CJC-1295 No DAC (Modified GRF 1-29): The GHRH Analogue — Mechanism, GH Physiology & Research Overview

What is CJC-1295 No DAC?

CJC-1295 without DAC — formally known as Modified GRF (1-29) or Mod GRF 1-29 — is a synthetic 29-amino-acid analogue of growth hormone releasing hormone (GHRH). It was developed as a stabilised version of the native GHRH (1-29) fragment, which has an extremely short half-life of only 2 minutes in vivo due to rapid enzymatic cleavage by dipeptidyl peptidase IV (DPP-IV) and other proteases [1].

The "No DAC" designation is critical and frequently misunderstood. It distinguishes this peptide from CJC-1295 with DAC — a version that incorporates a Drug Affinity Complex (a maleimidopropionic acid modification) that enables covalent binding to albumin in the bloodstream, extending the half-life to approximately 8 days. CJC-1295 no DAC has a short half-life of approximately 30 minutes, which is intentional: this brevity preserves the natural pulsatile pattern of GH secretion, which is physiologically important and cannot be replicated by long-acting GH-releasing agents.

CJC-1295 no DAC is one of the most widely studied GHRH analogues in the research literature and forms the foundational GHRH component of the extensively documented CJC-1295/Ipamorelin combination protocol. Its CAS number is 863288-34-0.

How it works: GHRH analogue mechanism

CJC-1295 no DAC works by mimicking the action of endogenous growth hormone releasing hormone — the hypothalamic signal that instructs the pituitary's somatotroph cells to secrete growth hormone. Understanding this mechanism requires a brief overview of the GH axis.

The GHRH receptor pathway

Under normal physiology, the hypothalamus releases pulses of GHRH every 90–120 minutes. Each GHRH pulse binds to GHRH receptors (GHRHR) on pituitary somatotroph cells, activating a cAMP-mediated cascade that culminates in GH exocytosis into the bloodstream. CJC-1295 no DAC replicates this signal with greater potency and stability than native GHRH (1-29), producing a sharp, transient GH pulse that mirrors the body's natural secretory pattern [1].

The four stabilising substitutions

Native GHRH (1-29) is almost instantly cleaved by DPP-IV, which cuts the His-Ala bond at positions 1-2 of the peptide. CJC-1295 no DAC incorporates four strategic amino acid substitutions that dramatically increase resistance to enzymatic degradation while preserving receptor binding affinity:

• Position 2: Ala → Tyr (primary DPP-IV resistance substitution)
• Position 8: Arg → Ala (increases plasma stability)
• Position 15: Gln → Ala (reduces amide hydrolysis)
• Position 27: Ala → Leu (enhances receptor binding)

These substitutions extend the functional half-life from ~2 minutes (native GHRH) to ~30 minutes — long enough to produce a robust GH pulse, but short enough that the pituitary returns to baseline between administrations, preserving the physiological pulsatile pattern [1,2].

Why pulsatility matters

Growth hormone's anabolic and lipolytic effects depend critically on pulsatile secretion. Continuous GH exposure leads to receptor desensitisation and paradoxically blunted downstream IGF-1 production — a phenomenon documented with CJC-1295 with DAC at sustained plasma concentrations [2]. CJC-1295 no DAC's short half-life is therefore a feature, not a limitation: it produces physiological GH pulses that keep receptor sensitivity intact across repeated administrations.

Documented research benefits

The following benefits are reported in the GHRH analogue literature. The majority of mechanistic data is from rodent models and early human studies; CJC-1295 no DAC specifically has been characterised in the context of the broader GHRH analogue class, which includes the longer-acting CJC-1295 (with DAC) studied by Teichman et al. [1] and Ionescu & Frohman [2].

Increased GH and IGF-1 levels

GHRH analogue administration consistently produces dose-dependent increases in peak GH secretion and, through downstream hepatic signalling, elevated IGF-1 levels. In the Teichman et al. 2006 human study of CJC-1295 (with DAC), a single injection produced mean GH increases of 2–10 fold above baseline, with IGF-1 elevations persisting for up to 14 days [1]. CJC-1295 no DAC produces shorter-duration but equivalent-amplitude GH pulses per administration.

Body composition improvements

In rodent models, GHRH analogue administration produced meaningful improvements in lean-to-fat mass ratio — consistent with GH's established anabolic (muscle-sparing) and lipolytic (fat-mobilising) actions. The Alba et al. 2006 mouse study demonstrated that CJC-1295 analogue administration normalised growth in GHRH-knockout mice [3], providing mechanistic evidence that the compound effectively substitutes for endogenous GHRH function.

Enhanced recovery and sleep quality

Approximately 70% of daily GH secretion occurs during slow-wave (deep) sleep, with the largest pulse occurring in the first 90 minutes after sleep onset. By administering CJC-1295 no DAC pre-sleep, researchers can align the exogenous GHRH signal with the natural somatotropic activity window, amplifying the nocturnal GH pulse. GH released during sleep drives tissue repair, protein synthesis, and metabolic housekeeping — functions that underlie its reputation for recovery enhancement in the research literature.

