# cjc1295buy.com # CJC-1295 Buy — Independent dossier on a halted GHRH analog and its supply landscape > What the published research, FDA Pharmacy Compounding Advisory Committee briefings, and WADA standards say about CJC-1295 — a long-acting GHRH analog whose Phase 2 program was terminated in 2006 and which the FDA placed in 503A Category 2 in 2023. An independent record of what published science, FDA committee briefings, and anti-doping authorities say about a research peptide that was never approved, whose only Phase 2 trial was halted in 2006, and whose U.S. supply remains restricted. ## The short version CJC-1295 is a synthetic version of the hormone that tells your pituitary gland to release growth hormone. Unlike the natural version, which clears from the bloodstream in about seven minutes, CJC-1295 DAC — the long-acting form — stays active for nearly a week by hitching a ride on a blood protein called albumin. The result is days of elevated growth hormone and IGF-1, the downstream signal that drives tissue repair and metabolism. It was never approved by the FDA. A Phase 2 clinical trial was terminated in 2006. The FDA's compounding advisory committee reviewed it in 2024 and did not recommend it for pharmacy compounding. It is prohibited by the World Anti-Doping Agency at all times. This dossier catalogs the peer-reviewed evidence: what the compound does in the lab, what the Phase 1 human data actually show, and where the regulatory record stands today. It also covers [what people using it in research settings report](/effects) — both the effects they describe and the cautions that matter. ## What CJC-1295 is, in one paragraph CJC-1295 is a 30-amino-acid synthetic analog of growth hormone-releasing hormone (GHRH) developed in the early 2000s by ConjuChem Biotechnologies. It is built on the first 29 amino acids of human GHRH with four protective substitutions — D-Ala at position 2, Gln at 8, Ala at 15, and Leu at 27 — that resist enzymatic degradation. The defining structural feature is a 31st modification: a maleimidopropionic acid group at the C-terminus that covalently bonds to the free thiol on Cys34 of circulating serum albumin after subcutaneous injection [1]. That albumin tether is what makes CJC-1295 long-acting; the mean plasma half-life in healthy adults is between 5.8 and 8.1 days, against the roughly seven-minute half-life of native GHRH [2]. The non-DAC version — sometimes sold as 'CJC-1295 without DAC' or 'modified GRF (1-29)' — omits the maleimide group and has a plasma half-life of approximately 30 minutes [8]. The two are pharmacokinetically distinct and frequently conflated in supplier copy. ## Why this site exists The phrase 'CJC-1295 buy' is a high-frequency search query. The pages that rank for it tend to be vendor product listings, not editorial summaries — which means anyone looking for the regulatory, clinical, and analytical record of the compound has to assemble it themselves from primary literature. This dossier is that assembly. It catalogs what peer-reviewed studies, FDA Pharmacy Compounding Advisory Committee briefings, World Anti-Doping Agency standards, and forensic mass-spectrometry papers actually say about CJC-1295 — its mechanism, its halted clinical program, its current regulatory status, and the supply landscape that has formed around it. The domain modifier 'buy' is editorial framing. It locates this publication relative to a particular search intent. It is not a claim about services this site offers. The site does not sell CJC-1295, does not facilitate its purchase, does not direct readers to vendors, and is not affiliated with any pharmacy, compounder, research-chemical supplier, or clinic. It is an independent editorial record. ## The regulatory record in five facts **One.** CJC-1295 is not approved by the U.S. Food and Drug Administration or by any other major regulator for any human indication. It has never been approved. **Two.** The only Phase 2 trial — NCT00267527, a 192-participant study in HIV-associated visceral adiposity sponsored by ConjuChem Biotechnologies — was terminated in October 2006 after a participant died from an acute coronary event approximately two hours after the eleventh weekly dose. An independent review attributed the event to pre-existing undiagnosed coronary artery disease and judged it unrelated to study drug, but the program was halted and primary efficacy endpoints were never published [7]. **Three.** In 2023, the FDA placed CJC-1295 in Section 503A Category 2 — substances not approved for routine compounding pending FDA review — which directly restricted the channels through which it can be lawfully supplied through traditional U.S. compounding pharmacies [13]. **Four.** At the October 29, 2024 meeting of the FDA Pharmacy Compounding Advisory Committee, members reviewed pharmacology, safety, and historical use data on CJC-1295 (five chemical forms across DAC and non-DAC variants) and did not recommend inclusion on the 503A bulk drug substances list. A follow-up briefing on December 4, 2024 consolidated public comment, manufacturer evidence submissions, and adverse-event signal review and reiterated insufficient evidence to support routine 503A access [13, 17]. **Five.** The World Anti-Doping Agency lists CJC-1295 on the 2025 Prohibited List under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics — at all times, both in-competition and out-of-competition. For any athlete subject to the WADA Code, possession alone constitutes an Anti-Doping Rule Violation under Article 2.6 [16]. ## The clinical record in three lines The published human evidence base for CJC-1295 is narrow. One Phase 1 pharmacokinetic and pharmacodynamic study in healthy adults established that single subcutaneous doses of 30 to 250 μg/kg produced mean plasma growth hormone elevations of two- to ten-fold for at least six days and mean IGF-1 elevations of 1.5- to three-fold for nine to eleven days; multiple-dose cohorts sustained IGF-1 elevation up to 28 days [2]. A companion paper from the same program demonstrated that GH secretion remained pulsatile during continuous CJC-1295 stimulation rather than being abolished, with trough GH levels rising approximately 7.5-fold while normal pulse architecture was preserved [6]. There are no published long-term human efficacy or safety randomized controlled trials. The Phase 2 program in HIV-associated visceral adiposity was the only registered clinical-stage efficacy study, and it was terminated before primary endpoint publication [7]. ## Where to read further The [research page](/research) walks through the mechanism, the published Phase 1 data, the pulsatility findings, and the comparator literature on the closely related FDA-approved GHRH analog tesamorelin. The [dosage page](/dosage) is a research-context summary only — doses studied in animal models and the published Phase 1 cohort, with no prescriptive dosing guidance. The [FAQ page](/faq) answers the questions that recur in search around buying, legality, vendor verification, the DAC versus non-DAC distinction, and what the WADA listing means in practice. The [references page](/references) is the full citation list — peer-reviewed papers, ClinicalTrials.gov entries, FDA briefing materials, and the WADA prohibited list — sortable by year and source category. The [about page](/about) explains who publishes this dossier and the editorial standards applied. