CJC 1295

CJC-1295 With DAC vs Without DAC: 2026 UK Guide — Order Now on JCSG.org

CJC-1295 with DAC and CJC-1295 without DAC (Modified GRF 1-29) share the same stabilised GHRH(1-29) backbone with one structural difference: the DAC variant carries a maleimidopropionic acid linker that covalently binds albumin's Cys34, extending the plasma half-life from roughly 30 minutes to about 6–8 days [14][26]. That single chemical modification separates a short-acting pulse mimetic from a once-weekly IGF-1 elevator — the albumin conjugate evades glomerular filtration and maintains receptor occupancy over days rather than minutes.

In the 2006 Teichman trial at 30–60 μg/kg, a single subcutaneous dose of CJC-1295 with DAC raised IGF-1 for 9–11 days, while Modified GRF 1-29 clears within hours and requires multiple daily injections to sustain pulsatile GH release [14][6]. This guide compares both compounds on structure, pharmacokinetics, research dosing context, and 2026 UK regulatory status — order Body Pharm CJC-1295 on JCSG.org once you have identified the right form for your research.

Key Takeaways

• CJC-1295 with DAC achieves a 6–8 day half-life through covalent albumin binding; the non-DAC form clears in ~30 minutes.
• The DAC linker is a maleimidopropionic acid group that undergoes Michael addition with serum albumin's Cys34.
• Teichman 2006 reported sustained IGF-1 elevation for 9–11 days from a single DAC dose; Modified GRF 1-29 requires 2–3 daily injections to mimic pulsatile GH release.
• Neither form is a licensed medicinal product in the UK; both are prohibited under WADA 2026 Section S2.
• ConjuChem's clinical programme was discontinued around 2006–2007 amid hypersensitivity concerns and non-titrable GH/IGF-1 exposure.
• Ready to order? Browse Body Pharm CJC-1295 on JCSG.org — fast UK dispatch, batch-tested purity certificates included.

CJC-1295 at a glance (2026)

CJC-1295 is a synthetic long-acting analogue of growth hormone-releasing hormone fragment 1-29 (GHRH(1-29)), engineered with four amino acid substitutions — D-Ala², Gln⁸, Ala¹⁵ and Leu²⁷ — that protect the peptide from dipeptidyl peptidase-IV cleavage and trypsin-like degradation [9][26]. It exists in two research forms: CJC-1295 with DAC, which carries a maleimidopropionic acid linker that covalently binds albumin's Cys34 for a 6–8 day half-life, and CJC-1295 without DAC, also sold as Modified GRF 1-29, which clears in roughly 30 minutes [1][6][26].

In the UK, neither form is a licensed medicinal product. The MHRA treats both as unauthorised medicines if marketed for human use, while permitting sale as laboratory reagents labelled research-only [15][17]. CJC-1295 is not a controlled drug under the Misuse of Drugs Act [16], but it is prohibited in sport under WADA 2026 Section S2 as a GHRH analogue [18].

The distinction matters because the DAC variant produces sustained, tonic IGF-1 elevation, whereas Modified GRF 1-29 preserves the natural GH pulse pattern. The closest licensed comparator is Tesamorelin. See our full peptide reference library for adjacent compounds.

Molecular structure and mechanism

CJC-1295 is a GHRH receptor (GHRHR) agonist on anterior pituitary somatotrophs. Binding triggers Gs-coupled adenylate cyclase activity, raises intracellular cAMP, and drives pulsatile growth hormone release into portal circulation. Hepatic GH receptors then transduce that signal into IGF-1 synthesis via JAK2/STAT5 [9][11]. The parent scaffold is the first 29 residues of human GHRH — the minimal fragment that retains full agonist potency, because shorter sequences lose critical receptor-contact residues.

Four amino acid substitutions distinguish the CJC-1295 backbone from native GHRH(1-29):

• D-Ala at position 2 blocks dipeptidyl peptidase-IV cleavage of the Tyr¹-Ala² bond
• Gln⁸ reduces asparagine deamidation
• Ala¹⁵ stabilises the α-helix presented to GHRHR
• Leu²⁷ (sometimes Nle²⁷) resists oxidation and trypsin-like proteolysis [7][11]

These four changes define "Modified GRF 1-29" as a distinct chemical entity from the unmodified fragment, and they are retained in both DAC and non-DAC forms.

What the DAC adds structurally

The Drug Affinity Complex (DAC) appends a maleimidopropionic acid (MPA) linker to the ε-amino group of a lysine side chain in the C-terminal region of the GRF(1-29) sequence via a stable amide bond [1][2]. The linker is a three-carbon propionic acid chain terminating in a maleimide ring.

