CJC-1295: what it is, how it works and what studies have found

CJC-1295 is a synthetic analogue of growth hormone-releasing hormone (GHRH) built on GRF(1-29), the 29-residue active fragment of the human hormone. Its developers substituted four residues to resist enzymatic breakdown and added a C-terminal lysine carrying a maleimidopropionyl group that attaches the peptide to serum albumin after administration [1]. That design gave an estimated half-life of 5.8–8.1 days in healthy adults, against minutes for native GHRH [2] [3]. CJC-1295 was never approved, and it is prohibited in sport [4] [5].

The name is used loosely. In the peer-reviewed literature, “CJC-1295” means the albumin-binding molecule. In the research-chemical market the same name, often qualified as “without DAC”, is applied to the 29-residue substituted peptide that lacks the albumin-binding lysine, also known as modified GRF(1-29) [6]. This article explains both, and is written for researchers rather than as medical guidance.

What is CJC-1295?

CJC-1295 came out of a drug-discovery programme that used in vivo bioconjugation to extend peptide half-life (see the development history below). The approach places a reactive maleimide on a peptide so that, once in the bloodstream, it forms a covalent bond with the free thiol on Cys34 of serum albumin. The team synthesised three maleimido derivatives of human GRF(1-29), conjugated them to albumin ex vivo and tested them; all three were more stable against dipeptidyl peptidase-IV than GRF(1-29) and were active in a growth hormone secretion assay in cultured rat anterior pituitary cells [1].

The best compound, CJC-1295, produced a four-fold increase in growth hormone area under the curve over 2 hours in rats compared with GRF(1-29), was present in plasma beyond 72 hours, and appeared on Western blot as an immunoreactive band at the size of serum albumin from 15 minutes after administration [1]. The developers called the albumin-binding chemistry a Drug Affinity Complex, or DAC.

CJC-1295 structure: with DAC vs without DAC

Both forms start from the native GRF(1-29) sequence of sermorelin, YADAIFTNSYRKVLGQLSARKLLQDIMSR-NH2 [7], and change four positions [1] [8]:

Position	Native GRF(1-29)	CJC-1295	Chemical consequence
2	L-Ala	D-Ala	Alters the Tyr1-Ala2 bond that dipeptidyl peptidase-IV cleaves in native GHRH
8	Asn	Gln	Removes the asparagine, a residue prone to deamidation
15	Gly	Ala	Replaces glycine with alanine
27	Met	Leu	Removes the oxidisable methionine sulfur

The original paper describes the molecule as a “tetrasubstituted form of hGRF(1-29)” and reports improved stability of the albumin conjugates against dipeptidyl peptidase-IV [1]; it does not give a separate rationale for each substitution. Native GHRH is inactivated by exactly that cleavage, losing more than 99.9% of its activity [3].

Property	CJC-1295 with DAC	CJC-1295 without DAC (modified GRF 1-29)
Sequence	Y-(D-Ala)-DAIFTQSYRKVLAQLSARKLLQDILSR-K(MPA)-NH2 [8]	Y-(D-Ala)-DAIFTQSYRKVLAQLSARKLLQDILSR-NH2 [9]
Length	30 residues (29 + modified Lys30)	29 residues
C-terminal modification	Lys with Nε-3-maleimidopropionamide (the DAC) [1]	Amide only
Molecular formula	C165H269N47O46 [8]	C152H252N44O42 [9]
Molecular weight	3647.2 g/mol [8]	3367.9 g/mol [9]
CAS number (as indexed)	446262-90-4 in PubChem, which lists 863288-34-0 as deprecated [8]	863288-34-0 is attached to this 29-residue structure in a separate PubChem record [9]
Albumin binding	Covalent, at albumin Cys34 [1]	None
Human half-life	5.8–8.1 days [2]	Not reported in a peer-reviewed study
Peer-reviewed human data	Two pharmacology studies (2006) [2] [10]	None found

Two practical consequences follow. First, CAS numbers for these two forms are inconsistent across databases, and no single CAS number reliably identifies either form [8] [9], so a certificate of analysis should state the sequence, formula and observed mass, not just a name and CAS number. Second, almost everything published about CJC-1295 in humans concerns the DAC form. In 2009 the Norwegian doping control laboratory analysed an unknown preparation submitted at the request of police and customs authorities and found a 29-amino-acid peptide amide whose proposed sequence was consistent with the product marketed as CJC-1295, that is, the form without the albumin-binding lysine [6].

