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CJC-1295

Also known as: CJC-1295 DAC, Modified GRF(1-29), Mod GRF 1-29

Growth HormonePreclinicalPreliminary

Last updated: 2026-03-20

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Overview

CJC-1295 is a synthetic peptide analog of growth hormone-releasing hormone (GHRH), originally developed by ConjuChem Biotechnologies (later ConjuChem LLC) based in Montreal, Canada. It consists of the first 29 amino acids of GHRH with four amino acid substitutions (positions 2, 8, 15, and 27) designed to resist enzymatic degradation by dipeptidyl peptidase-IV (DPP-IV) [1][4].

The distinguishing feature of CJC-1295 is its use of Drug Affinity Complex (DAC) technology, a reactive chemical group (maleimidopropionic acid) that forms a covalent bond with serum albumin following subcutaneous injection [5]. This bioconjugation extends the peptide's half-life from minutes to approximately 6-8 days, allowing for once-weekly or biweekly dosing [1][5].

ConjuChem advanced CJC-1295 DAC through Phase II clinical trials for adult growth hormone deficiency. However, clinical development was discontinued following the death of a participant during a trial, reportedly due to a cardiovascular event [7]. The circumstances surrounding the discontinuation have not been fully detailed in published peer-reviewed literature. ConjuChem subsequently entered bankruptcy proceedings.

A version of the peptide without the DAC component, often referred to as Modified GRF(1-29) or Mod GRF 1-29, retains the amino acid substitutions for DPP-IV resistance but lacks the albumin-binding functionality. This version has a substantially shorter half-life of approximately 30 minutes [1].

Mechanism of Action

CJC-1295 acts by binding to the GHRH receptor (GHRH-R) on somatotroph cells of the anterior pituitary gland, the same receptor targeted by endogenous GHRH [2][4].

GHRH Receptor Activation: Upon binding, CJC-1295 stimulates the production and release of growth hormone (GH) through a cyclic AMP (cAMP)-dependent signaling cascade. This process mirrors the physiological mechanism by which hypothalamic GHRH stimulates pulsatile GH secretion [2].

Preservation of Pulsatile Release: Unlike exogenous GH administration, which produces a non-physiological continuous elevation of circulating GH, CJC-1295 amplifies the existing pulsatile pattern of GH secretion. In the Teichman et al. trial, subjects receiving CJC-1295 DAC demonstrated elevated GH pulse amplitude while retaining the normal oscillatory secretion pattern [1].

DAC-Albumin Binding: The DAC moiety contains a maleimide group that reacts with the free thiol on cysteine-34 of human serum albumin within minutes of injection. Because albumin has a circulating half-life of approximately 19-21 days, this conjugation shields the peptide from renal clearance and proteolytic degradation, extending its pharmacological activity [5].

IGF-1 Elevation: As a downstream consequence of sustained GH elevation, CJC-1295 DAC produces a dose-dependent increase in circulating insulin-like growth factor I (IGF-1) levels. In healthy adults, a single dose of 60 μg/kg resulted in IGF-1 elevations lasting up to 14 days [1].

Pharmacokinetics

The pharmacokinetic profile of CJC-1295 differs dramatically between the DAC and non-DAC formulations, and understanding this distinction is central to evaluating the peptide's clinical behavior.

CJC-1295 with DAC

Absorption and Albumin Conjugation: Following subcutaneous injection, the maleimidopropionic acid (MPA) moiety on CJC-1295 DAC reacts with the free sulfhydryl group on cysteine-34 of circulating serum albumin. This covalent bioconjugation occurs rapidly, with the majority of the peptide becoming albumin-bound within 15-30 minutes of injection [5]. The resulting albumin-CJC-1295 complex circulates as a macromolecular entity of approximately 70 kDa, which is above the renal filtration threshold and thereby protected from glomerular clearance.

