CJC 1295

CJC 1295 is a synthetic GHRH(1‑29) analogue with four stabilising substitutions (D‑Ala², Gln⁸, Ala¹⁵, Leu²⁷). The DAC variant adds a maleimidopropionyl–lysine linker that binds serum albumin and extends half‑life to roughly 5.8–8.1 days in humans, versus ~30 minutes for the no‑DAC form [5][6]. In the UAE, both variants and the CJC 1295 + Ipamorelin combination are sold by research‑use‑only vendors such as PharmaLab Global UAE and UAE Peptide Research, priced in AED and shipped domestically [1][3][8]. Neither is a MoHAP‑registered medicine.

Key Takeaways

• CJC 1295 with DAC persists for 6–8 days via albumin binding; the no-DAC form clears in ~30 minutes and preserves pulsatile GH release
• Ipamorelin synergises with CJC 1295 by activating the GHS-R1a receptor, increasing GH pulse frequency while CJC 1295 raises pulse amplitude
• Current AED pricing and product specifications are available from UAE research vendors; regulatory status is research-use-only under UAE Federal Law No. 4 of 2016
• The most recent human pharmacokinetics data (Teichman et al. 2006) remains the primary reference; no peer-reviewed human trial has updated these parameters since 2020
• Storage in UAE summer heat (40–45 °C) requires insulated packaging and immediate refrigeration post-delivery

What Is CJC 1295? Structure and Mechanism

CJC 1295 is a synthetic 30-amino-acid analogue of growth hormone-releasing hormone, built on the Modified GRF 1-29 (Sermorelin) backbone with four amino acid substitutions that confer protease resistance: D-Ala², Gln⁸, Ala¹⁵ and Leu²⁷ [5]. These substitutions block dipeptidyl peptidase-IV cleavage at position 2 and trypsin-like cleavage at positions 11–12, raising plasma stability without altering receptor-binding topology [5].

The molecule agonises the GHRH receptor (GHRHR), a class B G-protein-coupled receptor expressed on anterior pituitary somatotrophs. Binding activates Gαs and elevates intracellular cAMP, triggering calcium-dependent exocytosis of stored growth hormone. Crucially, this preserves the pulsatile secretion pattern rather than producing a flat tonic release [5]. Circulating GH then drives hepatic IGF-1 synthesis through JAK2/STAT5 signalling, the downstream marker most studies use as a pharmacodynamic readout [5].

Distinction from endogenous GHRH(1-44)

Native GHRH is a 44-residue peptide, but only the first 29 residues are required for full receptor activation. CJC 1295 retains that 1-29 active fragment and discards the C-terminal 30-44 sequence, which plays no role in somatotroph stimulation [5]. The four amino acid swaps extend the in vivo half-life of the base (no-DAC) peptide from roughly 7 minutes for native GHRH to approximately 30 minutes [5][6]. Teichman et al. (2006, Journal of Clinical Endocrinology & Metabolism) remains the primary human pharmacology reference for these parameters and for the DAC-linker pharmacokinetics discussed below [5].

Position within the GHRH-analogue class

CJC 1295 sits alongside Tesamorelin and Sermorelin as a GHRHR agonist. Tesamorelin is an approved trans-3-hexenoyl GRF(1-44) analogue for HIV-associated lipodystrophy; CJC 1295 has never completed registration and remains a research compound in UAE vendor catalogues [7].

CJC 1295 With DAC vs. Without DAC

The decisive difference is half-life. CJC 1295 without DAC clears in roughly 30 minutes, while CJC 1295 with DAC persists for 6–8 days. A maleimidopropionic acid (MPA) linker on the Lys side chain forms a covalent thioether bond with Cys34 of circulating serum albumin, shielding the peptide from proteolysis and renal clearance [1][2]. That single structural addition reshapes every downstream pharmacokinetic and pharmacodynamic parameter worth weighing.

