CJC (no DAC)/Ipamorelin 5mg/5mg
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Research Use Only
These products are for laboratory research only and not intended for medical use. They are not FDA-approved to diagnose, treat, cure, or prevent any disease. By purchasing, you certify they will be used solely for research and not for human or animal consumption.
Bundle / Blend Research
This product contains CJC-1295 (no DAC) + Ipamorelin. Select a tab below to view the full Gold Standard research profile for each component.
Overview
Research Overview
CJC-1295 (no DAC), frequently referred to in the scientific literature as Modified GRF (1-29) or Mod GRF 1-29, is a synthetic peptide analog of endogenous growth hormone-releasing hormone (GHRH). It is derived from the first 29 amino acids of the native 44-amino acid GHRH molecule produced in the hypothalamus, representing the biologically active fragment responsible for stimulating growth hormone (GH) release from the anterior pituitary gland.[1][2] The peptide was originally developed by ConjuChem Biotechnologies Inc. (Montreal, Canada) as part of the CJC-1295 drug development program, where the tetrasubstituted core peptide served as the precursor to the long-acting DAC-conjugated variant.[4]
The term "tetrasubstituted" refers to four strategic amino acid substitutions in the native GHRH(1-29) sequence: D-Alanine at position 2, Glutamine at position 8, Alanine at position 15, and Leucine at position 27.[2][3] Each substitution serves a specific purpose: position 2 (D-Ala) prevents DPP-4 enzymatic cleavage, position 8 (Gln) reduces asparagine rearrangement or amide hydrolysis to aspartic acid, position 15 (Ala) enhances bioactivity, and position 27 (Leu) prevents methionine oxidation. These modifications collectively extend the half-life from the mere minutes characteristic of native GHRH to approximately 30 minutes for CJC-1295 (no DAC), dramatically improving bioavailability while preserving receptor binding characteristics.[1][5]
The "no DAC" designation is critically important for researchers to understand. CJC-1295 with DAC (Drug Affinity Complex) contains an N-epsilon-3-maleimidopropionyl-lysine linker that covalently binds to serum albumin, extending the half-life to 6–8 days and creating continuous, non-physiological GH stimulation.[4][8] In contrast, CJC-1295 (no DAC) lacks this conjugation entirely, producing pulsatile GH release that mimics the body's natural circadian rhythm. This pulsatile pattern is therapeutically preferred because it avoids receptor desensitization (downregulation) of GHRH receptors and minimizes side effects associated with chronic GH elevation.[5][6] The FDA, in its December 2024 Pharmacy Compounding Advisory Committee briefing, explicitly noted that many studies cited under the name "CJC-1295" actually utilized the DAC variant, and that no published human clinical trials or preclinical efficacy studies exist specifically for CJC-1295 without DAC.[9]
Research into CJC-1295 (no DAC) focuses on conditions driven by growth hormone deficiency (GHD) or age-related decline of the GH/IGF-1 axis. Key investigational areas include body composition and muscle hypertrophy (via GH-mediated protein synthesis and IGF-1 stimulation), lipid metabolism (GH-facilitated lipolysis and reduced visceral adipose tissue), tissue repair and injury recovery (collagen synthesis stimulation via the GH/IGF-1 axis), sleep physiology (GHRH analogs and slow-wave sleep enhancement), and anti-aging cellular function (restoring youthful GH pulsatility).[6][7][12] It is frequently studied in combination with Ipamorelin, a selective GH secretagogue that acts on a complementary receptor (the ghrelin/GHS receptor), for a synergistic effect on GH release.[12]
Forensic and analytical chemistry studies by Henninge et al. (2010) and Hartvig et al. (2014) have confirmed that products marketed as "CJC-1295" on the grey market frequently contain the no-DAC variant (Modified GRF 1-29) rather than the genuine CJC-1295 with DAC, underscoring the importance of precise nomenclature and rigorous analytical verification using RP-HPLC and LC-MS/MS.[1][3][13]
