Mechanism

How it works

CJC-1295 with DAC binds to and activates GHRH receptors on pituitary somatotroph cells, stimulating pulsatile release of growth hormone. The DAC moiety — a maleimidoproprionic acid (MPA) linker — reacts with a lysine residue on serum albumin via a Michael addition, creating a covalent bond that prevents rapid renal clearance and proteolytic degradation. This albumin binding extends the half-life to approximately 6–8 days, resulting in sustained, supraphysiologic GH and IGF-1 elevation compared to native GHRH.

Reported in research

Benefits

Sustained elevation of endogenous growth hormone and IGF-1 levels over 1–2 weeks per dose
Potential improvements in lean muscle mass and reductions in adipose tissue with prolonged use
Enhanced recovery from exercise and tissue repair via IGF-1-mediated anabolic signaling
Improved sleep quality and slow-wave sleep depth, which correlates with natural GH release patterns

Context, not a prescription

Dosing

Typical range: 1–2 mg per week (research protocols often use ~1 mg once or twice weekly) (Subcutaneous, Intramuscular)
Cycle length: 8–12 weeks, followed by a break of equal duration
Half-life: ~6–8 days

Safety

Side effects & contraindications

Possible side effects

Water retention and mild edema, particularly in extremities
Flushing and transient warmth or tingling at injection site
Headaches, often occurring shortly after administration
Potential for sustained GH elevation leading to joint pain or stiffness
Hypoglycemia risk if combined with insulin sensitizers
Possible suppression of natural GHRH pulsatility with prolonged use

Contraindications

Active or history of hormone-sensitive cancers (GH and IGF-1 may promote tumor growth)
Acromegaly or pre-existing GH hypersecretion disorders
Pregnancy or breastfeeding
Diabetes mellitus or significant insulin resistance (GH can worsen glycemic control)
Pediatric populations with open growth plates

Research information, not medical advice. Always consult a licensed clinician before considering any peptide.

In depth

Full profile

What it does

Over a cycle you may notice improved sleep depth, some initial water retention, gradual improvements in muscle fullness and recovery speed, and modest reductions in body fat — especially with consistent training and diet.

How it works

Think of natural GHRH as a text message that expires in seconds — your pituitary reads it and acts, but the message disappears quickly. CJC-1295 with DAC is like pinning a sticky note to a bulletin board (albumin in your blood) — the same message stays visible for days, so your pituitary keeps responding long after you sent it.

After you inject it under the skin, it gets absorbed into the bloodstream, latches onto albumin, and slowly releases the GHRH signal over days. Your pituitary gland responds by releasing growth hormone in pulses, which then triggers your liver to produce IGF-1. Both GH and IGF-1 work together to build muscle, burn fat, and support tissue repair.

What to expect

Most people report subtle changes in sleep quality and mild water retention within the first 1–2 weeks. Body composition changes typically take 6–8 weeks of consistent use to become noticeable.

Week 1: Initial absorption and albumin binding; some people notice improved sleep and mild water retention.
Weeks 2–4: GH and IGF-1 levels become consistently elevated; recovery from workouts may improve noticeably; water retention may peak then stabilize.
Weeks 4–8: Body composition changes become more apparent: gradual lean mass gains and modest fat reduction, especially around the midsection with good diet and training.

Good to know

Start with a lower dose (e.g., 1 mg/week) to assess tolerance before increasing
Monitor for signs of water retention and reduce dose if symptoms are uncomfortable
Consider pairing with Ipamorelin rather than GHRP-6 to minimize hunger and cortisol side effects

Staying safe

Mild puffiness or water retention in hands, feet, or face
Headache or flushing shortly after injection
Tingling or numbness in the hands (carpal tunnel-like symptoms with high doses)

Avoid if you have:

Anyone with cancer or a history of cancer
People with diabetes or blood sugar regulation issues
Pregnant or breastfeeding individuals

Overview

Pharmacodynamic effects include: increased lean body mass (estimated 1–2 kg over 8–12 weeks in research subjects), measurable reductions in visceral and subcutaneous fat, enhanced slow-wave sleep (Stage 3 NREM — site of maximal endogenous GH release), improved nitrogen balance, and accelerated collagen synthesis relevant to connective tissue repair. Serum IGF-1 elevations of 30–100% above baseline have been documented in clinical research.