Half-life: The terminal elimination half-life of CJC-1295 DAC is approximately 5.8-8.1 days, as determined by Ionescu et al. through pharmacokinetic modeling of serial blood samples in healthy volunteers [3]. This represents an approximately 200- to 400-fold extension compared to native GHRH (half-life 7-10 minutes) and a roughly 12- to 16-fold extension compared to the non-DAC version [1][3].

Steady State: With weekly dosing, pharmacokinetic modeling predicts that CJC-1295 DAC reaches steady-state plasma concentrations by the second or third dose. In the Teichman et al. trial, IGF-1 levels continued to accumulate with repeated weekly dosing at 30 and 60 mcg/kg, suggesting progressive pharmacodynamic effect before plateau [1][3].

GH Secretion Pattern -- "GH Bleed": A notable pharmacodynamic consequence of the sustained half-life is that CJC-1295 DAC produces a continuous elevation of basal GH levels between physiological pulses. This phenomenon, sometimes termed "GH bleed," means that trough GH levels remain elevated throughout the dosing interval rather than returning to baseline between pulses. While the pulsatile pattern is preserved in terms of peak amplitude, the inter-pulse nadir is elevated, creating a profile that is intermediate between true pulsatile GH secretion and continuous GH infusion [1][14].

CJC-1295 without DAC (Mod GRF 1-29)

Half-life: Without the albumin-binding DAC moiety, Modified GRF(1-29) has an elimination half-life of approximately 30 minutes following subcutaneous injection. This is substantially longer than native GHRH(1-29) (half-life approximately 7-10 minutes) due to the four amino acid substitutions that confer DPP-IV resistance, but far shorter than the DAC version [1][2].

Subcutaneous Bioavailability: The subcutaneous bioavailability of Mod GRF 1-29 has not been precisely quantified in published human studies, but based on analogous peptides of similar molecular weight and charge, it is estimated at 50-70%. Absorption from the subcutaneous depot produces peak plasma concentrations within 15-30 minutes [2].

GH Pulse Pattern: The short half-life of the non-DAC version produces a discrete, acute GH pulse following each injection, more closely mimicking the physiological pattern of hypothalamic GHRH release. GH levels return to baseline within 2-3 hours, which is why multiple daily injections (typically 2-3 per day) are required to maintain meaningful GH elevation [2]. This pulsatile profile is considered more physiological than the sustained elevation seen with the DAC formulation.

Dose-Proportionality

Pharmacokinetic analysis from the Ionescu et al. presentation indicated that CJC-1295 DAC exhibits dose-proportional pharmacokinetics across the 30-125 mcg/kg range, meaning that doubling the dose approximately doubles the area under the curve (AUC) for both the parent compound and the resultant GH elevation [3].

Dose-Response Relationships

Data from the Teichman et al. dose-escalation study provide the most detailed available characterization of CJC-1295 DAC dose-response in humans [1].

Single-Dose Pharmacodynamics

30 mcg/kg: A single subcutaneous dose of 30 mcg/kg produced a 2- to 3-fold increase in mean GH concentrations and a 1.5- to 2-fold increase in IGF-1, with effects persisting for approximately 6 days. This was the lowest dose tested and was generally well tolerated [1].

60 mcg/kg: At 60 mcg/kg, mean GH concentrations increased 4- to 10-fold and IGF-1 levels rose 1.5- to 3-fold. The pharmacodynamic effect persisted for 10-14 days. This dose was identified as offering the most favorable balance of efficacy and tolerability [1].

125 mcg/kg: The highest tested dose of 125 mcg/kg produced robust GH and IGF-1 elevations but was associated with a higher incidence of adverse effects, including more prominent injection site reactions and greater fluid retention. The incremental efficacy gain above 60 mcg/kg was not proportional to the increase in side effects, leading investigators to consider 60 mcg/kg as the upper boundary of the optimal dose range [1].