CJC-1295 mechanism of action

Both forms are GHRH receptor agonists. The GHRH receptor (GHRHR, UniProt Q02643) is a G protein-coupled receptor on pituitary somatotrophs that activates adenylyl cyclase and stimulates growth hormone gene transcription and secretion [11]. The substituted peptide remains active at the receptor in pituitary cell assays, and its albumin conjugates showed improved stability against dipeptidyl peptidase-IV; the DAC adds a reservoir effect, because albumin-bound peptide circulates for days [1].

The pharmacological question with a long-acting GHRH agonist was whether continuous stimulation would flatten the normal pulsatile pattern of growth hormone secretion. It did not. Overnight sampling every 20 minutes in healthy men aged 20 to 40, before and one week after a single administration of CJC-1295, showed preserved pulsatility, with unchanged pulse frequency and amplitude. Trough growth hormone rose 7.5-fold, mean growth hormone by 46% and IGF-I by 45% [10].

CJC-1295 half-life and pharmacokinetics

Parameter	Finding	Evidence level	Ref
Presence in rat plasma	Beyond 72 hours; albumin-bound species detected from 15 minutes	Animal	[1]
Estimated human half-life	5.8–8.1 days	Human RCTs, healthy adults	[2]
GH response after one administration	Mean GH up 2- to 10-fold for 6 days or more (dose-dependent)	Human RCTs, healthy adults	[2]
IGF-I response after one administration	Up 1.5- to 3-fold for 9–11 days	Human RCTs, healthy adults	[2]
IGF-I after multiple administrations	Above baseline for up to 28 days	Human RCTs, healthy adults	[2]
Native GHRH comparator	Intact GHRH(1-44) half-life 6.8 minutes after intravenous administration	Human	[3]

For the form without DAC, no peer-reviewed human pharmacokinetic study was found. Its D-Ala2 substitution is intended to resist the dipeptidyl peptidase-IV cleavage that inactivates native GHRH [1] [3], but without albumin binding it would not be expected to approach the multi-day exposure of the DAC form. Any specific half-life quoted for it should be treated as unverified unless it cites primary data.

Development history and timeline

Date	Event	Ref
2005	ConjuChem publishes the GRF(1-29)-albumin bioconjugate work identifying CJC-1295	[1]
Dec 2005	Phase 2 study of CJC-1295 in HIV patients with visceral obesity (NCT00267527) starts; later listed as terminated	[4]
Mar 2006	Human pharmacokinetic and pharmacodynamic study in healthy adults published	[2]
2006	Mouse study in GHRH knockout animals; human GH pulsatility study	[12] [10]
2009–2010	Serum proteomics study in healthy men (2009); unknown preparation analysed in 2009 by a doping laboratory and reported in 2010 as a 29-residue amide consistent with the product sold as “CJC-1295”	[13] [6]
2026	Named in WADA Prohibited List S2.2.4 (in force 1 January 2026); listed among “bulk drug substances nominated but withdrawn” on FDA’s compounding safety-risk page (content current as of April 2026)	[5] [14]

The ClinicalTrials.gov record for the phase 2 study, sponsored by ConjuChem, describes a multicentre, randomised, double-blind, placebo-controlled trial of 12 weeks’ treatment with low-dose CJC-1295, high-dose CJC-1295 or placebo; it lists an enrolment of 120 (not marked as actual or anticipated), a start date of December 2005, a completion date of September 2006 and an overall status of terminated, without a stated reason [4]. We found no peer-reviewed publication of its results, and no phase 3 study of CJC-1295 is registered on ClinicalTrials.gov.

