# cjc1295meds.com # CJC-1295: The GHRH Analog, Its DAC and No-DAC Variants, and What the Literature Measured > CJC-1295 is a 30-amino-acid GHRH analog. A single subcutaneous dose elevated growth hormone for 6+ days and IGF-1 for 9-11 days in healthy adults (Teichman 2006). A research digest. One pharmacokinetic trial drives most of what is known. The DAC variant ran ~8 days in plasma; the no-DAC variant ran ~30 minutes. Everything else on this site is the literature, in order, with citations. ## What the CJC-1295 literature actually contains CJC-1295 is a synthetic 30-amino-acid analog of growth hormone-releasing hormone (GHRH 1-29) carrying four amino-acid substitutions — D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27 — that block DPP-IV cleavage. An optional Drug Affinity Complex (DAC) maleimidopropionyl-lysine linker conjugates the peptide to Cys34 of serum albumin after subcutaneous injection, extending plasma residence from ~30 minutes to a published mean of 5.8-8.1 days [1]. The compound was developed by ConjuChem Biotechnologies and first described in human pharmacokinetic detail by Teichman and colleagues in 2006 [1]. The primary human dataset is small. A single ascending-dose study in 21- to 61-year-old healthy adults dosed subcutaneously at 30, 60, 125, and 250 mcg/kg measured dose-dependent 2- to 10-fold increases in mean plasma growth hormone for six or more days and 1.5- to 3-fold increases in mean plasma IGF-1 for nine to eleven days [1]. Subsequent multi-week dosing held IGF-1 above baseline for up to 28 days [1]. There is no published Phase 3 trial. There is no FDA-approved CJC-1295 drug product [13]. WADA prohibits the compound under Section S2 of its Prohibited List [10]. The rest of this digest is structured the same way. Mechanism on [CJC-1295 mechanism of action](/research#mechanism). Doses, half-life, and the DAC-vs-no-DAC pharmacokinetics on [CJC-1295 dosage](/dosage). Reported reactions and the regulatory record on [CJC-1295 side effects](/side-effects). Every quantitative claim ties to a numbered citation. ## CJC-1295: The peptide and its class CJC-1295 belongs to the GHRH-analog class. Native GHRH is a 44-amino-acid hypothalamic peptide that drives the anterior pituitary to synthesize and release growth hormone in pulses. The first 29 amino acids carry the bioactive sequence; sermorelin is GHRH (1-29) without modifications, with a plasma half-life of approximately 11-12 minutes [7]. CJC-1295 starts from the same 1-29 backbone and adds the four stabilizing substitutions described above, plus — in the with-DAC variant — the albumin-binding linker [1][6]. The mechanism is conserved across the class. The GHRH receptor on pituitary somatotrophs is a Gs-coupled receptor; agonism raises intracellular cAMP via adenylate cyclase activation, which drives GH synthesis and pulsatile release [4]. Downstream, hepatic IGF-1 rises. What CJC-1295 changes is not the pathway but the pharmacokinetics — the four substitutions resist DPP-IV cleavage, and the DAC linker turns a sub-hour molecule into a multi-day one [1][6]. ## Reported benefits in the research literature Reported outcomes in published CJC-1295 work are pharmacodynamic, not clinical. In healthy adults receiving a single subcutaneous CJC-1295 with DAC injection, mean plasma GH rose 2- to 10-fold over six days and IGF-1 rose 1.5- to 3-fold over nine to eleven days [1]. In GHRH-knockout mice given daily 2-mcg subcutaneous CJC-1295 from one week of age, weight and length normalized over five weeks of treatment; less-frequent dosing produced partial recovery [3]. Total pituitary RNA and GH mRNA rose, consistent with somatotroph proliferation [3]. The Ionescu and Frohman 2009 serum-proteomics paper found downstream protein-profile shifts in adults consistent with GH/IGF-1 axis activation rather than pleiotropic peptide effects [5]. Sigalos and colleagues in 2017 reported elevated IGF-1 in hypogonadal men receiving GH-secretagogue protocols, including GHRH analogs, alongside testosterone therapy [11]. These are the published outcomes. There are no FDA-registered indication trials, no Phase 3 efficacy endpoints, and no body-composition randomized trial for CJC-1295 itself — the closest clinical-grade GHRH-analog evidence comes from tesamorelin (a different molecule), which produced a 15-18% mean reduction in visceral adipose tissue in HIV-lipodystrophy trials [9]. For reproducibility purposes, the [CJC-1295 + ipamorelin combination](/research#ipamorelin-combination) protocols described in clinic case series have not been validated in a controlled randomized trial. ## What is CJC-1295? A synthetic 30-amino-acid analog of growth hormone-releasing hormone (GHRH 1-29) with four amino-acid substitutions designed to resist enzymatic degradation. The with-DAC variant adds a maleimidopropionyl-lysine linker that conjugates the peptide to serum albumin after injection. First described by ConjuChem Biotechnologies in the mid-2000s and characterized in healthy adults by Teichman et al. in the Journal of Clinical Endocrinology & Metabolism in 2006 [1]. ## What does CJC-1295 do to your body? Binds the GHRH receptor on pituitary somatotrophs, raises intracellular cAMP, and stimulates endogenous growth hormone synthesis and pulsatile release [4]. In Teichman 2006, a single subcutaneous CJC-1295 with DAC injection produced 2- to 10-fold elevations in mean plasma GH for at least six days and 1.5- to 3-fold elevations in mean plasma IGF-1 for nine to eleven days [1]. The DAC variant's effect is sustained because the peptide stays bound to serum albumin for a multi-day window. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # CJC-1295 Research: Mechanism, Trials, and the Modified GRF 1-29 Record > CJC-1295 mechanism of action, Teichman 2006 pharmacokinetics, the ipamorelin combination, modified GRF 1-29, and the sermorelin and tesamorelin comparison points — every claim cited. One human pharmacokinetic trial. One mouse growth-normalization study. A handful of analytical-chemistry and proteomic follow-ons. The published record, in order. ## CJC-1295 mechanism of action CJC-1295 mechanism of action is GHRH-receptor agonism on pituitary somatotrophs. The GHRH receptor is Gs-coupled; agonism activates adenylate cyclase, raises intracellular cAMP, and drives the cAMP/PKA cascade that produces GH synthesis and pulsatile release [4]. Bilezikjian and Vale characterized this pathway in purified rat somatotrophs in 1989, establishing the guanine-nucleotide-dependent activation kinetics (Ka ~10^-8 M) and the tight correlation between cAMP elevation and GH release [4]. What CJC-1295 adds to native GHRH biology is duration. The D-Ala-2 substitution blocks DPP-IV cleavage; Gln-8 reduces asparagine deamidation; Ala-15 enhances bioactivity; Leu-27 prevents methionine oxidation [6]. The optional DAC linker — a maleimidopropionyl-lysine group at the C-terminus — covalently binds free Cys34 of endogenous serum albumin within minutes of subcutaneous injection. Albumin's long circulating half-life (~19 days) then carries the peptide through plasma at a published mean of 5.8-8.1 days [1]. The no-DAC variant retains only the four substitutions; its half-life is approximately 30 minutes [6]. Downstream of the pituitary, the cascade is conventional. GH stimulates hepatic IGF-1 synthesis; serum IGF-1 is the standard biomarker for GH-axis activation in CJC-1295 trials [1][11]. Teichman 2006 reported preserved physiologic pulsatility under sustained CJC-1295 with DAC exposure — the molecule did not flatten the GH curve into a continuous infusion-like state, a concern that had been raised theoretically [1]. ## Outcomes reported in CJC-1295 studies The Teichman 2006 trial enrolled healthy adults aged 21-61 and dosed them at 30, 60, 125, and 250 mcg/kg as single subcutaneous CJC-1295 with DAC injections, with a separate ascending-dose multi-week arm. Single-dose results: dose-dependent 2- to 10-fold mean GH elevations for six or more days; 1.5- to 3-fold mean IGF-1 elevations for nine to eleven days [1]. Multi-dose results: weekly or biweekly dosing sustained IGF-1 above baseline for up to 28 days across 28- and 49-day study windows [1]. Reported as safe and relatively well tolerated, particularly at 30-60 mcg/kg [1]. Alba and colleagues in 2006 tested CJC-1295 in GHRH-knockout mice — animals that fail to grow without exogenous GHRH stimulation. Once-daily 2-mcg subcutaneous injections starting at one week of age normalized body weight and length over five weeks. Every-48-hour and every-72-hour dosing produced partial recovery without full normalization. Total pituitary RNA and GH mRNA rose, consistent with somatotroph proliferation [3]. Ionescu and Frohman in 2009 reported serum protein-profile shifts in normal adults receiving subcutaneous CJC-1295, consistent with downstream GH/IGF-1 axis activation rather than direct pleiotropic effects of the peptide [5]. Sigalos 2017 documented elevated IGF-1 in hypogonadal men receiving GH-secretagogue protocols (GHRH analogs and ghrelin-receptor agonists) alongside testosterone therapy [11]. ## Modified GRF 1-29 (no-DAC CJC-1295) Modified GRF 1-29 is the no-DAC variant. The name reflects the four amino-acid substitutions (D-Ala-2, Gln-8, Ala-15, Leu-27) modifying the native GHRH (1-29) backbone, without the DAC albumin-binding linker [6]. The Coy 1994 work established that the D-Ala-2 substitution alone increases half-life and decreases metabolic clearance of GHRH (1-29) in normal men [6]. Native GHRH (1-29) — sermorelin — has a plasma half-life of approximately 11-12 minutes [7]; modified GRF 1-29 extends to approximately 30 minutes [6]. The nomenclature crossover matters because researchers and analytical chemists frequently refer to the same molecule under different names. Henninge and colleagues in 2010 identified CJC-1295 in an unknown pharmaceutical preparation seized by Norwegian customs via LC-HRMS/MS, confirming the C-terminal amidated 29-amino-acid sequence consistent with both with-DAC and no-DAC CJC-1295 [8]. Modern anti-doping detection methods now distinguish the two forms [12][14]. ## CJC-1295 + ipamorelin: the studied combination Ipamorelin and CJC-1295 act on different receptors in the same axis. CJC-1295 is a GHRH-receptor agonist on pituitary somatotrophs; ipamorelin is a selective ghrelin-receptor (GHS-R1a) agonist. Raun and colleagues in 1998 characterized ipamorelin as the first selective GH secretagogue that releases GH without significantly elevating ACTH or cortisol — even at doses more than 200-fold above the ED50 for GH release [2]. The two pathways are parallel arms of the GH-release machinery, which is the mechanistic basis for combining them. The combination has not been validated in a controlled randomized trial. Most reports describing CJC-1295 plus ipamorelin protocols are clinic case-series, observational accounts, or analytical-chemistry detection reports — not Phase 3 efficacy studies. Sigalos 2017 measured IGF-1 elevation in hypogonadal men receiving combined GH-secretagogue therapy alongside testosterone replacement, suggesting the protocol produces a measurable GH-axis signal in human subjects, but the study was not a placebo-controlled CJC-1295-plus-ipamorelin RCT [11]. ## CJC-1295 vs ipamorelin: class difference CJC-1295 vs ipamorelin is a class-difference question, not a same-class comparison. CJC-1295 is a GHRH analog — a peptide-receptor agonist that mimics the hypothalamic input to the pituitary [1]. Ipamorelin is a pentapeptide GH secretagogue — it activates the ghrelin receptor (GHS-R1a) on the same somatotrophs [2]. Different receptor, different signaling, same downstream output. The selectivity profile is what made