CJC-1295 DAC Peptide Research – Complete Guide

Table of Contents

• Quick Facts
• What is CJC-1295 DAC?
• Molecular Structure and Core Properties
• Mechanisms of Action Being Investigated
• Major Areas of Research
• Pharmacokinetics and Biological Distribution
• Research Limitations and Evidence Gaps
• Regulatory and Research Status
• Key Research Findings
• Frequently Asked Questions
• References

Quick Facts (Research Snapshot)

• Primary Research Areas: Growth hormone secretion, IGF-1 axis modulation, metabolic research, body composition studies, GH deficiency models
• Developed By: ConjuChem Biotechnologies (mid-2000s)
• Molecular Weight: 3,647.8 g/mol
• CAS Number: 863288-34-0
• Amino Acid Count: 30 amino acids (modified GHRH 1-29 with DAC-lysine at C-terminus)
• Half-Life (Native GHRH): Approximately 7 minutes
• Half-Life (CJC-1295 DAC, human clinical data): 5.8 to 8.1 days
• Key Mechanisms: GHRH receptor activation, cAMP-PKA signaling, albumin-bound reservoir delivery, DPP-IV resistance
• Published Clinical Trials: Two randomized, placebo-controlled, double-blind Phase I trials in healthy adults (Teichman et al., 2006)
• Clinical Trial Status: Phase I completed; no Phase II or III trials published to date
• Regulatory Classification: Research use only; not approved for human therapeutic use by FDA or EMA

What is CJC-1295 DAC?

CJC-1295 DAC is a synthetic peptide analog of growth hormone-releasing hormone (GHRH), the hypothalamic signal that instructs the pituitary gland to release growth hormone (GH). The native form of GHRH degrades in blood within roughly seven minutes, making sustained GH stimulation through natural GHRH impractical for research or therapeutic applications. CJC-1295 DAC was engineered by ConjuChem Biotechnologies to solve that problem by attaching a chemical modification called a Drug Affinity Complex, or DAC, to the peptide’s C-terminal lysine residue.

The DAC modification enables the peptide to form a covalent bond with cysteine-34 of serum albumin, the most abundant protein in human blood. Once bound to albumin, the peptide circulates as a stable bioconjugate that resists enzymatic degradation and is cleared from the body at the same slow rate as albumin itself. The result is a plasma half-life of 5.8 to 8.1 days in human clinical studies, representing a greater than 1,000-fold extension compared to native GHRH [1].

CJC-1295 DAC belongs to the broader class of growth hormone secretagogues, compounds that stimulate the body’s own GH-producing cells rather than supplying exogenous GH directly. Unlike synthetic GH, GHRH analogs work upstream in the hormonal cascade, preserving the pituitary’s natural regulatory role. This distinction attracted significant preclinical and early clinical research interest beginning in the early 2000s.

Phase I human clinical trials published in 2006 established the compound’s pharmacokinetic profile and demonstrated dose-dependent GH and IGF-1 elevation in healthy adults lasting well beyond a single weekly injection [1]. These findings established CJC-1295 DAC as a reference compound for extended-release GHRH analog research. Subsequent preclinical work explored applications in GH deficiency models, body composition research, and metabolic studies across rodent and canine models.

All published research treats CJC-1295 DAC as a laboratory research compound. It has not advanced to Phase II or Phase III human clinical trials, and no regulatory authority has approved it for therapeutic use. Researchers studying the GH-IGF-1 axis, extended-release peptide delivery, or metabolic regulation use CJC-1295 DAC as a tool for controlled experimental investigation.

Molecular Structure and Core Properties

Chemical Structure and Specifications

Key Structural Features

CJC-1295 DAC differs from native GHRH at four amino acid positions. D-alanine replaces L-alanine at position 2, glutamine replaces serine at position 8, alanine replaces glycine at position 15, and leucine replaces methionine at position 27. These four substitutions collectively resist proteolytic cleavage by enzymes that rapidly degrade the native hormone in plasma [1].