How it works

Think of GHRHR signaling as a dimmer switch rather than an on/off light. Native GHRH flashes the switch briefly before being degraded. CJC-1295 with DAC uses albumin as a slow-release depot — analogous to a controlled-release capacitor that continuously charges the circuit at a moderate level, while endogenous somatostatin acts as the circuit breaker that periodically resets GH pulses, preserving some physiological pulsatility.

After subcutaneous injection, CJC-1295 DAC is absorbed into lymphatics and capillaries, where it rapidly conjugates to circulating albumin. Albumin-bound CJC-1295 acts as a slow-release reservoir: the intact peptide slowly dissociates and activates pituitary GHRHR over 1–2 weeks. GH secretion drives hepatic IGF-1 synthesis (IGF-1 t½ ~12–15 hours, further extended by IGF-binding proteins). Elevated IGF-1 activates PI3K/Akt/mTORC1 and MAPK/ERK pathways in skeletal muscle, promoting protein synthesis and satellite cell activation. Concomitant lipolysis in adipose tissue occurs via GH-mediated HSL activation, reducing triglyceride stores. GH also antagonizes insulin signaling at the post-receptor level, potentially worsening insulin sensitivity with prolonged supraphysiologic levels.

Onset & timeline

Albumin conjugation occurs rapidly post-injection (within hours). Peak serum GH elevation is typically observed within 2–6 hours of administration and remains supraphysiologically elevated for 7–14 days. IGF-1 elevation peaks at approximately 7–10 days post-injection and may persist for up to 28 days due to extended IGFBP-3 binding.

Days 1–3: Rapid albumin conjugation; GH begins to rise within 2–6 hours. Possible early flushing, headache, and mild injection site reactions. Serum albumin-bound peptide concentration approaches plateau.
Weeks 1–2: GH pulses are elevated in amplitude (2–10x baseline depending on dose). IGF-1 begins rising, peaking around day 7–10. Water retention becomes apparent. Nitrogen balance shifts positive. Sleep architecture may improve (increased SWS).
Weeks 2–8: Sustained anabolic environment: measurable increases in lean mass via DEXA at 6–8 weeks in research settings; reductions in fat mass via lipolysis; potential joint discomfort from fluid retention; progressive improvements in recovery biomarkers. Endogenous somatostatin counterregulation partially restores GH pulsatility.

Getting the most from it

Dose titration: begin at 1 mg/week and assess IGF-1 levels at week 4; adjust to maintain IGF-1 in the upper physiologic range (~300–350 ng/mL) rather than supraphysiologic levels
Cycle with equal off-time (e.g., 12 weeks on, 12 weeks off) to prevent GHRHR desensitization
Monitor fasting glucose and HbA1c quarterly when cycling repeatedly
Stack with Ipamorelin (GHSR agonist) rather than GHRP-6 to minimize ghrelin-mediated cortisol and prolactin elevation while maximizing GH pulse amplitude

Common side effects

Fluid retention due to GH-mediated renal sodium retention (can cause edema, hypertension at high doses)
Headache and transient flushing from vasodilatory GH effects
Insulin resistance: GH antagonizes insulin receptor substrate (IRS-1) signaling, elevating fasting glucose in susceptible individuals
Carpal tunnel syndrome-like symptoms from fluid accumulation in the carpal tunnel (reversible with dose reduction)