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # CJC-1295 reported effects, community signals, and safety cautions > What the research-use community reports about CJC-1295 — benefits, adverse effects, and the cited safety cautions that matter — in plain language, with the evidence clearly labeled. Community accounts from research-use settings, plainly described. Distinct from the clinical literature. Read alongside the dossier. ## The short version CJC-1295 is a research peptide that raises growth hormone (GH) for days — the DAC form can keep it elevated for up to a week from a single dose. Growth hormone touches a lot of systems: sleep, body composition, fluid balance, and metabolism. So the range of things people describe is wide. The published human evidence covers only short-term pharmacokinetics in small healthy-volunteer cohorts. There are no long-term human efficacy or safety trials. What follows is drawn from two distinct sources: community accounts from research-use forums and clinical write-ups (labeled throughout as anecdotal), and cited safety cautions that have a documented mechanistic or clinical basis. The two categories are clearly separated below. CJC-1295 is not approved for human use by the FDA or any major regulator [19]. It is prohibited at all times in sport under WADA Section S2 [16]. ## What people report **These are anecdotal, not clinical evidence.** They are drawn from research-use forums, wellness-clinic summaries of user feedback, and consumer peptide guides — not from controlled trials. They describe what users say, not what studies prove. **Deeper, more restful sleep** is the single most commonly reported effect. People often describe it as the first change they notice, sometimes within the first week — falling asleep faster, waking less, feeling more recovered in the morning. This fits the biology: growth hormone is released mainly during deep slow-wave sleep, and GHRH-axis stimulation is known to enhance that phase of sleep [12]. **Faster recovery from training and soreness** is frequently reported by people using the compound in fitness contexts. The mechanism is not established for CJC-1295 specifically; most community accounts attribute it to better sleep or to the general effects of elevated IGF-1 on tissue repair. **Gradual fat loss, especially around the midsection**, is frequently reported, typically described as a slow change over three to six weeks when accompanied by diet and exercise. The closest approved-drug evidence is from tesamorelin — a related GHRH analog — which produced significant visceral fat reduction in HIV-associated lipodystrophy over 26 weeks [14]. That finding is from a different drug in a different population and should not be extrapolated directly. **A leaner look and better muscle retention** while dieting is occasionally described. These accounts typically emphasize that results are subtle and take time, and that they require consistent training. **Water retention, bloating, and puffiness** is the most commonly reported downside. Communities widely note it is more pronounced with the long-acting CJC-1295 DAC form than with the short-acting no-DAC (Modified GRF 1-29) form, because the DAC keeps growth hormone elevated for days. Most accounts describe it as easing over a few weeks. **Tingling or numbness in the fingers and hands** is frequently reported and often compared to mild carpal tunnel. It is generally attributed to fluid retention pressing on nerves in the wrist. Reports describe it as dose-related. **Injection-site redness, itching, or mild swelling** is among the most consistently mentioned local effects. **Flushing or a warm head rush** shortly after dosing is occasionally reported, more often with the short-acting no-DAC form around injection time. Most accounts describe it as passing within minutes. **Fatigue or unusual drowsiness** is occasionally reported, sometimes shortly after a dose — though an equal number of users describe the opposite. **Increased appetite** is reported mainly when CJC-1295 is paired with ipamorelin; users on CJC-1295 alone report it far less often. ## Safety cautions The following cautions have a documented mechanistic or clinical basis. They are not personal advice. **CJC-1295 is not approved for human use and has no established long-term safety record.** Published human data are limited to two small Phase 1 pharmacokinetic studies in healthy adults. The compound is sold as a research chemical for laboratory use [2,19]. **Sustained elevation of IGF-1 carries a theoretical cancer-risk signal.** A large epidemiologic meta-analysis linked higher circulating IGF-1 to modestly increased risk of certain cancers [20]. CJC-1295 DAC keeps IGF-1 elevated for days per dose, so this mechanistic concern applies. The link is an association from population data, not proof that CJC-1295 causes cancer. **Growth hormone promotes sodium and water retention.** A clinical study confirmed that GH stimulates renal sodium reabsorption, expanding extracellular fluid volume [21]. This is the documented mechanism behind the water-retention and carpal-tunnel-like effects people report. Individuals with high blood pressure, heart conditions, or a tendency toward swelling should treat this as a real mechanism-based concern, not cosmetic bloating. **Sustained GH-axis stimulation can reduce insulin sensitivity and raise blood sugar.** A clinical study of a GHRH analog documented effects on endogenous GH pulsatility and insulin sensitivity [22]. Because growth hormone is glucose-sparing, this is particularly relevant for anyone with diabetes, prediabetes, or insulin resistance. **Immunogenicity was flagged by the FDA.** In 2024 briefing materials for the Pharmacy Compounding Advisory Committee, the FDA cited immunogenicity — the risk that the body mounts an immune response to the peptide — as part of the basis for not recommending CJC-1295 for the 503A compounding bulks list [17]. A current review of GHRH-analog pharmacology reinforces that long-acting albumin-binding designs carry this consideration [23]. **The original long-acting DAC program was discontinued, and a patient death during the development era is part of the public record.** The NCT00267527 Phase 2 trial was halted; the public record does not establish that CJC-1295 caused the death, and an independent safety review attributed it to pre-existing undiagnosed coronary artery disease [7]. The compound never advanced to approval. **The DAC and no-DAC forms are routinely confused, and the distinction matters for safety.** The DAC form (multi-day half-life) and Modified GRF 1-29 (minutes-to-hours half-life) behave very differently. The long-acting DAC form drives more sustained fluid retention, blood-sugar shifts, and IGF-1 exposure. Knowing which form is in hand is essential to interpreting any reported effect [1]. **CJC-1295 is prohibited in sport at all times.** It appears on the WADA 2025 Prohibited List under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics. Detection methods are established. Any tested athlete faces an anti-doping rule violation [16]. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # CJC-1295 Research — Mechanism, Phase 1 PK/PD, pulsatility, halted Phase 2, and forensic analytics > A peer-reviewed summary of CJC-1295 research: GHRH-receptor mechanism, DAC bioconjugate pharmacokinetics, the Teichman 2006 Phase 1 data, the Ionescu pulsatility paper, the halted NCT00267527 trial, and recent WADA analytical methodology. What twenty years of published work establishes — and what it explicitly does not. ## The research record, plainly The published science on CJC-1295 is narrower than its online reputation suggests. Two 2006 studies on healthy adults — one measuring pharmacokinetics, one examining whether normal pulsatile growth-hormone release is preserved — are the core of the human evidence base. Both were conducted by the same group, in small cohorts, before the Phase 2 clinical program was halted. What those studies showed: single subcutaneous doses raise growth hormone levels by two to ten times and keep IGF-1 elevated for up to eleven days. The natural rhythmic bursting of growth hormone secretion is preserved, not abolished. A mouse study from the same year confirmed that the compound can substitute for the animal's own growth-hormone-releasing hormone. What those studies did not show: long-term safety, efficacy for any health outcome, or any data beyond short-term pharmacokinetics in healthy volunteers. The Phase 2 trial that might have supplied efficacy data was terminated before those results were published. ## Mechanism: a GHRH receptor agonist on an albumin tether CJC-1295 binds the GHRH receptor (GHRHR), a class-B G-protein-coupled receptor expressed predominantly on somatotroph cells of the anterior pituitary. Activation initiates a Gs-protein, adenylyl-cyclase, cAMP, protein-kinase-A second-messenger cascade that upregulates growth hormone gene transcription and triggers pulsatile GH secretion [1]. Downstream, hepatic IGF-1 (somatomedin C) production rises in response to circulating GH, and IGF-1 becomes the primary biomarker of GH-axis activation [2]. What distinguishes CJC-1295 from native GHRH is the Drug Affinity Complex (DAC) — a maleimidopropionic acid group appended to the C-terminus that undergoes a Michael-addition reaction with the free thiol on Cys34 of circulating serum albumin after subcutaneous injection [1]. The covalent peptide-albumin bioconjugate is sterically shielded from peptidase degradation and from renal clearance. Native GHRH has a plasma half-life of approximately seven minutes; the four protective amino acid substitutions in the modified GRF (1-29) backbone extend that to roughly 30 minutes by resisting DPP-4 cleavage, deamidation, and oxidation [8]; the DAC bioconjugate extends it further still, to between 5.8 and 8.1 days in healthy adults [3]. The pharmacology is therefore not 'a more potent GHRH' but 'a GHRH-equivalent stimulus delivered over days rather than minutes.' That distinction matters for how the compound's effects on the GH/IGF-1 axis present in the literature. ## The Phase 1 record: Teichman 2006 The first and most-cited human pharmacokinetic study on CJC-1295 was published by Teichman and colleagues in the Journal of Clinical Endocrinology and Metabolism in 2006 [2]. Healthy adults received single subcutaneous injections at one of four dose levels — 30, 60, 125, or 250 μg/kg — and were followed for plasma GH, IGF-1, and pharmacokinetic parameters across cohorts. The findings, as reported: single-dose mean plasma GH rose two- to ten-fold above baseline and remained elevated for at least six days; mean IGF-1 rose 1.5- to three-fold above baseline and remained elevated for nine to eleven days. Multiple-dose cohorts dosed weekly or biweekly for 28 to 49 days sustained IGF-1 elevation across the dosing window, with no plateau observed within that interval [2]. Mean plasma half-life estimates fell between 5.8 and 8.1 days across dose cohorts [3]. No serious adverse events attributable to study drug were reported in the Phase 1 cohort. The most commonly reported events were injection-site reactions and transient facial flushing — both consistent with documented effects of GHRH receptor agonism. ## Pulsatility preserved: Ionescu and Frohman A second 2006 paper from the same program, by Ionescu and Frohman, addressed a mechanistically important question — whether continuous stimulation by a long-acting GHRH analog would abolish the natural pulsatile secretion of growth hormone, as exogenous recombinant GH effectively does, or whether somatotrophs would continue to fire in discrete pulses against an elevated baseline [6]. The finding was the latter. Single CJC-1295 injections raised basal (trough) GH levels approximately 7.5-fold while mean GH ran about 46% above baseline; pulsatile architecture — discrete GH bursts at characteristic intervals — persisted across the elevated baseline. The authors characterized this as a pharmacologically distinctive profile relative to recombinant GH administration [6]. This pulsatility preservation is the mechanism-level argument frequently invoked for why a GHRH analog might be theoretically preferable to exogenous GH in research contexts. The argument is mechanistic and rests on Phase 1 PK data, not on long-term human efficacy or safety trials, of which none exist. ## GHRH-knockout mouse model: Alba 2006 In the same year, Alba and colleagues published a study of CJC-1295 in GHRH-knockout mice — animals genetically unable to produce endogenous GHRH and consequently growth-impaired [4]. Once-daily subcutaneous injections of 2 μg per mouse for five weeks normalized linear growth, body weight, and lean body composition against untreated knockout controls. Less-frequent dosing at 48-hour and 72-hour intervals produced partial restoration. Pituitary somatotroph proliferation and GH mRNA expression both increased with treatment. The study is the cleanest mechanistic demonstration that CJC-1295 can substitute for endogenous GHRH in a deficient system. It does not establish efficacy for any human indication, but it grounds the molecular pharmacology in a whole-animal phenotype. ## The halted Phase 2: NCT00267527 The only registered Phase 2 trial of CJC-1295 — NCT00267527, sponsored by ConjuChem Biotechnologies and conducted in HIV-associated visceral adiposity — enrolled 192 participants on a weekly subcutaneous dosing schedule [7]. The trial was terminated in October 2006 after a participant died of an acute coronary event approximately two hours after the eleventh weekly dose. An independent safety review attributed the event to pre-existing undiagnosed coronary artery disease and judged it unrelated to study drug. The trial was not restarted. No further sponsor-funded clinical development of CJC-1295 has occurred since. Primary efficacy endpoints on visceral fat, the trial's named outcome, were never published in the peer-reviewed literature [7]. For context on the indication: the closely related FDA-approved GHRH analog tesamorelin produces a 15-20% reduction in visceral adipose tissue over 26 weeks of daily 2 mg subcutaneous dosing in HIV-associated lipodystrophy [14]. That benchmark — established in a separate molecule from the same pharmacological class — is the closest published efficacy reference point for what the CJC-1295 Phase 2 program might have measured, had it run to completion. ## Serum protein signatures: Sackmann-Sala 2009 A 2009 proteomic study by Sackmann-Sala and colleagues analyzed serum samples from eleven healthy young men one week after a single CJC-1295 injection [5]. Five differentially expressed serum proteins were identified: apolipoprotein A1 and transthyretin isoforms decreased; β-hemoglobin, albumin C-terminal fragments, and immunoglobulin fragments increased. The immunoglobulin and albumin-fragment spot correlated linearly with IGF-1 levels, suggesting a candidate biomarker panel for GH/IGF-1 axis activation downstream of GHRH-analog administration. The study is methodological — it identifies serum signatures of GH/IGF-1 axis activation rather than evaluating clinical outcomes — but it remains one of the few peer-reviewed human exposure analyses of CJC-1295 published after the Phase 2 termination. ## Forensic and anti-doping analytics The compound