Bone density

Animal models of GH deficiency and GHRH knockout show reduced bone mineral density, which GHRH analogue treatment partially reverses [3]. IGF-1 — the primary GH downstream effector — is a known osteogenic signal, and sustained IGF-1 elevation from GHRH analogue treatment correlates with bone density improvements in the preclinical literature. Human data on bone outcomes remain limited to GH-deficient populations rather than healthy research subjects.

The CJC-1295 / Ipamorelin combination: the most studied GHRH+GHRP pairing

CJC-1295 no DAC's primary research context is as the GHRH component of the GHRH + GHRP synergy protocol. Ipamorelin — a selective growth hormone releasing peptide (GHRP) — acts through the ghrelin receptor (GHSR-1a) to amplify the GH pulse that CJC-1295 no DAC initiates. The GHRH analogue primes and opens the pituitary "gate" for GH release; the GHRP simultaneously pulls the trigger via a separate receptor. This two-signal mechanism produces GH pulses substantially larger than either peptide alone, a synergy that has been documented across multiple GHRH+GHRP combination studies.

Dosing ranges in published literature

Published dosing for CJC-1295 no DAC specifically is limited; most human pharmacokinetic data comes from the related CJC-1295 with DAC studies (Teichman et al. 2006 [1], Ionescu & Frohman 2006 [2]). The no-DAC form's 30-minute half-life means that the key variable is not the dose per se but the timing relative to sleep and co-administration with a GHRP.

In the GHRH analogue human literature, 1–2 µg/kg SC administered pre-sleep is the most commonly referenced dosing context. For a 70 kg adult, this translates to roughly 70–140 µg per administration. Protocols in the published literature typically administer CJC-1295 no DAC 2–3 times per week; the short half-life means each dose produces a discrete GH pulse rather than sustained elevation, and this intermittent pattern is considered important for preventing receptor desensitisation [2].

Administration & reconstitution

Route and timing

CJC-1295 no DAC is administered by subcutaneous injection, typically into the abdominal subcutaneous fat. The timing of administration is arguably more important than the dose: most researchers in the published literature administer the peptide 15–30 minutes before sleep to align with the natural nocturnal GH pulse window. This pre-sleep administration strategy amplifies endogenous GH secretion rather than simply adding a pharmacological signal on top of a suppressed baseline [1,2].

Reconstitution protocol (lyophilised powder)

CJC-1295 no DAC is supplied as a lyophilised white powder. Standard reconstitution uses bacteriostatic water (0.9% benzyl alcohol in sterile water for injection).

1. Allow the vial to reach room temperature before opening
2. Add bacteriostatic water slowly down the side wall of the vial — do not inject directly onto the powder
3. Gently swirl; do not vortex or shake
4. Store reconstituted solution at 2–8°C, protected from light
5. Use within 28 days of reconstitution

A common research calculation: adding 2 mL of bacteriostatic water to a 2 mg vial yields a concentration of 1,000 µg/mL (1 mg/mL), making each 0.1 mL drawn into a syringe equal to 100 µg.

The CJC-1295 No DAC + Ipamorelin combination

The most-studied administration protocol combines CJC-1295 no DAC with Ipamorelin in a single pre-sleep injection. Ipamorelin activates the growth hormone secretagogue receptor (GHSR-1a) independently of the GHRH receptor, creating a two-axis amplification of GH release. The GHRH analogue provides the hypothalamic "permission" signal; Ipamorelin provides the pituitary "amplifier" signal. Administering both simultaneously in the same subcutaneous injection is standard in the published research protocol literature. See our Ipamorelin guide for the full pharmacology of the GHRP component.

Side effects and safety data

CJC-1295 no DAC's short half-life contributes to a generally clean adverse event profile compared to longer-acting GHRH analogues. Side effects are largely attributable to the downstream effects of elevated GH and IGF-1 rather than direct peptide toxicity.

Reported adverse effects in literature

• Water retention — the most common GH-elevation effect; transient and dose-dependent; typically resolves as the GH pulse clears
• Tingling or numbness in extremities — a carpal tunnel-like sensation associated with fluid shifts and GH-driven extracellular water redistribution; reported with GH class compounds at higher doses
• Hypoglycaemia risk near feeding — GH is counter-regulatory to insulin; administering pre-sleep (in a fasted state relative to the last meal) reduces this risk; feeding shortly after administration can produce mild glucose dysregulation
• Injection site reactions — mild, localised; consistent with any subcutaneous peptide injection
• Flushing or transient warmth — occasionally reported during peak GH elevation; brief and not considered clinically significant