Side-by-side comparison

Parameter	CJC 1295 without DAC	CJC 1295 with DAC
Plasma half-life	~30 minutes [1]	6–8 days [1][2]
Dosing frequency	Daily or twice-daily	Once weekly [2]
GH secretion pattern	Preserves pulsatile release	Sustained tonic elevation [2]
IGF-1 response	Acute peaks following each dose	Sustained 28-day elevation of 28–55% above baseline [1]
Typical research dose	100–200 µg per injection	1–2 mg per week [2]
Albumin binding mechanism	None	MPA linker → Cys34 covalent bond [1][2]

Interpreting the pulsatility trade-off

Teichman et al. (2006) reported that a single subcutaneous CJC 1295 with DAC injection in 65 healthy adults produced mean IGF-1 increases of 28–55% sustained across 28 days at dose groups spanning 30–120 µg/kg, with GH levels held above baseline for 6 or more days [1]. That sustained envelope is the appeal of the DAC variant for weekly dosing protocols. It also presents the principal concern: continuous GHRHR agonism flattens the endogenous pulse architecture that hepatic IGF-1 synthesis and receptor sensitivity normally depend on.

The no-DAC form behaves closer to physiological GHRH signalling. Each 100–200 µg injection produces a discrete cAMP-driven GH pulse that decays within an hour, allowing the somatotroph axis to reset between doses and preserving the diurnal rhythm that pairs cleanly with a ghrelin-mimetic such as Ipamorelin. Researchers prioritising pulsatility-dependent endpoints typically select no-DAC. Those modelling chronic IGF-1 exposure, as studied with Tesamorelin in lipodystrophy contexts, select the DAC variant.

One practical note for UAE buyers: DAC vials are usually supplied at 2 mg to match weekly dosing, while no-DAC is supplied at 2–5 mg to support daily reconstitution windows. Shelf stability post-reconstitution differs accordingly.

CJC 1295 + Ipamorelin Combination

Researchers stack CJC 1295 with Ipamorelin because the two peptides act on separate somatotroph receptors and produce additive GH release. CJC 1295 binds the GHRH receptor to amplify pulse amplitude. Ipamorelin binds the GHS-R1a ghrelin receptor to increase pulse frequency and suppress somatostatin tone [5][6]. The result is a larger, more frequent GH pulse than either compound generates alone.

Dual-receptor mechanism

GHRHR activation by CJC 1295 elevates intracellular cAMP in somatotrophs, raising the ceiling of each GH pulse. Ipamorelin, a pentapeptide with the sequence Aib-His-D-2-Nal-D-Phe-Lys-NH₂, acts through a phospholipase C / IP₃ pathway at GHS-R1a and concurrently dampens hypothalamic somatostatin output, removing the brake on pulse initiation [5]. Because the two signals converge on the same secretory cell through different second-messenger cascades, the GH output is mathematically additive rather than redundant.

Selectivity advantage over GHRP-6

Ipamorelin's selectivity for GHS-R1a is why it has displaced earlier ghrelin mimetics such as GHRP-6 in research protocols. Raun et al. (1998, European Journal of Endocrinology) characterised Ipamorelin as releasing GH with no measurable rise in cortisol, prolactin, or ACTH at GH-releasing doses [5], unlike GHRP-6 and hexarelin, which elevate all three. That clean endocrine profile makes the CJC 1295 + Ipamorelin pairing tractable for studies isolating GH-axis effects from confounding stress-hormone signalling.

Why no-DAC is preferred in the stack

The no-DAC variant is the standard pairing partner because its ~30-minute plasma window matches Ipamorelin's ~2-hour half-life, preserving the pulsatile architecture that combination protocols target. The DAC variant's multi-day albumin-bound exposure flattens pulses and negates the frequency benefit Ipamorelin provides. Researchers modelling the downstream GH → IGF-1 axis, or comparing GHRH-analogue stacks against monotherapy with Tesamorelin, typically default to no-DAC + Ipamorelin for this reason.

Sigalos & Pastuszak (2018, Sexual Medicine Reviews) synthesised GH secretagogue combination logic. That review is now eight years old; researchers should check 2024–2026 endocrinology literature for updated combination pharmacodynamics before finalising any protocol design [5].