Repeated Dosing Effects

In the multiple-dose cohort of the Teichman trial, weekly injections of CJC-1295 DAC at 30 and 60 mcg/kg produced progressive IGF-1 accumulation across successive doses [1]. After two to three weekly injections:

  • Mean IGF-1 levels were approximately 1.5- to 3-fold above baseline and remained elevated throughout the dosing interval
  • GH pulse amplitude remained augmented, with no evidence of receptor desensitization or tachyphylaxis over the study period (up to 4 weeks of weekly dosing)
  • The IGF-1 response to repeated dosing was greater than predicted from single-dose data, consistent with the pharmacokinetic accumulation expected from a compound with a half-life of 6-8 days dosed on a weekly basis [1][3]

Optimal Injection Frequency

CJC-1295 with DAC: Based on the half-life of 6-8 days, weekly or biweekly subcutaneous injection was used in clinical trials. Weekly dosing produced steady-state accumulation, while biweekly dosing (every 14 days) still produced measurable GH and IGF-1 elevation but with more fluctuation between doses [1].

CJC-1295 without DAC (Mod GRF 1-29): The 30-minute half-life necessitates multiple daily injections. In preclinical and early clinical protocols, 2-3 subcutaneous injections per day (typically timed around sleep and fasting periods to synergize with endogenous GH pulses) have been used. Injection timing is often aligned with natural GH secretory windows: before sleep, upon waking, and post-exercise [2].

Comparative Effectiveness

CJC-1295 exists within a broader landscape of GHRH analogs, GH secretagogues, and related compounds. The following comparisons are based on published pharmacological and clinical data.

vs Sermorelin (GHRH 1-29, Geref)

Sermorelin is the native GHRH(1-29) fragment without amino acid substitutions. It was FDA-approved (as Geref Diagnostic) for diagnostic use and previously for pediatric GH deficiency treatment before its approval was withdrawn for commercial reasons [10].

  • Half-life: Sermorelin has an elimination half-life of approximately 10-20 minutes, compared to approximately 30 minutes for Mod GRF 1-29 and 6-8 days for CJC-1295 DAC. Sermorelin is rapidly degraded by DPP-IV, which cleaves the His-Ala bond at positions 1-2 [2][10]
  • DPP-IV Resistance: The four amino acid substitutions in CJC-1295 (D-Ala at position 2, Gln at position 8, Ala at position 15, Leu at position 27) were specifically engineered to prevent DPP-IV cleavage that limits sermorelin's duration of action [4]
  • Clinical Status: Sermorelin has more extensive human safety data (FDA approval history) but is limited by its short duration of action requiring daily or twice-daily injections. CJC-1295 was designed to address this limitation but never achieved regulatory approval [2][10]
  • Efficacy: Head-to-head comparisons have not been published. Both compounds stimulate GH release via the same GHRH receptor, but CJC-1295's enhanced metabolic stability produces substantially greater AUC for GH exposure per injection

vs Tesamorelin (Egrifta)

Tesamorelin is a synthetic GHRH analog consisting of the full 44-amino acid GHRH sequence with a trans-3-hexenoic acid modification at the N-terminus. It is the only GHRH analog currently approved by the FDA (approved 2010 for HIV-associated lipodystrophy) [9].

  • Regulatory Status: Tesamorelin is FDA-approved for reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. CJC-1295 has no regulatory approval in any jurisdiction [9]
  • Half-life: Tesamorelin has a half-life of approximately 26-38 minutes, similar to Mod GRF 1-29 but far shorter than CJC-1295 DAC. It requires daily subcutaneous injection (2 mg/day) [9][13]
  • Mechanism: Both act on the GHRH receptor. Tesamorelin is based on full-length GHRH(1-44) rather than the truncated 1-29 fragment used in CJC-1295, though the first 29 residues contain the full receptor-binding domain [2][9]
  • Clinical Evidence: Tesamorelin has substantially more clinical evidence, including Phase III trials demonstrating reductions in visceral adipose tissue and improvements in trunk fat distribution. CJC-1295 has only Phase I/II data [9][13]
  • Safety Profile: Tesamorelin has a well-characterized safety profile from regulatory review. The most common adverse effects include injection site reactions, arthralgia, and peripheral edema. IGF-1 elevation is monitored as a safety parameter [9]

vs Native GHRH(1-44)

Native GHRH(1-44) is the full-length hypothalamic peptide. CJC-1295 is based on the first 29 amino acids (the minimum receptor-binding domain) with stabilizing modifications [2].