Mechanism of Action
Mechanism of Action
CJC-1295 (no DAC) functions as a selective GHRH receptor agonist that binds to growth hormone-releasing hormone receptors (GHRHr) on somatotroph cells in the anterior pituitary gland, initiating a cAMP-dependent signaling cascade that stimulates growth hormone (GH) gene transcription, synthesis, and pulsatile secretion.[7][8]
Primary Receptor Target & Binding Characteristics
| Property | Detail | Evidence |
|---|---|---|
| Primary Target | Growth Hormone-Releasing Hormone Receptor (GHRHr) on anterior pituitary somatotrophs | Teichman et al. (2006); Alba et al. (2006)[8] |
| Receptor Class | Class B1 (secretin family) G protein-coupled receptor (GPCR) | Established GHRH receptor pharmacology[7] |
| Binding Affinity | High affinity; mimics native GHRH structure with enhanced stability from tetrasubstitution | Jetté et al. (2005)[4] |
| Binding Reversibility | Reversible binding; crucial for maintaining physiological balance and preventing GH axis overstimulation | Pharmacokinetic profile[5] |
| Half-Life | ~30 minutes (vs. minutes for native GHRH; vs. 6–8 days for CJC-1295 with DAC) | Soule et al. (1994); Henninge et al. (2010)[2][1] |
| Selectivity | Highly selective for GHRHr on pituitary somatotrophs; possible low-level cross-reactivity within the secretin receptor family | 86% homology with endogenous GHRH[7] |
| DPP-4 Resistance | D-Alanine at position 2 prevents dipeptidyl peptidase-4 cleavage that rapidly degrades native GHRH | Jetté et al. (2005); Soule et al. (1994)[4][2] |
Downstream Signaling Cascade
| Step | Event | Molecular Detail |
|---|---|---|
| 1. Receptor Binding | CJC-1295 (no DAC) binds GHRHr on somatotroph cell surface | High-affinity, reversible "lock-and-key" interaction mimicking native GHRH[7] |
| 2. G-Protein Activation | Ligand-receptor interaction activates stimulatory G-proteins (Gs) | Gsα subunit dissociates and activates downstream effectors[7] |
| 3. cAMP Production | Gs activates adenylyl cyclase; ATP is converted to cyclic AMP (cAMP) | Intracellular cAMP levels increase significantly (dose-dependent)[7][14] |
| 4. PKA Activation | Elevated cAMP activates Protein Kinase A (PKA) phosphorylation cascades | PKA phosphorylates transcription factors including CREB[7] |
| 5. GH Gene Transcription | PKA cascade stimulates GH gene transcription and protein synthesis in somatotrophs | Increased GH mRNA and total pituitary RNA[7][8] |
| 6. Pulsatile GH Secretion | GH is released in a physiological pulse from anterior pituitary | ~30 min half-life produces pulsatile (not continuous) GH release[5][6] |
| 7. IGF-1 Stimulation | Released GH stimulates the liver to produce Insulin-like Growth Factor-1 (IGF-1) | GH/IGF-1 axis activation drives downstream anabolic effects[8] |
Alternative Signaling Pathways
While the Gs/cAMP/PKA cascade is the primary signaling pathway, CJC-1295 (no DAC) may also engage the MAPK (mitogen-activated protein kinase) and PI3K/Akt pathways, which contribute to anabolic effects (protein synthesis via mTOR), anti-apoptotic signaling, and cellular proliferation.[7]
Cellular and Tissue-Level Effects
| Effect | Detail | Evidence |
|---|---|---|
| Somatotroph Proliferation | Stimulates proliferation of pituitary somatotroph cells; increases total pituitary RNA and GH mRNA | Alba et al. (2006) (DAC variant)[8] |
| GH/IGF-1 Axis | Stimulates pulsatile GH release; liver produces IGF-1; dose-dependent GH and IGF-1 elevation | Teichman et al. (2006) (DAC variant)[8] |
| Lipolysis | GH promotes fat breakdown via hormone-sensitive lipase activation; inhibits lipogenesis | GH/IGF-1 axis pharmacology[7] |
| Protein Synthesis | Enhances muscle protein synthesis via mTOR pathway activation downstream of GH/IGF-1 | GH secretagogue literature[12] |
| Tissue Repair | Accelerates wound healing and connective tissue repair through collagen synthesis stimulation | GH/IGF-1 axis regenerative properties[12] |
| DNA Damage (Pituitary) | Intense cAMP stimulation by CJC-1295 in mouse pituitary cells induced DNA damage (H2AX phosphorylation and comet assays) | Ben-Shlomo et al. (2020) (likely DAC variant)[14] |
