range | Context | Source |
|---|---|---|---|
| subcutaneous | 30–120 µg/kg single dose (ascending) | Teichman 2006 Phase I ascending-dose; healthy adults 21–61, n=64. WITH-DAC variant — not directly translatable to Mod GRF 1-29. | PMID:16352683 |
| subcutaneous | 30–60 µg/kg twice or three times per week (repeat dosing) | Teichman 2006 Phase I/II repeat-dosing; WITH-DAC variant. Reported "well tolerated" at these doses. | PMID:16352683 |
| subcutaneous | 60–240 µg/kg weekly (escalating) | NCT00267527 Phase II HIV lipodystrophy; n=192; WITH-DAC variant. Trial TERMINATED after participant death. | NCT00267527 |
| subcutaneous | 10 µg/kg nightly × 16 weeks | [Nle27]GHRH(1-29)-NH2 — a related but NOT identical compound (position-27 differs). Chapman 1997, age-advanced adults. | PMID:9141536 |
Stability & handling
- Lyophilized shelf life
- ~24–36 months properly stored (manufacturer / vendor data; no independently validated peer-reviewed stability study specific to Mod GRF 1-29 identified)
- Lyophilized storage
- Freeze at −20°C (long-term) or 2–8°C (short-term, up to months); sealed, desiccated, protected from light. Do not open cold vials until equilibrated to room temperature — moisture condensation is the primary degradation risk.
- Reconstitution diluents
- Bacteriostatic water for injection (benzyl alcohol preserved) — standard for multi-dose research vials, Sterile water for injection (single-use only), Dilute acetic acid (0.1–1%) — occasionally used for poorly soluble lots
- Reconstituted (refrigerated)
- Up to ~30 days at 2–8°C (general peptide guideline; no Mod-GRF-1-29-specific analytical stability validation)
- Reconstituted (room temp)
- Degradation begins above 8°C; use within hours if not refrigerated. CJC-1295 WITH-DAC retained ~68% potency at 25°C/24h in one vendor stability report — a useful analog but not a direct Mod GRF 1-29 measurement.
- OK to refreeze
- No
- Light sensitive
- Yes — protect from light
Critical stability failure modes specific to this compound: (1) D-Ala at position 2 can racemize back toward L-Ala under heat / long storage, which restores DPP-IV susceptibility and collapses the ~30-min half-life back toward sermorelin's ~3–5 min — standard reverse-phase HPLC does NOT detect this, only chiral HPLC or amino acid analysis after hydrolysis does. (2) Gln at position 8 can deamidate to glutamate under near-neutral pH or elevated temperature, producing a +1 Da mass shift detectable by mass spec but often co-eluting on HPLC. (3) DAC contamination — the WITH-DAC variant differs by ~279 Da and can co-elute on standard HPLC; only mass spec can confirm absence of WITH-DAC in a product sold as "no-DAC." (4) Standard lyophilization uses TFA counterions from preparative HPLC — acetate salt form is preferable for injection but requires ion exchange; COAs should report counterion identity and net peptide content distinct from chromatographic purity %.
Frequently asked questions
Is CJC-1295 No DAC the same as CJC-1295 (with DAC)?
No. "CJC-1295" in published clinical literature (Teichman 2006, Ionescu 2006, Sackmann-Sala 2009, the terminated Phase II NCT00267527) refers to the WITH-DAC variant — a 30-amino-acid peptide that covalently binds albumin and has a half-life of 6–8 days. CJC-1295 No DAC (Modified GRF 1-29) is the first 29 amino acids of that compound without the albumin-binding extension; its half-life is approximately 30 minutes. They act through the same GHRH receptor but have completely different pharmacokinetic profiles. Nearly all clinical evidence cited online for "CJC-1295 No DAC" was actually generated on the WITH-DAC form.
What's the difference between CJC-1295 No DAC and sermorelin?