The defining structural element is the C-terminal lysine modified with an N-epsilon-3-maleimidopropionamide group, the DAC component itself. This reactive maleimide moiety forms a covalent thioether bond with the free sulfhydryl group on cysteine-34 of circulating serum albumin shortly after injection. The resulting peptide-albumin bioconjugate is the pharmacologically active circulating form of the compound.

The D-alanine substitution at position 2 confers specific resistance to dipeptidyl peptidase-IV (DPP-IV), the enzyme responsible for cleaving the first two residues from GHRH and rapidly inactivating it. Together, the four amino acid substitutions and the albumin-binding DAC modification create a molecule that retains high GHRH receptor selectivity while surviving in the circulation long enough to produce sustained hormonal effects [1,2].

Mechanisms of Action Being Investigated

CJC-1295 DAC activates the growth hormone-releasing hormone receptor on pituitary somatotroph cells, triggering an intracellular signaling cascade that elevates GH secretion. The DAC modification extends this receptor stimulation over days rather than minutes by creating a circulating peptide reservoir bound to serum albumin.

GHRH Receptor Activation and cAMP Signaling

CJC-1295 DAC binds selectively to GHRH receptors (GHRHR), G-protein-coupled receptors expressed on anterior pituitary somatotroph cells. Receptor binding activates adenylyl cyclase, the enzyme that converts ATP to cyclic AMP (cAMP). Elevated intracellular cAMP activates protein kinase A (PKA), which phosphorylates transcription factors including CREB. Phosphorylated CREB drives transcription of the GH1 gene and related somatotroph proteins, resulting in dose-dependent GH synthesis and secretion [1,3].

IGF-1 Axis Activation

GH released from pituitary somatotrophs enters systemic circulation and binds hepatic GH receptors. This activates the JAK-STAT signaling pathway in liver cells, driving insulin-like growth factor 1 (IGF-1) synthesis and secretion. IGF-1 then activates its own receptor tyrosine kinase, triggering both PI3K/Akt and MAPK/ERK downstream pathways. These pathways regulate protein synthesis, glucose metabolism, lipid utilization, and cell proliferation across multiple tissue types [1,4].

Human clinical trials confirmed that a single dose of CJC-1295 DAC elevates IGF-1 by 1.5- to 3-fold above baseline for 9 to 11 days. With repeated dosing, IGF-1 remained elevated above baseline for up to 28 days [1].

DAC Albumin-Binding Technology

The maleimidopropionamide group on CJC-1295 DAC’s C-terminal lysine reacts with cysteine-34 of serum albumin within minutes of subcutaneous injection. The bond formed is a covalent thioether linkage, making the peptide-albumin complex stable under physiological conditions. Albumin has a half-life of approximately 19 days in humans, and the bound peptide benefits from this extended circulatory lifespan.

Albumin binding provides two protective effects simultaneously. First, the large albumin molecule physically shields the peptide from proteolytic enzymes circulating in plasma. Second, albumin’s excluded volume limits glomerular filtration, preventing rapid renal clearance. Together these effects extend the peptide’s effective half-life from approximately 7 minutes to 5.8 to 8.1 days [1]. No significant binding to other plasma proteins has been reported in published research.

Pulsatile GH Secretion Preservation

A pharmacodynamically significant finding from clinical research is that the pituitary continues to release GH in pulses during sustained CJC-1295 DAC stimulation. Ionescu and Frohman confirmed this in a 2006 study using frequent blood sampling to characterize GH secretory patterns [2]. Pulsatile release is important because continuous receptor occupancy by a GH secretagogue can theoretically desensitize pituitary somatotrophs. The preservation of pulse architecture suggests that pituitary regulatory feedback mechanisms remain partially operative even under sustained GHRHR stimulation.