Comparison: CJC-1295 No DAC vs. Related Compounds
| Parameter | CJC-1295 No DAC (Mod GRF 1-29) | CJC-1295 With DAC | Native GHRH(1-29) / Sermorelin |
|---|---|---|---|
| Half-Life | ~30 minutes | 6–8 days | Minutes |
| GH Release Pattern | Pulsatile (physiological) | Continuous (non-physiological) | Pulsatile (very brief) |
| DPP-4 Resistance | Yes (D-Ala² substitution) | Yes (D-Ala² substitution) | No (rapidly cleaved) |
| Albumin Binding | None | Covalent (via MPA-Lys linker) | None |
| Receptor Desensitization Risk | Low (pulsatile clearance) | Higher (chronic stimulation) | Low (too brief to cause) |
| Clinical Trials | None identified for this specific compound | Phase I/II completed (Teichman 2006; Ionescu 2006) | FDA-approved (as Sermorelin, discontinued) |
Research Applications
Research Applications
CJC-1295 (no DAC) is utilized in laboratory research to investigate the effects of pulsatile GHRH receptor stimulation on the GH/IGF-1 axis across 5+ research domains. It is important to note that the FDA has identified no published clinical trials or preclinical efficacy studies specific to CJC-1295 without DAC; the research applications below reflect the broader GHRH analog literature and the known pharmacology of the GH/IGF-1 axis.[9]
Application Areas
- Body Composition & Muscle Hypertrophy — Research indicates that GHRH analog-stimulated GH release promotes protein synthesis and increases lean muscle mass through IGF-1 stimulation. CJC-1295 (no DAC) is frequently studied in the context of sarcopenia (age-related muscle loss) to determine if pulsatile GHRH stimulation can preserve muscle tissue and strength in aging populations.[6][12]
- Lipid Metabolism & Weight Management — Studies suggest that upregulation of GH secretion facilitates lipolysis (fat breakdown) and inhibits lipogenesis. Researchers investigate the utility of GHRH analogs in models of obesity and metabolic syndrome, focusing on improved energy expenditure and reduction of visceral adipose tissue.[6][12]
- Tissue Repair & Injury Recovery — Due to the regenerative properties of the GH/IGF-1 axis, this peptide is researched for its potential to accelerate the healing of connective tissues, including tendons and ligaments. It is hypothesized to enhance collagen synthesis and cellular repair mechanisms following acute injury or surgery.[6]
- Sleep Physiology — Growth hormone secretion is intimately linked with slow-wave sleep (SWS). Research explores the potential of GHRH analogs to deepen sleep cycles and improve restorative sleep states, as GHRH activity is necessary to initiate and maintain the deepest stages of non-REM sleep.[6]
- Anti-Aging & Cellular Function — Investigational uses focus on the peptide's ability to restore "youthful" GH pulsatility in aging populations, potentially mitigating physiological declines associated with the somatopause, including reduced skin elasticity, bone mineral density loss, and cognitive function decline.[6][12]
Evidence Summary by Application
| Application | Mechanism | Evidence Level | Key References |
|---|---|---|---|
| Muscle Hypertrophy / Sarcopenia | GH → IGF-1 → mTOR → protein synthesis | Preclinical (DAC variant); theoretical for no-DAC | Sinha et al. (2020)[12] |
| Lipid Metabolism / Obesity | GH → hormone-sensitive lipase → lipolysis; inhibited lipogenesis | Preclinical (DAC variant); theoretical for no-DAC | Sigalos & Pastuszak (2018)[7] |
| Tissue Repair / Connective Tissue | GH/IGF-1 → collagen synthesis stimulation | Theoretical; based on GH/IGF-1 axis physiology | GH axis pharmacology[6] |
| Sleep Enhancement | GHRH signaling → slow-wave sleep induction and maintenance | Theoretical; based on GHRH/SWS relationship | GHRH sleep physiology literature[6] |
| Anti-Aging / Somatopause | Restoration of pulsatile GH secretion; IGF-1 normalization | Theoretical; based on age-related GH decline | Sinha et al. (2020)[12] |
| Pituitary Biology / DNA Damage | cAMP stimulation → H2AX phosphorylation → DNA damage in somatotrophs | Preclinical in vitro/in vivo (likely DAC variant) | Ben-Shlomo et al. (2020)[14] |