Both are 29-amino-acid GHRH analogs that activate the GHRH receptor and stimulate pulsatile GH release. Sermorelin IS native hGHRH(1-29)-NH2; Modified GRF 1-29 adds four substitutions (D-Ala2, Gln8, Ala15, Leu27) that extend half-life from ~3–5 minutes to ~30 minutes and reduce enzymatic degradation. Sermorelin has an FDA approval history (approved for GH-deficiency diagnosis, then withdrawn from the US market around 2008; now available as a compounded preparation); Mod GRF 1-29 has never been FDA-approved. Practitioners often discuss them as interchangeable but the half-life difference means dosing schedules differ materially.
Why do people stack CJC-1295 No DAC with ipamorelin?
The two peptides act through different receptors: Mod GRF 1-29 activates the GHRH receptor (the pituitary "go" signal), while ipamorelin activates the GHS-R ghrelin receptor (a separate "go" signal that ALSO suppresses somatostatin, the counter-regulatory "stop" signal). In animal studies and extrapolation from GH-axis physiology, combining a GHRH-R agonist with a GHS-R agonist can produce supra-additive GH release. However, no human RCT has tested this specific combination. The 3–5-fold amplification figure cited online is receptor-pharmacology extrapolation, not a published clinical result.
Has anyone died from CJC-1295?
A participant in ConjuChem's Phase II study of CJC-1295 WITH-DAC (NCT00267527, HIV lipodystrophy) died of acute MI approximately 2 hours after the eleventh injection in 2006. The attending physician attributed the death to pre-existing coronary artery disease, not to the drug. ConjuChem halted the trial as a precaution and subsequently abandoned the compound entirely. No formal causal assessment was completed. The no-DAC variant has no similar trial history — because it has never been tested in an adequately-powered human trial.
What's the real half-life of CJC-1295 No DAC?
Approximately 30 minutes. Native hGHRH(1-29) has a plasma half-life of ~3–5 minutes due to rapid DPP-IV cleavage; the D-Ala2 substitution blocks that cleavage, extending half-life to roughly 30 minutes. IMPORTANT: this figure is not from a published PK study of Modified GRF 1-29 in humans — it is a mechanistic inference based on the compound's DPP-IV resistance and structural similarity to sermorelin. No direct human PK data for Mod GRF 1-29 has been published.
Will CJC-1295 No DAC show up on a drug test?
Yes, if the test panel covers GHRH analogs. CJC-1295 is explicitly prohibited under WADA category S2 and has LC-HRMS/MS detection methodology. Given the no-DAC form's short half-life, the detection window is substantially shorter than for the WITH-DAC form, but detection is possible for several hours post-injection. Athletes subject to WADA testing should treat CJC-1295 as prohibited at all times.
Is the evidence for "preserving pulsatile GH secretion" real?
The Ionescu & Frohman 2006 paper commonly cited for this claim is a study of CJC-1295 WITH-DAC — it demonstrated that GH pulsatility is preserved even under SUSTAINED WITH-DAC stimulation. The no-DAC form almost certainly also preserves pulsatility (it clears too quickly to impose sustained receptor occupancy), so the claim is mechanistically coherent. What is NOT demonstrated is that pulsatile profiles produced by Mod GRF 1-29 are clinically SUPERIOR to the elevated-but-pulsatile profiles produced by WITH-DAC. That comparative claim has no evidentiary basis.
What should I look for on a CJC-1295 No DAC COA?
Four things, separately reported: (1) MASS SPEC CONFIRMATION that the compound is no-DAC, not WITH-DAC — the two differ by ~279 Da and can co-elute on standard HPLC; a COA showing only HPLC purity cannot confirm the absence of WITH-DAC contamination. (2) CHIRAL CONFIRMATION of D-Ala at position 2 — reverse-phase HPLC does not detect D→L racemization, which silently collapses the half-life back to sermorelin's ~3–5 min; chiral HPLC or amino-acid analysis after hydrolysis is required. (3) NET PEPTIDE CONTENT distinct from HPLC chromatographic purity — TFA and acetate counterions plus residual water contribute to stated vial mass; COAs should report peptide content as a percentage of gross weight. (4) ENDOTOXIN (LAL) testing per USP <85> because the product is injectable. A COA showing only "≥98% purity by HPLC" without these four items has not characterized what's actually in the vial.
Last researched: Apr 21, 2026
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