CJC 1295 and IGF-1

CJC 1295 elevates IGF-1 indirectly by stimulating endogenous GH release from the pituitary, which drives hepatic IGF-1 synthesis. In the Teichman et al. 2006 phase I trial, single subcutaneous doses of CJC 1295 with DAC produced IGF-1 standard deviation (SD) score increases of approximately 0.3–0.6 across the 30, 60, and 90 µg/kg dose groups, with elevations sustained for 9–11 days post-injection [5]. This remains the most-cited quantitative human IGF-1 dataset for the molecule.

The GH → IGF-1 axis in context

GH secreted in response to GHRH-receptor activation binds hepatic GH receptors and induces IGF-1 transcription. Circulating IGF-1 then mediates the anabolic and metabolic signalling that body composition, tissue repair, and metabolic researchers study downstream. Because CJC 1295 acts upstream at the pituitary, the IGF-1 response is pulsatile-physiological in the no-DAC variant and tonic-elevated in the DAC variant [5][7]. Researchers modelling chronic exposure should weight this distinction when interpreting any IGF-1 SD-score change.

Endogenous elevation vs. direct IGF-1 administration

CJC 1295 is mechanistically distinct from exogenous IGF-1 analogues. Direct-acting peptides such as IGF-1 LR3 bypass the pituitary-hepatic cascade entirely and bind IGF-1 receptors directly, producing a pharmacokinetic and feedback profile that is not comparable to GHRH-analogue-driven elevation. Comparative protocols against other GHRH analogues such as Tesamorelin should isolate which arm of the axis is being interrogated before IGF-1 endpoints are interpreted.

The post-2020 evidence gap

No peer-reviewed human clinical trial published between 2020 and 2026 has updated or superseded the Teichman 2006 IGF-1 dataset [5][6]. Practitioner reviews and 2023–2024 educational syntheses continue to cite the original ConjuChem figures. Any researcher designing a 2026 protocol is working from a 20-year-old human pharmacokinetics reference and should treat the IGF-1 SD-score range accordingly.

CJC 1295 Research Protocols

The parameters below describe doses used in published research and vendor research-use-only labelling, not medical dosing advice. The Teichman 2006 phase I trial administered CJC 1295 with DAC subcutaneously at 30, 60, 90, and 120 µg/kg in healthy adults, the primary human pharmacokinetics dataset researchers benchmark against [5][6].

For the DAC variant, protocols cited in 2024 vendor and educational literature converge on 1–2 mg once weekly by subcutaneous injection, reflecting the albumin-bound half-life that sustains tonic GHRH-receptor activation across 5.8–8.1 days [1][6]. For the no-DAC variant, researchers report 100–200 µg per administration, one to three times daily. Timing is typically pre-sleep or fasted windows so the exogenous pulse aligns with endogenous nocturnal GH release [6][7].

Combination with Ipamorelin

CJC 1295 no-DAC is frequently co-administered with Ipamorelin at 200–300 µg per injection, exploiting the GHRH-analogue plus selective ghrelin-receptor agonist synergy described in mechanistic reviews [7][8]. Combination vials sold in the UAE research market commonly use a 7.5 mg CJC 1295 + 15 mg Ipamorelin ratio per blend [8]. Researchers comparing the GHRH arm against a pure GHRH analogue should review the Tesamorelin protocol parameters before designing the control arm. Researchers isolating the downstream IGF-1 response may prefer IGF-1 LR3 as a direct-acting comparator.

Reconstitution and storage

Lyophilised CJC 1295 is reconstituted with 1–2 mL of bacteriostatic water per vial. Calculate concentration against the labelled peptide mass on the Certificate of Analysis (CoA) [1][6]. Lyophilised powder is stable at room temperature for short transit windows; the reconstituted solution should be held at 2–8 °C and protected from light [1][6].

UAE climate consideration

UAE summer ambient temperatures routinely exceed 40 °C between June and September, with logged airport readings above 45 °C across Dubai and Abu Dhabi. Lyophilised peptides tolerate brief excursions, but reconstituted vials should never be left in vehicles or unconditioned storerooms. Researchers ordering domestically should request insulated packaging with gel packs and refrigerate immediately on receipt [1][6].