has continued to appear in the analytical chemistry literature, primarily through anti-doping and forensic-identification work. In 2010, Henninge and colleagues at an anti-doping laboratory used liquid chromatography high-resolution tandem mass spectrometry to determine the sequence of an unknown peptide pharmaceutical preparation seized through enforcement channels [9]. The compound was identified as CJC-1295. The paper is one of the first explicit confirmations in the literature that the compound is in distribution through gray-market channels and that confirming the identity of seized material requires sequence-level mass spectrometric analysis. In 2024, Thomas and colleagues published validated nano-LC quadrupole/Orbitrap mass spectrometry methods for screening and confirmation of CJC-1295 and related GHRH synthetic analogs in athlete urine, compliant with WADA technical requirements [11]. The work addresses two persistent analytical challenges — peptide instability through standard sample-preparation workflows and very low urinary concentrations of the parent peptide — and brings routine doping-control detection of CJC-1295 within reach of accredited laboratories. ## Documented patterns of unsupervised use Outside the published clinical literature, observational and qualitative work has documented patterns of CJC-1295 acquisition outside clinical channels. A 2016 netnographic analysis by Van Hout and Hearne of nine online bodybuilding forums and 23 discussion threads documented self-reported female use of CJC-1295 sourced through non-clinical channels [10]. Reported motivations included weight loss, muscle gain, skin appearance, sleep improvement, and injury recovery. The authors documented safety anxieties expressed by users themselves around gender differences in GH pulsatility and around product purity from unregulated sources — concerns the published clinical literature does not address, because no controlled studies of those use patterns exist. A mechanistic rationale frequently invoked in non-clinical discussion is the combination of a GHRH analog with a GHS-R1a (ghrelin receptor) agonist such as ipamorelin. The pharmacological basis for that pairing is documented: Bowers and colleagues demonstrated in 1990 that combined intravenous administration of GHRH and a ghrelin-receptor agonist produces a GH secretory response several-fold larger than either agent alone in healthy adults [15]. That study used native GHRH and GHRP-6, not CJC-1295 and ipamorelin specifically, but the dual-receptor mechanism is the same. ## What the literature does and does not establish The published literature establishes: that CJC-1295 binds GHRHR and activates the documented downstream signaling cascade [1]; that single doses in healthy adults produce sustained GH and IGF-1 elevation lasting days [2]; that the DAC bioconjugate produces a plasma half-life of 5.8 to 8.1 days in humans [3]; that natural pulsatile GH secretion is preserved during continuous stimulation [6]; that the compound normalizes growth in GHRH-knockout mice [4]; that the only Phase 2 program was terminated in 2006 and did not restart [7]; that the compound is distributed through gray-market channels and identifiable by mass spectrometry [9]; and that it is currently restricted from routine 503A compounding [13, 17] and prohibited by WADA at all times [16]. The published literature does not establish: long-term human efficacy for any indication; long-term human safety; comparative effectiveness against any approved therapy; appropriate dosing for any human use; or a published efficacy benchmark on visceral fat, lean mass, sleep architecture, or any other endpoint discussed in non-clinical settings. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # CJC-1295 Dosage Research — What animal and Phase 1 human studies reported > A research-context summary of the doses, routes, and intervals studied in published CJC-1295 work — Jetté 2005 rat PK, Alba 2006 GHRH-knockout mouse, Teichman 2006 Phase 1 human PK/PD. Not prescriptive guidance. CJC-1295 is not approved for any human indication. The doses recorded below are the doses administered in the published research literature, summarized in research context only. Nothing on this page is dosing guidance for human use. ## What doses were actually studied CJC-1295 is not approved for any human indication, so there is no labeled dose, no titration schedule, and no clinical practice guideline. This page describes only what was reported in published research — what investigators administered in controlled settings and what they observed. The human pharmacokinetic study used single subcutaneous doses of 30 to 250 micrograms per kilogram of body weight. At those doses, growth hormone rose two to ten times above baseline and IGF-1 rose one-and-a-half to three times, with effects lasting up to eleven days from a single dose. Multiple-dose cohorts in that trial maintained IGF-1 elevation for up to 28 days. Animal work used 2 micrograms per dose in GHRH-knockout mice (equivalent to roughly 80 micrograms per kilogram) at 24- to 72-hour intervals. The Phase 2 trial in humans — the only registered efficacy study — was terminated before specific dose data were published. Nothing on this page is prescriptive guidance. ## A note on what this page is CJC-1295 has never been approved by the FDA or any major regulator for human use. There is no labeled dose. There is no titration schedule. There is no clinical-practice guideline. This page summarizes the doses, routes, and intervals reported in published research — peer-reviewed PK/PD studies in healthy adult Phase 1 cohorts and in animal models. It is descriptive: what investigators administered, what they measured, what they reported. It is not prescriptive: it does not tell a reader what to administer, to whom, at what frequency, or for what purpose. Anyone using CJC-1295 in laboratory research should consult primary sources and applicable institutional and regulatory standards directly, not this page. The four published studies that contain explicit dose data are summarized below. ## Rat pharmacokinetics: Jetté 2005 The foundational pharmacokinetic identification of CJC-1295 was published by Jetté and colleagues in Endocrinology in 2005 [1]. The study evaluated several human GRF(1-29)-albumin bioconjugates in rats, characterizing receptor activation on the anterior pituitary and circulating bioactivity over time. Single subcutaneous bolus doses in the low-μg/kg range produced a four-fold increase in growth hormone area-under-the-curve over two hours relative to unconjugated peptide, with bioactivity remaining detectable beyond 72 hours [1]. This established the basic premise of the albumin-bioconjugate platform: a peptide that would otherwise clear in minutes was producing measurable bioactivity for days. The paper named CJC-1295 as the lead candidate among the conjugates evaluated. ## GHRH-knockout mouse: Alba 2006 Alba and colleagues administered 2 μg of CJC-1295 per injection to GHRH-knockout mice at three different dosing intervals — 24, 48, and 72 hours — over a five-week treatment period [4]. In a 25 g mouse, 2 μg corresponds to approximately 80 μg/kg. The once-daily (24 h) interval normalized linear growth, body weight, and lean body composition relative to untreated knockout controls. The 48-hour and 72-hour intervals produced partial restoration on the same outcomes. Pituitary somatotroph proliferation and GH mRNA expression both increased with treatment across intervals. No adverse effects on the measured outcomes were reported