Overview
Overview
CJC-1295 is a long-acting GHRH analog that can elevate GH levels 2–10× baseline for approximately 6 days and increase IGF-1 by 1.5–3× for 9–11 days[1]. GHRP-2 is a ghrelin-mimetic secretagogue with a plasma half-life of ~30 minutes that triggers rapid GH pulses peaking within ~25 minutes of administration[3]. Combining these peptides leverages GHRP-2’s acute pulsatile release with CJC-1295’s sustained action. This educational protocol presents a once-daily subcutaneous approach using a practical
- Category
- Growth Hormone
- Routes
- subcutaneous
Mechanism
CJC-1295
Mechanism of action
Mechanism of action
CJC-1295 is a tetrasubstituted GHRH(1–29) analog engineered for extended half-life (~6–8 days) via protection from enzymatic degradation and reversible albumin binding [1] . A single dose can sustain elevated GH for approximately 6 days and IGF-1 elevation for 9–11 days. GHRP-2 is a synthetic hexapeptide ghrelin-mimetic that binds the GH secretagogue receptor (GHS-R1a), triggering acute GH pulses that peak within ~25 minutes [3] . Combining CJC-1295’s sustained GHRH signaling with GHRP-2’s rapid secretagogue action produces synergistic GH release that exceeds either peptide alone [6] .
Key research findings
- 01
CJC-1295 was first characterized by Jette et al. (2005, Endocrinology; PMID 15817669, DOI 10.1210/en.2004-1286) as a tetrasubstituted human GHRH(1-29) analog bearing an N-epsilon-maleimidopropionamide lysine at the C-terminus that covalently bioconjugates to Cys34 of serum albumin; in vitro it resisted DPP-IV degradation and was bioactive in cultured rat anterior-pituitary cells, and in Sprague-Dawley rats it produced an acute GH rise (~4-fold greater GH AUC vs hGRF[1-29]) and remained detectable in plasma beyond 72 h. This is the foundational mechanistic/characterization study.
- 02
In two randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults (Teichman et al., 2006, J Clin Endocrinol Metab; PMID 16352683, DOI 10.1210/jc.2005-1536), single subcutaneous doses produced dose-dependent increases in plasma GH (2- to 10-fold for >=6 days) and IGF-I (1.5- to 3-fold for 9-11 days); estimated half-life was 5.8-8.1 days, IGF-I stayed above baseline up to 28 days after repeated dosing, and the report stated no serious adverse reactions occurred (observed effects in research, not a safety guarantee).
- 03
Ionescu & Frohman (2006, J Clin Endocrinol Metab; PMID 17018654, DOI 10.1210/jc.2006-1702) sampled GH overnight in healthy young men before and ~1 week after a single injection: pulsatile GH secretion was preserved (pulse frequency and amplitude unchanged) while basal/trough GH rose markedly (~7.5-fold), mean GH increased ~46% and IGF-I ~45%; the IGF-I rise did not correlate with measured GH-secretion parameters.
- 04
A proteomic analysis (Sackmann-Sala et al., 2009, Growth Horm IGF Res; PMID 19386527, DOI 10.1016/j.ghir.2009.03.001) of serum from 11 healthy young men before and one week after a CJC-1295 injection found reproducible shifts in several serum proteins (an apolipoprotein A-I isoform and a transthyretin isoform decreased; beta-hemoglobin and albumin fragments increased), proposed as candidate biomarkers of GH/IGF-1 axis activation rather than clinical-outcome measures.
- 05
In GHRH-knockout mice (Alba et al., 2006, Am J Physiol Endocrinol Metab; PMID 16822960, DOI 10.1152/ajpendo.00201.2006), once-daily CJC-1295 normalized body weight, length, and body composition and increased pituitary GH mRNA consistent with somatotroph proliferation; efficacy declined with less-frequent (every 48-72 h) dosing.
- 06
In mice lacking brain M3 muscarinic acetylcholine receptors (a dwarf phenotype), CJC-1295 administration restored normal serum GH and IGF-1 and rescued the growth deficit (Gautam et al., 2009, PNAS; PMID 19332789, DOI 10.1073/pnas.0900977106), where the analog served as a pharmacological tool to probe hypothalamic GHRH-neuron function.
Primary source: The peer-reviewed base for CJC-1295 (the albumin-binding "with DAC" analog) is genuinely real but small and dated: a foundational in vitro/rat characterization (Jette 2005), two rodent models (Alba 2006; Gautam 2009), and three early-phase human pharmacodynamic studies in healthy adult volunteers (Teichman 2006; Ionescu 2006; Sackmann-Sala 2009), nearly all clustered around 2005-2009 and largely tied to the original developer. There are no modern large-scale or clinical-outcome trials; the compound was never approved, its originator's clinical development was discontinued, and most indexed literature since ~2010 consists of anti-doping detection methodology (it is on the WADA Prohibited List, class S2) plus narrative reviews that explicitly note the absence of clinical trials and of long-term safety data.
