PerformanceDAC:GRFGRF 1-29 analog (with DAC)

CJC-1295

Long-acting GHRH analog · albumin-binding GH secretagogue

CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH) engineered for persistence: a stabilized GHRH(1-29) scaffold carrying a small chemical linker that covalently binds serum albumin in the bloodstream, stretching native GHRH's minutes-long half-life to roughly 6–8 days in humans. In first-in-human trials a single subcutaneous dose raised mean growth-hormone levels several-fold for at least six days and IGF-1 for over a week, while preserving the body's natural pulsatile GH rhythm. One identity point matters: the name "CJC-1295" properly refers to this long-acting DAC form (DAC:GRF), but the same name is widely sold as "CJC-1295 no-DAC," which is a chemically distinct, short-acting molecule (Mod-GRF 1-29) without the albumin linker — nearly all the human evidence below is for the DAC form. CJC-1295 never advanced past Phase 2 and is not an approved drug; it is prohibited in sport at all times (WADA).

The short version

CJC-1295 is a lab-made copy of part of GHRH — the natural hormone that tells the pituitary gland to release growth hormone — with chemistry added to make it last much longer in the body.

The trick is a small molecular hook that latches onto albumin, a carrier protein in the blood. Anchored to albumin, the peptide resists breakdown and stays in circulation for days instead of minutes, so a single injection can keep growth hormone and IGF-1 elevated for a week or more — and it does this while keeping the body's natural up-and-down rhythm of growth-hormone pulses intact.

Important: products labeled "CJC-1295" are not all the same molecule. The original long-acting version has that albumin hook (called "DAC"). A second version sold under the same name, "CJC-1295 no-DAC," leaves the hook off and only lasts about half an hour. Almost all of the published human research is on the long-acting DAC version.

It is not an approved drug — development stopped after early trials — and it is banned in competitive sport.

Molecular identity

Specs

Molecular weight: 3,647.2 g/mol (with DAC)
Molecular formula: C165H269N47O46 (with DAC)
Monoisotopic mass: 3,645.02 Da (with DAC)
CAS / UNII: 446262-90-4 · 62RC32V9N7 (with DAC)

No-DAC form: Mod-GRF(1-29): C152H252N44O42, 3,367.9 g/mol (monoiso 3,365.89 Da)PubChem CID 91976842
Structure / class: Long-acting GHRH(1-29) analog; maleimidopropionamide–albumin (DAC) linkerPMID 15817669
Molecular target: GHRH receptor (GHRHR) on pituitary somatotrophsPMID 16352683
Half-life: ~5.8–8.1 days (with DAC, human SC); ~30 min (no-DAC, secondary)PMID 16352683Half-life curve →
Regulatory status: Not FDA-approved (Phase 2 only) · WADA S2 prohibitedFDA / research literature

Plain English

Mechanism

CJC-1295 is an agonist (a molecule that switches a receptor on) at the GHRH receptor on the somatotroph cells — the growth-hormone-producing cells — of the anterior pituitary (the front part of the pituitary, the master hormone gland at the base of the brain). Binding the receptor drives the cAMP/PKA pathway (a chain of internal cell signals), which stimulates both the synthesis and the pulsatile release (release in natural bursts) of growth hormone — the same signal native GHRH carries, but from a molecule built to survive far longer in circulation.

Persistence comes from the "DAC" (Drug Affinity Complex) chemistry. The peptide carries a maleimidopropionamide group (a reactive chemical hook) that undergoes a Michael addition (a chemical bond-forming reaction) with the free thiol (a sulfur-containing chemical group) of cysteine-34 — a specific amino acid — on endogenous serum albumin (the body's own most abundant blood-carrier protein), forming a stable bioconjugate (a peptide permanently fused to a protein). Tethered to albumin, the peptide resists proteolysis (being chopped up by enzymes) and renal clearance (being filtered out by the kidneys), becoming a days-long circulating depot (a slow-release reservoir in the blood). In rats, CJC-1295 remained detectable in plasma (the liquid part of blood) beyond 72 hours and produced roughly four times the growth-hormone area-under-curve (total exposure over time) over two hours versus native GHRH(1-29). The underlying GHRH(1-29) scaffold also carries amino-acid substitutions (swapped building blocks) reported to confer resistance to enzymatic degradation (breakdown by the enzyme DPP-IV); these substitution identities are described in secondary literature and are consistent with the molecule's published formula.

