Growth hormone axis

CJC-1295 with DAC

Name: CJC-1295 with DAC: What the Research Actually Shows
Creator: Peptide Health Lab

FOR RESEARCH PURPOSES ONLY

Also known as: DAC:GRF, hGRF(1-29) albumin bioconjugate

Regulatory status: Research only
Evidence grade: Anecdotal reports only

Last reviewed September 1, 2026 · 13 sources

What CJC-1295 with DAC is and how it works

DAC stands for drug affinity complex, and the name is a description of a piece of chemistry rather than of a biological effect. The starting material is hGRF(1-29), the first 29 amino acids of human growth-hormone-releasing factor, which is the shortest fragment that still activates the GHRH receptor on pituitary somatotropes. Four amino-acid substitutions harden it against enzymes that would otherwise degrade it within minutes. Then a maleimidopropionyl group is attached at the C-terminus, and that group is the entire innovation: maleimide reacts selectively with free thiols, the most abundant free thiol in plasma sits on serum albumin, and the reaction forms a covalent bond.^[1]

What the conjugate produces is not a stronger signal at the receptor. It is a longer one. An unmodified GHRH peptide is cleared in minutes; albumin circulates for weeks, and a peptide bolted to albumin inherits that behavior. In the originating rat work three such bioconjugates were compared, and the one designated CJC-1295 produced a fourfold larger growth-hormone response than unmodified hGRF(1-29) while remaining detectable in plasma past 72 hours.^[1] In healthy human volunteers the half-life was estimated at between 5.8 and 8.1 days.^[2] The investigators of the pulsatility study described the binding as permanent, which is the practical meaning of a covalent adduct.^[3]

One naming point has to be settled before the evidence below can be read correctly, and then this page will leave it alone. The market and the analytical literature both use two names. The bare name refers to the unconjugated 29-amino-acid peptide, also sold as CJC-1295 without DAC or modified GRF(1-29). The name on this page refers to the albumin-binding bioconjugate. Doping-control method development treats them as two separate target peptides with separate metabolites and separate reference materials, which is the strongest available statement that they are not interchangeable.^[8] Everything below concerns the conjugate.

The distinction has a mechanistic consequence worth stating plainly. Normal GHRH signaling is episodic — bursts, then silence. This molecule converts an episodic signal into a continuous one that cannot be stopped once started, and whether continuous stimulation of a system evolved for intermittent stimulation is desirable is a question the pharmacology raises and the published evidence does not answer.

What the research actually shows

Two randomized trials, both measuring hormone concentrations. The core human evidence is a pair of randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults aged 21 to 61, conducted at two investigational sites over 28 and 49 days. Their stated outcome measures were peak concentration and area under the curve for GH and IGF-1 plus standard pharmacokinetic parameters. After one subcutaneous injection, mean plasma GH climbed two- to tenfold in a dose-dependent fashion and stayed up for six days or longer; mean plasma IGF-1 climbed 1.5- to threefold and stayed up for nine to eleven. Repeat dosing pushed IGF-1 above baseline for as long as 28 days, which the authors read as a cumulative effect. Nobody experienced a serious adverse reaction, and the authors' conclusion singled out the two middle doses as safe and relatively well tolerated.^[2]

The pulsatility study is more interesting than its title. Because pulsatile delivery is thought to matter for how growth hormone acts, a separate non-randomized study sampled healthy men every 20 minutes across a 12-hour overnight window, before and one week after a single injection. Pulse frequency and pulse magnitude were unchanged — the result the title reports. Underneath it, basal trough GH went up about 7.5-fold, which carried mean GH up 46% and IGF-1 up 45%, and the authors' conclusion assigned the IGF-1 gain to the raised trough rather than to the pulses. No parameter of GH secretion they measured tracked the IGF-1 change.^[3]

A proteomic study, designed to find doping biomarkers. Sera from eleven healthy young men before and one week after injection were separated by two-dimensional gel electrophoresis and the changed spots identified by mass spectrometry. An apolipoprotein A1 isoform and a transthyretin isoform fell; beta-hemoglobin and two albumin-fragment-containing spots rose, one of them tracking IGF-1 linearly. The authors framed all of this as candidate biomarkers of GH and IGF-1 action, motivated explicitly by the difficulty of detecting GH misuse — not as evidence that anything improved.^[5]

Animal work is a deficiency model. Mice with the GHRH gene ablated, treated once daily from one week of age for five weeks, reached normal body weight and length and held normal relative lean and subcutaneous fat mass; 48- and 72-hour intervals produced only partial catch-up.^[4] Correcting an engineered hormone deficiency in a growing animal is a different experiment from raising an already-normal axis in an adult, and no published study has run the second one.

