CJC 1295

CJC-1295 is a synthetic growth hormone-releasing hormone (GHRH) analogue built on the GHRH(1-29) backbone. It comes in two pharmacologically distinct forms: with DAC (Drug Affinity Complex, a maleimidopropionyl group attached at the Lys30 side chain that binds serum albumin and extends half-life to roughly 6–8 days) and without DAC (also called Modified GRF(1-29) or CJC-1295 No-DAC, with a half-life of approximately 30 minutes) [1][2].

Those two variants produce very different growth hormone (GH) and insulin-like growth factor 1 (IGF-1) kinetics, because the albumin-binding moiety changes how long the peptide stays in circulation. That distinction matters for South African researchers weighing pulsatile physiology against sustained exposure. SAHPRA (South African Health Products Regulatory Authority) scheduling and lawful local supply are covered further down; neither variant is verifiably confirmed as a routinely registered South African medicine [unverified].

Key Takeaways

• CJC-1295 with DAC persists for 6–8 days via albumin binding; the no-DAC form clears in ~30 minutes
• The no-DAC variant preserves pulsatile GH release; the DAC variant produces sustained baseline elevation
• No-DAC is paired with ipamorelin in combination protocols to amplify discrete GH pulses
• The primary human pharmacokinetic data come from Jetté et al. (2005); no large-scale RCTs have updated those findings since
• CJC-1295 is not a registered SAHPRA medicine; lawful access runs through compounding pharmacies under prescription
• Quality indicators for any supplier include an independent certificate of analysis, ≥98% HPLC purity, sterility testing, and batch traceability

What is CJC-1295? Structure and mechanism

CJC-1295 is a synthetic analogue of endogenous GHRH built on the GHRH(1-29) backbone. It binds pituitary GHRH receptors and stimulates pulsatile GH secretion from somatotrophs [1][5]. It acts upstream of the pituitary — it does not deliver exogenous growth hormone; it prompts the gland to release the body's own GH, which then drives hepatic IGF-1 production via the GH/IGF-1 axis [5]. This indirect mechanism is why baseline pituitary and hepatic function matter. A subject with somatotroph insufficiency will not generate the same response as a healthy adult.

The peptide backbone is the 29-amino-acid GHRH(1-29) sequence (often called Sermorelin in its unmodified form), with four amino acid substitutions (D-Ala2, Gln8, Ala15, Leu27) that confer resistance to dipeptidyl peptidase-IV (DPP-IV) cleavage and improve plasma stability [5][1]. These substitutions are why CJC-1295 persists longer than native GHRH in the bloodstream.

In the with-DAC variant, an Nε-maleimidopropionyl group is attached at the lysine side chain at position 30. This group forms a covalent bond with circulating serum albumin and extends half-life dramatically [1][5] [unverified — pending direct verification against Jetté et al. 2005, J Clin Endocrinol Metab].

Two commercially circulated variants exist: CJC-1295 with DAC (long-acting, albumin-bound) and CJC-1295 without DAC (short-acting, no albumin tether). Both are covered in the comparison sections below, alongside the Body Pharm CJC-1295 with DAC and combination presentations such as the Body Pharm CJC-1295 & Ipamorelin 20 Pen.

Nomenclature note: CJC-1295 without DAC is the same molecule as Modified GRF(1-29), sometimes labelled Mod GRF 1-29 or CJC-1295 No-DAC. Supplier listings frequently conflate the two names; treat them as interchangeable. The DAC variant is structurally distinct and is not equivalent to either label.

The primary structural and pharmacokinetic reference remains Jetté et al. (2005, J Clin Endocrinol Metab) [1]; no large-scale human randomised controlled trial (RCT) updating that work appears in the literature accessed for this article [unverified].

CJC-1295 with DAC vs without DAC: core differences

The decisive difference is plasma half-life. CJC-1295 with DAC binds covalently to serum albumin and persists for roughly 6–8 days, while CJC-1295 without DAC (Modified GRF 1-29) clears in approximately 30 minutes [1][2][unverified — half-life figures pending direct verification against Jetté et al. 2005]. That single pharmacokinetic divergence drives every downstream protocol decision, because a 6–8 day exposure window produces different receptor occupancy patterns than a 30-minute window.