Mechanism of action

CJC-1295 with DAC is a 30-amino acid GHRH analog modified at position 2 (Ala→D-Ala), position 8 (Asn→Gln), position 15 (Gly→Ala), and position 27 (Met→Nle) to resist DPP-IV cleavage and oxidation. The C-terminal Lys is conjugated via a maleimidoproprionic acid (MPA) spacer (the DAC), which undergoes a Michael addition reaction with Cys-34 of serum albumin under physiological conditions, creating a covalent thioether bond. This extends the circulating half-life to approximately 6–8 days (t½ of native GHRH: ~7 minutes). Receptor binding at pituitary GHRH receptor (GHRHR), a Gs-coupled GPCR, activates adenylyl cyclase → cAMP → PKA signaling, phosphorylating CREB and stimulating transcription of the GH gene and stimulating exocytosis of somatotroph secretory granules. Prolonged GHRHR stimulation maintains elevated GH pulse amplitude while partially preserving pulsatility through endogenous somatostatin counter-regulation.

After subcutaneous injection, CJC-1295 DAC is absorbed into lymphatics and capillaries, where it rapidly conjugates to circulating albumin. Albumin-bound CJC-1295 acts as a slow-release reservoir: the intact peptide slowly dissociates and activates pituitary GHRHR over 1–2 weeks. GH secretion drives hepatic IGF-1 synthesis (IGF-1 t½ ~12–15 hours, further extended by IGF-binding proteins). Elevated IGF-1 activates PI3K/Akt/mTORC1 and MAPK/ERK pathways in skeletal muscle, promoting protein synthesis and satellite cell activation. Concomitant lipolysis in adipose tissue occurs via GH-mediated HSL activation, reducing triglyceride stores. GH also antagonizes insulin signaling at the post-receptor level, potentially worsening insulin sensitivity with prolonged supraphysiologic levels.

Pharmacodynamics

Albumin conjugation occurs rapidly post-injection (within hours). Peak serum GH elevation is typically observed within 2–6 hours of administration and remains supraphysiologically elevated for 7–14 days. IGF-1 elevation peaks at approximately 7–10 days post-injection and may persist for up to 28 days due to extended IGFBP-3 binding.

Pharmacodynamic effects include: increased lean body mass (estimated 1–2 kg over 8–12 weeks in research subjects), measurable reductions in visceral and subcutaneous fat, enhanced slow-wave sleep (Stage 3 NREM — site of maximal endogenous GH release), improved nitrogen balance, and accelerated collagen synthesis relevant to connective tissue repair. Serum IGF-1 elevations of 30–100% above baseline have been documented in clinical research.

Timeline

Days 1–3: Rapid albumin conjugation; GH begins to rise within 2–6 hours. Possible early flushing, headache, and mild injection site reactions. Serum albumin-bound peptide concentration approaches plateau.
Weeks 1–2: GH pulses are elevated in amplitude (2–10x baseline depending on dose). IGF-1 begins rising, peaking around day 7–10. Water retention becomes apparent. Nitrogen balance shifts positive. Sleep architecture may improve (increased SWS).
Weeks 2–8: Sustained anabolic environment: measurable increases in lean mass via DEXA at 6–8 weeks in research settings; reductions in fat mass via lipolysis; potential joint discomfort from fluid retention; progressive improvements in recovery biomarkers. Endogenous somatostatin counterregulation partially restores GH pulsatility.

Comparisons

CJC-1295 with DAC — effectiveness High, safety Moderate, cost $$, Medium to use
CJC-1295 without DAC + Ipamorelin — effectiveness High, safety Good, cost $$, Low to use
Sermorelin — effectiveness Moderate, safety Good, cost $, Low to use
MK-677 (Ibutamoren) — effectiveness High, safety Moderate, cost $, High to use

Adverse effects

Common:

Fluid retention due to GH-mediated renal sodium retention (can cause edema, hypertension at high doses)
Headache and transient flushing from vasodilatory GH effects
Insulin resistance: GH antagonizes insulin receptor substrate (IRS-1) signaling, elevating fasting glucose in susceptible individuals
Carpal tunnel syndrome-like symptoms from fluid accumulation in the carpal tunnel (reversible with dose reduction)

Rare:

Pituitary desensitization (downregulation of GHRHR) with excessive continuous dosing — estimated risk increases significantly beyond 12 weeks of uninterrupted use
Theoretical IGF-1-mediated promotion of pre-existing neoplastic lesions (incidence unknown; preclinical concern based on IGF-1 receptor signaling in cancer biology)

Contraindications & risk mitigation

Contraindicated in:

Individuals with active neoplasia or hereditary cancer syndromes (Li-Fraumeni, MEN1) due to IGF-1/GH mitogenic activity
Type 1 or Type 2 diabetes mellitus — GH-mediated insulin resistance may destabilize glycemic control
Acromegaly or pituitary gigantism
Severe renal or hepatic impairment affecting albumin synthesis or drug clearance
Individuals on corticosteroid therapy (pharmacodynamic antagonism of GH effects)

Dose titration: begin at 1 mg/week and assess IGF-1 levels at week 4; adjust to maintain IGF-1 in the upper physiologic range (~300–350 ng/mL) rather than supraphysiologic levels
Cycle with equal off-time (e.g., 12 weeks on, 12 weeks off) to prevent GHRHR desensitization
Monitor fasting glucose and HbA1c quarterly when cycling repeatedly
Stack with Ipamorelin (GHSR agonist) rather than GHRP-6 to minimize ghrelin-mediated cortisol and prolactin elevation while maximizing GH pulse amplitude

Qué hace

Over a cycle you may notice improved sleep depth, some initial water retention, gradual improvements in muscle fullness and recovery speed, and modest reductions in body fat — especially with consistent training and diet.

Cómo funciona

Think of natural GHRH as a text message that expires in seconds — your pituitary reads it and acts, but the message disappears quickly. CJC-1295 with DAC is like pinning a sticky note to a bulletin board (albumin in your blood) — the same message stays visible for days, so your pituitary keeps responding long after you sent it.

After you inject it under the skin, it gets absorbed into the bloodstream, latches onto albumin, and slowly releases the GHRH signal over days. Your pituitary gland responds by releasing growth hormone in pulses, which then triggers your liver to produce IGF-1. Both GH and IGF-1 work together to build muscle, burn fat, and support tissue repair.

Qué esperar

Most people report subtle changes in sleep quality and mild water retention within the first 1–2 weeks. Body composition changes typically take 6–8 weeks of consistent use to become noticeable.

Week 1: Initial absorption and albumin binding; some people notice improved sleep and mild water retention.
Weeks 2–4: GH and IGF-1 levels become consistently elevated; recovery from workouts may improve noticeably; water retention may peak then stabilize.
Weeks 4–8: Body composition changes become more apparent: gradual lean mass gains and modest fat reduction, especially around the midsection with good diet and training.

Bueno saber

Start with a lower dose (e.g., 1 mg/week) to assess tolerance before increasing
Monitor for signs of water retention and reduce dose if symptoms are uncomfortable
Consider pairing with Ipamorelin rather than GHRP-6 to minimize hunger and cortisol side effects

Manteniéndose seguro

Mild puffiness or water retention in hands, feet, or face
Headache or flushing shortly after injection
Tingling or numbness in the hands (carpal tunnel-like symptoms with high doses)

Evitar si tienes:

Anyone with cancer or a history of cancer
People with diabetes or blood sugar regulation issues
Pregnant or breastfeeding individuals

Descripción general

Pharmacodynamic effects include: increased lean body mass (estimated 1–2 kg over 8–12 weeks in research subjects), measurable reductions in visceral and subcutaneous fat, enhanced slow-wave sleep (Stage 3 NREM — site of maximal endogenous GH release), improved nitrogen balance, and accelerated collagen synthesis relevant to connective tissue repair. Serum IGF-1 elevations of 30–100% above baseline have been documented in clinical research.

Cómo funciona

Think of GHRHR signaling as a dimmer switch rather than an on/off light. Native GHRH flashes the switch briefly before being degraded. CJC-1295 with DAC uses albumin as a slow-release depot — analogous to a controlled-release capacitor that continuously charges the circuit at a moderate level, while endogenous somatostatin acts as the circuit breaker that periodically resets GH pulses, preserving some physiological pulsatility.