Researchers note this distinguishes CJC-1295 DAC from continuous GH infusion, which suppresses endogenous pulsatility. However, the risk of receptor downregulation with very prolonged administration is an acknowledged concern in the literature, particularly when contrasting this compound with shorter-acting analogs like CJC-1295 without DAC [3].

Somatotroph Cell Effects in Deficiency Models

Preclinical research in GHRH knockout mice, which lack endogenous GHRH production and have underdeveloped pituitary somatotroph populations, showed that chronic CJC-1295 DAC administration increased total pituitary RNA content, GH mRNA expression, and apparent somatotroph cell number. These mice showed normalization of pituitary structure following treatment [4]. Effects were frequency-dependent, with daily administration producing greater restoration than intermittent dosing. These findings are confined to GH-deficient animal models and have not been replicated in normal human subjects.

Hormonal Selectivity

Clinical trial data confirmed that CJC-1295 DAC selectively activates the GH-IGF-1 axis without significantly elevating prolactin, cortisol, or ACTH in healthy adults at doses of 30 to 60 mcg/kg. This selectivity reflects the specificity of the GHRHR for its cognate ligand and distinguishes GHRH analogs from broader-spectrum GH secretagogues [1].

Major Areas of Research

CJC-1295 DAC research spans GH deficiency models, body composition studies, metabolic research, aging biology, and extended-release peptide delivery pharmacology. Most published work uses animal models or human Phase I data. No controlled human efficacy trials in disease states have been published.

Growth Hormone Deficiency Research

The most direct application for CJC-1295 DAC research is GH deficiency, where inadequate pituitary output causes impaired growth, altered body composition, and metabolic dysregulation. The compound’s ability to stimulate endogenous GH production makes it mechanistically distinct from recombinant GH replacement.

Alba et al. (2006) demonstrated that once-daily administration in GHRH knockout mice restored pituitary somatotroph populations, normalized body weight gain relative to controls, and corrected GH and IGF-1 deficits [4]. The frequency-dependence of these effects, greater restoration with daily versus intermittent dosing, informed subsequent research designs.

Human Phase I data confirmed GH and IGF-1 elevation in healthy adults, providing pharmacokinetic proof-of-concept for eventual deficiency trials. However, no published Phase II or III trials in GH-deficient patients exist as of current literature review.

Key Research Highlights:

• Pituitary somatotroph normalization in GHRH knockout mouse models
• Dose-dependent GH and IGF-1 elevation sustained over 6 to 11 days in healthy humans
• Cross-species pharmacodynamic confirmation in rats, dogs, and pigs

Body Composition and Metabolic Research

GH and IGF-1 both influence body composition through their effects on protein synthesis, lipolysis, and insulin sensitivity. CJC-1295 DAC’s ability to sustain GH elevation for days from a single dose makes it a useful research tool for studying these metabolic effects without requiring daily interventions.

Animal studies showed reduced body fat and increased lean mass in GH-deficient rodent models following CJC-1295 DAC treatment [4]. Researchers use these models to study how GH axis activation affects lipid mobilization from adipose tissue, protein accretion in skeletal muscle, and glucose utilization in peripheral tissues.

Sustained IGF-1 elevation is of particular interest in muscle biology research, as IGF-1 drives satellite cell activation, protein synthesis through Akt/mTOR signaling, and muscle fiber hypertrophy in animal models. The 28-day IGF-1 elevation observed with repeated dosing in human volunteers provides an extended window for studying these anabolic signaling effects [1].

Key Research Highlights:

• Reduced adiposity and normalized lean mass in GH-deficient animal models
• Sustained IGF-1 elevation providing a prolonged anabolic signaling window for metabolic studies
• Cross-species GH and IGF-1 dose-response relationships established in rats, dogs, and pigs

Extended-Release Peptide Delivery Research

CJC-1295 DAC serves as a proof-of-concept model for albumin-binding peptide delivery beyond GH biology. The DAC technology platform itself is a subject of pharmaceutical research interest, representing one approach to extending the effective half-life of otherwise short-lived therapeutic peptides.