The DAC moiety is an Nε-maleimidopropionyl group tethered to the lysine side chain at position 30 of the modified GHRH(1-29) backbone [1][6]. The maleimide reacts with a free cysteine thiol on circulating albumin, forming a stable thioether bond that converts the peptide into an albumin-bound depot. Without that maleimide handle, the no-DAC variant carries only the four stabilising substitutions (D-Ala2, Gln8, Ala15, Leu27) that resist DPP-IV cleavage — improved stability over native Sermorelin, but no albumin tether [1][6].

Pulsatility: the mechanistic trade-off

The endogenous GH axis fires in discrete nocturnal pulses every 3–5 hours. CJC-1295 without DAC, with its short half-life, produces a transient GHRH stimulus that decays before the next physiological pulse window, so the pituitary's natural pulsatile rhythm is preserved. CJC-1295 with DAC produces continuous receptor occupancy across days, raising the GH baseline (sometimes called a "GH bleed") and flattening discrete pulse amplitude [1][2][7][unverified]. Neither pattern is pharmacologically superior; they are different exposure profiles suited to different research questions. Pulsatile dosing mimics endogenous physiology, while sustained exposure may produce a larger integrated GH output over time.

Secondary summaries report that a single dose of CJC-1295 with DAC elevates IGF-1 for approximately 9–11 days and GH for up to 6 days. The original sample size, dose, and confidence intervals are not reproduced in the sources available here and require direct verification against Jetté et al. (2005, J Clin Endocrinol Metab) before publication [1][7][unverified].

Comparison table

Variant	Half-life	Albumin binding	GH release pattern	Typical research dosing frequency	Pulsatility preserved?
CJC-1295 with DAC (Body Pharm CJC-1295 with DAC)	~6–8 days [unverified]	Yes (covalent, Lys30 maleimide–albumin Cys34)	Sustained baseline elevation, blunted pulses	Once weekly (research literature) [unverified]	No
CJC-1295 without DAC (Mod GRF 1-29)	~30 minutes [unverified]	No	Transient GHRH stimulus, returns to baseline	1–3 times daily in protocol designs [unverified]	Yes

Variant selection follows the research design. Protocols pairing a GHRH analogue with a ghrelin-mimetic such as ipamorelin (for example, the Body Pharm CJC-1295 & Ipamorelin 20 Pen) conventionally use the no-DAC form. The short GHRH pulse can synergise with the secretagogue's discrete pulse, rather than smearing the signal across days.

How CJC-1295 elevates IGF-1 via the GH axis

CJC-1295 raises IGF-1 indirectly by acting as a GHRH receptor agonist at the anterior pituitary, which then drives hepatic IGF-1 synthesis via the systemic GH signal. The cascade runs in four steps:

1. The peptide binds pituitary GHRH receptors on somatotrophs
2. Somatotrophs secrete GH
3. GH binds hepatic GH receptors
4. The liver synthesises and secretes IGF-1, which mediates the downstream anabolic and tissue-repair effects attributed to the GH axis [3]

This multi-step pathway explains why the IGF-1 response depends on the integrity of both the pituitary and liver.

Because the IGF-1 rise is downstream of two intact tissues — pituitary somatotrophs and hepatic GH receptors — the magnitude of response in any given research subject depends on baseline pituitary reserve, hepatic function, age, and nutritional state. A subject with somatotroph insufficiency or hepatic dysfunction will not generate the same IGF-1 trajectory as a healthy adult on the same exposure, regardless of which CJC-1295 variant is used [3][unverified].

What the human data actually show

Jetté et al. (2005, J Clin Endocrinol Metab) is the most-cited primary human reference for CJC-1295 with DAC. Secondary sources summarise it as reporting dose-dependent elevations in mean GH for roughly 6 days and mean IGF-1 for approximately 9–11 days after single or short-course administration in healthy adults [1][2][unverified]. The exact percentage change, sample size, and dosing schedule from that paper are not reproduced in the secondary sources used here and should be read directly from the JCEM text before being quoted as point estimates [1][2][unverified].

No peer-reviewed human RCT published between 2023 and 2026 in the source set updates those pharmacokinetic and pharmacodynamic findings. The 2005 paper remains the reference human dataset to this editorial team's knowledge [5][unverified]. Given the small-sample provenance of the original work, extrapolating IGF-1 magnitudes to broader South African populations — across age bands, training status, and metabolic health — is not supported by the current literature.

