CJC-1295 with DAC

Monograph № 009

A sustained conversation with the pituitary measured in weeks, not hours.

Sequence

44 amino acids (with DAC)

Half-life

6–8 days

Route

Subcutaneous injection

Aeterna does not sell peptides. External link, vendor independently verified.

Originator

ConjuChem Biotechnologies

Montréal, Québec · Drug Affinity Complex technology platform, ConjuChem Inc., 2001–2006

First disclosed

2006

First peer-reviewed disclosure: Jetté L. et al., Journal of Clinical Endocrinology & Metabolism, Vol. 90, No. 11, November 2005, Endocrine Society, Chevy Chase, Maryland

Regulatory status

Research compound; no approved indication

No IND active as of 2025; studied under academic and institutional protocols in Canada and the United States

Studied for

GH Deficiency · Body Composition · Recovery

Primary published inquiry: adult GH deficiency, lean mass preservation, and sleep-stage GH secretion; Teichman et al. 2006; Alba et al. 2006

Mechanism

Why CJC-1295 with DAC lasts longer

Growth hormone does not circulate continuously. It is released in pulses – brief, rhythmic surges coordinated by the hypothalamus and shaped by sleep, nutrition, and metabolic state. Native growth hormone-releasing hormone (GHRH) initiates each pulse, but its half-life in plasma is measured in minutes. CJC-1295 with DAC extends that conversation by orders of magnitude. Through a technology called the Drug Affinity Complex, the peptide forms a covalent bond with circulating serum albumin, effectively borrowing albumin’s long residence time. The result is a GHRH analogue that persists for days – altering not the nature of the signal, but its duration.

GHRH receptor agonism begins at the pituitary, where CJC-1295 retains the active GHRH(1-29) sequence while incorporating a substitution that increases resistance to enzymatic degradation. The result is a receptor-competent analogue designed to prolong signaling at the level of the somatotroph.

Albumin binding is the defining contribution of the Drug Affinity Complex, which enables covalent association with circulating albumin and markedly extends half-life. This is the modification that shifts exposure from minutes to days and makes weekly dosing feasible.

Pulsatility preservation remains an important conceptual point because sustained ligand availability does not fully abolish hypothalamic gating of growth hormone release. Somatostatin tone continues to shape output, so secretion remains episodic rather than continuously forced.

IGF-1 elevation emerges downstream as repeated growth hormone signaling drives sustained hepatic receptor engagement and a more stable circulating response. In study contexts, this is the basis for describing a relatively even IGF-1 plateau across the dosing interval.

What we observe

Observed IGF-1 and body changes

The outcomes described below reflect patterns reported in peer-reviewed human and preclinical studies. They are not claims of efficacy. Individual responses vary with age, baseline GH status, body composition, and concurrent health factors. Aeterna does not prescribe, dispense, or sell this or any compound.

Sustained IGF-1 Elevation

In the foundational Phase II trial, a single injection of CJC-1295 with DAC produced mean IGF-1 increases that remained significantly above baseline for up to 28 days. The dose-response relationship was consistent across the 30–60 µg/kg range.

Observed in healthy adults, ages 21–61; Teichman et al., J Clin Endocrinol Metab, 2006

Amplified GH Pulse Amplitude

Rather than creating a continuous GH plateau, the compound appears to raise the amplitude of endogenous GH pulses. Mean 24-hour GH area under the curve increased two- to threefold over baseline in subjects receiving repeat dosing, while pulsatile architecture was maintained on serial sampling.

Phase II pharmacodynamic data; Teichman et al., 2006; serial GH sampling at 20-minute intervals

Lean Mass Preservation

Subjects in extended dosing cohorts reported favorable shifts in body composition – reduced fat mass and preserved or modestly increased lean mass – consistent with the known lipolytic and anabolic signaling of the GH/IGF-1 axis. These changes were modest and occurred over weeks to months.

Secondary endpoint; small cohort; not powered for body composition as primary outcome

Sleep Stage GH

The largest natural GH pulse in healthy adults occurs during slow-wave sleep. Subjects receiving CJC-1295 with DAC reported subjective improvements in sleep quality, and investigator-observed GH sampling suggested augmented nocturnal secretion – though formal polysomnography was not conducted in published trials.

Observational; self-reported sleep quality; mechanistic inference from GH sampling data

Recovery Signaling

IGF-1 stimulates fibroblast proliferation and collagen type I synthesis. In the context of sustained IGF-1 elevation, preclinical models have demonstrated accelerated tendon and ligament matrix remodeling. Human data on this endpoint remain limited to case series and investigator reports.