Synergistic Combination Research
CJC-1295 (no DAC) is frequently studied in combination with Ipamorelin, a selective growth hormone secretagogue that acts on the ghrelin/GHS receptor (a complementary pathway to GHRH). The rationale is that simultaneous GHRH receptor activation (via CJC-1295 no DAC) and GHS receptor activation (via Ipamorelin) produce a synergistic amplification of GH release beyond what either compound achieves alone.[12]
Analytical & Forensic Applications
CJC-1295 (no DAC) has been a subject of forensic and anti-doping research. Henninge et al. (2010) and Hartvig et al. (2014) developed LC-MS/MS methods to identify Modified GRF 1-29 in seized pharmaceutical preparations, confirming its widespread distribution in the grey market. These analytical methods also serve as the basis for WADA anti-doping testing protocols.[1][3][13]
Biochemical Characteristics
| Property | Value |
|---|---|
| Molecular Formula | C₁₅₂H₂₅₂N₄₄O₄₂ |
| Molecular Weight | 3367.95 g/mol |
| CAS Number | 863288-34-0 |
| PubChem CID | 56841945 |
| Sequence (1-Letter) | Y-a-D-A-I-F-T-Q-S-Y-R-K-V-L-A-Q-L-S-A-R-K-L-L-Q-D-I-L-S-R-NH₂ (a = D-Alanine) |
| Sequence (3-Letter) | Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH₂ |
| Structure | 29-amino acid linear peptide; tetrasubstituted analog of GHRH(1-29) with D-Ala², Gln⁸, Ala¹⁵, Leu²⁷ substitutions; C-terminal amide; lacks DAC (Drug Affinity Complex) moiety |
| Origin | Synthetic analog of human Growth Hormone-Releasing Hormone (GHRH) fragment 1-29, also known as Sermorelin. Developed by ConjuChem Biotechnologies Inc. (Montreal, Canada) |
| Classification | GHRH Analog / Growth Hormone Secretagogue / Research Peptide |
| Half-Life | Approximately 30 minutes (vs. 6–8 days for CJC-1295 with DAC; vs. minutes for native GHRH) |
| Bioavailability | Subcutaneous injection; resistant to DPP-4 enzymatic degradation; rapidly cleared from bloodstream |
Identifiers
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|---|---|
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| Alternate CAS | |
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| IUPAC Name |
Preclinical Research Summary
Research Summary
Clinical & Preclinical Data Status
According to a comprehensive FDA evaluation prepared for the Pharmacy Compounding Advisory Committee (December 2024), there are no published human clinical trials and no preclinical efficacy or toxicity studies specifically for CJC-1295 without DAC (Modified GRF 1-29). All prominent clinical trials associated with the name "CJC-1295" in medical literature were conducted using the DAC variant, which is pharmacokinetically distinct due to its albumin-binding Drug Affinity Complex.[9][10]
Key Studies on CJC-1295 (DAC Variant) — Often Misattributed to No-DAC
| Study | Model | Key Findings | Ref |
|---|---|---|---|
| Teichman et al. (2006) J Clin Endocrinol Metab | Healthy human adults; 30–250 mcg/kg SC; single or weekly/biweekly doses | Dose-dependent increases in mean plasma GH (2–10-fold for ≥6 days) and IGF-1 (1.5–3-fold for 9–11 days). Half-life 5.8–8.1 days. Note: DAC variant, not applicable to no-DAC. | [8] |
| Ionescu & Frohman (2006) J Clin Endocrinol Metab | Healthy human adults; CJC-1295 with DAC | Confirmed that pulsatile GH secretion persists during continuous stimulation by CJC-1295 (DAC). Note: DAC variant. | [15] |
| Jetté et al. (2005) Endocrinology | Sprague-Dawley rats; 1 µmol/kg SC | Described synthesis of tetrasubstituted GHRH core and DAC conjugation. Demonstrated GH elevation with half-life >72 hours. Note: DAC variant. | [4] |
| Alba et al. (2006) Am J Physiol | GHRH knockout mice; 2 µg/mouse daily | Normalized growth; increased body length and lean mass; increased pituitary GH mRNA and somatotroph proliferation. Note: DAC variant. | [8] |
| Ben-Shlomo et al. (2020) J Clin Invest | C57BL/6 mice and primary pituitary cultures; 10–50 ng/mL in vitro | Intense cAMP stimulation induced DNA damage in somatotrophs (H2AX phosphorylation, comet assays). Increased GH levels and pituitary weight in vivo. Note: Likely DAC variant per FDA assessment. | [14] |