Where the evidence is weak

Nothing a person would notice has ever been measured. Peak concentrations, areas under curves, pulse parameters, protein spots on a gel — that is the complete list of what the human literature on this molecule reports. Strength, lean mass, fat mass, sleep architecture, recovery from injury, skin: no published trial has looked. An independent narrative review of injectable peptide therapy for orthopaedic and sports medicine physicians reaches the same verdict, notes that the frequently quoted combination result pairing this analog with ipamorelin comes from mice with glucocorticoid-induced muscle loss, and states that indications, dosing, frequency, and duration remain unknown.^[10] That is why the compound-level grade on this page sits at the bottom despite one genuinely randomized finding: the grade tracks the claim people make for the compound, and no human study has tested that claim.

Three human studies, roughly two decades old, from a programme that stopped. The evidence base is a few dozen volunteers, generated during a development effort in the mid-2000s that never reached approval, and nothing since has replaced or extended it. Reviewing the same territory two decades later, a 2026 survey of peptide therapies promoted for musculoskeletal injury and athletic performance found the rigorous human evidence on unapproved molecules of this kind to be thin, and paired that finding with an explicit warning about the potential for serious harm.^[11]

The glycemic question is open, not closed. Growth hormone is a counter-regulatory hormone. A 2026 review of growth hormone and glycemic metabolism describes chronic GH and IGF-1 excess in acromegaly producing systemic insulin resistance through direct antagonism of insulin receptor signaling, increased lipolysis, and elevated free fatty acids, with impaired glucose tolerance or overt diabetes in as many as half of those patients.^[9] A disease of decades-long hormone excess is not a weeks-long pharmacology study in healthy volunteers, and the inference does not transfer directly. But this molecule's characterized effect is a sustained non-pulsatile elevation of exactly those hormones, and none of the three human studies reported a fasting glucose, an insulin, an oral glucose tolerance test, or an HbA1c.^[2] The honest description is uncharacterized, which is a different and less comfortable thing than characterized-and-benign.

Duration cuts both ways and only one direction is usually discussed. A 5.8-to-8.1-day half-life produced by an irreversible covalent bond means the exposure cannot be truncated. Most injectable peptides can effectively be stopped; this one runs its course.^[2] No published work describes managing an adverse response to it, because the studied exposures were short, small, and uneventful.

IGF-1 exposure epidemiology is not reassuring in the abstract. Pooled individual-participant analysis links higher circulating IGF-I to prostate cancer risk, and prospective UK Biobank analyses examined IGF-I against the incidence of 30 cancers.^[12]^[13] Neither study administered anything to anyone; both observe endogenous variation across large populations, which makes them background biology about the hormone rather than a risk estimate for the molecule. Background biology is still the right reason to put the malignancy question to a clinician instead of dismissing it.

Identity is unusually hard to confirm for this molecule specifically. The absence of a manufacturer's assay standard and release specification is the ordinary condition of an unapproved peptide. What is particular here is that the conjugate is genuinely difficult to detect even in a properly equipped laboratory: racing-industry analysts describe it as low in abundance, high in molecular weight, and bound to a range of different protein substrates, and needed immuno-affinity capture followed by tryptic digestion to confirm it in equine plasma.^[7] Separately, when a national doping-control laboratory sequenced an unknown preparation carrying the CJC-1295 name, what it contained was the unconjugated peptide.^[6] A label naming the conjugate is not, on this evidence, a strong claim about what is in the vial.