Once injected, the exposed maleimide undergoes Michael addition with the free thiol of cysteine-34 on circulating human serum albumin. Albumin's Cys34 is the only reduced surface cysteine on the protein, making it the sole free thiol available for nucleophilic attack. The resulting covalent peptide-albumin conjugate inherits albumin's ~19-day plasma residence, which stretches the functional half-life into the 6–8 day window reported by Teichman et al. [16].

The design is structurally economical: the receptor-binding N-terminus (residues 1-4 in particular) projects freely while the bulky albumin cargo tethers from the opposite end. This arrangement preserves agonist geometry at GHRHR because the linker length permits spatial separation of the binding domain from the albumin mass. Modified GRF 1-29 lacks this tether entirely, so it diffuses, signals, and degrades on the timescale of endogenous GHRH itself.

The closest licensed comparator with a documented receptor-binding profile in this family is Tesamorelin. Broader structural context for adjacent GHRH-axis compounds sits in our full peptide reference library.

CJC-1295 with DAC vs without DAC: side-by-side

CJC-1295 with DAC is a long-acting, albumin-tethered GHRH analogue with a reported ~6–8 day plasma half-life [15][14]. CJC-1295 without DAC (Modified GRF 1-29) is the same stabilised GRF(1-29) sequence without the MPA linker, with a reported half-life of roughly 30 minutes [1][2]. The structural difference is one linker; the pharmacokinetic difference is roughly three orders of magnitude, because the albumin conjugate prevents renal filtration and enzymatic degradation. Both half-life figures trace back to a thin primary-source base and warrant independent verification against Teichman et al. 2006 [15] and the older GRF(1-29) PK literature [5].

For the closest licensed GHRH-axis comparator, see Tesamorelin. Broader structural context across this family sits in our full peptide reference library.

Half-life and pharmacokinetics explained

The half-life gap between CJC-1295 with DAC (~6–8 days, Teichman 2006 [5]) and Modified GRF 1-29 (~30 minutes, up to 1–2 hours in published PK literature) drives every other downstream difference. Longer residence time permits sustained receptor occupancy and tonic hormone elevation.

Native GHRH sits at roughly 7 minutes of plasma half-life in older endocrine literature [10]. Even the non-DAC analogue represents a 4–8x extension, achieved purely through the four canonical amino-acid substitutions that block DPP-IV cleavage [9].

DAC pushes that extension by three orders of magnitude through a different mechanism: covalent capture by serum albumin via the maleimidopropionic acid linker reacting with Cys34 [27]. Albumin's 19-day circulating half-life and 66 kDa mass allow the conjugate to evade glomerular filtration. The slow off-rate from the receptor-binding pocket keeps GHRH-receptor occupancy tonically elevated rather than pulsed [26].

Why "GH bleed" is the contested term

The Teichman 2006 trial recorded GH staying elevated for ~6 days and IGF-1 for 9–11 days after a single 30–60 μg/kg subcutaneous dose [5]. The trial reported a 7.5-fold rise in basal GH but only ~46% rise in average GH and ~45% rise in IGF-1 across the dosing window [23].

That pattern — sustained basal elevation with preserved but blunted pulses — is what researchers call the GH bleed, because the hormone concentration does not return to baseline between endogenous pulses. The 2026 clinician commentary flagging CJC-1295 with DAC as high-risk specifically cites the non-titrable nature of this exposure: once injected, the peptide cannot be withdrawn for roughly a week [14].

Pulsatile signalling and IGF-1 kinetics

Modified GRF 1-29's ~30-minute window forces 2–3x daily dosing in research protocols [8]. This operational burden reproduces the burst-and-trough pattern of endogenous GHRH because the short half-life permits complete clearance between doses.

The pharmacological argument for the non-DAC form rests on receptor desensitisation theory: tonic GHRH-receptor occupancy from DAC may downregulate signalling, whereas pulsatile exposure permits resensitisation between doses [3].

For sourcing decisions, the closest licensed comparator with a documented receptor-binding profile remains Tesamorelin. Structural cousins across the GHRH family are catalogued in our full peptide reference library.

Research dosing context (not a recommendation)

No MHRA-approved dose exists for CJC-1295 in either form, because neither variant is a licensed medicinal product in the UK [11]. What follows describes doses reported in published trials and observed in research-vendor product formats. JCSG provides no clinical recommendation and does not endorse human administration.