Studies Specific to CJC-1295 No DAC (Analytical/Forensic Only)
| Study | Context | Key Findings | Ref |
|---|---|---|---|
| Henninge et al. (2010) Drug Test Anal | Norwegian Doping Control Laboratory; seized pharmaceutical preparations | Identified Modified GRF 1-29 (CJC-1295 without DAC) in seized products using mass spectrometry. Confirmed widespread distribution of no-DAC variant mislabeled as CJC-1295. | [1] |
| Hartvig et al. (2014) Scand J Forensic Sci | Danish authorities; doping compounds confiscated 2007–2013 | Identified CJC-1295 (no DAC) among confiscated peptide preparations. No therapeutic efficacy or safety data generated. | [3] |
| Fabresse et al. (2017) Toxicol Anal Clin | LC-HRMS/MS identification of CJC-1295 analogs | Developed high-resolution mass spectrometric methods for identifying CJC-1295 peptide analogs in analytical chemistry settings. | [13] |
FDA Assessment Summary (December 2024)
| Category | FDA Finding for CJC-1295 No DAC |
|---|---|
| Clinical Trials | None identified. No Phase I, II, or III trials for CJC-1295 (free base) or CJC-1295 acetate.[9] |
| Preclinical Pharmacology | None identified. No nonclinical pharmacological studies for this specific substance.[9] |
| Preclinical Toxicity | None identified. No acute toxicity, repeat-dose toxicity, genotoxicity, developmental/reproductive toxicity, or carcinogenicity studies.[9] |
| Safety Profile | Unknown in humans. Potential risks include immunogenicity and injection site reactions based on peptide characteristics.[9] |
| Regulatory Classification | Category 2. Significant safety risks or insufficient evidence; restricted from pharmacy compounding.[9][10] |
Dosage Overview (From Literature & Clinical Practice)
| Setting | Dose | Route / Schedule | Notes |
|---|---|---|---|
| In Vitro (pituitary cultures) | 10–50 ng/mL | Cell culture | Ben-Shlomo et al. (2020); likely DAC variant[14] |
| Animal (rats — DAC variant) | 1 µmol/kg SC | Subcutaneous injection | Jetté et al. (2005)[4] |
| Animal (mice — DAC variant) | 2 µg/mouse daily | Subcutaneous injection | Alba et al. (2006)[8] |
| Human (DAC variant) | 30–250 mcg/kg | SC; single or weekly/biweekly | Teichman et al. (2006)[8] |
| Human (no-DAC; clinical practice) | 100–300 mcg | SC; 1–3x daily or 5 days/week | Anecdotal protocols; not derived from clinical trials |
Safety Considerations
| Parameter | Finding |
|---|---|
| Clinical Safety Data | No submitted or identified clinical safety studies for CJC-1295 (free base) or acetate[9] |
| Preclinical Toxicity Data | No nonclinical toxicity studies (acute, repeat-dose, genotoxicity) identified[9] |
| Immunogenicity | Theoretical risk of antibody formation; 86% homology with endogenous GHRH[9] |
| Reported Adverse Effects (Anecdotal) | Injection site reactions, flushing, headache, transient hypotension, water retention[12] |
| Contraindications (General GHRH Analog) | Active malignancy (GH/IGF-1 may promote tumor growth), pregnancy/breastfeeding, hypersensitivity[7] |
| DAC Variant Safety Note | CJC-1295 with DAC was discontinued during Phase 2 trials after a patient death (attributed to underlying coronary artery disease, not the drug); no such event linked to the no-DAC variant[7] |
Important Disclaimer
This product is sold strictly for in-vitro research and laboratory use only. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. For Laboratory Research Only. Not for human use, medical use, diagnostic use, or veterinary use.
About This Research Profile
This research profile was compiled from peer-reviewed sources, regulatory documents (FDA briefing materials), forensic analytical chemistry publications, and established GHRH pharmacology literature. All citations have been verified against PubMed, DOI, and official regulatory repositories. It is important to note that the FDA has identified no clinical trials or preclinical efficacy/toxicity studies specific to CJC-1295 without DAC; the research context presented here is drawn from the broader GHRH analog literature and the pharmacology of the GH/IGF-1 axis. ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.