Legal and regulatory status

CJC-1295 with DAC is not approved by the FDA for any indication, and no approved product exists under this name or its synonyms in any jurisdiction. It is not an approved drug, nor is it a permissible dietary supplement ingredient. What circulates under the name moves as laboratory research material, and that is the basis for the research-only framing this page carries. The development programme behind the human trials began in the 2000s and did not complete a path to approval.^[2]

In tested sport the position is settled. Growth-hormone-releasing hormone and its synthetic analogs are prohibited by the World Anti-Doping Agency, and the method-development literature names this bioconjugate explicitly as one of four larger GHRH analogs targeted for detection, alongside the unconjugated peptide, sermorelin, and tesamorelin. Nineteen in vitro metabolites were identified, synthesized, and used as reference materials to build a liquid chromatography–tandem mass spectrometry assay reaching limits of detection generally at or below the WADA required performance limit. The same authors note that despite intelligence and admissions indicating use, these analogs had historically not been found in accredited laboratory samples — a detection gap that this work exists to close.^[8] Regulated animal sport has moved in parallel, with equine racing laboratories publishing their own confirmation methods.^[7]

For a reader, the practical content of the regulatory status is narrow: no label, no approved indication, no manufacturer standing behind a specification, and an enforceable prohibition in competition. Nothing on this property is for sale, and the question of how unapproved material moves is outside what PHL will address.

Questions to bring to a provider

The productive conversation is not whether to run this compound. It is what a person is actually trying to change, whether the growth-hormone axis is plausibly involved, and what evidence would settle it either way. Questions worth raising:

What symptom or measurement suggests the GH/IGF-1 axis is involved at all, and which test would confirm or rule that out before anything else is considered?
Given that a single injection commits to roughly a week of sustained exposure that cannot be interrupted, what is the plan if something goes wrong?^[2]
No human study of this molecule has reported a glycemic endpoint — would baseline and follow-up fasting glucose, insulin, and HbA1c be worth having before and after anything?^[9]
Because the conjugate holds IGF-I up continuously for days rather than restoring a pulse, how heavily should a cancer history — personal or in the family — weigh before starting, when large untreated cohorts tie higher circulating IGF-I to the incidence of several cancers?^[13]
Every endpoint in this conjugate's human record is a concentration in blood drawn over days. If the goal is something a person would actually notice — sleep, body composition, recovery from training — which measurement would be taken, on what schedule, and against which baseline?^[10]
For anyone subject to drug testing, has the current year's list been checked directly, and are the assays now sensitive enough that historical non-detection is no longer a guide?^[8]
Analytical work found the unconjugated peptide inside a preparation carrying this name — how would anyone confirm which molecule is actually present?^[6]

A provider whose answer is that the published record ends at a blood concentration has read the record accurately, and that is a useful place for the conversation to start rather than a reason to end it.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Prolonged elevation of growth hormone and IGF-1 in healthy adults

Human RCT evidence human RCT · human observational

This is the one claim on the page carrying randomized human evidence. Across two randomized, double-blind, placebo-controlled ascending-dose trials, a single subcutaneous injection produced dose-dependent increases in mean plasma GH of two- to tenfold sustained for six days or longer and increases in mean plasma IGF-1 of 1.5- to threefold sustained for nine to eleven days, with an estimated half-life of 5.8 to 8.1 days. A separate proteomic analysis in eleven healthy men found reproducible serum protein changes one week after injection, which independently confirms the axis was engaged. The claim is about hormone concentrations. It is not a claim about anything those concentrations went on to do.

[2] [5]

The multi-day duration attributable to albumin conjugation

Human RCT evidence animal · human RCT

The originating chemistry work in rats compared three hGRF(1-29)-albumin bioconjugates and identified the candidate designated CJC-1295, which produced a fourfold greater GH response than unmodified hGRF(1-29) and remained detectable in plasma past 72 hours. The randomized human trials then measured the half-life directly at 5.8 to 8.1 days. Duration is the best-supported property of this molecule and the only respect in which it clearly differs from every other GHRH analog — and duration is a pharmacokinetic parameter, not a benefit.

[1] [2]

Preserved pulsatility during continuous stimulation

Anecdotal reports only human observational

One non-randomized, single-site study in healthy men reported unchanged GH pulse frequency and magnitude one week after injection, alongside a 7.5-fold rise in trough GH, a 46% rise in mean GH, and a 45% rise in IGF-1. It has not been replicated, it enrolled a narrow age band, and the IGF-1 increase correlated with no measured parameter of GH secretion. The finding is real and worth knowing; it is not randomized evidence, and the preserved-pulsatility half of it is routinely quoted without the trough half.

[3]

Correction of growth failure in hormone-deficient animals

Animal studies only animal

In mice with the GHRH gene ablated, once-daily administration across five weeks normalized body weight and length and held relative lean and subcutaneous fat mass at normal values, while 48- and 72-hour intervals achieved only partial catch-up. This is a deficiency-correction result in growing animals with an engineered lesion. It does not address a hormonally intact adult, and the same caveat applies to the rat work that established the conjugation chemistry.