The Teichman 2006 trial administered single subcutaneous doses of 30–60 μg/kg CJC-1295 with DAC to healthy adults. GH elevated for ~6 days and IGF-1 for 9–11 days post-injection [7][15]. That extended exposure window is why community research protocols for the DAC form typically reference once- or twice-weekly administration.

Modified GRF 1-29's ~30-minute half-life pushes reported protocols to 2–3 subcutaneous administrations per day to approximate the pulsatile profile of endogenous GHRH [1][3].

Why Ipamorelin co-administration appears in protocols

The pairing of a GHRH analogue with the selective GHRP Ipamorelin is the most commonly documented combination in non-clinical literature. The rationale is that the two act on distinct receptors (GHRH-R and GHSR-1a) and produce additive GH release without the cortisol or prolactin rise associated with older GHRPs [3].

JCSG.org stocks both compounds from Body Pharm with batch-specific purity certificates. Order CJC-1295 or browse the full UK peptide catalogue to compare formats side by side. See the current price in the buy box on the product page.

Format choice follows half-life

The practical split is operational. The DAC conjugate's 5.8–8.1 day half-life [17][19] makes weekly schedules feasible but exposure non-titrable, because the long residence time prevents rapid dose adjustment. Modified GRF 1-29's sub-hour clearance permits same-day adjustment but demands disciplined injection timing [4].

Researchers comparing against a licensed reference point can review Tesamorelin. The wider GHRH-axis catalogue sits in our full peptide reference library.

Reported benefits in the research literature

The documented research signals for CJC-1295 cluster around sustained IGF-1 elevation, preserved GH pulsatility, and downstream effects inferred from those endocrine shifts. The strongest evidence sits with the endocrine markers themselves, not clinical endpoints — a distinction that matters when reading vendor copy, because marker elevation does not guarantee clinical benefit.

The headline finding is dose-dependent IGF-1 elevation. Teichman et al. (2006) reported that a single subcutaneous dose of CJC-1295 with DAC at 30–60 μg/kg in healthy adults produced a 1.5–3-fold rise in mean plasma IGF-1, with elevations persisting 9–11 days post-injection [10][19]. Secondary synthesis from Ionescu & Frohman, summarised in 2024 UK educational material, cites a 7.5-fold rise in basal GH, a 46% rise in average GH, and roughly 45% rise in IGF-1 from a single dose. Native pulsatile GH release was preserved rather than flattened [18].

Studied effects vs proven outcomes

Body-composition changes (lean mass gain, reduced adiposity) are routinely attributed to CJC-1295 in supplier monographs. The primary human data stop at GH and IGF-1 biomarkers because no long-term body-composition trial was completed. Animal-model and short-window human trials did not measure long-term body-composition endpoints, and the ConjuChem programme was discontinued before Phase III could test them [12][13].

CJC-1295 stimulates endogenous GH release via GHRH-R agonism rather than supplying exogenous GH [3] — a key distinction when evaluating research protocols.

Fertility-adjacent signals

Preliminary hypotheses around follicle growth and sperm maturation appear in published mechanistic literature on the rationale that IGF-1 modulates gonadal function. No controlled human trial of CJC-1295 has reported reproductive endpoints because such studies have not been conducted. Treat these as mechanistic speculation rather than evidence.

For a licensed GHRH-axis comparator with published indication-specific outcomes, see Tesamorelin. The wider peptide reference library covers adjacent secretagogues.

Reported side effects and safety signals

Reported side effects of CJC-1295 fall into local, vasomotor, and endocrine categories, with long-term human safety data still limited as of 2026. The most consistently reported effects across the 2006 Teichman trial and 2024–2025 secondary summaries are:

• Injection-site reactions (redness, itching, transient nodules)
• Facial flushing
• Headache
• Mild water retention
• Numbness or tingling in the extremities [1][2][20]

The Teichman 2006 Phase II data described CJC-1295 with DAC at 30–60 μg/kg as "safe and relatively well tolerated" over 28- and 49-day observation windows, with no serious acute adverse events recorded in that period [2]. ConjuChem's clinical programme was nevertheless wound down around 2006–2007. Secondary sources cite at least one hypersensitivity or immune-mediated reaction and concerns over prolonged, non-titrable GH/IGF-1 exposure as contributing factors [4]. Treat that discontinuation narrative as unverified at the primary-document level because the original regulatory correspondence has not been published.

Endocrine and theoretical signals

Elevated cortisol and prolactin are commonly raised as concerns in community discussion of GH secretagogues. These are more closely associated with non-selective GHRPs than with GHRH analogues, because GHRH-R activation does not directly trigger corticotroph or lactotroph release.