at the doses studied [4]. ## Human Phase 1: Teichman 2006 The published human dose-ranging data come from a single Phase 1 study by Teichman and colleagues [2]. Healthy adults aged 21 to 61 received single subcutaneous injections at one of four dose levels: 30, 60, 125, or 250 μg/kg. Separate multiple-dose cohorts received weekly or biweekly subcutaneous injections for 28 to 49 days. Reported pharmacodynamic outcomes at single dose were: mean plasma GH elevation of two- to ten-fold above baseline, sustained for at least six days; mean IGF-1 elevation of 1.5- to three-fold above baseline, sustained for nine to eleven days. Multiple-dose cohorts maintained IGF-1 elevation up to 28 days [2]. Mean plasma half-life across dose cohorts was estimated at 5.8 to 8.1 days, attributed to covalent albumin bioconjugation via the C-terminal maleimide group [3]. The Phase 1 study reported no serious adverse events attributable to study drug. The most commonly reported events were injection-site reactions and transient facial flushing. ## Phase 2: terminated before dosing schedules were fully disclosed The only registered Phase 2 trial of CJC-1295 — NCT00267527, in HIV-associated visceral adiposity, n=192 — was conducted on a weekly subcutaneous dosing schedule [7]. The specific μg/kg dose used in Phase 2 was not fully disclosed in the literature before the trial was terminated in October 2006. No primary endpoint publication exists. ## Route of administration Every reviewed human study and the predominant majority of animal studies administered CJC-1295 by subcutaneous injection [1, 2, 4]. Some rodent mechanistic work has used intraperitoneal administration. Intravenous administration appears in early comparator GHRH studies but not as a delivery route for CJC-1295 itself in the published clinical literature. The practical implication of the DAC bioconjugation mechanism is that delivery must give the peptide time to encounter circulating albumin and form the covalent bond at Cys34 before clearance. Subcutaneous administration provides that sustained-release profile and is the only route in the human PK record. ## Half-life: DAC vs non-DAC Native human GHRH has a plasma half-life of approximately seven minutes. The four amino acid substitutions in the modified GRF (1-29) backbone — D-Ala²/Gln⁸/Ala¹⁵/Leu²⁷ — confer resistance to DPP-4 cleavage, deamidation, and oxidation, extending in-vivo half-life of the non-DAC peptide to approximately 30 minutes while preserving GHRHR binding affinity [8]. The DAC variant adds the maleimide-Cys34 bioconjugation step. The reported mean plasma half-life of the bioconjugate in healthy adults is 5.8 to 8.1 days across the dose cohorts of the Teichman Phase 1 study [3]. The two compounds — DAC and non-DAC — are often conflated in supplier copy and discussion forums under the umbrella label 'CJC-1295,' but they are pharmacokinetically distinct by roughly two orders of magnitude in plasma persistence. ## Stability and handling notes from the research literature The DAC variant's bioactivity depends on covalent attachment to the free thiol of albumin Cys34, which occurs after subcutaneous administration. Reconstituted peptide is typically stored refrigerated for short-term laboratory use and frozen for longer-term storage; freeze-thaw cycles and elevated temperatures degrade activity, consistent with general peptide handling practice. The non-DAC variant degrades faster in solution because it lacks the albumin tethering that protects the DAC bioconjugate from peptidase activity. Reported research-context handling for non-DAC modified GRF (1-29) follows the same cold-chain principles but with shorter post-reconstitution working windows. ## What the dose record does not establish The published dose record establishes single-dose and short-course pharmacokinetic and pharmacodynamic parameters in healthy adult Phase 1 cohorts (n at the low double digits per dose level) and in animal models. It does not establish a safe long-term human dose for any indication, a comparative effectiveness benchmark, an appropriate dose for any clinical endpoint, or any dose recommendation outside the controlled research settings in which those doses were administered. The Phase 2 program that would have generated comparative efficacy data at a defined dose was terminated before it could publish those data [7]. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # CJC-1295 Buy — Frequently asked questions on legality, supply, vendors, and the WADA listing > Editorial answers to the questions that recur in search around buying CJC-1295: U.S. legal status, why compounding pharmacy supply is restricted, DAC vs non-DAC, vendor verification, anti-doping consequences, and what the published research actually shows. The questions below are the ones the search data shows readers asking about buying CJC-1295. The answers are editorial — what the literature, the FDA briefings, and the WADA standards say. They are not legal, medical, or purchasing advice. ## Is it legal to buy CJC-1295 in the United States? CJC-1295 is not a scheduled controlled substance under the U.S. Controlled Substances Act. It is also not an FDA-approved drug for any human indication. Those two facts together place it in a regulatory gray area that varies by transaction. The FDA placed CJC-1295 in Section 503A Category 2 in 2023 — substances not approved for routine pharmacy compounding pending FDA review [13]. At the October 2024 Pharmacy Compounding Advisory Committee meeting, members reviewed evidence on five chemical forms of the compound and did not recommend inclusion on the 503A bulk drug substances list; a December 2024 follow-up briefing reiterated insufficient evidence [13, 17]. The practical effect is that traditional U.S. compounding pharmacies cannot lawfully prepare CJC-1295 for individual patient prescriptions under 503A. The compound continues to appear in distribution channels labeled 'research chemical' — a designation that the suppliers themselves apply to indicate the product is not approved for human use and is sold for in vitro or non-human laboratory investigation only. The legality of any specific transaction depends on jurisdiction, on the seller's regulatory standing, on the buyer's stated purpose, and on whether the transaction crosses borders. This site does not provide legal advice and does not direct readers to vendors. ## Why has U.S. compounding pharmacy supply been restricted? Section 503A of the Federal Food, Drug, and Cosmetic Act allows traditional pharmacies to compound drug products for individual patient prescriptions. The bulk drug substances that may be used in 503A compounding are governed by FDA review and listing. CJC-1295 was placed in 503A Category 2 in 2023 — substances under FDA review and not approved for routine 503A compounding access. The FDA Pharmacy Compounding Advisory Committee took up CJC-1295 at its October 29, 2024 meeting. According to the public briefing materials, members considered the available pharmacology, safety, and historical-use evidence for five chemical forms across the DAC and non-DAC variants and did not recommend inclusion on the 503A bulks list [13]. A December 4, 2024 follow-up briefing on the broader GH-secretagogue peptide class consolidated public comment, manufacturer evidence submissions, and adverse-event signal review and reiterated insufficient evidence to support routine 503A access for the class [17]. CJC-1295 therefore remains in Category 2. ## What is the difference between CJC-1295 DAC and 'CJC-1295 without DAC'? Two distinct compounds