The pharmacokinetic properties of CJC-1295 DAC, particularly the pharmacodynamic disconnect between drug elimination and biological effect (IGF-1 elevation persisting beyond detectable peptide concentrations), illustrate important principles of depot-release pharmacology. Researchers studying long-acting biologics use this compound as a reference for understanding how albumin bioconjugation affects distribution, elimination, and downstream signaling kinetics [1].

Key Research Highlights:

• Greater than 1,000-fold half-life extension via covalent albumin binding established as research proof-of-concept
• Pharmacodynamic effects persist beyond detectable plasma peptide, suggesting continued bioactivity of albumin-bound reservoir
• DPP-IV resistance through D-alanine substitution demonstrated as a replicable structural strategy

Aging and GH Axis Research

GH and IGF-1 concentrations decline with age, a phenomenon linked to changes in body composition, bone density, immune function, and cognitive performance. CJC-1295 DAC has attracted interest as a research tool for studying whether restoring youthful GH-IGF-1 axis activity can reverse or slow age-associated changes in animal models.

Preclinical studies in aged rodents have examined whether GHRH analog treatment can restore muscle mass, reduce adiposity, or improve measures of physical performance. These studies remain in early stages, with most published work focusing on pharmacodynamic characterization rather than comprehensive outcome measurement. Human aging research using CJC-1295 DAC has not been published in peer-reviewed literature beyond the Phase I safety and pharmacokinetics data [1,4].

Key Research Highlights:

• GH and IGF-1 decline with aging established as the biological rationale for GHRH analog research in this area
• Preclinical models suggest potential for body composition improvements in GH-deficient states
• Human aging efficacy data absent from published literature

Pituitary Biology and Receptor Pharmacology

CJC-1295 DAC provides researchers with a long-acting GHRHR agonist for studying pituitary somatotroph biology, receptor desensitization dynamics, and GH pulse generation mechanisms. The ability to maintain sustained GHRHR stimulation without suppressing all pulsatility makes it a nuanced pharmacological tool.

Ionescu and Frohman’s pulsatility study used CJC-1295 DAC to probe how the pituitary integrates tonic receptor stimulation with its intrinsic GH pulse-generating circuitry [2]. This research area contributes to understanding the regulation of neuroendocrine axes more broadly, with implications for research into other hypothalamic-pituitary systems.

Key Research Highlights:

• Pulsatile GH secretion maintained during sustained GHRHR stimulation, distinguishing this compound from continuous GH infusion
• Receptor desensitization studied as a function of dosing frequency in animal models
• Pituitary somatotroph proliferation confirmed in deficiency models, raising questions about long-term gland effects

Pharmacokinetics and Biological Distribution

Absorption and Bioavailability

CJC-1295 DAC has been administered by subcutaneous injection in all published human clinical trials. Albumin bioconjugation occurs rapidly after injection as the maleimide DAC group reacts with circulating albumin. The rate of this conjugation step has not been reported precisely in public literature, but GH elevation is detectable within hours of injection, consistent with rapid systemic absorption and albumin binding [1].

No oral or intranasal bioavailability data for CJC-1295 DAC has been published. Peptides of this size and complexity are generally degraded in the gastrointestinal tract before systemic absorption.

Distribution and Metabolism

Once bound to serum albumin, CJC-1295 DAC distributes throughout the vascular compartment following albumin kinetics. The volume of distribution approximates plasma volume, reflecting the albumin-restricted distribution pattern. Tissue penetration is likely limited compared to smaller, unbound peptides, as albumin does not cross most biological membranes freely.

The extended half-life of 5.8 to 8.1 days reflects albumin turnover kinetics rather than rapid peptide degradation. Proteolytic breakdown is significantly reduced by both the structural amino acid modifications and the physical shielding provided by albumin binding. DPP-IV, the primary enzyme responsible for GHRH degradation, cannot readily cleave the modified N-terminus of CJC-1295 DAC [1,2].