ipamorelin notable in 1998: GH release without the cortisol or prolactin elevations seen with earlier GH secretagogues [2]. ## CJC-1295 vs sermorelin Sermorelin is GHRH (1-29) with no stabilizing modifications — the unmodified bioactive sequence. Plasma half-life is approximately 11-12 minutes after IV or subcutaneous administration; subcutaneous bioavailability is approximately 6% [7]. Despite the rapid peptide clearance, the GH pulse sermorelin triggers persists 2-4 hours, with peak GH at 30-60 minutes post-injection [7]. Sermorelin was approved by the FDA in 1997 (Geref, sermorelin acetate) for pediatric GH deficiency; the labeled product has since been discontinued in the US for commercial reasons unrelated to safety. CJC-1295 was engineered to overcome sermorelin's pharmacokinetic limitation. The four substitutions extend the no-DAC half-life to ~30 minutes; the DAC linker extends the with-DAC half-life to ~8 days [1][6]. Same receptor, same downstream cascade. Different duration. ## CJC-1295 vs recombinant HGH Recombinant human growth hormone is GH itself, administered exogenously. CJC-1295 is upstream of GH — a GHRH-receptor agonist that stimulates the pituitary to release endogenous GH in pulses [1]. The downstream IGF-1 elevation is similar in kind but differs in pattern. Teichman 2006 reported preserved GH pulsatility under CJC-1295 with DAC, whereas exogenous recombinant GH bypasses the pituitary regulatory loop entirely [1]. Tesamorelin — a different GHRH analog, approved by the FDA in 2010 for HIV-associated lipodystrophy — produced a 15-18% mean reduction in visceral adipose tissue versus placebo in pivotal trials, establishing the clinical-grade evidence ceiling for GHRH-receptor agonism [9]. ## What is modified GRF 1-29? An alternative name for CJC-1295 without DAC. The four amino-acid substitutions at positions 2, 8, 15, and 27 that stabilize the molecule against DPP-IV cleavage are the 'modifications' the name references [6]. Half-life is approximately 30 minutes — short compared with the ~8-day DAC variant, longer than native GHRH (1-29) at ~10 minutes [6][7]. ## How does CJC-1295 work? Agonist at the pituitary GHRH receptor [4]. The DAC-bearing variant covalently binds serum albumin via the maleimide linker, producing a sustained plasma residence of approximately 5.8-8.1 days and a multi-day GH 'bleed' [1]. The no-DAC variant clears within ~30 minutes, producing a pulse closer to native GH physiology [6]. ## How does CJC-1295 differ from ipamorelin? Different receptor targets. CJC-1295 is a GHRH-receptor agonist; ipamorelin is a selective ghrelin-receptor (GHSR-1a) agonist [2]. They act on different signaling pathways within the same GH-release axis, which is the mechanistic basis for combination protocols [11]. ## What does CJC-1295 + ipamorelin do? Combination protocols pair GHRH-receptor agonism (CJC-1295) with ghrelin-receptor agonism (ipamorelin) to engage two parallel arms of GH-release physiology [1][2]. Most data is from clinic case series rather than controlled trials; Sigalos 2017 documented a measurable GH-axis signal in human subjects receiving combined GH-secretagogue therapy [11]. ## How does CJC-1295 compare to sermorelin? Both are GHRH analogs. Sermorelin is GHRH (1-29) with no stabilizing modifications and an 11-12 minute half-life [7]. CJC-1295 carries four substitutions that extend half-life — to approximately 30 minutes for the no-DAC variant, and to a published mean of 5.8-8.1 days for the with-DAC variant via covalent albumin binding [1][6]. ## What is the difference between CJC-1295 and HGH? Recombinant HGH is the growth hormone itself, administered exogenously. CJC-1295 is a GHRH-receptor agonist — it stimulates the pituitary to release the body's own GH in a more physiologically patterned way [1]. Different point of action on the GH/IGF-1 axis; different downstream pulsatility profile. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # CJC-1295 Dosage in the Research Literature > CJC-1295 dosage in published research: Teichman 2006 single-dose pharmacokinetics at 30, 60, 125, 250 mcg/kg; the ~8-day DAC half-life vs the ~30-minute no-DAC half-life; reconstitution and route. Doses studied. Routes used. Half-life numerals. Reconstitution as described in published protocols. None of this is a recommendation for human use. ## Doses used in published research CJC-1295 dosage in the research literature reduces to a small set of numbers. Teichman 2006 dosed healthy adult subjects (ages 21-61) at 30, 60, 125, and 250 mcg/kg as single subcutaneous CJC-1295 with DAC injections, plus a separate ascending-dose multi-week arm [1]. Alba 2006 dosed GHRH-knockout mice at 2 mcg per injection at 24-, 48-, or 72-hour intervals for five weeks, starting at one week of age [3]. These are the published controlled-trial dose ranges for the with-DAC variant. Observational reports from clinic protocols describe no-DAC variant administration in the range of 100-300 mcg subcutaneously, several times per week; the with-DAC variant in clinic protocols typically appears as a once-weekly injection. These observational protocols are not from controlled trials and do not appear in the peer-reviewed pharmacokinetic literature [15]. The FDA Pharmacy Compounding Advisory Committee briefing materials reviewed reconstitution and clinic-protocol patterns in its 2024 docket but did not endorse any dose range [13]. ## CJC-1295 with DAC vs no-DAC CJC-1295 with DAC vs no-DAC is fundamentally a pharmacokinetic split. DAC (Drug Affinity Complex) is a maleimidopropionyl-lysine linker covalently bound to the C-terminus of the peptide that reacts with free Cys34 of endogenous serum albumin within minutes of subcutaneous injection [1]. The peptide then circulates as an albumin conjugate. Plasma half-life: approximately 5.8-8.1 days [1]. The no-DAC variant — also known as modified