Theoretical considerations

• IGF-1 elevation at pharmacological levels — chronic supraphysiological IGF-1 is theoretically associated with cancer promotion; no documented evidence exists at the doses used in research protocols, and the pulsatile, non-continuous nature of CJC-1295 no DAC administration means IGF-1 elevations are transient rather than sustained
• Pituitary desensitisation — with very frequent administration, GHRH receptor downregulation is theoretically possible; the pulsatile, 2–3× weekly protocol in the literature is designed specifically to prevent this

Interactions & contraindications

No formal drug interaction studies have been published for CJC-1295 no DAC specifically. Based on its mechanism, the following considerations are documented in the GHRH analogue and GH class literature:

• Ipamorelin and other GHRPs — synergistic, well-documented, and considered the standard research combination; the amplified GH pulse means side effects (water retention, tingling) may be more pronounced than with either peptide alone
• Insulin — GH is counter-regulatory to insulin action; co-administration with exogenous insulin requires glucose monitoring; the pre-sleep, fasted-state protocol reduces but does not eliminate this interaction
• Glucocorticoids — corticosteroids suppress GH secretion at the pituitary level and may substantially reduce CJC-1295 no DAC's efficacy; the clinical relevance depends on the corticosteroid dose and duration
• Other GHRH analogues (sermorelin, tesamorelin) — combining multiple GHRH receptor agonists produces additive receptor stimulation with no documented safety data for the combination; not studied
• Somatostatin analogues (octreotide, lanreotide) — these compounds act at the pituitary to suppress GH release and would directly antagonise CJC-1295 no DAC's effect

Storage & stability

CJC-1295 no DAC is a relatively stable peptide in lyophilised form, with resistance to oxidation that makes it easier to handle than some longer, more structurally complex peptides. Reconstituted stability is good when refrigerated and protected from light.

Frequently asked questions

What is the difference between CJC-1295 with DAC and without DAC?

The DAC (Drug Affinity Complex) modification is a maleimidopropionic acid group that covalently binds to albumin in the bloodstream after injection, extending the half-life from ~30 minutes (no DAC) to ~8 days (with DAC). CJC-1295 with DAC produces a continuous, sustained elevation of GH rather than discrete pulses. This may sound beneficial, but continuous GH elevation leads to receptor desensitisation and potentially blunts downstream IGF-1 production over time — an effect documented by Ionescu & Frohman 2006 [2]. CJC-1295 no DAC's short half-life produces physiological GH pulses that keep receptor sensitivity intact.

Why is CJC-1295 no DAC almost always paired with Ipamorelin?

CJC-1295 no DAC and Ipamorelin activate two different receptor pathways that converge on the same outcome — pituitary GH release — but through distinct mechanisms. CJC-1295 no DAC works via the GHRH receptor; Ipamorelin works via the ghrelin receptor (GHSR-1a). When both signals reach the somatotroph cell simultaneously, the GH pulse produced is substantially larger than either peptide could produce alone. Additionally, Ipamorelin's selectivity for GH release (without significantly stimulating cortisol or prolactin, unlike older GHRPs) makes it a clean amplifier. The combination is one of the most thoroughly characterised GHRH+GHRP pairings in the published literature.

Does CJC-1295 no DAC directly increase muscle mass?

CJC-1295 no DAC itself does not directly stimulate muscle protein synthesis. It stimulates GH release, which in turn drives hepatic IGF-1 production. IGF-1 is the primary anabolic effector that promotes muscle protein synthesis and satellite cell activation. So the pathway is: CJC-1295 no DAC → GH pulse → IGF-1 elevation → anabolic signalling in muscle. The magnitude of the muscle-building effect depends on many variables including baseline GH status, training stimulus, nutrition, and the magnitude and duration of IGF-1 elevation [1].

How is CJC-1295 no DAC different from synthetic HGH?

Recombinant human growth hormone (rhGH, synthetic HGH) is the hormone itself — it produces a continuous, supraphysiological elevation of circulating GH and IGF-1 that bypasses the pituitary entirely. CJC-1295 no DAC is a secretagogue — it tells the pituitary to release its own GH. This distinction matters because: (1) the pituitary's own GH release is subject to negative feedback from elevated IGF-1, which acts as a natural safety mechanism; (2) pulsatile GH release from a functioning pituitary is more physiologically appropriate than continuous supraphysiological exposure from exogenous HGH; (3) CJC-1295 no DAC is significantly less potent than exogenous HGH at comparable research doses.

Is CJC-1295 no DAC legal in India?

CJC-1295 no DAC is not an approved pharmaceutical in India and is not listed as a scheduled substance under the Drugs and Cosmetics Act 1940. It is available as a research compound for laboratory use. PEPTIGRID carries it from two GMP-certified manufacturers — see our Denik Pharm and Gold Bond Labs product pages. See our introductory peptide guide for a fuller discussion of the Indian regulatory context for research peptides.