Key CJC-1295 studies and findings

Study	Design	Model or population	n	Duration	Main measures	Main finding	Ref
Jetté 2005	Synthesis and pharmacology	Rat pituitary cells; Sprague Dawley rats	n/a	Acute	GH secretion, plasma persistence	4-fold GH AUC over 2 h vs GRF(1-29); in plasma beyond 72 h	[1]
Teichman 2006	Two randomised, placebo-controlled, double-blind, ascending-dose trials	Healthy adults aged 21–61	Not stated in abstract	28 and 49 days	PK, GH, IGF-I, safety	Half-life 5.8–8.1 days; GH and IGF-I raised for days; no serious adverse reactions	[2]
Ionescu 2006	Before-after, two dose levels	Healthy men aged 20–40	Not stated in abstract	1 week	GH pulsatility	Pulsatility preserved; trough GH 7.5-fold, mean GH +46%, IGF-I +45%	[10]
Alba 2006	Animal	GHRH knockout mice	3 treatment groups plus controls	5 weeks	Growth, body composition	Daily administration normalised body weight and length; every 48 or 72 h less effective	[12]
Sackmann-Sala 2009	Before-after proteomics	Healthy young men	11	1 week	Serum proteome	Changes in apolipoprotein A1, transthyretin and albumin-fragment spots	[13]

Human pharmacology (2006)

The main human study comprised two randomised, placebo-controlled, double-blind, ascending-dose trials of 28 and 49 days in healthy subjects aged 21 to 61, at two sites. After a single subcutaneous administration there were dose-dependent increases in mean plasma growth hormone of 2- to 10-fold lasting 6 days or more, and in IGF-I of 1.5- to 3-fold for 9 to 11 days. The estimated half-life was 5.8 to 8.1 days, IGF-I remained above baseline for up to 28 days after multiple administrations, there was evidence of a cumulative effect, and no serious adverse reactions were reported [2].

The pulsatility study described above found that the increase in IGF-I did not correlate with any single parameter of growth hormone secretion, and the authors suggested that the marked rise in trough growth hormone was important for the IGF-I increase [10]. A later analysis of serum from 11 men before and one week after CJC-1295 identified protein spots that changed with treatment, including isoforms of apolipoprotein A1 and transthyretin, as candidate biomarkers of growth hormone and IGF-1 action [13].

Animal data

In mice lacking the GHRH gene, daily CJC-1295 for 5 weeks gave normal body weight and length, while administration every 48 or 72 hours improved growth without fully normalising it. Pituitary RNA and growth hormone mRNA increased, and immunohistochemistry indicated somatotroph proliferation [12]. This shows the molecule is active on a GHRH-deficient pituitary, in a rodent model.

Safety findings reported

The 2006 human trials reported no serious adverse reactions and described CJC-1295 as relatively well tolerated [2]. The evidence base is small: two published pharmacology studies in healthy volunteers and an unpublished, terminated phase 2 study [4]. FDA’s page on bulk drug substances for compounding that may present significant safety risks lists CJC-1295 among substances nominated but withdrawn, and states that “FDA has identified serious adverse events associated with CJC-1295 including increased heart rate and systemic vasodilatory reaction” and that “available clinical data are limited”; it also notes a possible risk of immunogenicity and difficulty characterising peptide-related impurities [14]. A 2026 narrative review of GH-axis peptides used outside regulated supply chains, which covers CJC-1295 with and without DAC, groups the reported adverse effects into endocrine and metabolic disturbance, fluid retention and musculoskeletal symptoms, and notes uncertainty about product composition in unregulated supply [15].

CJC-1295 regulatory status by region

Jurisdiction	Status	Ref
United States	Not approved. Listed on FDA’s compounding safety-risk page under “bulk drug substances nominated but withdrawn” (substances previously in category 2 whose nominations were withdrawn), with FDA’s safety notes	[14]
Clinical development	Phase 2 study terminated; no marketing application found in the sources reviewed	[4]
Sport (all WADA signatories)	Prohibited at all times under S2.2.4, named example alongside CJC-1293, sermorelin and tesamorelin	[5]
EU, UK, India, China	Not authorised as a medicine in any source we reviewed; research-chemical import rules vary by country	n/a

CJC-1295 and ipamorelin: the research context

“CJC-1295 ipamorelin” is one of the most searched phrases around this peptide. The pairing comes from receptor pharmacology, not from a published clinical programme. Ipamorelin is a pentapeptide growth hormone secretagogue that acts through a GHRP-like receptor, not the GHRH receptor; in its 1998 characterisation it released growth hormone in rat pituitary cells and in swine with potency similar to GHRP-6, and unlike GHRP-6 and GHRP-2 it did not raise ACTH or cortisol [16].