GRF 1-29 — retains the four stabilizing amino-acid substitutions (D-Ala-2, Gln-8, Ala-15, Leu-27) without the linker [6]. Plasma half-life: approximately 30 minutes [6]. The pharmacodynamic consequence is different GH-release patterns: with-DAC produces sustained mean GH elevation across days; no-DAC produces a pulse closer to native GH physiology, clearing within hours [1][6]. Neither variant has FDA-approved status [13]. Both are WADA-prohibited under Section S2 [10]. ## CJC-1295 no-DAC (modified GRF 1-29) CJC-1295 no-DAC is the variant without the albumin-binding linker. The literature also refers to it as modified GRF 1-29, mod GRF 1-29, or tetrasubstituted GRF (1-29). The four amino-acid substitutions (D-Ala-2, Gln-8, Ala-15, Leu-27) confer DPP-IV resistance and extend plasma half-life to approximately 30 minutes versus the sub-10-minute half-life of native GHRH (1-29) [6][7]. Without DAC, GH release is pulsatile and short-acting — closer to the physiologic pattern triggered by endogenous GHRH pulses. ## CJC-1295 half-life CJC-1295 half-life is variant-dependent. With DAC, mean plasma half-life is 5.8-8.1 days following a single subcutaneous injection in healthy adults [1]. Without DAC, plasma half-life is approximately 30 minutes [6]. The native GHRH (1-29) comparison point — sermorelin — runs 11-12 minutes [7]. The order-of-magnitude difference between the no-DAC and with-DAC variants is entirely attributable to the DAC linker's covalent albumin binding [1]. ## Plasma persistence and washout The with-DAC variant remains detectable in plasma for approximately two weeks after a single dose, given the ~8-day half-life [1]. Multi-week dosing windows in Teichman 2006 sustained IGF-1 above baseline for up to 28 days [1]. The no-DAC variant clears within hours; pharmacodynamic GH elevation is also short [6]. The DAC variant's long residence is the practical reason discontinuation is described in clinic monographs as a delayed washout rather than an immediate clearance. ## Injection route used in studies Subcutaneous injection in every published human CJC-1295 pharmacokinetic study, with the abdomen or thigh as the typical injection site in research protocols [1]. Alba 2006 used subcutaneous administration in the GHRH-knockout mouse model [3]. Some preclinical rodent work used intraperitoneal injection. No published trial has used oral, intranasal, sublingual, or transdermal routes — the peptide's size and structure make oral bioavailability negligible [1]. ## Reconstitution in published protocols CJC-1295 is supplied as a lyophilized (freeze-dried) powder. Reconstitution in published research and pharmacy monographs uses bacteriostatic water — sterile water containing 0.9% benzyl alcohol as a preservative — as the diluent. Vial concentrations depend on the powder mass: pharmacy monographs and published protocols describe 1-2 mL of bacteriostatic water per 5-mg vial [13]. The reconstituted solution is stored refrigerated; stability data in monographs supports approximately 30 days of refrigerated stability. ## How long does CJC-1295 stay in your system? With-DAC variant: detectable in plasma for approximately two weeks after a single dose given the ~8-day half-life [1]. No-DAC variant: clears within hours [6]. The downstream IGF-1 elevation extends beyond pure peptide clearance because IGF-1 has its own circulating half-life (~16 hours) and the GH-axis activation cascade persists for days after a DAC-variant dose [1]. ## What is the typical CJC-1295 dosage used in research? Teichman 2006 dosed healthy adult subjects at 30, 60, 125, and 250 mcg/kg as a single subcutaneous injection [1]. Subsequent observational reports describe clinic-protocol no-DAC dosing in the 100-300 mcg subcutaneous range, several times per week, and once-weekly with-DAC dosing — none of these clinic protocols are from controlled trials [13]. ## What is the half-life of CJC-1295? With DAC: approximately 5.8-8.1 days in plasma [1]. Without DAC (modified GRF 1-29): approximately 30 minutes [6]. The difference is the DAC linker's covalent binding to serum albumin Cys34, which extends residence by roughly two orders of magnitude [1]. ## How is CJC-1295 injected in research protocols? Subcutaneous injection. The abdomen or thigh is the typical injection site in published human pharmacokinetic studies [1]. Subcutaneous administration was also used in the Alba 2006 GHRH-knockout mouse growth-normalization study [3]. ## How is CJC-1295 reconstituted? Lyophilized powder reconstituted with bacteriostatic water (sterile water with 0.9% benzyl alcohol preservative). Published protocols and pharmacy monographs describe 1-2 mL of bacteriostatic water per 5-mg vial; final concentration scales with vial size and diluent volume [13]. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # CJC-1295 Side Effects in the Research Literature > CJC-1295 side effects documented in Teichman 2006, the Van Hout 2016 netnography, and the 2024 FDA Pharmacy Compounding Advisory Committee briefing — injection-site reactions, flushing, headache, water retention, plus the systemic vasodilatory concern. What controlled trials reported. What clinic case-series logged. What the FDA's 2024 PCAC review explicitly flagged. No long-term safety data exists. ## Side effects reported in clinical literature CJC-1295 side effects documented in the published record cluster into a small set. Teichman 2006 reported the compound as 'safe and relatively well tolerated' across the dose range studied, with the cleanest tolerability profile at 30-60 mcg/kg [1]. The trial enrolled healthy adults aged 21-61 and ran 28- and 49-day study windows; specific adverse events at higher doses (125 and 250 mcg/kg) included transient injection-site reactions [1]. The Van Hout and Hearne 2016 netnography of female CJC-1295 users in online community discussions