Authors & Attribution
✍️ Article Author
Lucie Jetté, PhD
Lucie Jetté, PhD, was a lead researcher at ConjuChem Biotechnologies Inc. (Montreal, Canada), the company that developed the CJC-1295 peptide class. She and her team synthesized the tetrasubstituted growth hormone-releasing hormone (GHRH) analog known as Modified GRF (1-29), which serves as the core peptide for both CJC-1295 (no DAC) and CJC-1295 (with DAC). Her foundational 2005 paper in Endocrinology described the structural modifications (tetrasubstitution at positions 2, 8, 15, and 27) that grant the peptide resistance to DPP-4 enzymatic degradation, and characterized the Drug Affinity Complex (DAC) albumin-binding mechanism designed to extend the peptide's half-life. This work established the pharmacological foundation for all subsequent CJC-1295 research, including the clinical trials conducted by Teichman et al. (2006). Her key publication is "Human Growth Hormone-Releasing Factor (hGRF)1-29-Albumin Bioconjugates Activate the GRF Receptor on the Anterior Pituitary in Rats: Identification of CJC-1295 as a Long-Lasting GRF Analog" (2005, Endocrinology). Lucie Jetté is being referenced as one of the leading scientists involved in CJC-1295 (no DAC) research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
🎓 Scientific Journal Author
Lawrence A. Frohman, MD
Lawrence A. Frohman, MD (1935–2018), was a distinguished neuro-endocrinologist and one of the foremost authorities on growth hormone-releasing hormone (GHRH) physiology and pharmacology. He served as the Edmund F. Foley Professor and Chairman of the Department of Medicine at the University of Illinois College of Medicine in Chicago (1992–2001), and previously directed the Division of Endocrinology and Metabolism at the University of Cincinnati (1981–1992). His extensive career spanned foundational research on GHRH discovery, regulation, and clinical applications. As a senior investigator on the landmark Teichman et al. (2006) and Ionescu & Frohman (2006) clinical trials, he established the dose-dependent pharmacokinetic and pharmacodynamic profile of CJC-1295, demonstrating sustained GH and IGF-1 elevation in healthy adults. His key publications include "Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295" (2006, J Clin Endocrinol Metab) and "Pulsatile secretion of growth hormone persists during continuous stimulation by CJC-1295" (2006, J Clin Endocrinol Metab). Lawrence A. Frohman is being referenced as one of the leading scientists involved in CJC-1295 (no DAC) research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
🔬 Contributing Researcher
Anat Ben-Shlomo, MD
Anat Ben-Shlomo, MD, is an endocrinologist and researcher at Cedars-Sinai Medical Center (Los Angeles, California) and a member of the Melmed Research Lab, one of the world's preeminent pituitary research groups. She earned her medical degree from Tel Aviv University and specializes in the study of genomic changes underlying the development and progression of pituitary tumors, particularly growth hormone-secreting somatotroph adenomas that lead to acromegaly. Her landmark 2020 study in The Journal of Clinical Investigation demonstrated that intense cAMP stimulation by CJC-1295 in mouse pituitary cells induced DNA damage, as measured by H2AX phosphorylation and comet assays. This work revealed a critical link between GHRH receptor-mediated secretory activity and cellular stress in somatotrophs, showing that somatic copy number alterations (SCNAs) rather than genetic mutations are hallmarks of these tumors. Her key publication is "DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas" (2020, The Journal of Clinical Investigation). Anat Ben-Shlomo is being referenced as one of the leading scientists involved in CJC-1295 (no DAC) research. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Pure US Peptide and this doctor.
Referenced Citations
Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Testing and Analysis, 2(11-12), 647-650, 2010.
DOISoule S, King JA, Millar RP. Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men. The Journal of Clinical Endocrinology and Metabolism, 79(4), 1208-1211, 1994.
DOIHartvig RA, Holm NB, Dalsgaard PW, Reitzel LA, Müller IB, Linnet K. Identification of peptide and protein doping related drug compounds confiscated in Denmark between 2007-2013. Scandinavian Journal of Forensic Science, 20(2), 42-49, 2014.