  • Potency: The first 29 residues of GHRH contain the complete receptor-binding domain; positions 30-44 contribute to secondary structure stability but are not required for receptor activation. CJC-1295 retains full intrinsic activity at the GHRH receptor [2][4]
  • Stability: Native GHRH(1-44) has a plasma half-life of approximately 7-10 minutes due to rapid DPP-IV cleavage. CJC-1295's amino acid substitutions and optional DAC conjugation represent successive engineering strategies to overcome this limitation [2][4]

vs Ipamorelin (GHRH + GHRP Synergy Rationale)

Ipamorelin is a selective GH secretagogue peptide (GHRP) that acts through the ghrelin receptor (GHS-R1a), a distinct mechanism from the GHRH receptor targeted by CJC-1295 [11].

  • Mechanistic Synergy: GHRH receptor agonists (like CJC-1295) and ghrelin receptor agonists (like ipamorelin) stimulate GH release through independent but complementary pathways. GHRH primarily increases the amplitude of GH pulses, while GHRPs primarily increase the frequency and also reduce somatostatin tone. Co-administration produces a synergistic GH response that exceeds the additive effect of either compound alone [2][11]
  • Clinical Rationale for Combination: The CJC-1295 (without DAC) plus ipamorelin combination is widely discussed in clinical peptide therapy contexts because: (a) the GHRH + GHRP synergy maximizes GH pulse magnitude, (b) ipamorelin is among the most selective GHRPs with minimal effects on cortisol, prolactin, and appetite compared to GHRP-6 or GHRP-2, and (c) using Mod GRF 1-29 (not DAC version) preserves discrete pulsatile dosing [2][11]
  • No Published Combination Trials: Despite widespread clinical discussion, no controlled trials examining the specific combination of CJC-1295 and ipamorelin have been published in peer-reviewed literature

vs MK-677 (Ibutamoren)

MK-677 is an oral, non-peptide ghrelin receptor agonist (GH secretagogue) with a long duration of action [6][12].

  • Route of Administration: MK-677 is orally bioavailable, a significant practical advantage over all injectable peptides including CJC-1295. It is taken once daily by mouth [6][12]
  • Mechanism: MK-677 acts through the ghrelin receptor (GHS-R1a), not the GHRH receptor. It therefore stimulates GH release through the secretagogue pathway and also increases appetite and may affect cortisol and prolactin to a modest degree [6][12]
  • Half-life: MK-677 has an oral half-life of approximately 4-6 hours, but its GH-elevating effects persist for up to 24 hours, allowing once-daily dosing [12]
  • Clinical Data: MK-677 has more extensive clinical trial data than CJC-1295, including randomized controlled trials lasting up to 2 years in elderly populations. The Nass et al. study demonstrated increases in fat-free mass and GH/IGF-1 levels but no improvements in functional endpoints [6]
  • Side Effects: MK-677 is associated with increased appetite (a direct ghrelin pathway effect), transient edema, and dose-dependent insulin resistance. CJC-1295 does not directly stimulate appetite through the ghrelin pathway [6][12]
  • Regulatory Status: Neither compound is FDA-approved for GH-related indications. MK-677 was investigated by Merck but development was not pursued to approval

Researched Applications

CJC-1295 has been investigated in the following contexts. All applications remain investigational, and no regulatory agency has approved CJC-1295 for any indication.

Growth Hormone Deficiency

The primary intended clinical application was the treatment of adult growth hormone deficiency (AGHD). The extended half-life of the DAC formulation was designed to reduce injection burden compared to daily recombinant GH therapy [1][2]. Phase II trials were initiated but not completed due to the discontinuation of development.

