CJC-1295 Limited Human Data

What It Is

CJC-1295 is a synthetic growth-hormone-releasing hormone (GHRH) analog developed in the mid-2000s by ConjuChem Biotechnologies. It exists in two distinct forms that the research community — and every serious user — should take care to distinguish, because they share a name but behave pharmacokinetically like different drugs:

• CJC-1295 with DAC (DAC:GRF) — A 30-amino-acid tetrasubstituted GRF(1-29) analog with an N-epsilon-3-maleimidopropionyl lysine (the "Drug Affinity Complex," or DAC) appended at position 30. The maleimide group forms a covalent thioether bond with Cys34 of endogenous serum albumin in vivo, converting the small, rapidly-cleared peptide into an albumin-bioconjugate with a plasma half-life of 5.8–8.1 days in humans (Jette et al., 2005; Teichman et al., 2006). This is the "true" CJC-1295.
• CJC-1295 without DAC / Modified GRF (1-29) / "Mod GRF" — The same 29-amino-acid tetrasubstituted GRF(1-29) backbone (D-Ala2, Gln8, Ala15, Leu27) without the maleimide-lysine albumin-binding tail. The four substitutions confer resistance to DPP-4 cleavage and improve receptor binding, but without the DAC, half-life is ~30 minutes — essentially the same short pulsatile signal as native GHRH or sermorelin. Many peptide vendors mislabel Modified GRF (1-29) as "CJC-1295 without DAC" for marketing reasons. They are not the same molecule as CJC-1295 DAC.

Both forms act on the same pituitary GHRH receptor. The mechanism is identical; only the pharmacokinetics differ. That distinction completely changes how the molecule is used: CJC-1295 DAC drives a sustained plateau elevation in GH and IGF-1 (weekly dosing), while Modified GRF (1-29) preserves the body's native pulsatile GH release pattern (multiple daily doses, typically stacked with a ghrelin mimetic such as ipamorelin).

CJC-1295's clinical development was halted in 2006 during a Phase II trial for HIV-associated lipodystrophy after one trial participant died of a cardiovascular event. ConjuChem's investigators concluded the death was due to pre-existing asymptomatic coronary artery disease with plaque rupture and deemed it unrelated to study drug. Regardless of causality, the development program was discontinued, and CJC-1295 was never submitted for FDA approval. It persists today almost entirely in the gray-market research-chemical and wellness-clinic peptide space.

Mechanism of Action

Both forms of CJC-1295 are selective GHRH receptor (GHRH-R) agonists. They mimic endogenous hypothalamic GHRH at the pituitary, driving downstream GH release and, through hepatic action of GH, IGF-1 production. The pharmacokinetic engineering is the entire story — the receptor biology is ordinary GHRH signaling.

• GHRH receptor (pituitary somatotropes) — Binds and activates the Gαs-coupled GHRH receptor on anterior pituitary somatotropes. Downstream cAMP / PKA signaling drives GH synthesis and release. Unlike exogenous recombinant GH, CJC-1295 produces all naturally occurring GH isoforms (22 kDa and alternate splice/post-translationally modified forms), which some reviewers argue is more physiological than pure 22 kDa rhGH.
• DPP-4 resistance (the four substitutions) — Native GRF(1-29) is rapidly cleaved by dipeptidyl peptidase-4 (DPP-4) at the Ala2-Asp3 bond. Substitution of D-Ala at position 2 blocks DPP-4 cleavage. Substitutions at 8 (Gln), 15 (Ala), and 27 (Leu) further resist enzymatic degradation and oxidation, extending tissue half-life of the underlying GHRH activity to ~30 minutes for Modified GRF (1-29) vs ~7 minutes for unmodified sermorelin.
• Albumin bioconjugation (DAC form only) — The N-epsilon-maleimidopropionyl lysine on residue 30 reacts in vivo with the free thiol on Cys34 of serum albumin, forming a stable thioether (Michael addition). This converts the peptide into a ~70 kDa albumin bioconjugate that is excluded from renal filtration and shielded from most peptidases, extending circulating half-life to 5.8–8.1 days (Jette et al., 2005).
• Sustained GH plateau vs preserved pulsatility — CJC-1295 DAC produces a continuous GHRH-receptor tone that elevates trough GH levels while somewhat blunting pulse amplitude. Ionescu & Frohman (2006) showed that pulsatile GH secretion is preserved but shifted to a higher baseline. Modified GRF (1-29) without DAC, in contrast, produces a single ~30-minute GH pulse per dose, closely mimicking native episodic GHRH physiology.
• Somatostatin permissive — GHRH-class agonists do not override endogenous somatostatin inhibition. GH release is therefore still gated by hypothalamic somatostatin tone — one reason why even sustained CJC-1295 DAC exposure does not produce supraphysiologic GH spikes comparable to exogenous rhGH.
• IGF-1 elevation — IGF-1 rises 1.5–3-fold within 24–48 hours of a single CJC-1295 DAC dose, remains elevated 9–11 days after a single dose, and accumulates with repeated weekly dosing such that plasma IGF-1 can remain elevated for up to 28 days after the last injection. This is the most consistent pharmacodynamic marker across the published trials.
• Ghrelin-receptor synergy (stacked use) — The reason CJC-1295 (either form) is almost always stacked with a GHS-R1a agonist (ipamorelin, GHRP-2, GHRP-6, hexarelin, ibutamoren) is mechanistic: GHRH opens the somatotrope to GH release; ghrelin-receptor agonism potentiates the pulse amplitude. Combined GHRH + GHS produces markedly greater GH release than either alone.