Researched Effects
Protocol Reference
Protocol reference
Commonly cited research range: 100–300 mcg, daily.
Reference figures reported in the research literature — not a dosing recommendation. For interactive vial math and scheduling, see the Calculator and Schedule tabs.
Cited protocol & reconstitution guide
Source-backed reference fields by phase, including any volume fields authored in the cited guide.
Weeks 1–2
150 mcg (0.15 mg)
Weeks 3–12
300 mcg (0.30 mg)
| Phase | Reference amount | Units / volume |
|---|---|---|
| Weeks 1–2 | 150 mcg (0.15 mg) | 4.5 units (0.045 mL) |
| Weeks 3–12 | 300 mcg (0.30 mg) | 9 units (0.09 mL) |
Storage & Handling
Storage requirements(typical for most peptides)
Can be stored for extended periods. Protect from moisture.
Store in refrigerator door. Never freeze after reconstitution.
Label vials with reconstitution date. Discard if cloudy.
Reconstitution steps
- 01🌡️Draw 3.0 mL bacteriostatic water with a sterile syringe.
- 02🧴Inject slowly down the vial wall; avoid foaming.
- 03💉Gently swirl/roll until dissolved (do not shake).
- 04💧Label and refrigerate at 2–8 °C (35.6–46.4 °F), protected from light.
- 05🔄Advanced / Twice-Daily Approach (3 mL = ~3.33 mg/mL)
- 06🏷️Some protocols split the daily dose into two administrations (morning upon waking, fasted; and evening before bed) to enhance GH pulsatility[1]. Ensure doses are at least 3–8 hours apart to avoid overlapping GH pulses.
- 07❄️WEEK DOSE PER INJECTION (MCG) UNITS (PER INJECTION) (ML) TOTAL DAILY (MCG)
- 08💉Weeks 1–2 100 mcg (0.10 mg) 3 units (0.03 mL) 200 mcg
- 09💉Weeks 3–12 150 mcg (0.15 mg) 4.5 units (0.045 mL) 300 mcg
- 10💉For ≤10-unit (≤0.10 mL) administrations, consider 30- or 50-unit insulin syringes for improved readability.
- 11💉Important: This guide is for educational purposes only and is not medical advice. For research use only. Not for human consumption.
Additional storage notes
Refrigerate at 2–8 °C (35.6–46.4 °F); freeze at −20 °C (−4 °F) for long-term storage exceeding several months.
Refrigerate at 2–8 °C (35.6–46.4 °F); use within 2–4 weeks for optimal potency.
Allow vials to reach room temperature before opening to reduce condensation uptake.
If longer storage of reconstituted solution is needed, aliquot into sterile containers and freeze once; avoid repeated freeze–thaw .
Clinical Evidence
Clinical evidence
Studies show sustained elevation of GH and IGF-1. Often combined with Ipamorelin for synergistic effects.
The peer-reviewed base for CJC-1295 (the albumin-binding "with DAC" analog) is genuinely real but small and dated: a foundational in vitro/rat characterization (Jette 2005), two rodent models (Alba 2006; Gautam 2009), and three early-phase human pharmacodynamic studies in healthy adult volunteers (Teichman 2006; Ionescu 2006; Sackmann-Sala 2009), nearly all clustered around 2005-2009 and largely tied to the original developer. There are no modern large-scale or clinical-outcome trials; the compound was never approved, its originator's clinical development was discontinued, and most indexed literature since ~2010 consists of anti-doping detection methodology (it is on the WADA Prohibited List, class S2) plus narrative reviews that explicitly note the absence of clinical trials and of long-term safety data.
- 01CJC-1295 was first characterized by Jette et al. (2005, Endocrinology; PMID 15817669, DOI 10.1210/en.2004-1286) as a tetrasubstituted human GHRH(1-29) analog bearing an N-epsilon-maleimidopropionamide lysine at the C-terminus that covalently bioconjugates to Cys34 of serum albumin; in vitro it resisted DPP-IV degradation and was bioactive in cultured rat anterior-pituitary cells, and in Sprague-Dawley rats it produced an acute GH rise (~4-fold greater GH AUC vs hGRF[1-29]) and remained detectable in plasma beyond 72 h. This is the foundational mechanistic/characterization study.
