Peptide fact-sheet · English

CJC-1295

Synthetic GHRH analog (long-acting via albumin conjugation in the DAC variant)

Long-acting GHRH analog with two variants (DAC and Mod-GRF 1-29); investigational, no regulatory approval, WADA-prohibited.

Translated and adapted from the canonical Portuguese version: /peptideos/cjc-1295.

Quick answer

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH) developed by ConjuChem in the early 2000s. It exists in two principal variants. The DAC (Drug Affinity Complex) variant carries a maleimidopropionyl group that forms a covalent bond with cysteine 34 of serum albumin, extending the half-life to approximately 8 days. The non-DAC variant — also called Mod-GRF 1-29 — lacks the albumin-conjugating group and has a half-life of approximately 30 minutes, preserving the pulsatile pattern of endogenous GH secretion. The seminal pharmacokinetic study (Teichman 2006, Journal of Clinical Endocrinology & Metabolism, PMID 16352683, n=43 across two trials, 28 and 49 days) reported dose-dependent GH elevations of 2-10 fold sustained for more than 6 days and IGF-1 elevations of 1.5-3 fold sustained for 9-11 days after a single subcutaneous dose of CJC-1295 with DAC in healthy adults. The complementary study by Ionescu and Frohman (PMID 17018654, n=20 healthy men) demonstrated that endogenous GH pulsatility is preserved during continuous receptor stimulation by CJC-1295. As of May 2026, CJC-1295 has no regulatory approval in any country and is listed by name on the WADA 2026 Prohibited List under category S2.2.4 (growth hormone-releasing factors), prohibited at all times. The published human evidence base is restricted to three small studies in healthy adults published between 2006 and 2009. No randomized clinical trial in any patient population — adults with GH deficiency, older adults with sarcopenia, athletes, or adults with HIV-associated lipodystrophy — has been published in peer-reviewed indexed literature.

What it is

CJC-1295 is a synthetic peptide analog of human growth hormone-releasing hormone (GHRH 1-29) developed by ConjuChem in the early 2000s. Four amino acid substitutions in the GHRH 1-29 sequence confer resistance to degradation by dipeptidyl peptidase-4 (DPP-4), the enzyme that inactivates endogenous GHRH within minutes of secretion.

Two variants exist:

CJC-1295 with DAC (Drug Affinity Complex) — carries a maleimidopropionyl group at the N-terminus that forms a covalent bond with cysteine 34 of serum albumin upon injection. The albumin-conjugated peptide circulates with a half-life of approximately 8 days, producing sustained elevation of IGF-1 — a pharmacokinetic profile with no physiologic equivalent.
CJC-1295 without DAC (also called Mod-GRF 1-29 or modified GRF 1-29) — contains the four amino-acid substitutions without the albumin-conjugating group. Half-life is approximately 30 minutes. Endogenous pulsatile GH secretion is preserved, more closely mirroring the hypothalamic GHRH signaling pattern. Requires more frequent administration in research protocols.

CJC-1295 has never been registered as a finished drug product by FDA, EMA, or any other regulatory authority. It has no INN. The complete human published evidence base consists of three small studies in healthy adults from 2006-2009 and a 2020 proteomic follow-up. Material labeled "CJC-1295" is distributed through "research peptide" suppliers and compounding pharmacies in some jurisdictions.

Mechanism of action

Endogenous GHRH is secreted by the hypothalamus in pulses every 3-4 hours and binds the GHRH receptor (GHRH-R) on somatotrophs in the anterior pituitary. Receptor activation triggers adenylyl cyclase, elevates intracellular cAMP, and releases stored growth hormone (GH).

CJC-1295 occupies the same receptor with preserved affinity. The mechanistic difference between the variants is the duration of receptor exposure. CJC-1295 with DAC, bound to circulating albumin, exposes the GHRH receptor to near-continuous stimulation for days, overlaid on the endogenous pulsatile pattern. The result, demonstrated by Ionescu and Frohman in 2006, is an approximately 7.5-fold elevation in basal GH with preservation of pulse frequency and amplitude — a key mechanistic distinction from exogenous recombinant GH, which suppresses endogenous secretion through hypothalamic-pituitary feedback.

GH released by the pituitary stimulates hepatic IGF-1 production, which mediates a substantial part of the anabolic effects of the somatotropic axis. In the DAC variant, IGF-1 remains elevated for 9-11 days after a single dose (Teichman 2006). This sustained IGF-1 profile is the distinguishing pharmacologic feature of CJC-1295 with DAC and the basis for both its therapeutic hypothesis and the safety concerns about prolonged IGF-1 elevation.

A mechanistic detail relevant to interpretation: somatostatin feedback continues to inhibit GH release intermittently even under continuous GHRH-R stimulation, preserving some degree of physiologic modulation. This is the basis for the Ionescu-Frohman observation that endogenous pulses persist during continuous DAC stimulation.

What the trials show

The published human clinical literature on CJC-1295 consists of a small number of studies in healthy adults conducted between 2006 and 2009. No randomized controlled trial in any clinical population has been published in peer-reviewed indexed literature.

Teichman 2006 — pharmacokinetics in healthy adults (Journal of Clinical Endocrinology & Metabolism, PMID 16352683). Two randomized double-blind placebo-controlled dose-escalation trials, durations 28 and 49 days, combined n=43 healthy adults aged 21-61. Single subcutaneous doses of CJC-1295 with DAC produced dose-dependent GH elevations of 2-10 fold sustained for more than 6 days and IGF-1 elevations of 1.5-3 fold sustained for 9-11 days. Estimated half-life 5.8-8.1 days. The seminal pharmacokinetic study. Limitation: small sample of healthy adults; no clinical-population data on outcomes such as body composition, metabolic function, or symptoms.