A defining pharmacodynamic feature (how the drug affects the body) is that this sustained stimulation does not flatten the body's natural rhythm. In healthy men, continuous receptor stimulation by the DAC form preserved growth-hormone pulse frequency and amplitude (how often and how big the bursts are) while raising the trough (baseline, the low point between bursts) level — trough GH rose roughly 7.5-fold, mean (average) GH about 46%, and IGF-1 about 45%.

The short-acting no-DAC form (Mod-GRF 1-29) shares the receptor-agonist mechanism but, lacking the albumin linker, clears in roughly half an hour (a figure reported in secondary sources rather than a primary pharmacokinetic — drug-handling — trial).

Sources:PMID 15817669 PMID 17018654 PubChem CID 91971820

Why people reach for it

Potential benefits

CJC-1295 is the long-acting GHRH half of the classic growth-hormone stack — here's what draws people to it.

Raise your own growth hormone, not inject it — CJC-1295 signals the pituitary to make and release the body's own GH rather than replacing it from outside — in first-in-human trials a single dose lifted mean GH several-fold and IGF-1 for over a week.
A steady GH floor that lasts (DAC form) — The albumin-binding DAC chemistry stretches GHRH's minutes-long half-life to roughly 6–8 days, so the long-acting form holds GH and IGF-1 elevated from one weekly injection.
Keeps the body's natural pulse intact — In healthy men the DAC form raised the baseline GH level while preserving the natural frequency and size of GH bursts — it lifts the floor without flattening the rhythm.
Leaner body composition and recovery support — Sustained GH/IGF-1 elevation is what people reach for it for — body-composition and training-recovery goals, where IGF-1 drives protein synthesis.
The natural partner for a GHRP — Because it works the GHRH receptor, it pairs cleanly with a ghrelin-receptor peptide for a bigger combined pulse — most famously Ipamorelin, the canonical CJC-1295 + Ipamorelin night stack.

Sources:PMID 16352683 PMID 17018654 PMID 15817669

What people reach for CJC-1295 for, drawn from what the research reports (the human evidence is for the DAC form) and how it's used — not proven outcomes or medical claims.

Implied timing

Best time to dose

Implied best time

Bedtime (empty stomach)

Most people inject the short-acting (no-DAC) form at bedtime on an empty stomach; the long-acting DAC form is once-weekly, so time-of-day matters far less.

These GHRH analogs amplify the body's own GH release, and the single largest natural GH pulse fires in early slow-wave (deep) sleep — dosing at bedtime stacks the peptide's signal on top of that nocturnal surge.
Food is the reason for the empty stomach: a meal raises insulin and somatostatin (GH's off-switch), both of which blunt the pulse, so the no-DAC dose goes ~2 hours clear of eating.
This applies to the short, pulsatile no-DAC form (Mod-GRF 1-29, ~30 min). The long-acting DAC form keeps GH elevated across the whole week, so its once-weekly injection can go any time of day — bedtime is convention, not a requirement.
Morning and/or post-workout doses are common secondary no-DAC injections, but the bedtime dose is the anchor.

No study establishes an ideal time of day for CJC-1295 — this is reasoned from its GHRH mechanism and how it's used. As a rule of thumb peptide dosing lands in the midday-to-evening window; for the short-acting form the lean is bedtime, fasted.

Sources:PMID 16352683 PMID 17018654

How to run it

Dosing & protocol

The defining decision for CJC-1295 is which form you have: the long-acting DAC form (once-weekly dosing, sustained GH elevation) or the short-acting no-DAC form / Mod-GRF(1-29) (daily pulsatile dosing, always paired with a GHRP). Unlike most research peptides, the DAC form was actually dosed in first-in-human trials — the practical numbers here lean on that real human data. The no-DAC form has no primary human trial; its protocol is practitioner convention. Both forms are subcutaneous injections.

Community/practitioner convention: no trial has set a "recommended" regimen for either form. The DAC figures come from Phase 1/2 trials that were never completed to approval; no-DAC figures are practitioner extrapolation. CJC-1295 is not an FDA-approved drug and is prohibited by WADA (S2) at all times.

Tiered dose ranges

The two forms are dosed on completely different schedules — pick the right column before measuring anything.