documented self-reported events: injection-site redness, swelling, and itching; facial flushing; headache; dizziness; transient nausea; mild water retention [15]. These are observational, self-reported, and not from a controlled clinical trial — but they are the largest single inventory of community-reported events in the open literature. The FDA Pharmacy Compounding Advisory Committee briefing in 2024 specifically referenced 'systemic vasodilatory reaction' as a safety concern for CJC-1295 in its review of non-approved peptide compounding [13]. The PCAC materials also flagged immunogenicity, impurities, and limited human clinical data as ongoing concerns for the substance class [13]. The compound was removed from Category 2 of the interim 503A bulks list in September 2024 following nominator withdrawal, pending further PCAC review [16]. ## Is CJC-1295 considered safe in the literature? Short-term human exposure data is limited. Teichman 2006 — weeks of single-dose and multi-dose exposure in healthy adults — reported the compound as well tolerated at the doses studied, with the cleanest profile at 30-60 mcg/kg [1]. There is no published long-term human safety dataset. The compound has never received FDA approval for any indication [13][16]. The FDA's 2024 PCAC briefing identified immunogenicity, impurities, limited human data, and a noted systemic vasodilatory reaction profile as the principal safety concerns relevant to compounding [13]. WADA prohibits the substance under Section S2 of its Prohibited List, in-competition and out-of-competition [10]. ## Why CJC-1295 causes flushing Histamine release and vasodilation following subcutaneous injection are the proposed mechanisms cited in pharmacy monographs and the FDA PCAC briefing [13]. The PCAC materials specifically reference 'systemic vasodilatory reaction' as a noted safety concern [13]. Facial flushing is one of the more frequently reported community events in the Van Hout 2016 netnography [15]. The reaction is typically transient — minutes to an hour post-injection — and is not consistently dose-related across the small published data. ## Hair loss reports Hair loss has not been documented as a side effect in published controlled trials of CJC-1295 [1]. The community-discussion record summarized by Van Hout 2016 contains scattered references to hair-related concerns, but these typically reference downstream IGF-1 elevation as a hypothesized mechanism rather than the peptide itself [15]. No quantitative incidence data exists in the peer-reviewed CJC-1295 literature. ## Weight changes and water retention Mild water retention is reported in the observational Van Hout 2016 netnography record [15]. The Teichman 2006 trial did not report significant weight change as a primary outcome — the study endpoints were pharmacokinetic (plasma GH, plasma IGF-1) rather than body-composition [1]. The closest body-composition signal in the broader GHRH-analog class comes from tesamorelin (a different molecule with FDA approval for HIV-associated lipodystrophy): 15-18% mean reduction in visceral adipose tissue versus placebo, with mild water retention reported as a class-typical effect [9]. ## Effect on testosterone CJC-1295 acts on the GH/IGF-1 axis, not the hypothalamic-pituitary-gonadal (HPG) axis. Published trials measured GH and IGF-1 as primary endpoints; significant changes in testosterone have not been reported as a primary outcome [1]. The Sigalos 2017 paper documented elevated IGF-1 in hypogonadal men receiving combined GH-secretagogue and testosterone-replacement therapy — but the testosterone component came from exogenous administration in that protocol, not from CJC-1295 itself [11]. ## Discontinuation in clinical reports GH and IGF-1 levels return toward baseline as the compound clears. The with-DAC variant's long half-life (~8 days) means residual activity persists for approximately one to two weeks after the last dose, with downstream IGF-1 normalization extending beyond pure peptide clearance [1]. The no-DAC variant clears within hours; pharmacodynamic GH effects are correspondingly short [6]. The DAC variant's long residence is one reason the FDA PCAC materials flagged acute discontinuation as a class concern: residual albumin-bound drug is not rapidly recoverable from plasma [13]. ## What are the side effects of CJC-1295? Reported in published trials and case reports: injection-site reactions (redness, swelling, itching), facial flushing, headache, dizziness, transient nausea, and mild water retention [1][15]. The FDA PCAC 2024 briefing referenced cardiovascular concerns including systemic vasodilatory reaction [13]. Immunogenicity, impurities, and limited long-term human data are flagged as class concerns [13]. ## Does CJC-1295 cause hair loss? Not documented as a side effect in published controlled trials of CJC-1295 [1]. Hair-related concerns in community discussion typically reference downstream IGF-1 elevation as a hypothesized mechanism rather than the peptide itself [15]. No quantitative incidence data exists in the peer-reviewed literature. ## Does CJC-1295 cause weight gain? Mild water retention is reported in observational sources [15]. Studied outcomes in published GH-axis research focus on body-composition shifts (lean-mass changes, adipose-tissue changes) rather than scale weight per se [9]. Teichman 2006 did not report scale weight as a primary endpoint [1]. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # CJC-1295 FAQ: Mechanism, Half-Life, Dosage, Side Effects, Regulatory Status > Direct answers to the most-searched CJC-1295 questions — what it is, how it works, the DAC vs no-DAC difference, half-life, dosage in research, side effects, FDA status, WADA status — each answer cited. Twenty-six direct answers to the most-searched CJC-1295 questions, each one tied back to the underlying study or regulatory record. ## What is CJC-1295? A synthetic 30-amino-acid analog of growth hormone-releasing hormone (GHRH 1-29) with four amino-acid substitutions to resist enzymatic degradation; first described by ConjuChem in the mid-2000s and characterized in healthy adults by Teichman et al. in JCEM 2006 [1][17]. ## What does CJC-1295 do to your body? Binds pituitary GHRH receptors and stimulates endogenous growth hormone release; in healthy adults receiving a single subcutaneous with-DAC injection, mean plasma GH rose 2- to 10-fold for six or more days and IGF-1 rose 1.5- to 3-fold for nine to eleven days [1]. ## How does CJC-1295 work? Agonist at the pituitary GHRH receptor. The DAC-bearing variant covalently binds serum albumin via a maleimide linker, producing a plasma half-life of 5.8-8.1 days and a sustained GH 'bleed' [1]. The no-DAC variant clears within ~30 minutes, producing pulses closer to native GH physiology [6]. ## What is the difference between CJC-1295 with DAC and CJC-1295 no DAC? DAC (Drug Affinity Complex) is a maleimide linker that conjugates CJC-1295 to albumin in vivo, extending plasma half-life from ~30 minutes (no-DAC) to a mean of 5.8-8.1 days (with-DAC) [1][6]. With-DAC produces sustained GH elevation; no-DAC (also called modified GRF 1-29) produces pulsatile GH release closer to physiologic patterns. ## What is modified GRF 1-29? An alternative name for CJC-1295 without DAC. 'Modified' refers to the four amino-acid substitutions at positions 2, 8, 15, and 27 (D-Ala, Gln, Ala, Leu) that stabilize the molecule against DPP-IV cleavage [6]. ## What are the side effects of CJC-1295? Reported in published trials and case reports: injection-site reactions (redness, swelling, itching), facial flushing, headache, dizziness, transient nausea, and mild water retention [1][15]. The FDA's 2024 PCAC briefing also references systemic vasodilatory reaction and increased heart rate among class-level cardiovascular concerns [13]. ## Is CJC-1295 safe? Short-term human trials (Teichman 2006, weeks of exposure) reported it as well tolerated at studied doses, particularly at 30-60 mcg/kg [1]. Long-term human safety data does not exist. The compound is not FDA-approved for any indication and is subject to ongoing PCAC review [13][16]. ## Is CJC-1295 FDA approved? No. CJC-1295 has never received FDA approval for any clinical indication [13]. The FDA's 2024 PCAC briefing categorizes it among non-approved peptides under review for compounding eligibility, and the substance was removed from Category 2 of the interim 503A bulks list in September 2024 [13][16]. ## What is the typical CJC-1295 dosage used in research? Teichman 2006 dosed healthy adult subjects at 30, 60, 125, and 250 mcg/kg as a single subcutaneous CJC-1295 with DAC injection [1]. Subsequent observational reports describe clinic protocols of 100-300 mcg subcutaneously, 5 days per week, for the no-DAC variant — these are not from controlled trials [15]. ## What is the half-life of CJC-1295? CJC-1295 with DAC: mean plasma half-life of 5.8-8.1 days [1]. CJC-1295 without DAC (modified GRF 1-29): approximately 30 minutes — longer than native GHRH (1-29) at ~10 minutes, far shorter than the DAC variant [6][7]. ## How does CJC-1295 differ from ipamorelin? Different receptor targets. CJC-1295 is a GHRH-receptor agonist; ipamorelin is a selective ghrelin-receptor (GHSR-1a) agonist [2]. They act on different signaling pathways within the same GH-release axis, which is the mechanistic basis for combination protocols [11]. ## How is CJC-1295 injected in research protocols? Subcutaneous injection in published human pharmacokinetic studies. The abdomen or thigh is the typical injection site in research protocols [1]. The Alba 2006 GHRH-knockout mouse model also used subcutaneous administration [3]. ## Time to effect in pharmacokinetic studies Teichman 2006 measured GH elevation within hours of a single CJC-1295 with DAC injection, with sustained elevation across the multi-day pharmacokinetic window [1]. Onset characteristics for the no-DAC variant follow a pulsatile pattern over minutes to hours [6]. ## Discontinuation in clinical reports GH and IGF-1 levels return toward baseline as the compound clears. The DAC variant's long half-life means residual activity persists for roughly one to two weeks after the last dose [1]. The no-DAC variant clears within hours [6]. ## Hair loss reports Not documented as a side effect in published controlled trials of CJC-1295 [1]. Hair-related concerns in community discussion typically reference downstream IGF-1 elevation rather than the compound itself [15]. ## Effect on testosterone CJC-1295 acts on the GH/IGF-1 axis, not the HPG axis. Published trials measured GH and IGF-1 endpoints; significant changes in testosterone have not been reported as a primary outcome [1][11]. ## Weight changes and water retention Mild water retention is reported in observational sources [15]. Studied outcomes in published GH-axis research focus on body-composition shifts (lean-mass, adipose-tissue) rather than scale weight per se [9]. ## Why CJC-1295 causes flushing Histamine release and vasodilation following injection are the proposed mechanisms cited in pharmacy monographs [13]. The FDA's 2024 PCAC briefing specifically references 'systemic vasodilatory reaction' as a safety concern. ## Plasma persistence and washout With-DAC variant: detectable in plasma for approximately two weeks after a single dose given the ~8-day half-life [1]. No-DAC variant clears within hours [6]. ## CJC-1295 + ipamorelin combination Combination protocols pair GHRH-receptor agonism (CJC-1295) with ghrelin-receptor agonism (ipamorelin) to engage two arms of GH-release physiology [1][2]. Most data is from clinic case series rather than controlled trials [11]. ## Reconstitution in published protocols Lyophilized powder reconstituted with