[4] [1]

Any clinical outcome in humans — body composition, recovery, sleep, injury healing

Anecdotal reports only review

No published trial of this bioconjugate has measured a clinical outcome of any kind. Every human study on this page reports concentrations: peak and area-under-curve values for GH and IGF-1, pulsatility parameters, protein spots on a gel. There is no published result for strength, lean mass, fat mass, sleep architecture, recovery from injury, skin, or anything else a person would notice. Independent narrative review of injectable peptide therapy reaches the same conclusion and notes that the one commonly cited combination result — this analog paired with ipamorelin, improving maximum tetanic tension under glucocorticoid-induced muscle loss — is a murine finding, with indications, dosing, frequency, and duration all still unknown.

[10] [11]

Effect on glucose homeostasis and insulin sensitivity

Anecdotal reports only review · human RCT

Unmeasured rather than reassuring. No published human study of this molecule reported a glycemic endpoint. The background pharmacology is well characterized in the opposite direction: growth hormone antagonizes insulin action, and chronic GH and IGF-1 excess is an established cause of insulin resistance and impaired glucose tolerance in acromegaly. What a much smaller, weeks-long, pharmacologically sustained elevation does to glucose handling in a healthy adult is an open question that the existing studies were not designed to answer.

[9] [2]

Claim area	Evidence & sources	What the research shows
Prolonged elevation of growth hormone and IGF-1 in healthy adults	Human RCT evidence human RCT · human observational [2] [5]	This is the one claim on the page carrying randomized human evidence. Across two randomized, double-blind, placebo-controlled ascending-dose trials, a single subcutaneous injection produced dose-dependent increases in mean plasma GH of two- to tenfold sustained for six days or longer and increases in mean plasma IGF-1 of 1.5- to threefold sustained for nine to eleven days, with an estimated half-life of 5.8 to 8.1 days. A separate proteomic analysis in eleven healthy men found reproducible serum protein changes one week after injection, which independently confirms the axis was engaged. The claim is about hormone concentrations. It is not a claim about anything those concentrations went on to do.
The multi-day duration attributable to albumin conjugation	Human RCT evidence animal · human RCT [1] [2]	The originating chemistry work in rats compared three hGRF(1-29)-albumin bioconjugates and identified the candidate designated CJC-1295, which produced a fourfold greater GH response than unmodified hGRF(1-29) and remained detectable in plasma past 72 hours. The randomized human trials then measured the half-life directly at 5.8 to 8.1 days. Duration is the best-supported property of this molecule and the only respect in which it clearly differs from every other GHRH analog — and duration is a pharmacokinetic parameter, not a benefit.
Preserved pulsatility during continuous stimulation	Anecdotal reports only human observational [3]	One non-randomized, single-site study in healthy men reported unchanged GH pulse frequency and magnitude one week after injection, alongside a 7.5-fold rise in trough GH, a 46% rise in mean GH, and a 45% rise in IGF-1. It has not been replicated, it enrolled a narrow age band, and the IGF-1 increase correlated with no measured parameter of GH secretion. The finding is real and worth knowing; it is not randomized evidence, and the preserved-pulsatility half of it is routinely quoted without the trough half.
Correction of growth failure in hormone-deficient animals	Animal studies only animal [4] [1]	In mice with the GHRH gene ablated, once-daily administration across five weeks normalized body weight and length and held relative lean and subcutaneous fat mass at normal values, while 48- and 72-hour intervals achieved only partial catch-up. This is a deficiency-correction result in growing animals with an engineered lesion. It does not address a hormonally intact adult, and the same caveat applies to the rat work that established the conjugation chemistry.
Any clinical outcome in humans — body composition, recovery, sleep, injury healing	Anecdotal reports only review [10] [11]	No published trial of this bioconjugate has measured a clinical outcome of any kind. Every human study on this page reports concentrations: peak and area-under-curve values for GH and IGF-1, pulsatility parameters, protein spots on a gel. There is no published result for strength, lean mass, fat mass, sleep architecture, recovery from injury, skin, or anything else a person would notice. Independent narrative review of injectable peptide therapy reaches the same conclusion and notes that the one commonly cited combination result — this analog paired with ipamorelin, improving maximum tetanic tension under glucocorticoid-induced muscle loss — is a murine finding, with indications, dosing, frequency, and duration all still unknown.
Effect on glucose homeostasis and insulin sensitivity	Anecdotal reports only review · human RCT [9] [2]	Unmeasured rather than reassuring. No published human study of this molecule reported a glycemic endpoint. The background pharmacology is well characterized in the opposite direction: growth hormone antagonizes insulin action, and chronic GH and IGF-1 excess is an established cause of insulin resistance and impaired glucose tolerance in acromegaly. What a much smaller, weeks-long, pharmacologically sustained elevation does to glucose handling in a healthy adult is an open question that the existing studies were not designed to answer.