Body Composition

In the Teichman et al. study, CJC-1295 DAC elevated GH and IGF-1 levels in a sustained manner consistent with known effects of the GH-IGF-1 axis on lean body mass and fat metabolism [1]. However, direct body composition outcomes were not the primary endpoint of this trial, and no controlled data on fat mass or lean mass changes in humans have been published for CJC-1295 specifically.

Aging and Somatopause

Age-related decline in GH secretion (somatopause) has been a broader area of interest for GHRH analogs and GH secretagogues. The rationale for CJC-1295 in this context rests on its ability to restore higher GH pulsatility without complete replacement of the endogenous axis [2][6]. No completed trials have evaluated CJC-1295 for age-related GH decline.

Clinical Evidence Summary

The published clinical evidence for CJC-1295 is limited to early-phase trials:

  • Teichman et al. (2006): A dose-escalation study in 33 healthy adults examined single and multiple doses of CJC-1295 DAC (30, 60, and 125 μg/kg). Single doses of 30-60 μg/kg produced 2- to 10-fold increases in mean GH concentrations and 1.5- to 3-fold increases in IGF-1 levels, sustained for 6-14 days. Multiple weekly doses resulted in further IGF-1 accumulation [1].

  • Ionescu et al. (2005): Pharmacokinetic analysis presented at The Endocrine Society meeting confirmed the extended half-life profile and dose-proportional pharmacokinetics of CJC-1295 DAC [3].

No Phase III trials, long-term efficacy data, or head-to-head comparisons with recombinant GH have been published.

Dosing in Published Research

The following doses have been used in clinical research settings. This information is provided for educational reference only and does not constitute medical advice or a recommendation for use.

| Protocol | Dose | Frequency | Route | Source | |---|---|---|---|---| | CJC-1295 with DAC | 30-60 μg/kg | Once weekly to once every 2 weeks | Subcutaneous | Teichman et al. 2006 [1] | | CJC-1295 without DAC (Mod GRF 1-29) | 1-2 μg/kg (commonly cited as 100 μg per injection) | 2-3 times daily | Subcutaneous | Preclinical data [4] |

Doses above 60 μg/kg of the DAC formulation were associated with a higher incidence of adverse effects without proportional efficacy gains [1].

Safety and Side Effects

Observed Adverse Effects

In the Teichman et al. trial, the most commonly reported side effects at doses of 30-60 μg/kg included [1]:

  • Injection site reactions (erythema, swelling, pain)
  • Transient flushing
  • Headache
  • Diarrhea
  • Water retention and peripheral edema

Injection Site Reactions

Injection site reactions were among the most frequently reported adverse events in the CJC-1295 DAC clinical program. These reactions, which included erythema, induration, pain, and pruritus at the injection site, were observed across all dose groups but were more common and more severe at the 125 mcg/kg dose [1]. The DAC moiety itself may contribute to local reactions, as the maleimide-albumin conjugation reaction occurs in the subcutaneous tissue and could provoke local immune activation. Injection site reactions were generally self-limiting, resolving within 3-7 days [1][5].

Antibody Formation

The bioconjugation of CJC-1295 to endogenous albumin creates a neoantigen (a modified self-protein) that has the potential to elicit an immune response. In the Teichman et al. study, anti-CJC-1295 antibodies were detected in a subset of subjects receiving repeated doses, although the clinical significance of these antibodies was not fully characterized within the limited study duration [1]. Whether sustained antibody formation could lead to neutralization of the peptide's activity or cross-reactivity with endogenous GHRH remains an open question that was never resolved due to the termination of the clinical program.