are routinely sold under the 'CJC-1295' label. The pharmacokinetic difference between them is roughly two orders of magnitude in plasma persistence. CJC-1295 with DAC — the original ConjuChem compound — is the 30-amino-acid GHRH analog with a C-terminal maleimidopropionic acid group that covalently binds to the free thiol on Cys34 of serum albumin after subcutaneous injection [1]. The mean plasma half-life of the resulting bioconjugate in healthy adults is between 5.8 and 8.1 days [3]. CJC-1295 without DAC — also called modified GRF (1-29) or mod GRF 1-29 — is the same 29-amino-acid backbone with the four protective substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) but without the maleimide-albumin bond. Its plasma half-life is approximately 30 minutes [8]. The two compounds were sometimes used in different research designs for different reasons. Vendors and discussion forums frequently conflate them. They are not interchangeable from a pharmacokinetic standpoint. ## Why is CJC-1295 commonly sold paired with ipamorelin? The 'CJC-1295 + ipamorelin' pairing has a documented mechanistic basis. CJC-1295 binds the GHRH receptor. Ipamorelin binds GHS-R1a, the ghrelin receptor. The two receptors converge on growth hormone release through distinct signaling pathways, and combined activation produces a GH secretory response several-fold larger than either agent alone [15]. The foundational study demonstrating this dual-receptor synergy was Bowers and colleagues in 1990, who administered native GHRH and the ghrelin-receptor agonist GHRP-6 to healthy adults [15]. The CJC-1295 + ipamorelin pairing extends that mechanism to longer-acting analogs and is the most commonly co-listed peptide blend in research-chemical supplier catalogs. No controlled human efficacy or safety studies of the CJC-1295 + ipamorelin combination at the doses or schedules sold in research-chemical channels have been published. ## How can a buyer verify the identity of CJC-1295 from a vendor? The peer-reviewed analytical literature establishes that the only definitive identification of CJC-1295 in a finished pharmaceutical preparation is by sequence-level mass spectrometric analysis. In 2010, Henninge and colleagues used liquid chromatography high-resolution tandem mass spectrometry to identify CJC-1295 in an unknown pharmaceutical preparation seized through enforcement channels [9]. In 2024, Thomas and colleagues published validated nano-LC Orbitrap mass spectrometry methods for routine detection of CJC-1295 and related GHRH analogs in athlete urine [11]. In practical terms: paper certificates of analysis provided by vendors are documents about a batch, not the specific vial in a buyer's hand. The literature documents that the identity, purity, and sterility of peptides in non-pharmaceutical channels are not assured — the seized-material analysis was published precisely because what was on the label and what was in the preparation could not otherwise be confirmed [9]. A buyer who needs to confirm identity has to submit a sample to a qualified analytical laboratory. ## What are the documented risks of acquiring CJC-1295 from unregulated vendors? The published literature documents three categories of concern. First, identity: an unknown pharmaceutical preparation seized through enforcement channels was confirmed to contain CJC-1295 only after sequence-level mass spectrometric analysis [9]. The implication — that the contents of unregulated preparations cannot be confirmed from labeling alone — is general to the gray-market peptide channel. Second, purity and sterility: peptide products distributed through research-chemical channels are not subject to pharmacopoeial standards for impurity profiles, residual solvents, endotoxin content, or sterility. The 2024 FDA Pharmacy Compounding Advisory Committee briefings explicitly cited absence of quality-controlled supply as part of the safety evaluation for the GH-secretagogue peptide class [13, 17]. Third, the documented behavioral pattern: a 2016 netnographic analysis of nine online bodybuilding forums documented user-reported safety anxieties around product purity and around the absence of clinical oversight when acquiring CJC-1295 through non-clinical channels [10]. The published clinical literature does not address long-term consequences of unsupervised use because no controlled studies of those use patterns exist. ## Is CJC-1295 a prescription drug? CJC-1295 is not an FDA-approved drug for any human indication. It therefore has no FDA-approved labeled use under which a U.S. clinician could prescribe it on-label. It is also not a scheduled controlled substance under the Controlled Substances Act. Prior to the 2023 503A Category 2 designation, the compound was reportedly available through some compounding pharmacies for individual patient prescriptions; the FDA's Category 2 placement and the 2024 PCAC committee declining to add the compound to the 503A bulks list have restricted that channel [13, 17]. The compound continues to appear in distribution channels labeled 'research chemical' that explicitly exclude human-use claims. ## Does buying CJC-1295 have anti-doping consequences? For any athlete subject to the World Anti-Doping Code, the consequences are direct. CJC-1295 is listed on the 2025 WADA Prohibited List under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics — at all times, both in-competition and out-of-competition [16]. Article 2.6 of the WADA Code establishes that possession of a prohibited substance by an athlete or athlete support personnel is sufficient for an Anti-Doping Rule Violation. Detection is no longer the analytical challenge it once was. The Thomas 2024 methodology paper documents validated nano-LC Orbitrap mass spectrometry methods for routine detection of CJC-1295 in urine at sub-nanogram-per-milliliter limits, meeting WADA technical requirements [11]. For individuals not subject to the WADA Code, there is no anti-doping consequence by definition. Other consequences — employer testing policies, insurance, professional licensing — are jurisdiction- and context-specific and are outside the scope of this dossier. ## What does the published clinical literature actually show? The published human evidence base is narrow. A single Phase 1 dose-ranging study in healthy adults established that subcutaneous CJC-1295 produces sustained mean GH and IGF-1 elevation lasting days after single doses, with a mean plasma half-life of 5.8 to 8.1 days [2, 3]. A companion paper established that pulsatile GH secretion is preserved during continuous CJC-1295 stimulation [6]. A proteomic study identified candidate serum biomarkers of GH/IGF-1 axis activation downstream of CJC-1295 administration [5]. The only Phase 2 trial — NCT00267527, in HIV-associated visceral adiposity — was terminated in October 2006 after a participant died of an acute coronary event that an independent review judged unrelated to study drug. The trial did not restart, and primary efficacy endpoints were never published [7]. There are no published long-term human efficacy or safety randomized controlled trials of CJC-1295. ## Why does this site exist if it doesn't sell CJC-1295? Because the search query 'CJC-1295 buy' is dominated by vendor product listings, and the regulatory, clinical, and analytical record of the compound is genuinely informative public-interest material that is harder to find than a vendor catalog. This site is an editorial dossier that catalogs what the peer-reviewed and regulatory record says. It does not sell CJC-1295, does not facilitate its