Delivery Methods Under Investigation

• Subcutaneous injection: Standard route in all human clinical trials; rapid albumin conjugation and systemic distribution confirmed
• Intraperitoneal injection: Used in rodent research models; systemic distribution and GH response confirmed across multiple animal species
• Intravenous administration: Used in some preclinical pharmacokinetic studies; not established as a preferred route in published clinical research

Excretion and Clearance

Elimination of CJC-1295 DAC from the body follows albumin catabolism pathways. Albumin is primarily degraded intracellularly following endocytosis by vascular endothelial cells and hepatocytes. Amino acid recycling from peptide degradation likely follows standard pathways. Specific excretion data for CJC-1295 DAC or its metabolites has not been published in available literature [1].

A pharmacodynamically notable feature of CJC-1295 DAC is the disconnect between plasma drug concentrations and biological effect duration. IGF-1 elevation persisting for 28 days with repeated dosing exceeds what would be expected from the 5.8 to 8.1 day half-life alone, suggesting either continued bioactivity from the albumin-bound reservoir or sustained downstream signaling that outlasts measurable peptide concentrations. This pharmacodynamic disconnect is described as a characteristic feature of the albumin bioconjugate approach [1].

Research Limitations and Evidence Gaps

Current Research Gaps

Human Clinical Data

CJC-1295 DAC has completed only Phase I trials in healthy adult volunteers. No Phase II or Phase III trials in any disease state, including GH deficiency, have been published. The available human safety data covers 28 to 49 day study periods, leaving long-term safety in humans completely uncharacterized. Optimal dosing parameters for any potential clinical application remain unknown. The high rate of adverse events at doses above 60 mcg/kg, combined with the lack of efficacy trials, creates significant uncertainty about the compound’s therapeutic index [1].

Mechanistic Understanding

The specific receptor desensitization dynamics during extended CJC-1295 DAC administration are incompletely characterized. The risk of pituitary somatotroph downregulation with prolonged use represents a theoretical concern that has not been systematically studied in humans. The relationship between sustained GH elevation and downstream tissue effects beyond IGF-1 production is not well-characterized in published human research. The pharmacodynamic disconnect between plasma half-life and IGF-1 elevation duration is documented but not mechanistically explained in detail [1,2].

Methodological Considerations

Most efficacy data comes from animal models with significant physiological differences from humans. The two published human Phase I trials enrolled relatively small numbers of healthy adults and were not designed to assess efficacy in disease states. Cross-species pharmacodynamic data from rats, dogs, and pigs supports the GH response but cannot reliably predict the magnitude or duration of effects across all human populations. Excretion pathways for the peptide and its metabolites are incompletely characterized.

Areas Needing Further Investigation

• Phase II and III trials in GH-deficient patient populations: the critical gap separating preclinical promise from clinical validation
• Long-term safety with extended administration beyond 49 days: entirely absent from published literature
• Drug interaction profiles: no published data on interactions with insulin, sex hormones, thyroid hormones, or other clinically relevant compounds
• Receptor desensitization thresholds: the point at which sustained GHRHR stimulation causes clinically meaningful somatotroph downregulation has not been established in humans
• Specific excretion pathways and metabolite characterization: relevant to safety assessment in populations with renal or hepatic impairment

Regulatory and Research Status

Current Classification

FDA Status

CJC-1295 DAC is not approved by the FDA for human therapeutic use in any indication. The compound is classified as an unapproved new drug under FDA regulations. It is available for legitimate laboratory and preclinical research purposes under appropriate institutional oversight. No IND applications for CJC-1295 DAC in advanced clinical development have been publicly reported since the original Phase I work by ConjuChem Biotechnologies.

WADA Status

The World Anti-Doping Agency prohibits CJC-1295 DAC in competitive sport. The compound falls under the prohibited list category of peptide hormones, growth factors, related substances, and mimetics, specifically as a GHRH analog. Athletes subject to anti-doping testing must not use this compound regardless of administration route or purpose.