CJC-1295 WITH DAC — starting dose:: ~1 mg (1,000 mcg) subcutaneously, once weekly. This maps to roughly 30–60 mcg/kg for a 70–80 kg person — the range the Phase 1/2 trials identified as best tolerated. A single injection keeps GH elevated for ≥6 days and IGF-1 elevated for 9–11 days.
CJC-1295 WITH DAC — higher range:: Up to ~2 mg (2,000 mcg) once weekly, mirroring the upper end of the trial cohort (up to ~60 µg/kg for a 70 kg person). Practitioner ceiling. The sustained GH elevation is less pulsatile than the no-DAC form — it raises the trough floor rather than amplifying individual peaks.
CJC-1295 WITHOUT DAC (Mod-GRF 1-29) — standard:: 100 mcg subcutaneously, 1–3× daily. Short-acting (~30 min half-life, secondary-sourced); each injection produces a discrete GH pulse. Almost always paired in the same syringe with a GHRP (e.g. Ipamorelin 100–200 mcg) at injection time — the two-signal trigger amplifies the pulse above what either achieves alone.
CJC-1295 WITHOUT DAC — timing note:: Inject on an EMPTY STOMACH — ideally the primary daily dose at bedtime to stack with the body's largest natural GH pulse in slow-wave sleep. Keep a ~2-hour food window before and after: insulin and somatostatin (GH's off-switch) released by a meal directly blunt the GH pulse. Morning and/or post-workout are common secondary doses.

Subcutaneous administration

Both forms are injected subcutaneously into fat; the vial math differs because the doses are on different scales.

Injection site:: The abdomen (2–3 cm clear of the navel), the love-handle area, or the outer thigh. Rotate sites between doses to prevent lipohypertrophy (fatty lumps from repeated injections to the same spot).
Measuring the dose (DAC form, standard mix):: Reconstitute a 10 mg vial with 2 mL bacteriostatic water = 5,000 mcg/mL. For a 1 mg (1,000 mcg) dose on a U-100 insulin syringe: 20 IU. For a 2 mg dose: 40 IU. The on-page calculator uses this vial's default (100 mcg dose; adjust to your actual dose).
Measuring the dose (no-DAC form):: Using the same 10 mg vial + 2 mL mix (5,000 mcg/mL), 100 mcg = 2 IU on a U-100 syringe. The calculator default (100 mcg) is set for no-DAC co-injection with a GHRP.
Time of day:: DAC form: any time of day — once-weekly schedule, timing matters less because GH elevation spans the entire week. No-DAC form: bedtime is the primary anchor dose; a morning dose and/or a post-workout dose are common additions on a multi-dose schedule.
Food window (no-DAC form):: At minimum a 2-hour fast before the no-DAC injection and 30 minutes after. Carbohydrates and dietary fat elevate insulin and trigger somatostatin release — both suppress pituitary GH output and will blunt the peptide's effect. The DAC form's persistent stimulation is less sensitive to the food window, though a fasted window is still considered better practice.

Cycle & washout

The DAC and no-DAC forms run on different cycle lengths because their pharmacokinetics are completely different.

DAC form cycle:: 8–12 weeks of once-weekly dosing is the common block length. The Phase 2 trial data showed IGF-1 remaining elevated for up to ~4 weeks of repeated weekly dosing, which is the practical logic for a multi-week cycle. After 8–12 weeks, take a 4-week break before reassessing.
No-DAC form cycle:: 5 days on / 2 days off is a common rotation (mirrors some practitioner protocols for GHRP/GHRH pairs). Alternatively, 8–12 weeks continuous daily dosing followed by a 4-week washout — similar to other GH secretagogues.
Washout rationale:: GHRH-receptor stimulation theory: continuous agonism may downregulate pituitary sensitivity over time; a break is thought to reset responsiveness. The washout period is convention — no desensitization study for CJC-1295 specifically was located.
Lab check:: IGF-1 is the relevant marker for both forms. A baseline IGF-1 before starting and a re-check at 6–8 weeks (within the cycle) shows whether the signal is landing. An IGF-1 above the age-adjusted reference range is a signal to reduce dose or pause.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for the standard Ki 10 mg vial:

Standard mix:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg/mL. On a U-100 (1 mL / 100-unit) syringe: 100 mcg = 2 IU · 500 mcg = 10 IU · 1,000 mcg = 20 IU · 2,000 mcg = 40 IU.
Alternative mix for no-DAC (easier small-dose measuring):: 10 mg vial + 5 mL bacteriostatic water = 2,000 mcg/mL: 100 mcg = 5 IU — spreads small doses across more syringe units, reducing dosing error.