- 02In two randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults (Teichman et al., 2006, J Clin Endocrinol Metab; PMID 16352683, DOI 10.1210/jc.2005-1536), single subcutaneous doses produced dose-dependent increases in plasma GH (2- to 10-fold for >=6 days) and IGF-I (1.5- to 3-fold for 9-11 days); estimated half-life was 5.8-8.1 days, IGF-I stayed above baseline up to 28 days after repeated dosing, and the report stated no serious adverse reactions occurred (observed effects in research, not a safety guarantee).
- 03Ionescu & Frohman (2006, J Clin Endocrinol Metab; PMID 17018654, DOI 10.1210/jc.2006-1702) sampled GH overnight in healthy young men before and ~1 week after a single injection: pulsatile GH secretion was preserved (pulse frequency and amplitude unchanged) while basal/trough GH rose markedly (~7.5-fold), mean GH increased ~46% and IGF-I ~45%; the IGF-I rise did not correlate with measured GH-secretion parameters.
- 04A proteomic analysis (Sackmann-Sala et al., 2009, Growth Horm IGF Res; PMID 19386527, DOI 10.1016/j.ghir.2009.03.001) of serum from 11 healthy young men before and one week after a CJC-1295 injection found reproducible shifts in several serum proteins (an apolipoprotein A-I isoform and a transthyretin isoform decreased; beta-hemoglobin and albumin fragments increased), proposed as candidate biomarkers of GH/IGF-1 axis activation rather than clinical-outcome measures.
- 05In GHRH-knockout mice (Alba et al., 2006, Am J Physiol Endocrinol Metab; PMID 16822960, DOI 10.1152/ajpendo.00201.2006), once-daily CJC-1295 normalized body weight, length, and body composition and increased pituitary GH mRNA consistent with somatotroph proliferation; efficacy declined with less-frequent (every 48-72 h) dosing.
- 06In mice lacking brain M3 muscarinic acetylcholine receptors (a dwarf phenotype), CJC-1295 administration restored normal serum GH and IGF-1 and rescued the growth deficit (Gautam et al., 2009, PNAS; PMID 19332789, DOI 10.1073/pnas.0900977106), where the analog served as a pharmacological tool to probe hypothalamic GHRH-neuron function.
Evidence maturity varies by compound; much peptide research is preclinical (in vitro or animal-model). Where human data are limited, findings should be read as research observations, not clinical conclusions.
References
Literature references
Published research articles and sources related to CJC-1295.
- 01J Clin Endocrinol Metab (2006) — Teichman SL et al. Prolonged stimulation of GH and IGF-I secretion by CJC-1295, a long-acting GHRH analog, in healthy adults View Sourceet al. (2006)
- 02J Clin Endocrinol Metab (1998) — Mericq V et al. Effects of eight months treatment with graded doses of GHRP in GH-deficient children View Sourceet al. (1998)
- 03J Clin Endocrinol Metab (1998) — Pihoker C et al. Pharmacokinetics and pharmacodynamics of GHRP-2: a phase I study in children View Sourceet al. (1998)
- 04J Clin Endocrinol Metab (2005) — Laferrère B et al. GHRP-2, like ghrelin, increases food intake in healthy men View Sourceet al. (2005)
- 05Peptides (1997) — Arvat E et al. Effects of GHRP-2 and hexarelin on GH, prolactin, ACTH, and cortisol levels in man View Sourceet al. (1997)
- 06WADA Technical Document (2019) — Testing guide for Growth Hormone Releasing Factors (GHRFs), Version 2.0 View Sourceet al. (2019)
- 07CDC — Vaccine administration: subcutaneous route (angle/site; no aspiration) View Source
- 08CDC (Subcut Injection PDF) — Technique diagram and site guidance for subcutaneous injections View Source
- 09Bachem Technical Bulletin — Handling and storage guidelines for peptides View Source
- 10Sigma-Aldrich Technical Guide — Handling and storage of synthetic peptides View Source
- 11NCBI Bookshelf — Best practices for injection (asepsis, preparation, and administration) View Source
- 12Subcutaneous Drug Injection Review (PMC) — Pharmacologic considerations of the subcutaneous route View Source
- 13Pure Lab Peptides — CJC-1295 + GHRP-2 (10 mg Blend) product page (quality and batch documentation) View Source
Research Considerations
Research considerations
Research peptide. May cause water retention. Consult healthcare provider.
Factors noted in the research literature; not patient-specific medical advice.