FOR RESEARCH PURPOSES ONLY

Typical protocol range in the research

Two randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults aged 21 to 61, run at two investigational sites over 28 and 49 days, with peak concentration and area under the curve for GH and IGF-1 as the stated outcome measures

Subcutaneous administration in one of four ascending single doses in the first trial, and in two or three doses given weekly or every second week in the second; the authors concluded the compound was safe and relatively well tolerated particularly at 30 and 60 micrograms per kilogram of body weight [2]
Non-randomized overnight pulsatility study in healthy men aged 20 to 40, with blood drawn every 20 minutes across a 12-hour window before and again one week after a single injection

A single subcutaneous dose of either 60 or 90 micrograms per kilogram of body weight; the investigators observed no significant difference between the responses to the two [3]
Growth-hormone-releasing-hormone knockout mice, dosed from one week of age for five weeks, as a model of correcting an engineered hormone deficiency

2 micrograms per animal at 24-, 48-, or 72-hour intervals; only the 24-hour interval brought body weight and length to normal [4]

Every human figure above is weight-normalized and was chosen to characterize a pharmacokinetic curve, not to treat anything. No published trial has established a dose of this bioconjugate for any indication in any population, and no published trial has compared one dose against another for an outcome a person would notice. Fixed milligram-per-week figures circulate in community discussion; they trace to no published study and are therefore absent from this page.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

A sustained non-pulsatile growth-hormone floor

Observed one week after a single injection in healthy men · The headline of the pulsatility study is usually read as reassurance — pulse frequency and pulse magnitude were unaltered. The finding underneath it is that basal trough growth hormone rose roughly 7.5-fold, and the investigators attributed the IGF-1 rise to that trough elevation rather than to the pulses. Endogenous GH secretion spends most of the day near zero between pulses. Replacing those low troughs with a continuously raised floor is the pharmacological signature of this molecule, and no study has followed what that floor does beyond a single overnight sampling window.

[3]
IGF-1 elevation that accumulates across doses

Reported in every human study of this bioconjugate · A single injection raised mean plasma IGF-1 by 1.5- to 3-fold for nine to eleven days; after repeated doses IGF-1 stayed above baseline for as long as 28 days, which the authors described as a cumulative effect. Separately, and in people taking nothing at all, large prospective cohort work associates higher circulating IGF-1 with the incidence of several cancers, most consistently prostate cancer. That is exposure epidemiology, not a measured risk of this compound, and it is the reason a personal or family malignancy history belongs in a clinician conversation before any growth-hormone-axis compound is considered.

[2] [12] [13]
Glucose handling: unmeasured in every human study of this molecule

Never characterized in any published human study · None of the three published human studies reported fasting glucose, insulin, an oral glucose tolerance test, or HbA1c; their endpoints were hormone concentrations and serum protein spots. That gap is pointed here rather than incidental. A 2026 review of growth hormone and glycemic metabolism describes sustained GH and IGF-1 excess in acromegaly as producing systemic insulin resistance through direct antagonism of insulin receptor signaling, increased lipolysis, and elevated free fatty acids, with impaired glucose tolerance or overt diabetes in up to half of those patients. A weeks-long pharmacology study in healthy volunteers is a far smaller and shorter exposure than a disease of chronic hormone excess, and no inference runs directly from one to the other — but the direction of the effect this bioconjugate is designed to produce is the same direction, and nobody measured it. Existing diabetes, prediabetes, or any glucose-lowering medication is a provider-discussion flag.

[2] [9]
No human exposure on record beyond seven weeks

Not established · The longest controlled human exposure ran 49 days and reported no serious adverse reactions across a few dozen volunteers. That is an absence of findings across weeks in a small sample, which cannot speak to uncommon events or to anything with a long latency. Independent review of peptides marketed direct to patients characterizes rigorous human safety data for unapproved compounds in this class as scarce and flags potential for serious harm.