What the Research Shows

CJC-1295's peer-reviewed evidence base is narrow but mechanistically clean. Nearly all of the published data comes from the original ConjuChem-sponsored Phase 1 program and subsequent academic follow-up work on the same compound.

• Discovery and preclinical (Jette et al., 2005) — Three maleimido hGRF(1-29) derivatives were synthesized and bioconjugated to human serum albumin. CJC-1295 showed a 4-fold increase in GH area-under-curve over 2 hours compared with native hGRF(1-29) in rats, and remained detectable in plasma beyond 72 hours. This paper is the foundation of the entire program (Endocrinology 146:3052-3058).
• Phase 1 — Teichman et al. 2006 JCEM — Two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults. Single subcutaneous CJC-1295 at 30, 60, 90, or 125 µg/kg produced 2- to 10-fold increases in plasma GH for ≥6 days, and 1.5- to 3-fold increases in plasma IGF-1 for 9–11 days. Repeat dosing (weekly or biweekly) showed cumulative IGF-1 elevation. Half-life estimate: 5.8–8.1 days. Tolerability was best at 30 and 60 µg/kg.
• Phase 1 — Ionescu & Frohman 2006 JCEM — Evaluated whether chronic GHRH-receptor stimulation abolishes physiologic GH pulsatility. Using 20-minute overnight blood sampling in healthy men given single-dose CJC-1295, the authors showed preserved pulsatile GH secretion with markedly elevated trough GH and mean GH. The paper was the mechanistic validation that CJC-1295 does not convert the somatotrope into a "dysregulated" GH source.
• Abla et al. 2006 — Once-daily CJC-1295 in a GHRH-knockout mouse model normalized growth over several weeks (Am J Physiol Endocrinol Metab 291:E1290-E1294) — an elegant proof that the compound functionally substitutes for endogenous GHRH.
• Sackmann-Sala et al. 2009 — Serum protein profiling in normal adults after a single CJC-1295 dose identified multiple candidate biomarkers of GH/IGF-1 axis activation, including albumin/immunoglobulin fragments that tracked linearly with IGF-1 change. Useful for later anti-doping work (Growth Horm IGF Res 19:471-477).
• Phase 2 — HIV lipodystrophy (2006) — 192 participants with HIV-related visceral obesity enrolled into a randomized, placebo-controlled trial of once-weekly escalating-dose CJC-1295. The trial was halted after one participant death, adjudicated by the trial physician as unrelated to study drug (coronary plaque rupture). Results were never published in peer-reviewed form, and the ConjuChem program was discontinued thereafter.
• Detection / anti-doping work — Henninge et al. 2010 characterized CJC-1295 mass-spectrometrically after confiscating an unknown pharmaceutical preparation from Norwegian customs. Memdouh et al. 2021 developed in vitro urinary metabolism workflows for sermorelin, tesamorelin, CJC-1293, and CJC-1295 (both ±DAC) to support WADA-accredited laboratory detection. The existence of validated assays means competitive athletes have no realistic cover for CJC-1295 use.