After subcutaneous injection, CJC-1295 DAC is absorbed into lymphatics and capillaries, where it rapidly conjugates to circulating albumin. Albumin-bound CJC-1295 acts as a slow-release reservoir: the intact peptide slowly dissociates and activates pituitary GHRHR over 1–2 weeks. GH secretion drives hepatic IGF-1 synthesis (IGF-1 t½ ~12–15 hours, further extended by IGF-binding proteins). Elevated IGF-1 activates PI3K/Akt/mTORC1 and MAPK/ERK pathways in skeletal muscle, promoting protein synthesis and satellite cell activation. Concomitant lipolysis in adipose tissue occurs via GH-mediated HSL activation, reducing triglyceride stores. GH also antagonizes insulin signaling at the post-receptor level, potentially worsening insulin sensitivity with prolonged supraphysiologic levels.

Inicio y cronología

Albumin conjugation occurs rapidly post-injection (within hours). Peak serum GH elevation is typically observed within 2–6 hours of administration and remains supraphysiologically elevated for 7–14 days. IGF-1 elevation peaks at approximately 7–10 days post-injection and may persist for up to 28 days due to extended IGFBP-3 binding.

Days 1–3: Rapid albumin conjugation; GH begins to rise within 2–6 hours. Possible early flushing, headache, and mild injection site reactions. Serum albumin-bound peptide concentration approaches plateau.
Weeks 1–2: GH pulses are elevated in amplitude (2–10x baseline depending on dose). IGF-1 begins rising, peaking around day 7–10. Water retention becomes apparent. Nitrogen balance shifts positive. Sleep architecture may improve (increased SWS).
Weeks 2–8: Sustained anabolic environment: measurable increases in lean mass via DEXA at 6–8 weeks in research settings; reductions in fat mass via lipolysis; potential joint discomfort from fluid retention; progressive improvements in recovery biomarkers. Endogenous somatostatin counterregulation partially restores GH pulsatility.

Cómo aprovecharlo al máximo

Dose titration: begin at 1 mg/week and assess IGF-1 levels at week 4; adjust to maintain IGF-1 in the upper physiologic range (~300–350 ng/mL) rather than supraphysiologic levels
Cycle with equal off-time (e.g., 12 weeks on, 12 weeks off) to prevent GHRHR desensitization
Monitor fasting glucose and HbA1c quarterly when cycling repeatedly
Stack with Ipamorelin (GHSR agonist) rather than GHRP-6 to minimize ghrelin-mediated cortisol and prolactin elevation while maximizing GH pulse amplitude

Efectos secundarios comunes

Fluid retention due to GH-mediated renal sodium retention (can cause edema, hypertension at high doses)
Headache and transient flushing from vasodilatory GH effects
Insulin resistance: GH antagonizes insulin receptor substrate (IRS-1) signaling, elevating fasting glucose in susceptible individuals
Carpal tunnel syndrome-like symptoms from fluid accumulation in the carpal tunnel (reversible with dose reduction)

Mecanismo de acción

CJC-1295 with DAC is a 30-amino acid GHRH analog modified at position 2 (Ala→D-Ala), position 8 (Asn→Gln), position 15 (Gly→Ala), and position 27 (Met→Nle) to resist DPP-IV cleavage and oxidation. The C-terminal Lys is conjugated via a maleimidoproprionic acid (MPA) spacer (the DAC), which undergoes a Michael addition reaction with Cys-34 of serum albumin under physiological conditions, creating a covalent thioether bond. This extends the circulating half-life to approximately 6–8 days (t½ of native GHRH: ~7 minutes). Receptor binding at pituitary GHRH receptor (GHRHR), a Gs-coupled GPCR, activates adenylyl cyclase → cAMP → PKA signaling, phosphorylating CREB and stimulating transcription of the GH gene and stimulating exocytosis of somatotroph secretory granules. Prolonged GHRHR stimulation maintains elevated GH pulse amplitude while partially preserving pulsatility through endogenous somatostatin counter-regulation.