[2] [11]
An effect that cannot be withdrawn once given

Structural consequence of the conjugation chemistry · The covalent bond to albumin is not reversible on any useful timescale, and the estimated plasma half-life in healthy adults was 5.8 to 8.1 days. Most injectable peptides clear within minutes to hours, so stopping is a meaningful intervention. Here it is not: once an injection has been given, the exposure runs its course over days regardless of anything that happens afterward. No published study describes managing an adverse response to this molecule, because none has had to.

[2] [3]
Prohibited at all times in tested sport, and in regulated animal sport

Standing status · Growth-hormone-releasing hormone and its synthetic analogs are prohibited by the World Anti-Doping Agency, and the analytical literature treats CJC-1295 with drug affinity complex as one of its named target analogs alongside the unconjugated peptide, sermorelin, and tesamorelin. Racing-industry laboratories have developed their own confirmation methods for equine plasma. Any competitor in a tested sport should confirm the current year's list rather than rely on a reference page.

[8] [7]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage: The freeze-dried bioconjugate precursor is conventionally held refrigerated at 2–8 °C and shielded from light, with frozen holding used for longer intervals. Nothing in the published literature on this molecule addresses powder shelf life. What the literature does characterize is the opposite end of the process — how long the peptide survives in circulation once it has attached itself to albumin — and a multi-day plasma half-life says nothing about how a sealed vial behaves on a shelf.
Reconstituted storage: Solutions of lyophilized peptides are conventionally kept refrigerated, protected from light, and treated as short-dated. No published stability work assigns this bioconjugate an in-solution shelf life, so any interval quoted for it comes from general peptide practice rather than from a study of this molecule.
Reconstitution diluent: Bacteriostatic water — sterile water preserved with 0.9% benzyl alcohol — is the conventional diluent for lyophilized research peptides and is the default for material carrying this name. Unpreserved sterile water is used where a preservative is contraindicated and is treated as single-use.
Reconstitution & handling: Conventional handling only: sanitize the stopper before it is pierced, introduce the diluent slowly against the inside wall of the vial rather than jetting it onto the powder, and allow the cake to go into solution on its own. Gentle swirling is conventional; shaking is not. A clear solution is the expected result, and anything cloudy, tinted, or carrying visible particulate is discarded. PHL publishes no volume or unit arithmetic — that is a dosing decision and dosing decisions sit with a licensed clinician.
Handling notes: The maleimide group that defines this molecule is a reactive chemical handle — that reactivity is what lets it couple to a free thiol on albumin after injection, and reactive handles are generally less forgiving of heat, light, and repeated warming than an inert peptide would be. No published work quantifies that for this compound. With no approved manufacturer there is also no label, no beyond-use date, and no lot release testing behind any of these conventions; treat them as convention rather than specification.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

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Citations

13 sources · every identifier checked against PubMed

[1] 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. Animal study
[2] Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults · The Journal of Clinical Endocrinology & Metabolism, 2006. Human RCT
[3] Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog · The Journal of Clinical Endocrinology & Metabolism, 2006. Human observational study
[4] 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. Animal study
[5] 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. Human observational study
[6] Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation · Drug Testing and Analysis, 2010. In vitro study
[7] A method for confirming CJC-1295 abuse in equine plasma samples by LC-MS/MS · Drug Testing and Analysis, 2019. In vitro study
[8] Advances in the detection of growth hormone releasing hormone synthetic analogs · Drug Testing and Analysis, 2021. In vitro study
[9] Growth hormone and glycemic metabolism · Vitamins and Hormones, 2026. Review
[10] Injectable peptide therapy: a primer for orthopaedic and sports medicine physicians · The American Journal of Sports Medicine, 2026. Review
[11] Safety and efficacy of approved and unapproved peptide therapies for musculoskeletal injuries and athletic performance · Sports Medicine, 2026. Review
[12] A meta-analysis of individual participant data reveals an association between circulating levels of IGF-I and prostate cancer risk · Cancer Research, 2016. Human observational study
[13] Circulating insulin-like growth factor-I concentrations and risk of 30 cancers: prospective analyses in UK Biobank · Cancer Research, 2020. Human observational study

Before you act on any of this

This page is educational only and is not medical advice. It does not diagnose, treat, or prescribe. Review it with a licensed provider before making any health decision. Peptide Health Lab does not sell peptides.

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