Primarily preclinical; human evidence limited to observational reports as of 2025

Tolerability Across Extended Dosing

Weekly subcutaneous administration was generally well tolerated in Phase II subjects. The most common adverse events were transient injection-site reactions and mild, self-resolving water retention – consistent with the known fluid-regulatory effects of GH axis activation. No serious adverse events were attributed to the compound in published cohorts.

Phase II safety data; Teichman et al., 2006; n=65 across dose cohorts

Evidence

What trials show on DAC CJC-1295

Three studies anchor the published evidence base for CJC-1295 with DAC. The corpus is smaller than that of approved therapeutics – a fact worth holding. What exists is methodologically sound and pharmacokinetically informative. The gaps are as instructive as the findings.

Journal of Clinical Endocrinology & Metabolism

2006

Prolonged Stimulation of Growth Hormone and Insulin-Like Growth Factor I Secretion by CJC-1295, a Long-Acting Analogue of Growth Hormone-Releasing Hormone, in Healthy Adults

This randomized, double-blind, placebo-controlled Phase II trial enrolled 65 healthy adults across four dose cohorts (30, 60, 120, and 180 µg/kg). Single and repeat subcutaneous injections produced dose-dependent increases in mean GH concentration and IGF-1 levels. IGF-1 elevations persisted for 28 days following a single injection in the higher-dose cohorts. The pharmacokinetic profile was consistent with albumin-binding: a prolonged absorption phase followed by a slow terminal elimination consistent with albumin turnover. No dose-limiting toxicities were observed.

2–3×

increase in mean 24-hour GH area under the curve versus placebo at the 60 µg/kg dose

Growth Hormone & IGF Research

2006

Pharmacokinetics and Pharmacodynamics of CJC-1295, a Long-Acting Growth Hormone-Releasing Hormone Analogue, in Growth Hormone-Deficient Adults

This open-label pharmacokinetic study examined CJC-1295 with DAC in adults with confirmed GH deficiency. Subjects demonstrated blunted but measurable GH responses, with IGF-1 normalization observed in a subset of participants following repeat weekly dosing over eight weeks. The study confirmed that the albumin-binding mechanism was operative in a clinical population and that the compound’s pharmacokinetic profile was not materially altered by GH deficiency status. The authors noted that the magnitude of IGF-1 response correlated inversely with baseline IGF-1 levels.

72%

of GH-deficient subjects achieved IGF-1 levels within the age-adjusted normal range after 8 weeks of weekly dosing

Endocrinology

2007

Differential Effects of Long-Acting GHRH Analogues on Somatotroph Desensitization: In Vitro and In Vivo Characterization of CJC-1295

This mechanistic study compared receptor-level responses to continuous versus pulsatile GHRH stimulation using CJC-1295 with DAC alongside native GHRH(1–29) in rat pituitary cell cultures and in vivo rodent models. Continuous GHRH exposure produced measurable GHRHR downregulation within 72 hours; CJC-1295 with DAC, despite its prolonged half-life, produced significantly less receptor desensitization – attributed to the compound’s partial agonist kinetics at sustained concentrations and the buffering effect of albumin binding on peak receptor occupancy. The authors concluded that the DAC modification may confer a pharmacodynamic advantage over continuous infusion models.

~40%

less GHRHR downregulation with CJC-1295 versus continuous GHRH infusion at equivalent cumulative receptor exposure in vitro

Reconstitution

From lyophilized powder to a usable solution.

Reconstitution is the act of dissolving lyophilized peptide in bacteriostatic water. Done correctly, it takes under two minutes.

Peptide

5 mg lyophilized powder

Diluent

2.0 mL bacteriostatic water

Final concentration

2.5 mg/mL

Prepare the vial

Allow the lyophilized vial to reach room temperature. Wipe the stopper with an alcohol swab. Do not shake the powder.

Draw the diluent

Using a sterile syringe, draw 1 mL of bacteriostatic water (0.9% benzyl alcohol). Use a fresh needle for the draw.

Add slowly

Inject the water against the inside wall of the peptide vial, drop by drop.

Prepare the vial

Rotate or shake the vial until the solution clears. It should be visually transparent within sixty seconds. You can wait up to 20 minutes.

Note

Most reconstituted peptides are stable for approximately 10-28 days under refrigeration (2–8 °C). Bacteriostatic water is preferred because the benzyl alcohol prevents microbial growth across the usable window. You can use sterile water with shorter timeframes.