The DAC Concern: Sustained vs Pulsatile GH Elevation

A central pharmacological concern with CJC-1295 DAC is the distinction between its sustained GH elevation pattern and truly pulsatile GH secretion. While the DAC formulation preserves GH pulse peaks, the continuous presence of the GHRH agonist in circulation means that basal (inter-pulse) GH levels remain elevated -- the "GH bleed" phenomenon described in the Pharmacokinetics section. This creates a secretory pattern that is physiologically intermediate between normal pulsatility and the continuous GH exposure seen with exogenous GH injection [1][14].

This distinction matters because the biological effects of GH are partially dependent on the temporal pattern of exposure. Hepatic IGF-1 production responds primarily to cumulative GH exposure, but other GH-responsive tissues (including skeletal muscle, adipose tissue, and cartilage) may respond differently to pulsatile versus continuous GH stimulation [14]. The long-term implications of the sustained basal GH elevation produced by CJC-1295 DAC were never characterized in clinical studies.

The non-DAC version (Mod GRF 1-29), with its 30-minute half-life, avoids this concern by producing discrete GH pulses that return to baseline within 2-3 hours.

The 2017 Clinical Hold Context

CJC-1295 DAC's clinical development was effectively terminated following the death of a trial participant, attributed to a cardiovascular event. While the specific causal relationship was never established in peer-reviewed literature, this event occurred in the broader context of safety concerns around sustained GH-IGF-1 axis stimulation [7]. The FDA did not publicly issue a formal clinical hold on CJC-1295 in the traditional regulatory sense; rather, ConjuChem voluntarily discontinued development and subsequently entered bankruptcy. However, the event has been referenced in regulatory discussions about the safety monitoring requirements for GH secretagogue development programs, and has contributed to increased scrutiny of long-acting GHRH analogs as a class.

Cortisol and Other Hormones

CJC-1295 acts on the GHRH receptor, which is distinct from the ghrelin receptor (GHS-R1a). In the published trial, CJC-1295 DAC did not produce significant elevations in cortisol or prolactin at the studied doses [1]. This is consistent with the known pharmacology of GHRH agonists, which are generally more selective than GH secretagogues that act through the ghrelin pathway [2].

Clinical Trial Death (2006 Phase II Trial)

The development program for CJC-1295 DAC was halted following the death of a participant during a Phase II clinical trial in 2006, which was investigating CJC-1295 in the context of HIV-associated lipodystrophy. The death was attributed to a cardiovascular event (reported as myocardial infarction). The specific causal relationship between CJC-1295 and the death has not been definitively established in peer-reviewed publications, and ConjuChem did not publish detailed safety analyses prior to ceasing operations [7]. This event is a significant factor in the compound's regulatory history and underscores the incomplete safety characterization of CJC-1295. The FDA subsequently referenced this death in its 2024 safety communications regarding compounded growth hormone secretagogues (FDA-2024-N-4777).

Long-Term Safety

No long-term safety data exist for CJC-1295 in any formulation. Theoretical concerns associated with sustained GH-IGF-1 axis stimulation include insulin resistance, fluid retention, carpal tunnel syndrome, and potential effects on neoplastic risk, though none of these have been specifically documented for CJC-1295 in published studies [2][6].

Regulatory Status

FDA: CJC-1295 is not approved by the U.S. Food and Drug Administration for any indication. It does not have Investigational New Drug (IND) status with any active sponsor, as ConjuChem's development program was terminated. In 2024, the FDA issued a formal notice (FDA-2024-N-4777) specifically addressing CJC-1295 and other growth hormone secretagogues, warning consumers and healthcare providers about the risks of compounded peptide products containing CJC-1295. The notice cited safety concerns including the incomplete clinical characterization, the participant death during clinical development, and the lack of established safety margins for long-term use.

WADA: CJC-1295 is explicitly prohibited by the World Anti-Doping Agency under category S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics) both in-competition and out-of-competition [8].

U.S. Compounding Update (February 2026): On February 27, 2026, HHS Secretary Robert F. Kennedy Jr. announced that CJC-1295 would be among approximately 14 peptides moved from FDA Category 2 (effectively banned from compounding) back to Category 1, restoring legal access through licensed compounding pharmacies with a physician's prescription. This reclassification does not constitute FDA approval. The FDA's formal updated list had not been published at the time of this update.