Sources:PMID 16352683 PMID 17018654 PMID 15817669

Substrate the signal needs

Nutritional cofactor precision

CJC-1295 works by stimulating the pituitary to release more GH — and GH release is gated by somatostatin, the body's own 'off-switch.' The most useful cofactors either relieve that brake, offset the metabolic cost of elevated GH (higher blood glucose, lower insulin sensitivity), or supply the raw material the raised GH/IGF-1 signal needs to build tissue.

Reasoned from GH-axis physiology and general GH-secretagogue class logic — not a CJC-1295-specific nutrition study. Supplement doses are common community convention, not CJC-1295-specific trial findings.

AMPLIFY / relieve the somatostatin brake

Somatostatin is GH's off-switch. These compounds lower somatostatin tone, giving the peptide more to work with.

L-arginine:: 3–6 g taken 30–60 minutes before the injection (especially the bedtime no-DAC dose). Arginine suppresses somatostatin release from the hypothalamus, widening the window for GH output. Best taken on an empty stomach so it isn't competing with dietary amino acids for transport.
Glycine:: 3–10 g taken at bedtime. Like arginine, glycine is associated with reduced somatostatin tone; it also improves slow-wave sleep quality — directly protecting the natural nighttime GH pulse that the no-DAC bedtime injection is designed to amplify.
Alpha-GPC:: 300–600 mg taken 30–60 minutes before the injection. Alpha-GPC raises acetylcholine, which stimulates GH release through a separate hypothalamic pathway and further suppresses somatostatin. Particularly useful in the no-DAC protocol where each pulse amplitude matters.

MITIGATE the cost — GH-driven glucose rise

Elevated GH transiently raises blood glucose and reduces insulin sensitivity. These offset that effect over a multi-week cycle.

Berberine:: 500 mg with meals, 2–3× daily. Berberine activates AMPK — the cell's fuel-sensing switch — and improves insulin sensitivity, directly countering the glucose-raising effect of sustained GH elevation. A practical first-line metabolic counter during a DAC-form cycle.
Alpha-lipoic acid (ALA):: 600 mg with a meal. ALA increases glucose uptake into muscle tissue via GLUT4 translocation and has antioxidant effects that support mitochondrial function under anabolic load.
Magnesium glycinate:: 200–400 mg elemental magnesium at bedtime. Magnesium supports insulin receptor signaling and glucose metabolism. The glycinate form also promotes sleep quality, protecting the slow-wave GH pulse window the no-DAC form targets.

SUPPLY the substrate — protein and GH-axis minerals

GH and IGF-1 are instructions to synthesize protein and remodel tissue. Without the raw material, the signal has nothing to build from.

Dietary protein:: 1.6–2.0 g per kg body weight per day (roughly 0.7–0.9 g per lb), distributed across meals. IGF-1's primary job is to drive protein synthesis — leucine-rich protein sources (meat, eggs, dairy, or leucine-supplemented plant protein) are most effective at triggering muscle protein synthesis. The DAC form keeps IGF-1 elevated continuously, so total daily protein matters more than peri-injection timing.
ZMA (zinc + magnesium + vitamin B6):: A standard ZMA formula (typically ~30 mg zinc, 450 mg magnesium, 10 mg B6) taken on an empty stomach 30–60 minutes before bed. Zinc deficiency is associated with lower IGF-1 output; B6 supports GH synthesis. This also reinforces the sleep-quality cofactor described above.
Vitamin D3 + K2:: Vitamin D is associated with healthy IGF-1 levels and musculoskeletal tissue quality — dose to maintain serum 25(OH)D in the sufficient range (typically 50–80 ng/mL). K2 (MK-7, ~100–200 mcg/day) directs calcium to bone rather than soft tissue during periods of elevated GH/IGF-1.

Combinations + timing

Stacking notes + timing windows

CJC-1295 is a GHRH-receptor agonist — it supplies one of the two signals the pituitary needs to fire a GH pulse. The canonical stack is a GHRH analog + a GHRP (ghrelin-receptor agonist): two different receptors, both on the same somatotroph cells, firing together for a synergistic pulse. Pairing CJC-1295 with another GHRH analog (Sermorelin, Tesamorelin) would push the same receptor twice — redundant, not synergistic.