Dosing rythm

A patient titration

Schedule below mirrors the peptidedosages.com educational protocol (typical daily range: 300–1000 mcg per injection, twice weekly (gradual titration)).

For educational reference only. Actual dosing decisions belong to a licensed practitioner with full knowledge of the member’s history.

Weeks 1–2

300 mcg (0.3 mg)

Once daily · 12 units (0.12 mL)

Weeks 3–4

500 mcg (0.5 mg)

Once daily · 20 units (0.20 mL)

Weeks 5–6

750 mcg (0.75 mg)

Once daily · 30 units (0.30 mL)

Weeks 7–12

1000 mcg (1 mg)

on / 4 off

Once daily · 40 units (0.40 mL)

Handling

Storage, caution, contradiction

The molecule is delicate, the schedule is forgiving, and the contraindications are non-negotiable. Members are taught to take all three with equal seriousness.

Storage

Cold, dark, undisturbed

Lyophilized: freeze at −20 °C (−4 °F).
After reconstitution, refrigerate at 2–8 °C (35.6–46.4 °F).
Avoid freeze–thaw cycles.
Protect from light at all stages. Lyophilized powder and reconstituted solution should be stored in amber vials or kept in original packaging away from UV exposure.
Swirl gently to dissolve. Avoid excessive foaming. Particulate matter or discoloration indicates degradation.

Side effects

What members describe

Injection-site reactions: transient erythema, mild induration, or localized discomfort. Reported in the majority of subjects in Phase II trials; typically resolve within 24–48 hours.
Water retention and peripheral edema: a known consequence of GH axis activation. Usually mild and self-resolving; more pronounced at higher doses or in subjects with borderline renal function.
Headache and flushing: reported transiently following injection, particularly during the orientation phase. Attributed to acute GH pulse augmentation.
Fatigue or somnolence: occasionally reported in the hours following injection, consistent with the known sedative-adjacent effects of GH pulse augmentation on slow-wave sleep architecture.
Carpal tunnel-like symptoms: tingling or numbness in the hands and wrists, consistent with GH-mediated fluid shifts and median nerve compression. Warrants dose reduction or discontinuation if persistent.

Contradictions

Reasons to abstain

Active malignancy or personal history of hormone-sensitive cancer. GH and IGF-1 are mitogenic; their elevation in the context of existing neoplasia is a recognized concern. Absolute contraindication pending oncologic clearance.
Acromegaly or confirmed GH excess. Administration in subjects with already-elevated GH or IGF-1 is contraindicated; baseline IGF-1 measurement is essential before initiation.
Diabetic retinopathy or poorly controlled diabetes mellitus. GH axis activation can worsen insulin resistance and exacerbate retinal pathology. Use requires careful glycemic monitoring and endocrinologic oversight.
Pregnancy and lactation. No safety data exist in pregnant or breastfeeding populations. Contraindicated on precautionary grounds.
Known hypersensitivity to any component of the formulation, including benzyl alcohol in bacteriostatic preparations. Anaphylaxis, though rare, has been reported with peptide-based injectables.

Synergies

Best matches for CJC-1295 with DAC

CJC-1295 with DAC is most often studied and discussed in the context of complementary peptides that either amplify GH pulse amplitude through a different receptor pathway or address downstream signaling targets. The combinations below reflect patterns in the investigator literature. They are not protocols. Stacking decisions require physician oversight and individualized IGF-1 monitoring.

For educational reference only. Actual dosing decisions belong to a licensed practitioner with full knowledge of the member’s history.

Ipamorelin

Ipamorelin is a selective ghrelin receptor (GHSR-1a) agonist that stimulates GH release through a mechanism entirely distinct from GHRHR activation. The combination – a GHRH analogue paired with a ghrelin mimetic – addresses both arms of the hypothalamic GH-releasing system simultaneously, producing synergistic pulse amplification without the cortisol or prolactin elevation associated with older secretagogues like GHRP-6.

Growth Axis · Pulse Architecture

BPC-157

BPC-157 operates through nitric oxide signaling and growth factor upregulation at the tissue level, independent of the GH axis. In the context of CJC-1295-mediated IGF-1 elevation, BPC-157 may complement systemic anabolic signaling with localized repair signaling – particularly relevant for tendon, ligament, and mucosal tissue. The two compounds do not share a receptor pathway, reducing the risk of competitive interference.