Pairing with selective ghrelin agonists such as Ipamorelin is described in supplier and clinic literature as a way to avoid the cortisol/prolactin spillover seen with older GHRPs. A head-to-head human trial confirming this for CJC-1295 specifically has not been located.

Sustained IGF-1 elevation across 9–11 days following a single DAC dose [27] is the main theoretical concern: chronically raised IGF-1 is mechanistically linked in the wider endocrine literature to mitogenic risk because IGF-1 activates signalling pathways that promote cell proliferation. No long-term CJC-1295 cohort study has tested this endpoint.

For a licensed GHRH-axis comparator with published safety data, Tesamorelin is the closest analogue. Adjacent secretagogue profiles sit in our full peptide reference library.

UK regulatory status in 2026

CJC-1295, with or without DAC, is not a licensed medicine in the United Kingdom in 2026 and is not scheduled under the Misuse of Drugs Act 1971 [10][11]. That places it in the same regulatory category as most research peptides: lawful to hold as a laboratory reagent, unlawful to market or supply for human administration without a marketing authorisation from the MHRA.

The MHRA's general position on unlicensed medicinal products applies here. Any UK clinic, compounding pharmacy, or online vendor that promotes CJC-1295 with therapeutic claims supplies an unauthorised medicinal product under the Human Medicines Regulations 2012 and risks enforcement action [10]. This is why compliant UK suppliers label vials "for research use only" and avoid dosing instructions or treatment language. JCSG.org sells Body Pharm CJC-1295 strictly as a laboratory reagent — view the product page for the full specification and current pricing.

Importation for personal use sits in a grey area: there is no specific MHRA carve-out for GHRH analogues, and Border Force can detain shipments presented as medicines because they fall under the definition of medicinal products. Possession itself is not criminalised, but supply for human use is the trigger for regulatory action.

Anti-doping status

For competing athletes, the position is unambiguous. The WADA 2026 Prohibited List bans growth hormone-releasing factors and synthetic GHRH analogues under Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). UKAD educational materials name CJC-1295 explicitly as a prohibited GH secretagogue [13][14]. The ban applies in and out of competition because GHRH analogues confer performance advantage through sustained GH elevation.

This section is informational, not legal advice. For a licensed GHRH-axis comparator, see Tesamorelin. Adjacent profiles are catalogued in our full peptide reference library.

How CJC-1295 compares to other GHRH-axis peptides

CJC-1295 sits within a small family of GHRH-axis research peptides that differ mainly in receptor target, half-life, and regulatory status.

Tesamorelin is the only licensed GHRH analogue in this group, approved for HIV-associated lipodystrophy. It is structurally a stabilised GRF(1-44) rather than a 1-29 fragment, meaning it contains 15 additional C-terminal residues that may confer different receptor-binding kinetics. It carries a marketing authorisation that CJC-1295 lacks, which is why it dominates the clinical literature on visceral fat reduction. For a structural and pharmacokinetic profile, see our Tesamorelin reference page.

Sermorelin is the unmodified GHRH(1-29) parent fragment. Without the stabilising substitutions (D-Ala², Gln⁸→Glu, Ala¹⁵, Leu²⁷) that define Modified GRF 1-29, sermorelin is degraded by DPP-IV within minutes — a shorter functional window than even CJC-1295 without DAC [14].

Ipamorelin is mechanistically distinct. It is a selective ghrelin-receptor (GHS-R1a) agonist rather than a GHRH analogue, so it stimulates GH release through a separate pathway. It is frequently studied alongside Modified GRF 1-29 in dual-peptide research protocols to probe additive pulse amplitude because the two receptors operate independently.

Put simply: tesamorelin is the licensed comparator, sermorelin is the unstabilised ancestor, ipamorelin is the complementary mechanism, and CJC-1295 (DAC or no-DAC) is the stabilised middle ground. Adjacent monographs are catalogued in our full peptide reference library.

Order CJC-1295 on JCSG.org — UK Stock, Fast Dispatch

JCSG.org is the UK destination for Body Pharm research peptides, including both CJC-1295 with DAC and CJC-1295 without DAC (Modified GRF 1-29). Go to the CJC-1295 product page now — select your preferred form, check the current price in the buy box, and add to cart. Every order ships with a batch-specific certificate of analysis confirming purity.

Comparing forms? Use the guide above to choose the right variant for your protocol, then head straight to JCSG.org/uk/peptides/cjc-1295/ to place your order. For the licensed GHRH-axis comparator, see the Tesamorelin reference page. Browse the entire catalogue at our full UK peptide library.

For research use only. Not for human consumption.