purchase, does not link to vendors, and is not affiliated with any pharmacy, compounder, research-chemical supplier, or clinic. The 'buy' in the domain name is a marker of the search intent the page addresses editorially, not a description of services the site offers. ## What labeling and documentation accompany legitimately-supplied research peptide? Material distributed under the 'research chemical' designation is conventionally labeled for research use only and accompanied by some form of certificate of analysis describing identity, purity by HPLC or mass spectrometry, and sometimes residual solvent and endotoxin testing. A certificate of analysis is a document about a batch, prepared by or for the supplier, not an independent verification of the specific vial in a buyer's possession [9]. For research peptide acquired by a legitimately funded laboratory operating under institutional oversight, the more durable documentation chain runs through purchase orders, accession records, freezer logs, and — where the research design requires it — confirmatory analytical work performed independently of the supplier. None of that is purchasing advice; it is a description of how published research-grade peptide is conventionally documented in academic and contract-research settings. ## Was the 2006 Phase 2 death caused by CJC-1295? The independent safety review of the NCT00267527 trial attributed the participant's acute coronary event to pre-existing undiagnosed coronary artery disease and judged it unrelated to study drug [7]. The trial was nonetheless terminated and was not restarted, and ConjuChem Biotechnologies did not pursue further clinical development of CJC-1295. Primary efficacy endpoints from the trial were never published. The formal regulatory record therefore reads: a participant death adjudicated as unrelated to study drug, in the only Phase 2 trial of the compound, after which sponsor-funded clinical development ceased. The published peer-reviewed literature does not contain a contradictory finding. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # CJC-1295 References — Peer-reviewed papers, regulatory filings, and analytical standards > Full citation list for the CJC-1295 dossier: peer-reviewed PK/PD and mechanism papers from 2005-2024, the ClinicalTrials.gov record for NCT00267527, FDA Pharmacy Compounding Advisory Committee briefings from 2024, and the 2025 WADA Prohibited List. Every numbered citation in the research, dosage, FAQ, and index pages of this dossier corresponds to a row in the table below. Sortable by year, by source category, and by indication. ## How this list is organized Eighteen primary sources are cited in the body of the dossier and indexed below. Sources fall into four categories: **peer-reviewed clinical and preclinical literature** (Jetté 2005, Teichman 2006, Ionescu 2006, Alba 2006, Sackmann-Sala 2009, Stanley 2014, Bowers 1990, Steiger 1992), **forensic and anti-doping analytical chemistry** (Henninge 2010, Thomas 2024), **observational and qualitative work** (Van Hout 2016), and **regulatory and standards documents** (ClinicalTrials.gov NCT00267527, FDA PCAC October 2024, FDA PCAC December 2024, WADA 2025 Prohibited List). All links resolve to primary publishers (PubMed, ClinicalTrials.gov, FDA.gov, wada-ama.org). No links resolve to vendor pages or commercial intermediaries. ## Primary citation table The full numbered citation list is rendered as a sortable table below — sort by year ascending or descending, filter by source category. The same list is also available as plain markdown for crawlers and reading clients at `/references.md`. ## References [1] Jetté L, Léger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, Pham K, Bridon DP. 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. https://pubmed.ncbi.nlm.nih.gov/15817669/ [2] 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. Journal of Clinical Endocrinology and Metabolism. 2006;91(3):799-805. https://pubmed.ncbi.nlm.nih.gov/16352683/ [3] Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Estimated plasma half-life and PK profile of CJC-1295 across single-dose cohorts (5.8-8.1 days). Journal of Clinical Endocrinology and Metabolism. 2006;91(3):799-805. https://pubmed.ncbi.nlm.nih.gov/16352683/ [4] 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. American Journal of Physiology - Endocrinology and Metabolism. 2006;291(6):E1290-E1294. https://pubmed.ncbi.nlm.nih.gov/16822960/ [5] Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. 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 Hormone & IGF Research. 2009;19(6):471-477. https://pubmed.ncbi.nlm.nih.gov/19386527/ [6] Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. Journal of Clinical Endocrinology and Metabolism. 2006;91(12):4792-4797. https://pubmed.ncbi.nlm.nih.gov/17018654/ [7] ConjuChem Biotechnologies Inc. A study to evaluate CJC-1295 in HIV patients with visceral obesity. ClinicalTrials.gov identifier NCT00267527. Terminated October 2006. https://clinicaltrials.gov/study/NCT00267527 [8] Jetté L, Léger R, Thibaudeau K, et al. Mechanistic basis for the ~30-minute plasma half-life of modified GRF (1-29) — D-Ala²/Gln⁸/Ala¹⁵/Leu²⁷ substitutions confer DPP-4 resistance and preserve GHRHR binding. Endocrinology. 2005;146(7):3052-3058. https://pubmed.ncbi.nlm.nih.gov/15817669/ [9] 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. 2010;2(11-12):647-650. https://pubmed.ncbi.nlm.nih.gov/21204297/ [10] Van Hout MC, Hearne E. Netnography of female use of the synthetic growth hormone CJC-1295: pulses and potions. Substance Use & Misuse. 2016;51(1):73-84. https://pubmed.ncbi.nlm.nih.gov/26771670/ [11] Thomas A, Walpurgis K, Tretzel L, Brinkkötter P, Fußhöller G, Görgens C, Geyer H, Thevis M. Chromatographic-mass spectrometric analysis of peptidic analytes (2-10 kDa) in doping control urine samples. Journal of Mass Spectrometry. 2024;59(2):e4996. https://pubmed.ncbi.nlm.nih.gov/38197510/ [12] Steiger A, Guldner J, Hemmeter U, et al. Growth hormone-releasing hormone (GHRH) and sleep regulation. Psychoneuroendocrinology. 1992;17(2-3):203-209. https://pubmed.ncbi.nlm.nih.gov/1438644/ [13] U.S. Food and Drug Administration. October 29, 2024 Meeting of the Pharmacy Compounding Advisory Committee — CJC-1295 Briefing Materials. FDA Docket FDA-2024-N-4777. https://www.fda.gov/media/182088/download [14] Stanley TL, Feldpausch MN, Oh J, Branch KL, Lee H, Torriani M, Grinspoon SK. Effects of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. JAMA. 2014;312(4):380-389. https://pubmed.ncbi.nlm.nih.gov/25027139/ [15] Bowers CY, Reynolds GA, Durham D, Barrera CM, Pezzoli SS, Thorner MO. Combined administration of GHRH and GHRP-6 acts in synergy on growth hormone (GH) release in humans. Journal of Clinical Endocrinology and Metabolism. 1990;70(4):975-982. https://pubmed.ncbi.nlm.nih.gov/2107173/ [16] World Anti-Doping Agency. World Anti-Doping Code International Standard — The 2025 Prohibited List. Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics. https://www.wada-ama.org/en/prohibited-list [17] U.S. Food and Drug Administration. December 4, 2024 Pharmacy Compounding Advisory Committee Meeting — Follow-up Briefing on GH Secretagogue Peptides. FDA Docket FDA-2024-N-4777-FOLLOWUP. https://www.fda.gov/media/183819/download [18] Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Documentation of gray-market peptide acquisition through online research-chemical vendors operating outside conventional pharmacy oversight; identification of seized illicit preparations as CJC-1295. Drug Testing and Analysis. 