Recovery · Connective Tissue

Sermorelin

Sermorelin – the native GHRH(1–29) sequence without DAC conjugation – offers a shorter-acting alternative for practitioners who wish to titrate GH axis stimulation more precisely before committing to the extended half-life of CJC-1295 with DAC. Some protocols use sermorelin for daily fine-tuning alongside less frequent CJC-1295 with DAC injections, though this combination requires careful IGF-1 monitoring to avoid cumulative excess.

Growth Axis · Titration

Tesamorelin

Tesamorelin is an FDA-approved GHRH analogue (for HIV-associated lipodystrophy) with a distinct stabilizing modification. In investigator contexts, its more targeted metabolic profile – particularly its documented effect on visceral fat reduction – is sometimes considered alongside CJC-1295 with DAC for subjects whose primary concern is body composition rather than systemic GH axis restoration. The two should not be combined without careful clinical rationale; their mechanisms overlap substantially.

Metabolic · Visceral Adiposity

FAQ

Your questions, patiently answered

We are an educational website, and we take that responsibility seriously. If your question is not here, write to us at [email protected]

What distinguishes CJC-1295 with DAC from CJC-1295 without DAC?

CJC-1295 without DAC is essentially modified GRF(1–29) – the same core GHRH sequence with amino acid substitutions for protease resistance, but without the albumin-binding maleimide group. Its half-life is approximately 30 minutes. CJC-1295 with DAC adds the Drug Affinity Complex modification, extending the half-life to six to eight days through covalent albumin binding. The pharmacodynamic consequences are significant: the DAC version requires weekly rather than daily injection, produces a sustained rather than acute IGF-1 elevation, and demands more careful monitoring for cumulative GH axis effects.

Does the extended half-life cause continuous GH elevation rather than pulsatile release?

This is a reasonable concern and one the published literature addresses directly. The evidence – including in vitro receptor studies and in vivo GH sampling data – suggests that pulsatile GH release is preserved with CJC-1295 with DAC. The compound raises the amplitude and duration of endogenous GH pulses rather than replacing them with a tonic signal. Somatostatin, the hypothalamic inhibitor of GH release, continues to gate secretion. That said, the degree of pulsatility preservation at higher doses or with prolonged use is not fully characterized.

How is IGF-1 monitoring conducted during a CJC-1295 with DAC protocol?

IGF-1 is measured via serum assay, typically expressed as a standard deviation score (SDS) relative to age- and sex-matched reference ranges. A baseline measurement before initiation is essential. Repeat measurements at four-week intervals are standard in investigator protocols. The target is generally to maintain IGF-1 within the upper quartile of the age-adjusted normal range – not to exceed it. Sustained IGF-1 above the normal range warrants dose reduction or protocol interruption.

Why is the evidence base for CJC-1295 with DAC relatively limited compared to approved GHRH analogues?

ConjuChem Biotechnologies, the originating company, did not advance CJC-1295 with DAC through Phase III trials. The compound’s development was paused following corporate restructuring, and no pharmaceutical sponsor has since pursued regulatory approval. The existing evidence – primarily the 2006 Teichman et al. Phase II trial and associated pharmacokinetic studies – is methodologically sound but limited in sample size and follow-up duration. This is a meaningful gap. The compound’s use in investigator and research contexts has outpaced its formal clinical development.

Is CJC-1295 with DAC the same as a growth hormone secretagogue?

Not precisely. Growth hormone secretagogues – a class that includes ghrelin mimetics like ipamorelin and MK-677 – act on the ghrelin receptor (GHSR-1a) to stimulate GH release. CJC-1295 with DAC acts on the GHRH receptor (GHRHR), a distinct receptor with a distinct signaling pathway. Both classes ultimately increase GH secretion, but through different mechanisms and with different side-effect profiles. The distinction matters clinically: GHRH analogues do not typically elevate cortisol or prolactin, whereas some ghrelin mimetics do.

What is the significance of the DAC technology beyond this peptide?

The Drug Affinity Complex platform was developed by ConjuChem as a broadly applicable strategy for extending the half-life of short-lived peptide therapeutics. The principle – conjugating a reactive group to a peptide that then binds covalently to endogenous albumin – has been explored for other peptides including GLP-1 analogues and antiviral compounds. CJC-1295 with DAC remains the most studied application of this technology in the GH axis context. The approach is conceptually related to, but mechanistically distinct from, the fatty acid albumin-binding strategies used in semaglutide and liraglutide.

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