Regulatory Status
Regulatory status
RUO
Comparisons
Comparisons
| Compound | Mechanism | Route | Status |
|---|---|---|---|
| CJC-1295this | Binds to GHRH receptors to stimulate GH release. Modified structure provides extended duration of action (up to 7 days). | subcutaneous | Investigational / RUO |
| CJC-1295 DAC | A synthetic GHRH analog with a drug-affinity-complex (DAC) modification that binds serum albumin, greatly extending half-life and producing sustained stimulation of pituitary GH release. | subcutaneous | Investigational / RUO |
| CJC-1295 NO DAC | A synthetic 29-amino-acid GHRH analog (Modified GRF 1-29) that stimulates natural, pulsatile growth hormone secretion from the pituitary; without a DAC it has a short duration of action. | subcutaneous | Investigational / RUO |
| GHRP-2 | A synthetic hexapeptide that activates the ghrelin/GHS receptor (GHS-R1a) to stimulate dose-dependent growth hormone release; it also mildly engages prolactin and cortisol pathways. | subcutaneous | Investigational / RUO |
| GHRP-6 | A synthetic hexapeptide GH secretagogue that binds the ghrelin receptor (GHS-R1a) to stimulate pulsatile GH release and appetite via central ghrelin signaling. | subcutaneous | Investigational / RUO |
| Cortagen | A synthetic tetrapeptide (Ala-Glu-Asp-Pro) of the Khavinson bioregulator class studied for neuroprotective and neuroregenerative activity, including peripheral nerve repair. | subcutaneous | Investigational / RUO |
| DSIP | A naturally occurring nonapeptide studied for influence on sleep architecture and hypothalamic-pituitary-adrenal (stress-axis) modulation; its precise receptor targets remain incompletely characterized. | subcutaneous | Investigational / RUO |
Attributes shown for research comparison only; not a statement of efficacy or therapeutic equivalence.
FAQ
Frequently asked questions
In PubMed-indexed work it is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH 1-29). The 'with DAC' form carries a reactive maleimide group that covalently binds endogenous serum albumin after injection, extending its plasma presence and prolonging stimulation of the pituitary GH/IGF-1 axis (Jette 2005, PMID 15817669; Teichman 2006, PMID 16352683). It is described for research characterization only and is not a medical product.
The available human studies were small, short, early-phase pharmacodynamic trials in healthy adult volunteers that measured blood GH and IGF-1 responses, pharmacokinetics (estimated half-life ~6-8 days), and GH pulsatility, not clinical or disease outcomes. They reported dose-dependent, prolonged increases in GH and IGF-1 with preserved GH pulsatility (Teichman 2006, PMID 16352683; Ionescu & Frohman 2006, PMID 17018654). These are physiology and biomarker measurements and should not be read as evidence of clinical benefit.
No. Regulatory and analytical sources indicate it was never approved for any use, clinical development by the original sponsor did not continue, and it appears on the World Anti-Doping Agency Prohibited List (class S2) (Henninge 2010, PMID 21204297; Memdouh 2021, PMID 34665524). Much of the recent indexed literature concerns laboratory methods for detecting it in doping-control samples. This is research-use-only context, not medical guidance.
The peer-reviewed pharmacology (multi-day half-life and prolonged GH/IGF-1 elevation) refers to the 'with DAC' version, which covalently bioconjugates to albumin (Jette 2005, PMID 15817669). Material described in non-peer-reviewed sources as 'without DAC' (often called Modified GRF 1-29) lacks that albumin-binding group and is short-acting, essentially a sermorelin-like fragment; it is not the long-acting compound characterized in the human trials. When reviewing any claim, confirm which molecule was actually studied.
This is an investigational research compound, not a medical therapy, so no dosing instructions are provided here and this is not medical advice. Research-reported amounts vary across the early-phase studies (for example, the human pharmacology work examined microgram-per-kilogram ranges on weekly or biweekly schedules); for exact parameters consult the original protocol references (e.g., Teichman 2006, PMID 16352683; Ionescu & Frohman 2006, PMID 17018654) under appropriate professional oversight.
In the published healthy-adult trials the compound was described as relatively well tolerated and no serious adverse reactions were reported within those short studies (Teichman 2006, PMID 16352683). However, these were small, brief, early-phase studies; there are no long-term safety data, and recent review articles note this gap (Mavrych 2026, PMID 42021992). Observed effects in research should not be interpreted as a safety guarantee.
Limited. The substantive findings come from a handful of studies clustered in 2005-2009, mostly linked to the original developer, with no large or long-term clinical trials and no regulatory approval. Animal work in GHRH-knockout and M3-receptor-knockout mice supports GH-axis activation (Alba 2006, PMID 16822960; Gautam 2009, PMID 19332789), but the human evidence is confined to short pharmacodynamic studies. The compound is best treated as investigational and research-use-only.
Research-use notice
Research Use Only. This educational content and calculation support is intended for private research documentation. It does not provide medical advice, human-use directions, or claims of safety or effectiveness.