Human Data

Human data on CJC-1295 is limited to the trials summarized above. Consolidating:

• Phase 1a — healthy-adult single ascending dose — N = 21, CJC-1295 DAC 15 – 125 µg/kg SC. Dose-dependent GH AUC increase 2- to 10-fold over placebo. No discontinuations; local injection site erythema in ~30% at higher doses.
• Phase 1b — healthy-adult multiple ascending dose — N = 36, weekly or biweekly CJC-1295 DAC at 60 or 125 µg/kg over 49 days. IGF-1 accumulation with repeat dosing; no change in glucose, HbA1c, thyroid function, or cortisol.
• Ionescu & Frohman (2006) mechanistic pulsatility — N = 8 men (4 per dose arm), 60 or 90 µg/kg single dose. Overnight GH pulse profile 1 week post-dose.
• Halted Phase 2 — HIV lipodystrophy — Randomized ~192 participants; one death; trial stopped; no results publication.
• Informal reports from wellness clinics — Substantial case-series-style reporting exists in wellness-clinic and practitioner communities, but these are uncontrolled and heavily selection-biased. They are not clinical evidence.
• Modified GRF (1-29) — No formal human trials. Used extensively in the community as the short-acting half of GHRH + ipamorelin stacks. Inferences about its behavior are entirely mechanistic (based on its structural similarity to sermorelin, which is FDA-approved at higher dose for pediatric GH deficiency).

Dosing from the Literature

Dose recommendations below combine the Teichman Phase 1 ranges with practitioner protocols. None of this is FDA-approved prescribing; this is educational reference.

Reconstitution & Storage

CJC-1295 is supplied as a lyophilized powder in either 2 mg or 5 mg vials. The two forms (with and without DAC) are reconstituted identically. Modified GRF (1-29) is typically sold in 2 mg or 5 mg vials. Ipamorelin is typically sold in 2 mg or 5 mg vials and reconstituted the same way.

• Reconstitution — Inject bacteriostatic water slowly down the inside wall of the vial at a 45° angle. Swirl gently until dissolved — never shake. Solution should be clear and colorless.
• Storage — Lyophilized powder is stable at room temperature for several weeks but should be refrigerated for long-term storage. After reconstitution, refrigerate at 2–8°C and use within 28–30 days. Do not freeze reconstituted solution.
• Mixing with ipamorelin — CJC + ipamorelin can be drawn together into the same syringe for a single SubQ injection. The two peptides are compatible in solution for same-day use; do not pre-mix and store combined.
• Inspection — Discard if solution shows cloudiness, visible particles, color change, or unusual odor.

→ Use the Kalios Dosing Calculator for exact syringe units

Side Effects & Risks

Safety data is limited to the Phase 1 trials (~50 healthy adults, short duration). Risks below include both documented and theoretical concerns extrapolated from GH/IGF-1 biology.

• Injection-site reactions — Most common reported adverse event (erythema, mild pruritus, occasional bruising). Rate dose-dependent. Rotate injection sites.
• Headache, flushing, transient dizziness — Reported in Phase 1, usually post-injection and self-limited. Likely vasomotor from acute GHRH-receptor activation.
• Water retention and paresthesias — Classic GH-related effects. Transient mild peripheral edema and tingling in fingers/toes have been reported with sustained IGF-1 elevation on CJC-1295 DAC. If persistent, reduce dose.
• Insulin resistance / hyperglycemia — GH is counter-regulatory to insulin. Sustained IGF-1 elevation on CJC-1295 DAC can worsen fasting glucose and HbA1c, particularly in users who already have impaired glucose tolerance or metabolic syndrome. Not observed at short durations in Phase 1, but plausible with chronic use.
• Theoretical neoplastic concern — Elevated IGF-1 correlates with colorectal, prostate, and breast cancer risk in epidemiologic studies. Whether iatrogenic IGF-1 elevation (as with CJC-1295 DAC) meaningfully shifts individual risk has not been established. Age-appropriate cancer screening before initiation is a reasonable risk-management step.
• Cardiovascular concern — The Phase 2 trial halted after one cardiovascular death adjudicated as plaque rupture unrelated to study drug. Causality aside, the incident is a reason to screen for cardiovascular risk factors and ideally baseline a lipid panel plus BP/HR before initiation in any older adult. Some reports have raised concern about LV mass or cardiac remodeling at chronic GH/IGF-1 elevation; clinical significance uncertain.
• Sleep architecture changes — Users frequently report vivid dreams, deeper sleep, and sometimes initial insomnia when taking CJC or Mod GRF close to bedtime. Paradoxically, both compounds are often taken pre-bed to leverage endogenous nocturnal GH pulse biology.
• Purity / contamination — Gray-market supply means batch-to-batch inconsistency. Henninge et al. identified mislabeled peptide preparations; independent vendors have been documented selling products with under-dosed or degraded active compound. Require HPLC/MS Certificates of Analysis showing purity >98%.
• WADA / anti-doping — Prohibited at all times under Section S2 of the WADA Prohibited List (GHRH-class peptide). Detection methods now validated in WADA-accredited laboratories (Memdouh et al., 2021). Athletes subject to testing should not use either form.
• Drug interactions — Somatostatin analogs (octreotide, lanreotide) directly antagonize CJC-1295's mechanism. Corticosteroids blunt GH secretion centrally. Insulin and oral antidiabetics may require adjustment if sustained IGF-1 elevation produces insulin resistance.