bacteriostatic water. Concentration depends on vial size; published protocols and pharmacy monographs use 1-2 mL of bacteriostatic water per 5-mg vial [13]. ## Is CJC-1295 a steroid? No. CJC-1295 is a peptide hormone analog, structurally and pharmacologically distinct from anabolic-androgenic steroids. It acts on the GHRH receptor, not on androgen receptors [1]. ## Legal status of CJC-1295 Not FDA-approved as a drug [13][16]. Listed by WADA among prohibited substances for competitive athletes (Section S2, in-competition and out-of-competition) [10]. Legal status for research use varies by jurisdiction; included in the FDA's 2023-2024 review of non-approved compounding peptides [13]. ## CJC-1295 vs sermorelin Both are GHRH analogs. Sermorelin is GHRH (1-29) with no stabilizing modifications and a very short half-life (~11-12 minutes) [7]. CJC-1295 carries four substitutions that extend half-life — to ~30 minutes for no-DAC, and dramatically (~8 days) for with-DAC via covalent albumin binding [1][6]. ## Oral bioavailability No oral bioavailability has been established in published research. Peptides of this size are degraded by gastric proteases; all human trials used subcutaneous injection [1]. ## CJC-1295 vs recombinant HGH Recombinant HGH is growth hormone itself, administered exogenously. CJC-1295 is a GHRH-receptor agonist — it stimulates the pituitary to release the body's own GH in a more physiologically patterned way [1]. Teichman 2006 reported preserved pulsatility under CJC-1295 with DAC [1]. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # CJC-1295 References: Cited Sources in the Research Digest > Complete citation list for the CJC-1295 research digest — Teichman 2006, Alba 2006, Coy 1994, Raun 1998, Henninge 2010, Van Hout 2016, FDA PCAC 2024, WADA 2024, with DOIs and PubMed URLs. Every claim in the digest ties back to one of these entries. DOIs and PubMed identifiers where available. ## Sources cited in the CJC-1295 research digest Every quantitative claim on this site — every dose, half-life, percent change, study population — ties to one of the entries below. The list is rendered as a numbered reference index in the assembler. CJC-1295 has a small primary-source footprint; the Teichman 2006 JCEM trial is the single dominant human pharmacokinetic study, with the Alba 2006 GHRH-knockout mouse paper as the principal preclinical anchor [1][3]. The remaining entries are analytical-chemistry detection methods, regulatory documents, comparison-compound benchmarks (sermorelin, tesamorelin), and the Van Hout 2016 netnography of community-reported use patterns [7][9][15]. For the latest regulatory state, the FDA's 2024 Pharmacy Compounding Advisory Committee briefing and the September 2024 Category 2 removal announcement are the two primary federal-record entries [13][16]. WADA's 2024 Prohibited List is the source for the Section S2 status [10]. ## References [1] Teichman 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. J Clin Endocrinol Metab. 2006;91(3):799-805. https://pubmed.ncbi.nlm.nih.gov/16352683/ [2] Raun K, Hansen BS, Johansen NL, Thogersen H, Madsen K, Ankersen M, Andersen PH. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. https://pubmed.ncbi.nlm.nih.gov/9849822/ [3] Alba M, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290-E1294. https://pubmed.ncbi.nlm.nih.gov/16822960/ [4] Bilezikjian LM, Vale WW. Growth hormone-releasing factor-sensitive adenylate cyclase system of purified somatotrophs: effects of guanine nucleotides, somatostatin, calcium, and magnesium. Endocrinology. 1989. https://pubmed.ncbi.nlm.nih.gov/2562826/ [5] Ionescu M, Frohman LA. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Horm IGF Res. 2009. https://www.sciencedirect.com/science/article/abs/pii/S1096637409000409 [6] Coy DH, Murphy WA, Lance VA, Heiman ML. Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men. J Clin Endocrinol Metab. 1994. https://pubmed.ncbi.nlm.nih.gov/7962295/ [7] Sermorelin pharmacokinetics — product monograph and review. FDA-approved labeling, Geref (sermorelin acetate). 1997. https://www.sciencedirect.com/topics/medicine-and-dentistry/sermorelin [8] Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11-12):647-650. https://pubmed.ncbi.nlm.nih.gov/21204297/ [9] Falutz J, Allas S, Blot K, Potvin D, Kotler D, Somero M, Berger D, Brown S, Richmond G, Fessel J, Turner R, Grinspoon S. Effects of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. N Engl J Med. 2007. https://pubmed.ncbi.nlm.nih.gov/18000167/ [10] World Anti-Doping Agency. World Anti-Doping Code International Standard — The Prohibited List. 2024. https://www.wada-ama.org/en/prohibited-list [11] Sigalos JT, Pastuszak AW, Allison A, Ohlander SJ, Herati A, Lindgren MC, Lipshultz LI. Growth Hormone Secretagogue Treatment in Hypogonadal Men Raises Serum Insulin-Like Growth Factor-1 Levels. Am J Mens Health. 2017. https://pubmed.ncbi.nlm.nih.gov/28830317/ [12] Memdouh S, Ghosh D, Petrou M, Daly L, Cowan D, Brailsford AD. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Test Anal. 2021. https://pubmed.ncbi.nlm.nih.gov/34665524/ [13] U.S. Food and Drug Administration. FDA Briefing Document — Pharmacy Compounding Advisory Committee (PCAC) Meeting — Peptide bulk drug substances review. Regulations.gov docket FDA-2024-N-4777. 2024. https://downloads.regulations.gov/FDA-2024-N-4777-0002/attachment_7.pdf [14] Esposito S, Deventer K, Van Eenoo P. Chromatographic-mass spectrometric analysis of peptidic analytes (2-10 kDa) in doping control urine samples. Drug Test Anal / J Chromatogr B. 2024. https://pubmed.ncbi.nlm.nih.gov/38197510/ [15] Van Hout MC, Hearne E. Netnography of Female Use of the Synthetic Growth Hormone CJC-1295: Pulses and Potions. Subst Use Misuse. 