International Perspective

The European Medicines Agency has not approved CJC-1295 DAC for human use. Across major research markets, the compound is classified as a research chemical. Regulatory status for veterinary applications varies by jurisdiction, and researchers should verify local requirements before initiating studies.

Research Community Approach

Academic and pharmaceutical researchers who study the GH-IGF-1 axis, extended-release peptide pharmacology, or growth hormone deficiency use CJC-1295 DAC as a laboratory research tool. All legitimate research requires institutional review board oversight for any human study protocols, appropriate biosafety classification for laboratory handling, and compliance with applicable national and institutional regulations governing research peptide use.

ConjuChem Biotechnologies, the original developer, pursued the compound through Phase I trials but did not advance to efficacy trials. No major pharmaceutical company has publicly disclosed continued clinical development of CJC-1295 DAC as of available literature. The DAC technology platform, however, continues to influence extended-release peptide design across the field [1].

Future Research Directions

The most consequential unmet need in CJC-1295 DAC research is a controlled efficacy trial in GH-deficient patients, a population where the compound’s mechanism of action has clear theoretical relevance. Researchers also identify aging-associated GH decline as a candidate indication for future investigation. The DAC albumin-binding platform itself may find application in other peptide therapeutics, making mechanistic research into this delivery approach independently valuable regardless of CJC-1295 DAC’s clinical future.

Key Research Findings

Phase I Pharmacokinetics and Safety: Teichman et al. (2006)

Research Focus: Dose escalation safety, pharmacokinetics, and pharmacodynamics of CJC-1295 DAC in healthy adult volunteers Key Results: Two randomized, placebo-controlled, double-blind trials in adults aged 21 to 61 years. Single doses produced 2- to 10-fold increases in plasma GH sustained for at least 6 days. IGF-1 rose 1.5- to 3-fold above baseline and remained elevated for 9 to 11 days. Multiple doses kept IGF-1 elevated for up to 28 days. Estimated half-life was 5.8 to 8.1 days. Adverse events occurred in 94% of active-treated subjects but were mild to moderate and resolved without intervention. No antibody formation, ECG changes, or clinically meaningful laboratory value shifts were observed. Significance: Established the primary pharmacokinetic dataset for CJC-1295 DAC in humans and confirmed dose-dependent GH-IGF-1 axis activation with extended duration Limitations: Healthy adults only; no GH-deficient patients; study durations of 28 to 49 days; no long-term follow-up data [1]

Pulsatility Preservation: Ionescu and Frohman (2006)

Research Focus: Characterization of GH secretory patterns during sustained CJC-1295 DAC stimulation Key Results: Frequent blood sampling in human subjects confirmed that pulsatile GH secretion persists during continuous GHRHR stimulation from CJC-1295 DAC. Pulse architecture was maintained rather than suppressed, distinguishing this compound from continuous GH infusion. Significance: Established a pharmacodynamically important distinction between CJC-1295 DAC and exogenous GH, suggesting that some degree of pituitary self-regulation is preserved under extended GHRHR agonism Limitations: Small study; characterization only, not linked to clinical outcome measurements [2]

Somatotroph Normalization in Deficiency Models: Alba et al. (2006)

Research Focus: Effects of once-daily CJC-1295 DAC on pituitary structure and function in GHRH knockout mice Key Results: Chronic administration restored somatotroph cell populations, increased total pituitary RNA and GH mRNA expression, normalized body weight gain relative to controls, and corrected GH and IGF-1 deficits in GH-deficient animals. Daily dosing outperformed intermittent dosing. Significance: Provided preclinical proof-of-concept for CJC-1295 DAC in GH deficiency, establishing the frequency-dependence of somatotroph restoration as a relevant pharmacodynamic variable Limitations: GHRH knockout mouse model; results not replicable to human GH deficiency without clinical confirmation [4]