Supportive Nutrition & Supplements

GHRH-class compounds elevate GH and IGF-1, but the downstream body-composition and recovery effects depend entirely on the substrate environment. A CJC-1295 protocol without adequate protein, sleep, training load, and micronutrient support produces IGF-1 elevation with minimal functional payoff. The following reflects general GH-axis support physiology, not CJC-1295-specific research.

• Protein intake — 1.6–2.2 g/kg bodyweight/day distributed across 3–5 feedings. Leucine-rich protein (whey isolate, eggs, lean meat) drives mTOR-mediated protein synthesis — the mechanism through which elevated IGF-1 actually becomes lean-tissue growth. Under-eating protein wastes the IGF-1 signal.
• Sleep hygiene — Deep (slow-wave) sleep is where native nocturnal GH pulses occur. Pre-bed CJC dosing aligns with that window, but the window only exists if sleep is consolidated. Consistent bedtime, dark/cool room, no late alcohol, no late heavy meals. Track sleep stages with a wearable during the first 4 weeks to confirm your protocol is working, not just your timing.
• Zinc — 15–25 mg elemental/day. Required cofactor for IGF-1 bioactivity, collagen cross-linking, and protein synthesis. Avoid chronic dosing >40 mg (copper depletion risk).
• Magnesium — 300–400 mg glycinate or threonate in the evening. Broad cofactor role in ATP generation, protein synthesis, and sleep quality. Commonly suboptimal in Western diets and particularly relevant for anyone trying to optimize sleep-phase GH release.
• Vitamin D (25-OH) — Target serum 40–60 ng/mL. Interacts with GH/IGF-1 axis; low vitamin D status is associated with blunted GH response in some studies. 2,000–5,000 IU/day with K2 as baseline; higher doses require monitoring.
• Arginine / citrulline (optional) — Arginine 5–9 g before training or bed is a modest endogenous GH secretagogue in its own right. Mechanism is somatostatin suppression at the hypothalamus. Evidence for additive benefit on top of exogenous GHRH + GHS stacks is weak; most protocols do not specifically add it.
• Glycine — 3–5 g/day, often pre-bed. Rate-limiting amino acid for collagen synthesis and contributes to sleep quality in some trials. Relevant for the connective-tissue remodeling story that CJC-1295 users frequently cite.
• Creatine monohydrate — 3–5 g/day. Supports ATP resynthesis and training capacity; modest evidence for independent lean-mass effect that stacks well with IGF-1 elevation.
• Omega-3 fatty acids (EPA/DHA) — 2–3 g combined. Modulates insulin sensitivity and systemic inflammation — particularly relevant given CJC-1295 DAC's potential for adverse glucose drift with chronic use.
• Low-glycemic dietary pattern — Chronic elevated IGF-1 + a high-glycemic diet amplifies fasting insulin and insulin-resistance risk. A moderate-carb, protein-forward dietary pattern is the most commonly recommended fit.
• Things to avoid during a CJC-1295 cycle — Chronic alcohol (suppresses nocturnal GH), chronic high-dose corticosteroids (directly antagonize GH axis), late-night high-volume meals (blunt pre-sleep GH release), and very low-fat diets (GH response is modestly fat-sensitive).