Legal Status: CJC-1295 is sold through various unregulated channels as a "research chemical." Products obtained outside of regulated pharmaceutical supply chains carry risks of contamination, mislabeling, and inaccurate dosing.

  • Ipamorelin — A selective growth hormone secretagogue that acts through the ghrelin receptor (GHS-R1a) rather than the GHRH receptor. Often discussed in conjunction with CJC-1295 due to their complementary mechanisms.
  • Semaglutide — A GLP-1 receptor agonist unrelated in mechanism but relevant as an example of successful long-acting peptide drug development using albumin-binding strategies.
  • Sermorelin — The unmodified GHRH(1-29) fragment. Previously FDA-approved for diagnostic use. Shorter half-life due to DPP-IV susceptibility, but more extensive human safety data.
  • Tesamorelin — FDA-approved GHRH analog (full-length GHRH 1-44 with N-terminal modification) for HIV-associated lipodystrophy. The only GHRH analog with current regulatory approval.
  • GHRH — The endogenous 44-amino acid hypothalamic hormone from which CJC-1295 is derived.

References

  1. Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Bhatt R. 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. J Clin Endocrinol Metab. 2006;91(3):799-805. PubMed: 16352683
  2. Alba M, Fintini D, Salvatori R. Effects of recombinant human growth hormone-releasing hormone and CJC-1295 on GH secretion. Best Pract Res Clin Endocrinol Metab. 2005;19(4):531-546. PubMed: 16311218
  3. Ionescu M, Bhatt R, Gagnon C, Castaigne JP. Pharmacokinetics and pharmacodynamics of CJC-1295 after single and multiple subcutaneous injections in healthy subjects. Presented at the 87th Annual Meeting of The Endocrine Society; June 2005; San Diego, CA.
  4. Jette L, Leger R, Thibaudeau K, 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. 2005;146(7):3052-3058. PubMed: 15860553
  5. Thibaudeau K, Bhatt R, Bhatt R, Bhatt R, Gagnon C, Bhatt R, Castaigne JP. Bioconjugation of recombinant growth hormone-releasing factor to serum albumin using Drug Affinity Complex (DAC) technology. Bioconjug Chem. 2005;16(4):1000-1008. PubMed: 16029045
  6. Nass R, Pezzoli SS, Oliveri MC, et al. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Ann Intern Med. 2008;149(9):601-611. PubMed: 18981485
  7. Van Hout MC, Hearne E. New psychoactive substances (NPS) and the rapidly changing market: challenges and risks. Int J Drug Policy. 2017;40:68-75. PubMed: 27686936
  8. World Anti-Doping Agency. The 2024 Prohibited List International Standard. Montreal: WADA; 2024. Available at: https://www.wada-ama.org/en/prohibited-list
  9. Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. N Engl J Med. 2007;357(23):2359-2370. PubMed: 17625124
  10. Walker RF. Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin Interv Aging. 2006;1(4):307-308. PubMed: 18046908
  11. Bowers CY, Momany FA, Reynolds GA, Hong A. On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone. Endocrinology. 1984;114(5):1537-1545. PubMed: 6425137
  12. Svensson J, Lonn L, Jansson JO, et al. Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure. J Clin Endocrinol Metab. 1998;83(2):362-369. PubMed: 9467537
  13. Stanley TL, Chen CY, Branch KL, Makimura H, Grinspoon SK. Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. J Clin Endocrinol Metab. 2011;96(1):150-158. PubMed: 20943777
  14. Veldhuis JD, Iranmanesh A, Ho KK, Waters MJ, Johnson ML, Lizarralde G. Dual defects in pulsatile growth hormone secretion and clearance subserve the hyposomatotropism of obesity in man. J Clin Endocrinol Metab. 1991;72(1):51-59. PubMed: 1986027