Body Pharm CJC 1295 with DAC 2

The Body Pharm CJC 1295 with DAC 2 listing on JCSG is a 2 mg lyophilised vial of the DAC-modified GHRH(1-29) analogue, supplied for in-vitro research use only and shipped within the UAE with insulated cold-chain packaging. Current AED pricing is available at jcsg.org/ae/peptides/cjc-1295/body-pharm-cjc-1295-with-dac-2 (verify live price at publication).

Specifications

Each vial contains 2 mg of CJC 1295 with DAC in lyophilised powder format, manufactured by Body Pharm, a research peptide brand stocked alongside other GHRH analogues on UAE-facing research catalogues. Purity is stated ≥98% by HPLC per the manufacturer's Certificate of Analysis; request and cross-check this against the labelled mass before reconstitution calculations [6]. The DAC modification is the maleimidopropionyl (MPA) group on the Lys side chain that covalently binds serum albumin, the structural feature underpinning the multi-day half-life referenced throughout this article [5][6].

Shipping and regulatory status

JCSG dispatches domestically across the UAE with gel-pack insulation suitable for short transit windows in ambient conditions above 40 °C. Researchers comparing this DAC product against a non-albumin-binding GHRH analogue can review the Tesamorelin listing, or trace the downstream axis via IGF-1 LR3.

Disclaimer: This product is sold for laboratory research purposes only. CJC 1295 with DAC is not registered or approved by the UAE Ministry of Health and Prevention (MoHAP) or any other regulatory authority for human therapeutic, diagnostic, or cosmetic use.

How CJC 1295 Compares to Other GHRH Analogues

CJC 1295 with DAC sits at the long-half-life end of the GHRH analogue spectrum, while Tesamorelin and Sermorelin are short-acting and more clinically validated. For researchers evaluating which analogue suits a given protocol, the differentiators are sequence length, protease-resistance modifications, plasma persistence, and depth of regulatory evidence.

CJC 1295 vs. Tesamorelin

Tesamorelin is a GHRH(1-44) analogue carrying a trans-3-hexenoic acid N-terminal modification. It received FDA approval in 2010 as Egrifta for HIV-associated lipodystrophy. Its plasma half-life is approximately 26 minutes, so daily subcutaneous administration is required to sustain GH pulsatility. CJC 1295 with DAC has a 5.8–8.1-day half-life via albumin conjugation [5], permitting weekly or twice-weekly dosing in research models. The trade-off is regulatory weight: Tesamorelin has a registered human indication and post-marketing data; CJC 1295 remains an unregistered research compound under MoHAP framing.

CJC 1295 (No DAC) vs. Sermorelin

Sermorelin is the unmodified GHRH(1-29) parent sequence and the structural predecessor to CJC 1295 without DAC. CJC 1295 (no DAC) retains the same 29-residue backbone but introduces four substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) that confer protease resistance, extending plasma half-life from minutes (Sermorelin) to roughly 30 minutes [5][7]. Researchers tracking the downstream signal can cross-reference the IGF-1 LR3 monograph for the effector arm of the axis.

Regulatory Status in the UAE

CJC 1295 is not registered as an approved medicinal product by MoHAP or the Dubai Health Authority (DHA). It is supplied in the UAE strictly as a research chemical for in-vitro and laboratory use. UAE-facing peptide vendors consistently label CJC 1295 with and without DAC as "for research use only" and explicitly state it is not an approved medication [1][3][8].

The governing framework is UAE Federal Law No. 4 of 2016 on Medical Products, Pharmacy Profession and Pharmaceutical Establishments. Under this law, any unregistered product intended for human use falls within MoHAP and customs enforcement scope. Synthetic GHRH analogues including CJC 1295 and Ipamorelin are not named in the UAE narcotic or psychotropic schedules as of 2025. They are treated as unscheduled but unregistered medicinal products, not controlled substances, not freely tradeable supplements.

Practical implications for UAE researchers

JCSG dispatches CJC 1295 to verified research endpoints only. No therapeutic claim, dosing recommendation, or clinical indication is made or implied. Researchers comparing GHRH analogues for protocol design should consult the Tesamorelin monograph, which carries a distinct regulatory profile (FDA-approved indication, no MoHAP registration). The IGF-1 LR3 page covers the downstream effector arm.

Frequently Asked Questions