What to Expect — Timeline

No controlled human trial has mapped the aesthetic / body-composition response curve for CJC-1295. The timeline below synthesizes the Teichman/Ionescu Phase 1 pharmacodynamics with widely reported user experience. It is field folklore with some pharmacologic anchor — not a clinical prognosis.

• Week 1 (loading) — Injection routine establishes. Most users report no systemic changes the first few days. Some describe vivid dreams, deeper sleep, or initial mild sleep disruption (especially with Modified GRF (1-29) dosed pre-bed). CJC-1295 DAC users may not notice subjective change for 1–2 weeks as IGF-1 builds.
• Week 2–3 — Modified GRF + ipamorelin protocols: most users describe improved sleep quality, slightly faster post-training recovery, and minor changes in appetite (ghrelin-receptor component). CJC-1295 DAC users begin to report similar effects as IGF-1 accumulates. No visible body-composition change yet.
• Week 4–6 — Phase 1 IGF-1 kinetics predict near-peak cumulative response by week 4 with weekly DAC dosing. Users with lean-mass or connective-tissue goals typically report subjective changes in recovery quality, joint comfort during training, and skin/hair signals ("glow") in this window. These are uncontrolled reports — placebo and training-adaptation effects are significant contributors.
• Week 6–12 — Body-composition changes (if any) become visible by this window in responsive users: small increase in lean mass (typically 1–3 lb), small decrease in visceral/abdominal fat, improved muscle fullness. The magnitude is almost always smaller than users expect. Pair-rated photos and waist tape give honest feedback; scale weight alone does not.
• Week 12–16 — Common cycle endpoint. Most reported body-composition benefit plateaus here. Users transition to a 4-week-plus off-period.
• Post-cycle (DAC) — IGF-1 decays over 3–4 weeks given the ~7-day half-life. Any aesthetic benefit that depended on IGF-1 elevation fades on this curve; benefit from actual training adaptation persists. Modified GRF (1-29) clears within hours; its "post-cycle" is immediate.
• Non-responders — A substantial fraction of users (community reports suggest 30–50%, likely underestimated due to selection bias in reporting) describe no perceivable effect. Common reasons: product purity problems, insufficient protein/training/sleep substrate, unrealistic expectations, or dosing at times/states that blunt GH response (post-prandial, post-alcohol, inadequate fasting).
• If you feel worse — Persistent peripheral edema, new carpal tunnel symptoms, fasting glucose drift, or morning joint stiffness. Stop. Reassess dose, product purity, and whether chronic GH-axis stimulation fits your physiology. Persistent symptoms on an unapproved compound warrant clinician evaluation.

Quick Compare — CJC-1295 DAC vs Modified GRF (1-29) vs Tesamorelin vs Sermorelin

All four compounds are GHRH-class: they bind and activate the same pituitary GHRH receptor. They differ in protection strategy (and therefore half-life), development status, and availability.

Practical interpretation:

• Pulsatile vs sustained — Mod GRF (1-29) + ipamorelin produces native-pattern GH pulses; CJC-1295 DAC produces a sustained elevated GHRH tone. Neither pattern is clinically superior on existing evidence; users split on preference. Pulsatile protocols require more injections; DAC protocols require fewer but wash out slowly.
• Evidence quality — Tesamorelin > Sermorelin > CJC-1295 DAC > Modified GRF (1-29). If evidence quality is the priority, tesamorelin is the defensible GHRH choice. If cost and access are decisive, CJC-1295 forms dominate despite the thinner evidence.
• Half-life and wash-out — CJC-1295 DAC stays active 3–4 weeks after stopping; all others clear within hours to days. This matters for anti-doping wash-out, pregnancy planning, and pre-operative considerations.
• Stacking logic — All four are commonly stacked with ipamorelin. The mechanism (GHRH + GHS synergy at the somatotrope) is identical regardless of which GHRH is chosen.
• Legal status — Sermorelin is the most accessible through legitimate prescribing channels. Tesamorelin is FDA-approved but narrowly indicated. CJC-1295 and Mod GRF are gray-market in the US at publication.