DOIJetté L, et al. Human Growth Hormone-Releasing Factor (hGRF)1-29-Albumin Bioconjugates Activate the GRF Receptor on the Anterior Pituitary in Rats: Identification of CJC-1295 as a Long-Lasting GRF Analog. Endocrinology, 146(7), 3052-3058, 2005.
DOILance VA, Murphy WA, Sueiras-Diaz J, Coy DH. Super-active analogs of growth hormone-releasing factor (1-29)-amide. Biochemical and Biophysical Research Communications, 119(1), 265-272, 1984.
DOIVan Hout MC, Hearne E. Netnography of Female Use of the Synthetic Growth Hormone CJC-1295: Pulses and Potions. Substance Use & Misuse, 51(1), 73-84, 2016.
PubMedSigalos JT, Pastuszak AW. The Safety and Efficacy of Growth Hormone Secretagogues. Sexual Medicine Reviews, 6(1), 45-53, 2018.
PubMedTeichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. The Journal of Clinical Endocrinology & Metabolism, 91(3), 799-805, 2006.
DOIFood and Drug Administration. FDA Evaluation of CJC-1295 Related Bulk Drug Substances. FDA Briefing Document: Pharmacy Compounding Advisory Committee (PCAC) Meeting, December 4, 2024.
FDA.govFood and Drug Administration. Final Summary Minutes of the Pharmacy Compounding Advisory Committee Meeting. Center for Drug Evaluation and Research, December 4, 2024.
FDA.govWorld Anti-Doping Agency. The 2024 Prohibited List: International Standard. World Anti-Doping Code, 2024.
SourceSinha DK, Balasubramanian A, Tatem AJ, Kovac JR, Pastuszak AW, Lipshultz LI. Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Translational Andrology and Urology, 9(Suppl 2), S149-S159, 2020.
PubMedFabresse N, Grassin-Delyle S, Etting I, Alvarez JC. Identification of a GHRH peptide analogue, the CJC-1295, using LC-HRMS/MS. Toxicologie Analytique et Clinique, 29(2), 205-211, 2017.
DOIBen-Shlomo A, et al. DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas. The Journal of Clinical Investigation, 130(11), 5738-5755, 2020.
SourceIonescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. The Journal of Clinical Endocrinology & Metabolism, 91(12), 4792-4797, 2006.
DOIMemdouh S, Gavrilović I, Ng K, Cowan D, Abbate V. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Testing and Analysis, 13(11-12), 1871-1887, 2021.
DOIStorage & Handling
Summary
Lyophilized: -20°C (long-term) or 2–8°C (short-term); Reconstituted: 2–8°C, use within 14–28 days; avoid freeze-thaw cycles.
Lyophilized Powder
Store at -20°C for long-term stability. The lyophilized form is stable at refrigerated temperatures (2–8°C) or even room temperature for shorter periods but should be kept sealed, away from moisture and direct light for optimal preservation.
Reconstituted Solution
Reconstitute with bacteriostatic water (preferred for multi-use) or sterile water for injection. Once reconstituted, refrigerate at 2–8°C and use within 14–28 days depending on the solvent used and storage conditions. Bacteriostatic water generally allows longer storage compared to sterile water.
Handling
White to off-white lyophilized powder. When reconstituting, inject the solvent slowly down the side of the vial and swirl gently — do NOT shake, as this may damage the peptide structure. Purity: ≥98% by RP-HPLC. Identity: LC-MS/MS (~3367.95 Da). The tetrasubstitution modifications provide resistance to DPP-4 enzymatic degradation, extending functional half-life to approximately 30 minutes from the mere minutes characteristic of native GHRH.
RUO Disclaimer
For Research Use Only (RUO). This product is intended solely for in-vitro research and laboratory experimentation. It is not a drug, food, cosmetic, or medical device and has not been approved by the FDA for any human or veterinary use. It must not be used for therapeutic, diagnostic, or any other non-research purpose. Pure US Peptide does not condone or encourage the use of this product for anything other than strictly defined research applications. Users assume full responsibility for compliance with all applicable regulations and guidelines.
Certificate of Analysis (COA)
Every batch is strictly tested by accredited third-party laboratories (ISO 17025) to ensure 99%+ purity.
Latest Lab Report
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