After subcutaneous injection, CJC-1295 DAC is absorbed into lymphatics and capillaries, where it rapidly conjugates to circulating albumin. Albumin-bound CJC-1295 acts as a slow-release reservoir: the intact peptide slowly dissociates and activates pituitary GHRHR over 1–2 weeks. GH secretion drives hepatic IGF-1 synthesis (IGF-1 t½ ~12–15 hours, further extended by IGF-binding proteins). Elevated IGF-1 activates PI3K/Akt/mTORC1 and MAPK/ERK pathways in skeletal muscle, promoting protein synthesis and satellite cell activation. Concomitant lipolysis in adipose tissue occurs via GH-mediated HSL activation, reducing triglyceride stores. GH also antagonizes insulin signaling at the post-receptor level, potentially worsening insulin sensitivity with prolonged supraphysiologic levels.

Farmacodinamia

Albumin conjugation occurs rapidly post-injection (within hours). Peak serum GH elevation is typically observed within 2–6 hours of administration and remains supraphysiologically elevated for 7–14 days. IGF-1 elevation peaks at approximately 7–10 days post-injection and may persist for up to 28 days due to extended IGFBP-3 binding.

Pharmacodynamic effects include: increased lean body mass (estimated 1–2 kg over 8–12 weeks in research subjects), measurable reductions in visceral and subcutaneous fat, enhanced slow-wave sleep (Stage 3 NREM — site of maximal endogenous GH release), improved nitrogen balance, and accelerated collagen synthesis relevant to connective tissue repair. Serum IGF-1 elevations of 30–100% above baseline have been documented in clinical research.

Cronología

Days 1–3: Rapid albumin conjugation; GH begins to rise within 2–6 hours. Possible early flushing, headache, and mild injection site reactions. Serum albumin-bound peptide concentration approaches plateau.
Weeks 1–2: GH pulses are elevated in amplitude (2–10x baseline depending on dose). IGF-1 begins rising, peaking around day 7–10. Water retention becomes apparent. Nitrogen balance shifts positive. Sleep architecture may improve (increased SWS).
Weeks 2–8: Sustained anabolic environment: measurable increases in lean mass via DEXA at 6–8 weeks in research settings; reductions in fat mass via lipolysis; potential joint discomfort from fluid retention; progressive improvements in recovery biomarkers. Endogenous somatostatin counterregulation partially restores GH pulsatility.

Comparaciones

CJC-1295 with DAC — efectividad High, seguridad Moderate, costo $$, Medium de usar
CJC-1295 without DAC + Ipamorelin — efectividad High, seguridad Good, costo $$, Low de usar
Sermorelin — efectividad Moderate, seguridad Good, costo $, Low de usar
MK-677 (Ibutamoren) — efectividad High, seguridad Moderate, costo $, High de usar

Efectos adversos

Comunes:

Fluid retention due to GH-mediated renal sodium retention (can cause edema, hypertension at high doses)
Headache and transient flushing from vasodilatory GH effects
Insulin resistance: GH antagonizes insulin receptor substrate (IRS-1) signaling, elevating fasting glucose in susceptible individuals
Carpal tunnel syndrome-like symptoms from fluid accumulation in the carpal tunnel (reversible with dose reduction)

Raros:

Pituitary desensitization (downregulation of GHRHR) with excessive continuous dosing — estimated risk increases significantly beyond 12 weeks of uninterrupted use
Theoretical IGF-1-mediated promotion of pre-existing neoplastic lesions (incidence unknown; preclinical concern based on IGF-1 receptor signaling in cancer biology)

Contraindicaciones y mitigación de riesgos

Contraindicado en:

Individuals with active neoplasia or hereditary cancer syndromes (Li-Fraumeni, MEN1) due to IGF-1/GH mitogenic activity
Type 1 or Type 2 diabetes mellitus — GH-mediated insulin resistance may destabilize glycemic control
Acromegaly or pituitary gigantism
Severe renal or hepatic impairment affecting albumin synthesis or drug clearance
Individuals on corticosteroid therapy (pharmacodynamic antagonism of GH effects)

Dose titration: begin at 1 mg/week and assess IGF-1 levels at week 4; adjust to maintain IGF-1 in the upper physiologic range (~300–350 ng/mL) rather than supraphysiologic levels
Cycle with equal off-time (e.g., 12 weeks on, 12 weeks off) to prevent GHRHR desensitization
Monitor fasting glucose and HbA1c quarterly when cycling repeatedly
Stack with Ipamorelin (GHSR agonist) rather than GHRP-6 to minimize ghrelin-mediated cortisol and prolactin elevation while maximizing GH pulse amplitude

Reference data

Specifications

Molecular formula: C₁₆₅H₂₆₉N₄₇O₄₆
Molecular weight: 3647.1 Da (approximate; varies by salt form)
Half-life: ~6–8 days
Route: Subcutaneous, Intramuscular
Cycle length: 8–12 weeks, followed by a break of equal duration
Storage: Lyophilized (powder) form: store at 2–8°C (refrigerated), protected from light and moisture; stable for up to 24 months. After reconstitution with bacteriostatic water: store at 2–8°C and use within 28–30 days. Do not freeze reconstituted peptide.
Legal status: Research chemical; not approved by the FDA or EMA for human therapeutic use. Banned by WADA in competitive sports. Legal to purchase for laboratory/research purposes in many jurisdictions; regulations vary by country.

FAQ

Common questions

Does the continuous GHRHR stimulation by CJC-1295 DAC blunt natural GH pulsatility?

Ionescu & Frohman (2006, JCEM 91:4792) demonstrated that despite continuous GHRHR stimulation, somatostatin-mediated counter-regulation partially preserves GH pulsatility. However, prolonged continuous stimulation beyond 12 weeks raises theoretical concerns about GHRHR downregulation, which is why cyclic protocols are recommended.

What is the clinical evidence base for CJC-1295 DAC?

Teichman et al. (2006, JCEM 91:799-805) conducted the key Phase 1/2 human trial demonstrating dose-dependent GH and IGF-1 elevation, extended half-life (~6-8 days), and tolerability in healthy adults. No Phase 3 trials have been completed, making this a human-limited evidence profile. All extrapolations to athletic or anti-aging applications remain off-label and research-grade.

How does CJC-1295 DAC compare pharmacokinetically to modified GRF (1-29) without DAC?

Modified GRF 1-29 (CJC-1295 without DAC) has a half-life of approximately 30 minutes, requiring daily or twice-daily injections. The DAC extends this to ~6-8 days via covalent albumin binding, allowing once-weekly dosing. The trade-off is a more physiologically constant (less pulsatile) GH signal, which may not fully replicate the anabolic benefit of pulsatile secretion.

What is the evidence level?

This compound is classified as Limited human data. Some human data exists but trials are small, short-term, or not yet replicated.

Research

Research & sources

Limited human

Current evidence for CJC-1295 with DAC is rated as Limited human data. Limited human data is available.

1. Teichman SL et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor 1 secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults (2006) — Journal of Clinical Endocrinology & Metabolism, 91(3):799-805. DOI: 10.1210/jc.2005-1258
2. Ionescu M & Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog (2006) — Journal of Clinical Endocrinology & Metabolism, 91(12):4792-4797. DOI: 10.1210/jc.2006-1702
3. Alba M et al. Once-monthly administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse (2006) — American Journal of Physiology-Endocrinology and Metabolism, 291(6):E1290-4. DOI: 10.1152/ajpendo.00201.2006

Explore

Often discussed alongside

Ipamorelin · growth GHRP-6 · growth GHRP-2 · growth BPC-157 · healing TB-500 · healing