2010;2(11-12):647-650. https://pubmed.ncbi.nlm.nih.gov/21204297/ [19] Safety and efficacy of approved and unapproved peptide therapies for musculoskeletal conditions. Sports Med. 2026. https://pubmed.ncbi.nlm.nih.gov/41966639/ [20] Renehan AG, Zwahlen M, Minder C, O'Dwyer ST, Shalet SM, Egger M. Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis. Lancet. 2004;363(9418):1346-1353. https://pubmed.ncbi.nlm.nih.gov/15110491/ [21] GH increases extracellular volume by stimulating sodium reabsorption in the distal nephron. J Clin Endocrinol Metab. 2002. https://pubmed.ncbi.nlm.nih.gov/11932310/ [22] Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity. J Clin Endocrinol Metab. 2011. https://pubmed.ncbi.nlm.nih.gov/20943777/ [23] Granata R, Leone S, Zhang X, Gesmundo I, et al. Growth hormone-releasing hormone and its analogues in health and disease. Nat Rev Endocrinol. 2025;21(3):180-195. https://pubmed.ncbi.nlm.nih.gov/39537825/ --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # About CJC-1295 Buy — Independent editorial publisher, not a vendor or a clinic > CJC-1295 Buy is an independent editorial dossier on the published research, regulatory, and analytical record of CJC-1295. The site is not a clinic, does not employ clinicians, does not provide medical advice, and does not sell or distribute any product. An independent editorial publisher that summarizes peer-reviewed research and regulatory filings on CJC-1295. We do not sell anything. We do not employ clinicians. We do not provide medical advice. ## What CJC-1295 Buy is CJC-1295 Buy is an independent editorial project that publishes summaries of the peer-reviewed research literature, the FDA regulatory record, and the anti-doping standards relating to CJC-1295. 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. Our work is editorial commentary on publicly available science. The domain modifier 'buy' is editorial framing — a position the publisher occupies relative to the high-volume search query around purchasing CJC-1295, not a claim about services this site offers. The dossier exists because the regulatory, clinical, and analytical record of the compound is genuinely informative public-interest material that is otherwise difficult to find behind a wall of vendor product listings. ## What this site is not This site is not a pharmacy. It does not compound, dispense, ship, broker, or take payment for any peptide, drug, or chemical preparation. This site is not a clinic, telehealth service, or medical practice. There are no physicians on staff. There are no pharmacists on staff. There are no nurses on staff. The site does not offer consultations, prescriptions, dosing recommendations, treatment protocols, or any other clinical service. This site is not affiliated with any manufacturer, compounding pharmacy, research-chemical vendor, telehealth platform, or wellness clinic. We do not accept advertising. We do not run affiliate links. We do not direct readers to vendors. This site does not, anywhere in its pages, recommend the use of CJC-1295 by any person for any purpose. ## Editorial standards Every quantitative claim on every page cites a primary source — a peer-reviewed paper, a ClinicalTrials.gov record, an FDA briefing document, or a published anti-doping standard. The full citation list appears at /references and is reproduced as a plain markdown file at /references.md for crawlers and reading clients. Where the published record contradicts non-clinical or vendor-channel claims about CJC-1295, the dossier presents the published record. Where the published record is silent — for example, on long-term human safety and efficacy outcomes — the dossier says so explicitly rather than filling the gap with inference. The dossier does not use brand names of FDA-approved drugs in other classes. Compounds are referred to by their international nonproprietary names or recognized chemical identifiers. ## Sourcing methodology The citation set assembled for this dossier covers the published peer-reviewed literature on CJC-1295 from the 2005 Jetté identification paper through the 2024 Thomas analytical methodology paper, the ClinicalTrials.gov record for NCT00267527, the October 2024 and December 2024 FDA Pharmacy Compounding Advisory Committee briefings, and the 2025 WADA Prohibited List. Adjacent comparator literature — the Stanley 2014 tesamorelin paper on visceral fat, the Bowers 1990 GHRH-plus-GHRP synergy paper, the Steiger 1992 GHRH-sleep paper — is included where it provides essential context for findings reported on CJC-1295 itself. Where primary sources disagree, the dossier presents the disagreement explicitly rather than selecting a single interpretation. ## Disclaimer Everything published on this site is for research and informational purposes only and is not intended as medical advice. Nothing on this site is an offer to sell, an invitation to purchase, or a recommendation to use any compound, drug, or peptide preparation. CJC-1295 is not approved by the FDA or any other major regulator for human use. The site is not affiliated with any vendor, manufacturer, pharmacy, clinic, or telehealth service. Readers seeking medical guidance should consult a licensed healthcare professional. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295. --- # Contact CJC-1295 Buy — Editorial corrections and source suggestions > Editorial contact for CJC-1295 Buy. Use this form for factual corrections, new source suggestions, and editorial questions. We do not respond to vendor outreach, purchasing inquiries, or requests for medical advice. Use this form for factual corrections, new source suggestions, and editorial questions about the dossier. We do not respond to vendor outreach, purchasing inquiries, or requests for medical advice. ## What we respond to We read every editorial message that arrives through this form. We respond to: factual corrections to the dossier (with a citation to a primary source that supports the correction); suggestions of peer-reviewed papers, ClinicalTrials.gov entries, FDA briefings, or anti-doping standards that should be added to the references; questions about editorial scope; and questions about the entity that publishes the dossier. We do not respond to: requests to purchase CJC-1295; requests for vendor recommendations; requests for dosing guidance, treatment recommendations, or any other medical advice; vendor outreach asking to be linked, listed, mentioned, or advertised on the site; affiliate program proposals; or partnership offers from telehealth, compounding, or wellness operators. ## Editorial contact form A simple form follows below. Required fields are name, email, message category, and message. Submissions arrive at our editorial inbox and are reviewed within seven days. We do not subscribe submitters to any mailing list, and we do not share submitted information with third parties. If you prefer plain email, the editorial address is published in the form's accessible label and in the footer of every page. ## Disclaimer This contact form is not a medical-advice service. We are not clinicians. We do not provide individual guidance on the use of CJC-1295 or any other compound. We do not sell CJC-1295. We do not refer readers to vendors. Readers seeking medical guidance should consult a licensed healthcare professional. Readers seeking to acquire any peptide or pharmaceutical should pursue that through channels appropriate to their jurisdiction and circumstance; this site is not such a channel. --- An independent editorial record of what the published literature, the FDA, and WADA say about CJC-1295.