Ionescu and Frohman 2006 — pulsatility (Journal of Clinical Endocrinology & Metabolism, PMID 17018654). Open-label clinical trial with serial blood sampling over 12 hours at 20-minute intervals, n=20 healthy men aged 20-40. Mean GH increased 46%, IGF-1 increased 45%, basal GH increased 7.5-fold, with frequency and amplitude of endogenous pulses preserved. The mechanistic counterpoint to the assumption that continuous receptor stimulation would suppress endogenous secretion as exogenous GH does.

Sackmann-Sala 2009 — proteomic profile (Growth Hormone & IGF Research, PMID 19386527). Proteomic analysis (2D electrophoresis and mass spectrometry) of serum pre- and post-injection in 11 healthy young men. Five proteins with significant change after CJC-1295, including a linear correlation between an albumin/immunoglobulin fragment and IGF-1 levels. Hypothesis-generating, not confirmatory.

What does not exist in peer-reviewed indexed literature: a randomized trial in adults with growth hormone deficiency, in adults with obesity, in older adults with sarcopenia, or in adults with HIV-associated lipodystrophy. The last comparison is worth noting — tesamorelin, another GHRH analog, is FDA-approved specifically for HIV-associated lipodystrophy on the basis of robust phase 3 RCTs. CJC-1295 has not undergone an equivalent program. The chemistry is similar, the mechanism is the same, but the clinical evidence in defined populations belongs to tesamorelin, not to CJC-1295. Generalizing across molecules without direct trials is an extrapolation the published literature does not authorize.

Pharmacokinetics

DAC variant subcutaneous half-life: approximately 8 days (Teichman 2006: 5.8-8.1 days).
Non-DAC variant (Mod-GRF 1-29) subcutaneous half-life: approximately 30 minutes.
Route in published studies: subcutaneous injection. No oral, intranasal, or transdermal formulation has been characterized in peer-reviewed indexed literature.
Dosing in published trials: single doses of 30, 60, 125, and 250 μg/kg in the Teichman dose-escalation studies. No validated multi-dose chronic regimen exists in human peer-reviewed literature.

Safety and adverse events

The safety database is limited to fewer than 75 healthy adults across all published human studies, with follow-up of at most 49 days. The events described in published trials fall into three categories:

Acute and local — transient facial flushing, mild fluid retention, paresthesia or discomfort at the injection site, occasional headache. Described as mild and self-limited in the Teichman and Ionescu studies, more frequent at doses above 60 μg/kg.
Systemic, somatotropic axis-related — transient elevation of plasma glucose and potential insulin resistance with prolonged use, a mechanistically plausible effect given the known anti-insulin actions of GH. The sustained IGF-1 elevation characteristic of the DAC variant raises a theoretical concern in individuals with IGF-1-sensitive conditions, though the available trials lack the power to detect such an outcome.
Long-term uncertainties — no published human follow-up beyond 49 days. Prolonged IGF-1 signaling, in animal models and in clinical conditions such as acromegaly, is associated with cardiovascular and neoplastic risk. How much of this translates to intermittent CJC-1295 use in humans is unknown. Absence of data is not absence of risk; it is documented ignorance.

Regulatory status (international)

FDA: no approval. CJC-1295 is not listed in 503A or 503B bulk substances categories as a permissible compounding substance and is not registered as a finished drug product.
EMA: no marketing authorization.
INN (WHO): not assigned.
WADA: prohibited by name in the 2026 Prohibited List under category S2.2.4 (growth hormone-releasing factors), at all times (in and out of competition), alongside CJC-1293, sermorelin, and tesamorelin. Athletes testing positive face automatic sanctions under the World Anti-Doping Code.

Distribution through "research peptide" suppliers and compounding pharmacies in some jurisdictions does not constitute regulatory approval. Identity, purity, and endotoxin content of material outside a regulated pharmaceutical supply chain are not assured.

What we still don't know

Clinical effectiveness in any patient population — no published RCT exists in adults with GH deficiency, sarcopenia, obesity, or any other indication.
Long-term safety beyond 49 days of follow-up.
Cardiovascular and neoplastic risk under sustained IGF-1 elevation in humans.
Comparative effectiveness versus tesamorelin (the only FDA-approved GHRH analog) or versus recombinant GH in defined populations.
Whether any clinical trial program in a regulated framework is in development. As of May 2026, no phase 2 or phase 3 program for CJC-1295 in any indication is registered on ClinicalTrials.gov or EudraCT.

Why it matters

CJC-1295 occupies a position in the peptide commerce ecosystem disproportionate to its clinical evidence base. The published human literature consists of three small studies in healthy adults from 2006-2009, none addressing clinical outcomes in any patient population. No regulatory authority has approved the molecule for any indication. WADA prohibits it by name in sport. The mechanistic plausibility — and the structural similarity to tesamorelin, which does have phase 3 evidence and FDA approval in HIV-associated lipodystrophy — should not be confused with established clinical effectiveness or safety for CJC-1295 itself.

For international clinical readers, the comparison with tesamorelin is the editorial point. Where tesamorelin has earned regulatory approval through a defined trial program in a specific indication, CJC-1295 has not. The two molecules are not interchangeable as evidence, and the published literature does not authorize generalization from one to the other.