2016;51(1):73-84. https://www.tandfonline.com/doi/abs/10.3109/10826084.2015.1082595 [16] U.S. Food and Drug Administration. FDA removes certain peptide bulk drug substances from Category 2 of interim 503A bulks list and sets dates for PCAC review. Federal Register / FDA announcement. 2024. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks [17] National Center for Biotechnology Information. CJC-1295 — PubChem CID 91971820. 2024. https://pubchem.ncbi.nlm.nih.gov/compound/Cjc-1295 --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # About CJC-1295 Meds: An Editorial Reading Desk for the CJC-1295 Literature > CJC-1295 Meds is an independent editorial project that publishes plain-language summaries of the peer-reviewed CJC-1295 research literature. Not a clinic. Not a vendor. Not a prescription. An independent editorial reading desk for the peer-reviewed CJC-1295 research literature. ## What this site is CJC-1295 Meds is an independent editorial project that publishes plain-language summaries of the peer-reviewed research literature on CJC-1295 — the synthetic GHRH analog characterized by Teichman et al. in 2006 and its associated with-DAC and no-DAC variants. The site reads as a shader-lit research digest: every section is structured around the underlying study, every quantitative claim ties to a numbered citation, and every page exists to translate the published record into something a careful general reader can follow. We are not a clinic. We do not employ clinicians and we do not provide medical advice. We do not manufacture, sell, or distribute any product. We do not write prescriptions. Our work is editorial commentary on publicly available science. ## What 'meds' means in the domain name The 'meds' modifier in cjc1295meds.com is editorial framing — a position the publisher occupies relative to the research literature, not a claim about services this site offers. CJC-1295 is not FDA-approved as a medication; it is a research compound with a small primary-source footprint and a sprawling commercial-search landscape. Treating the substance with the rigor it would receive in a real research-pharmacology reference — citation-forward, mechanism-first, dose-and-half-life-precise — is what 'meds' signals here. It is not an offer to provide medical products. ## Editorial standards Every quantitative claim on this site cites a study in the references index. Every page is built from peer-reviewed primary sources or named federal regulatory documents — Teichman 2006 in the Journal of Clinical Endocrinology & Metabolism, Alba 2006 in the American Journal of Physiology - Endocrinology and Metabolism, Coy 1994 in JCEM, Raun 1998 in the European Journal of Endocrinology, the FDA's 2024 Pharmacy Compounding Advisory Committee briefing, the WADA Prohibited List, and the small set of analytical-chemistry detection papers that anchor the anti-doping literature. We do not write claims that cannot be cited. We do not extrapolate clinical recommendations from preclinical or observational data. We do not endorse the compound, recommend its use, or rank vendors. ## What the shader-lit register is doing The visual register of this site — dark ink ground, cyan and magenta accent rules, mono shader-debug eyebrows, polished chrome image vocabulary — is a deliberate departure from the warm clinic-marketing tone that dominates the CJC-1295 search landscape. The intent is to mark this site as a research reference rather than a sales surface. The aesthetic vocabulary draws from contemporary motion-design studios (Active Theory, Studio Tendril, Field.io) rather than from pharmaceutical marketing or wellness branding. Same content discipline as a textbook. Different visual register. --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription. --- # Contact CJC-1295 Meds: Editorial Inquiries Only > Contact CJC-1295 Meds for editorial inquiries — corrections, citations, source suggestions. We do not provide medical advice, do not sell products, and cannot answer clinical questions about CJC-1295. Editorial inquiries only. Corrections, citation suggestions, and source-flagging are welcome. ## What we can answer CJC-1295 Meds is an editorial project. We can respond to inquiries that fall inside the editorial scope of the site: corrections to a cited claim, suggestions for sources we should add, questions about how we read a specific paper, and notes on broken or stale citations. If you find an error on the site — a misattributed study, a mistyped half-life figure, a citation that no longer resolves — please flag it. We respond to editorial messages on a rolling basis, time permitting. We do not provide same-day responses and we do not run a help desk. ## What we cannot answer We cannot answer questions about your individual health, about whether CJC-1295 is appropriate for you, about dosing for your specific situation, about drug interactions with medications you take, or about where to obtain the compound. We do not provide medical advice. We do not write prescriptions. We do not employ clinicians. We do not maintain a clinical staff. Questions of this kind should be directed to a licensed healthcare provider — we cannot route or refer them. We also do not sell CJC-1295, do not source or distribute it, do not recommend vendors, and cannot evaluate the quality, identity, or purity of any product offered for sale. Inquiries about purchasing will not receive a response. ## Editorial inquiries form Use the form below for editorial inquiries. Please include the URL of the page you are referencing and the specific claim or citation in question. Messages are reviewed by the editorial desk and answered when within scope. (Form fields rendered by the assembler: name, email, page URL, message body, submit button. No tracking pixels, no third-party analytics on this form.) --- A shader-lit reading of the published CJC-1295 record — telemetry from the literature, debug-frame editorial, not a clinic and not a prescription.