Cross-Species Pharmacodynamic Confirmation

Research Focus: Dose-dependent GH and IGF-1 responses across multiple species Key Results: Animal studies in rats, dogs, and pigs all confirmed dose-dependent GH elevation and sustained IGF-1 responses following CJC-1295 DAC administration. Response magnitudes and durations varied by species but were directionally consistent. Significance: Cross-species pharmacodynamic data strengthened confidence in the mechanism prior to human trials and supported the hypothesis that albumin-binding kinetics drive the extended response regardless of species Limitations: Cross-species extrapolation carries inherent uncertainty; dose-response relationships differ significantly across species and cannot be directly applied to human dosing contexts [1,4]

Hormonal Selectivity Confirmation

Research Focus: Assessment of off-target hormonal activation in human Phase I trials Key Results: CJC-1295 DAC administration at doses of 30 to 60 mcg/kg produced no significant elevations in prolactin, cortisol, or ACTH. GH and IGF-1 axis activation was selective. Significance: Selectivity data reduces concern about non-GH hormonal perturbation and supports the specificity of the GHRHR agonist mechanism in humans Limitations: Assessed only in healthy adults at specific dose ranges; selectivity at higher doses or in patient populations with altered pituitary function is not established [1]

Adverse Event Profile at Phase I Doses

Research Focus: Safety characterization and adverse event frequency at multiple dose levels Key Results: Mild to moderate adverse events occurred in 94% of actively treated subjects versus 29% of placebo subjects. Injection site reactions including erythema, induration, and pain occurred in approximately 70% of subjects. Headache occurred in 63% and diarrhea in 43%. Systemic vasodilatory effects including flushing and transient hypotension occurred in approximately 30%. All events resolved spontaneously. Rates and severity were higher at doses of 125 to 250 mcg/kg, with 30 to 60 mcg/kg identified as the better-tolerated range. Significance: Characterizes the tolerability profile relevant to future clinical development and research protocol design Limitations: Short observation window; no long-term safety data; healthy adult population only [1]

Frequently Asked Questions

What is CJC-1295 DAC?

CJC-1295 DAC is a synthetic peptide designed to stimulate the pituitary gland to release growth hormone. It is a modified version of the body’s own growth hormone-releasing hormone, engineered with a chemical attachment called a Drug Affinity Complex that allows it to bind to a blood protein called albumin, dramatically extending how long it remains active in the body.

How long has CJC-1295 DAC been studied?

CJC-1295 DAC was developed by ConjuChem Biotechnologies in the mid-2000s. The landmark human clinical trials were published in 2006, and preclinical animal research was conducted around the same period. Research on the compound has continued in laboratory settings since then, though no major new human clinical trials have been published since the original Phase I studies.

What makes CJC-1295 DAC different from regular CJC-1295?

The key difference is the DAC modification. CJC-1295 without DAC has a plasma half-life of approximately 30 minutes to 2 hours, while the DAC version extends this to 5.8 to 8.1 days by binding to serum albumin in the bloodstream. This produces a much longer window of growth hormone and IGF-1 elevation from a single dose compared to the non-DAC version.

What did human research studies find about CJC-1295 DAC?

Published Phase I clinical trials in healthy adults found that a single dose elevated plasma growth hormone by 2- to 10-fold for at least 6 days, and raised IGF-1 by 1.5- to 3-fold for 9 to 11 days. With repeated doses, IGF-1 remained elevated for up to 28 days. Adverse events were mostly mild and resolved without treatment, though they occurred in the majority of study participants. No Phase II or Phase III efficacy trials in disease states have been published.

Is CJC-1295 DAC approved for human use?

No. CJC-1295 DAC is not approved by the FDA, EMA, or any major regulatory authority for human therapeutic use. It is prohibited by the World Anti-Doping Agency for use in competitive sports. It is classified as a research-use-only compound, and all published research treats it in that context.

References

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2. Ionescu, M., & Frohman, L.A. (2006). Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. Journal of Clinical Endocrinology & Metabolism, 91(12), 4792-4797. PubMed

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