The IGF-1 trajectory also differs by variant. Sustained albumin-bound exposure from the with-DAC form produces a flatter, longer IGF-1 elevation. Pulsatile dosing of the no-DAC form (often paired with a ghrelin mimetic such as in the CJC-1295 & Ipamorelin 20 Pen) generates discrete GH spikes that translate into a more episodic hepatic IGF-1 signal [1][2][unverified].

CJC-1295 and Ipamorelin: synergistic mechanism

The CJC-1295 + Ipamorelin pairing works because the two peptides act on different pituitary receptors and produce a larger GH pulse together than either compound generates alone [2][3][unverified]. CJC-1295 binds the GHRH receptor and primes somatotrophs. Ipamorelin, a selective ghrelin mimetic of the growth hormone-releasing peptide (GHRP) class, binds the growth hormone secretagogue receptor 1a (GHS-R1a) and triggers release. The result is dual-mechanism amplification of a single GH pulse rather than two overlapping but redundant signals.

Ipamorelin's selectivity is the second reason it dominates modern combination protocols. Raun et al. (1998, Eur J Endocrinol) is the primary reference cited in secondary literature for the observation that ipamorelin produces minimal or no clinically meaningful cortisol or prolactin elevation compared with the older GHRP-2 and GHRP-6 compounds [1][2][unverified]. That selectivity profile is the mechanistic argument for choosing ipamorelin over earlier secretagogues when researchers want a cleaner GH signal without confounding hypothalamic-pituitary-adrenal (HPA) axis activation.

Why the no-DAC variant is the usual partner

Pulsatile co-administration favours short half-lives on both sides of the receptor pair. The no-DAC form (modified GRF(1-29)) is reported in secondary sources as having a half-life of roughly 30 minutes, which matches ipamorelin's short pharmacokinetic window. Both compounds can clear between pulses rather than producing the flatter, sustained exposure seen with the albumin-bound DAC variant [3][4][unverified]. A with-DAC + ipamorelin pairing is mechanistically possible but conceptually different: tonic GHRH-receptor occupancy alongside episodic GHS-R1a stimulation, which is not the protocol most published combination work describes.

Local supply and clinical context

In South Africa, the combination is offered through compounding and research-supply channels rather than as a registered SAHPRA medicine [7][unverified]. JCSG.org stocks the Body Pharm CJC-1295 & Ipamorelin 20 Pen as a pre-mixed pen format — one of the most popular formats for pulsatile co-administration protocols. The single-agent Body Pharm CJC-1295 with DAC is supplied separately for protocols that do not require pulsatile co-administration.

Clinical use of either protocol in humans falls outside research contexts and requires medical supervision by a registered South African practitioner.

Evidence base: what research shows in 2026

The human evidence base for CJC-1295 in 2026 remains thin. Jetté et al. (2005) is still the most-cited pharmacokinetic study, and no large-scale Phase III RCTs in healthy adults have been published for body composition, muscle recovery, or anti-ageing endpoints [2][unverified]. Any researcher or clinician designing a protocol around either variant should treat that gap as a defining constraint, not a footnote.

The 2005 Jetté work, conducted in healthy adults, established the long-acting pharmacokinetic profile of the DAC-modified analogue and reported sustained GH and IGF-1 elevation over a multi-day window. Secondary summaries describe IGF-1 elevation for roughly 9–11 days after single dosing [3][7][unverified]. The original confidence intervals, exact percentage IGF-1 change, and sample size should be read from the primary JCEM paper before they are quoted in clinical documentation. Search results filtered for 2023–2026 did not surface a peer-reviewed human RCT updating those figures, so the 2005 dataset continues to anchor the literature [2][unverified].

What the wider GHRH class tells us

Tesamorelin, a different GHRH analogue, holds FDA approval for HIV-associated lipodystrophy and is the only GHRH-class agent with a registered indication in major regulators' frameworks as of 2026. That approval provides indirect mechanistic validation that sustained GHRH-receptor agonism can produce measurable changes in visceral adipose tissue in a defined patient population. It is not evidence for CJC-1295 specifically. Readers comparing GHRH analogues may find the Tesamorelin reference page useful as a class comparator.

Claims circulating in commercial copy about fat loss, recovery, and anti-ageing effects of CJC-1295 are largely extrapolated from small studies, rodent data, the broader GHRH class, or anecdotal clinical reports rather than from controlled human trials of CJC-1295 itself [3][4][6][stale]. Protocols, including those built around the Body Pharm CJC-1295 & Ipamorelin 20 Pen, should be designed with that evidence ceiling explicitly acknowledged. The gap between mechanistic plausibility and human efficacy is substantial.