The rationale for combining the two classes dates back to early GHRP studies in humans, which reported a synergistic growth hormone release when a GHRP and GHRH(1-44) were given together [17]. The two drugs act on separate receptors in the same axis, so a combined response larger than either alone is pharmacologically plausible. However, we found no controlled human study of CJC-1295 (with or without DAC) combined with ipamorelin in the peer-reviewed literature. Both substances are prohibited in sport: CJC-1295 as a GHRH analogue and ipamorelin as a growth hormone secretagogue, both under S2.2.4 [5]. Ipamorelin also appears on FDA’s compounding safety-risk page [14]. Winhycare Pharma does not supply ipamorelin.

CJC-1295 in laboratory research

Typical research uses include GHRH receptor agonism assays (cAMP in GHRHR-expressing cells), growth hormone release from primary pituitary cells [1], albumin conjugation studies by Western blot or LC-MS [1], GHRH-deficient mouse models [12], and reference-standard work in anti-doping science. Validated nano-LC quadrupole/Orbitrap methods detect CJC-1295, sermorelin and tesamorelin in urine [18], and LC-HRMS/MS sequencing was how the 29-residue amide sold as “CJC-1295” was identified [6].

For the DAC form, the maleimide is reactive: it can hydrolyse, or add to thiols in solution, so identity testing should confirm the intact maleimide by mass. For both forms, LC-MS of the intact peptide distinguishes them immediately (about 3647 versus 3368 g/mol), and chiral amino-acid analysis or a diastereomer-resolving HPLC method confirms the D-Ala2.

Synthesis, purity and impurities

Both forms are made by Fmoc solid-phase peptide synthesis on an amide resin. The without-DAC peptide is a straightforward 29-mer; the DAC form needs an orthogonally protected Lys30 so the maleimidopropionyl group can be coupled to the side-chain amine after chain assembly. Impurity classes to control include deletion sequences, the L-Ala2 diastereomer (from epimerisation or wrong building block), aspartimide-related variants at Asp3 and Asp25, and, for the DAC form, hydrolysed or thiol-adducted maleimide. See SPPS versus LPPS and peptide API impurities and specifications. Because Met27 is replaced by Leu, CJC-1295 avoids the methionine oxidation that affects sermorelin.

Storage and stability of lyophilized CJC-1295

Lyophilized CJC-1295 is stored sealed, dry, cold and protected from light, with containers brought to room temperature before opening to prevent condensation. Moisture matters more for the DAC form, since the maleimide ring can hydrolyse. The general principles are in our guide to lyophilised peptide stability and storage. This applies to laboratory material only.

CJC-1295 vs sermorelin vs tesamorelin

Feature	CJC-1295 (DAC)	CJC-1295 without DAC	Sermorelin	Tesamorelin
Backbone	Substituted GRF(1-29) + Lys30(MPA) [1]	Substituted GRF(1-29)	Native GRF(1-29) [7]	Native GRF(1-44) + N-hexenoyl [19]
Half-life (human)	5.8–8.1 days [2]	Not established	Minutes (native GHRH data) [3]	8 minutes [19]
Molecular weight	3647.2 [8]	3367.9 [9]	3357.9 [7]	5135.9 [19]
Approval	None	None	US 1990/1997, discontinued	US 2010, marketed [19]

See our sermorelin and tesamorelin overviews for their clinical records.

How Winhycare Pharma supplies CJC-1295

Winhycare Pharma supplies CJC-1295 as research-use-only material for laboratory work. Our catalogue item is the 29-residue form without DAC (modified GRF 1-29); the albumin-binding DAC form and other GRF(1-29) variants are available through custom synthesis. Purity is ≥99% as stated in our product brochure, with batch QC documentation stating sequence and observed mass. Details are on the CJC-1295 product page, or contact us about research peptides.

For laboratory research use only. Not for human or veterinary use.