Practitioner combinations reasoned from receptor complementarity — no primary interaction or synergy trial has been located for any of these pairings. Doses are community convention. "Commonly combined for" describes where users reach, not a proven indication.

CJC-1295 + Ipamorelin

The canonical GH-secretagogue stack — the GHRH half and the GHRP half of the pituitary's two-signal trigger.

Why it works:: Ipamorelin is a selective GHRP (ghrelin-receptor agonist) that activates the GHS-R1a receptor on pituitary somatotrophs — a completely different docking site from the GHRH receptor CJC-1295 occupies. Stimulating both simultaneously produces a synergistic GH pulse larger than either achieves alone, mimicking the two-signal system the body uses to fire natural pulses. Ipamorelin is the preferred GHRP partner because it is highly selective — minimal cortisol or prolactin elevation at standard doses.
The protocol (no-DAC form):: CJC-1295 no-DAC 100 mcg + Ipamorelin 100–200 mcg, drawn into the same U-100 syringe and injected subcutaneously together, 1–3× daily. The bedtime dose (empty stomach, 2-hour food window) is the anchor. Both peptides have similar subcutaneous onset windows, so co-injection is standard practice.
The protocol (DAC form):: CJC-1295 DAC ~1 mg subcutaneously once weekly + Ipamorelin 100–200 mcg subcutaneously 1–3× daily on its own schedule. The DAC form provides a steady GH floor all week; Ipamorelin adds pulsatile peaks on top. Different schedules — they are not co-injected.
Outcome:: Commonly combined for lean body composition, recovery from training, and sleep-quality improvement. The best-studied combination pattern in the GHRH/GHRP practitioner literature.

CJC-1295 + BPC-157 (+ TB-500)

The body-composition GH stack paired with a local tissue-repair signal — useful when the goal is both anabolic environment and structural repair.

Why it works:: BPC-157 promotes tendon, ligament, and gut-lining repair through a separate set of receptors with no overlap with the GH axis. TB-500 (Thymosin β4) drives cell migration into injured tissue. CJC-1295 + Ipamorelin provides the anabolic backdrop — elevated GH/IGF-1 accelerates collagen synthesis and satellite cell recruitment systemically, while BPC-157 and TB-500 work locally at the injury site. Three different levers: systemic anabolic signal + structural repair + cell migration.
The protocol:: CJC-1295 no-DAC 100 mcg + Ipamorelin 100–200 mcg at bedtime. BPC-157 250–500 mcg once daily, subcutaneously near the target area. TB-500 on its own loading/maintenance schedule (typically a higher weekly dose for the first 2–4 weeks, then a maintenance dose).
Outcome:: Commonly combined for soft-tissue injuries, post-surgical recovery, and training-related wear where both an anabolic environment and direct tissue repair are wanted.

What NOT to stack: another GHRH analog

Sermorelin and Tesamorelin are both GHRH-receptor agonists — the same lever as CJC-1295. Combining them adds no synergy.

Why it's redundant:: Sermorelin and Tesamorelin activate the same GHRH receptor on the same somatotroph cells. Adding a second GHRH analog while already running CJC-1295 does not open a new pathway — it just increases load on the same receptor without the two-signal amplification you get from a GHRP partner. The correct second agent is always a GHRP (ghrelin-receptor agonist), not another GHRH analog.
The honest call:: If a protocol suggests combining CJC-1295 with Sermorelin or Tesamorelin, that is a marketing stack, not a mechanistic one. Choose one GHRH analog and pair it with a GHRP.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.02 mL
Doses per vial: 100
Concentration: 5 mg/mL

One vial lasts

Daily: 100 days
Every other day: 200 days
5×/week: 140 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

In the early human trials of the DAC form, CJC-1295 was reported as safe and relatively well tolerated — no serious adverse reactions (harmful side effects), particularly at the 30–60 µg/kg subcutaneous doses. Injection-site reactions (redness, soreness, or swelling where the needle goes in) are commonly cited for this class; the published trials emphasized overall tolerability without itemizing local-reaction counts.