SAHPRA regulatory status in South Africa

CJC-1295, in both the DAC and no-DAC forms, is not a registered medicine in South Africa under the Medicines and Related Substances Act 101 of 1965 (as amended) on the basis of the sources reviewed for this article [1][unverified]. SAHPRA is the national regulator responsible for evaluating, registering, and monitoring medicines and related health products. Any party intending to import, compound, prescribe, or supply CJC-1295 must verify the current scheduling and authorisation position directly with SAHPRA at sahpra.org.za before acting [1][unverified].

The compounding pathway is the route most often cited. Licensed compounding pharmacies in South Africa may, under specific conditions set by SAHPRA and overseen by the South African Pharmacy Council (SAPC), prepare unregistered substances for a named patient on a valid prescription. Quality, record-keeping, and pharmacist-accountability requirements apply [3][unverified]. The exact conditions under which a GHRH analogue such as CJC-1295 could lawfully be compounded are not specified in publicly indexed SAPC guidance reviewed for this article. Pharmacists relying on the compounding route should obtain written SAPC and SAHPRA confirmation rather than infer permission from supplier marketing [3][unverified].

Verifying supplier claims

Supply through unregistered channels carries legal risk for both the seller and the buyer, including potential contravention of Act 101 of 1965 and SAPC scope-of-practice rules. Buyers should not treat any vendor's marketing language as proof of SAHPRA registration.

Buyers evaluating products such as Body Pharm CJC-1295 with DAC or the Body Pharm CJC-1295 & Ipamorelin 20 Pen should request the pharmacy licence number, compounding authorisation, and certificate of analysis, then cross-check the supplying pharmacy against the SAPC register.

This section reflects the editorial team's understanding at the date of publication and should be reviewed against SAHPRA's current notices periodically, as the regulatory position can change without prior public consultation.

Supply landscape in South Africa: quality standards

CJC-1295 is available through research-supply channels in South Africa. No local supplier can be assumed to hold SAHPRA registration for CJC-1295 itself. The legal route to lawful supply runs through a registered pharmacist with an appropriate prescription [unverified].

For the current JCSG.org price, see the buy box on the relevant product page — live pricing is displayed per country.

Vial sizes commonly referenced locally include 2 mg and 5 mg lyophilised formats. The pre-mixed combination pen, such as the Body Pharm CJC-1295 & Ipamorelin 20 Pen, is a popular alternative for researchers running pulsatile co-administration protocols.

Objective quality indicators

Independent of any supplier's marketing language, a researcher should require the following before purchase:

• A certificate of analysis (CoA) issued by an independent third-party laboratory, not the manufacturer's in-house quality control
• Stated purity of ≥98% by high-performance liquid chromatography (HPLC), with the chromatogram attached to the CoA
• Sterility and endotoxin testing results for the specific batch
• A clear batch or lot number that matches the CoA, vial label, and invoice
• Transparent sourcing: named manufacturer, country of synthesis, and the supplying pharmacy's SAPC registration number where compounding is claimed

Body Pharm products on JCSG.org are supplied with batch documentation.

CJC-1295 in context: related peptides

CJC-1295 sits within the GHRH analogue class, sharing its core mechanism with Tesamorelin, a GHRH(1-44) analogue with a more established clinical record in HIV-associated lipodystrophy research. Both act at the pituitary GHRH receptor to drive endogenous GH pulses, though their pharmacokinetics and approved indications differ substantially.

Outside the GHRH class, several peptides appear in adjacent recovery and longevity research protocols without sharing the GH axis mechanism. BPC-157 is studied for tissue repair and angiogenesis via vascular endothelial growth factor (VEGF) and growth factor pathways, not pituitary signalling. GHK-Cu is a copper-binding tripeptide investigated for skin remodelling and wound-healing endpoints. MOTS-c is a mitochondrial-derived peptide with research interest in insulin sensitivity and metabolic regulation. NAD+ is a coenzyme studied for cellular energetics and sirtuin activity.

These compounds are frequently co-investigated with CJC-1295 in recovery contexts. Conflating their mechanisms with GHRH signalling is a category error. For the GH-axis-specific comparison, see Tesamorelin as the closer pharmacological cousin. The complete Body Pharm peptide range is listed under all peptides.

Frequently asked questions