One program-level safety event deserves mention: a 2006 Phase 2 trial (a mid-stage human study) in HIV-associated lipodystrophy (an abnormal redistribution of body fat seen with HIV treatment) was halted after a participant died, with the cause of death and its relationship to the study drug reported as under investigation at the time. The developer (ConjuChem) later discontinued development. This account comes from secondary reporting rather than a primary trial publication, and no causal link (proven cause-and-effect) to CJC-1295 was established. There is no long-term human safety data, and the no-DAC form has no primary safety trial at all.

Sources:PMID 16352683 aidsmap 2006

As reported in literature

Research dosing ranges

These are the doses actually used in the published studies — the evidence the practical figures above lean on, shown separately so research data is never mistaken for an official human dose. Reported doses are for the long-acting DAC form and come from early human trials in healthy adults plus a rat pharmacokinetic study; no primary dosing trial was located for the short-acting no-DAC form. Subcutaneous doses are reported per kilogram of body weight (1 kg ≈ 2.2 lb). These are research-literature figures, not a validated therapeutic regimen.

Dose	Route	Model	Outcome	Sources:
30–60 µg/kg	Subcutaneous	Human (DAC; healthy, 21–61 y)	GH up 2–10× for ≥6 d; IGF-1 up 1.5–3× for 9–11 d; best-tolerated 30–60 µg/kg	PMID 16352683
60–90 µg/kg	Subcutaneous	Human (DAC; healthy men)	Preserved GH pulsatility; trough GH +7.5×, mean GH +46%, IGF-1 +45%	PMID 17018654
Single injection	Injection	Rat (DAC; Sprague-Dawley)	Plasma detectable >72 h; ~4× GH AUC over 2 h vs native GHRH	PMID 15817669

Quick answers

Frequently asked

What is the difference between CJC-1295 "with DAC" and "no-DAC"?

They are two different molecules sold under one name. The DAC version carries an albumin-binding linker (Drug Affinity Complex) that extends its half-life to roughly 6–8 days; this is the original CJC-1295 and the form behind nearly all the human research. The "no-DAC" version (chemically Mod-GRF 1-29) leaves the linker off and is short-acting (about 30 minutes, per secondary sources). They differ in formula, molecular weight, and pharmacokinetics.

How does CJC-1295 last so much longer than natural GHRH?

A small maleimide linker on the peptide reacts with cysteine-34 on serum albumin, forming a stable covalent bond. Anchored to this abundant blood-carrier protein, the peptide resists the enzymes and kidney clearance that break native GHRH down within minutes, so it circulates for days instead.

Does CJC-1295 disrupt the body's natural growth-hormone rhythm?

In a controlled human study, continuous stimulation by the DAC form preserved the frequency and amplitude of natural growth-hormone pulses while raising the baseline (trough) level — it lifted the floor without flattening the rhythm.

Is CJC-1295 an approved drug?

No. It never advanced past Phase 2 and is not approved for any indication. A U.S. FDA review placed it on, and later removed it from, the interim list of bulk substances considered for pharmacy compounding — it remains non-approvable for compounding. It is also prohibited in sport by WADA at all times. This page presents research literature only and makes no therapeutic claims.

What is CJC-1295's half-life?

For the long-acting DAC form, the estimated human half-life is about 5.8–8.1 days. The short-acting no-DAC form (Mod-GRF 1-29) is reported to clear in roughly 30 minutes, though that figure is secondary-sourced rather than from a published pharmacokinetic trial.

Primary sources

References

PubChem CID 91971820PubChem CID 91971820 (CJC-1295 with DAC)
PubChem CID 91976842PubChem CID 91976842 (CJC-1295 without DAC / Mod-GRF 1-29)
PMID 16352683J Clin Endocrinol Metab 2006 (CJC-1295 human PK/PD/safety, multi-day GH/IGF-1)
PMID 17018654J Clin Endocrinol Metab 2006 (preserved GH pulsatility under continuous stimulation)
PMID 15817669Endocrinology 2005 (hGRF(1-29)-albumin bioconjugate; original CJC-1295 ID, rat)
WADAWADA Prohibited List (S2, GHRH analogues prohibited at all times)
FDAFDA — bulk drug substances under section 503A (Category 2 history)
aidsmap 2006aidsmap (Jul 2006) — Phase 2 lipodystrophy trial halted after participant death

Research use only · Not medical advice · Updated 2026-06-01