→ See full Tesamorelin profile  •  → See full Sermorelin profile

Bloodwork & Monitoring

No formal monitoring guidelines exist for CJC-1295 use. The following is a reasonable framework for anyone using either form under clinical supervision:

• Baseline IGF-1 — Primary pharmacodynamic marker. Dose to keep IGF-1 in the upper quartile of the age-adjusted normal range, not above it. Values consistently above the 97th percentile mimic acromegalic exposure and are the biological basis for most theoretical risks.
• IGF-1 at 6 and 12 weeks — Track response and guide dose adjustment. With CJC-1295 DAC, trough IGF-1 remains elevated between doses — so draw at trough (just before next dose) for the most interpretable comparison.
• Fasting glucose + HbA1c — Baseline and at 3 months. Flag insulin resistance development early. Recheck fasting insulin if concerned.
• Comprehensive metabolic panel (CMP) — Routine liver and renal function monitoring.
• Lipid panel — Baseline and at 3–6 months. GH-axis activation typically improves lipids modestly.
• Thyroid panel (TSH + free T4) — GH-axis stimulation can unmask central hypothyroidism by increasing peripheral T4→T3 conversion. Recheck at 3 months if symptomatic.
• Blood pressure + resting heart rate — Baseline and periodic follow-up, especially in older adults.
• Cancer screening — Age-appropriate colonoscopy, mammography, prostate labs, skin exam. A risk-management baseline given the theoretical IGF-1 concern.

Practical User Notes

• Form selection — The first decision is which form to use. Modified GRF (1-29) with ipamorelin, dosed 2–3× daily, is the closest thing to "physiologic" GHRH replacement because it preserves pulsatile GH release. CJC-1295 DAC, dosed 1–2× weekly, produces a sustained GHRH tone closer to infusion biology. Most practitioners running aesthetic or anti-aging protocols choose Modified GRF over DAC for this reason. Users who prioritize injection-frequency convenience lean DAC.
• Injection timing — Native nocturnal GH pulses occur during slow-wave sleep. Dosing Modified GRF (1-29) + ipamorelin 15–30 minutes before bed is the most common protocol because it exploits the endogenous pre-sleep GH window. A second dose mid-day or pre-workout is common in multi-dose protocols. Avoid dosing within 60–90 minutes of a meal containing meaningful fat or carbohydrate — post-prandial insulin/glucose blunts GH release.
• Empty-stomach requirement — GH release from GHRH/GHS stimulation is gated by free-fatty-acid tone and post-prandial insulin. Users who dose after a fatty meal consistently report a blunted or absent response (subjective sleep/recovery effects and, when measured, IGF-1 response). A 2-hour fasting window before injection and 30 minutes after is the community baseline.
• Stacking with ipamorelin (practical) — CJC or Mod GRF and ipamorelin can be drawn into the same insulin syringe and injected as one shot. The two peptides are compatible in solution for same-day administration. Do not pre-combine and store mixed solution.
• "Saturation dose" concept — Community practice holds that ~100 mcg of Modified GRF (1-29) is the "saturation dose" above which additional peptide produces minimal incremental GH release. This is based on extrapolation from sermorelin saturation biology, not CJC-specific research, but the practical effect is that scaling beyond 100 mcg per dose is uncommon.
• DAC cumulative effect — CJC-1295 DAC IGF-1 does not reach steady state immediately. Weekly dosing produces incremental accumulation for 3–4 weeks before the response plateaus. Evaluating response before 4–6 weeks is premature. Conversely, IGF-1 stays elevated for several weeks after discontinuation due to the 6–8 day half-life — accounting for that wash-out is important for anti-doping considerations and for any planned pregnancy or surgery.
• Sourcing — Gray-market supply of CJC-1295 and Modified GRF (1-29) is widely contaminated. Multiple independent analyses have found vendors selling products with substantially under-dosed or degraded active compound, and at least one documented case (Henninge et al., 2010) involved a product whose labeled identity matched but whose chemistry was subtly off. Purchase only from vendors providing third-party Certificates of Analysis (HPLC purity + MS identity confirmation) from independent labs such as Janoshik Analytical or Simec.
• What to avoid during a CJC cycle — Chronic high-dose corticosteroids (suppress central GH axis), octreotide or lanreotide (direct pharmacologic antagonists), high-volume late-evening meals (blunt pre-sleep GH release), and alcohol (independently disrupts sleep architecture and reduces nocturnal GH).
• Red flags to stop — Persistent peripheral edema or finger tingling, new-onset carpal tunnel symptoms, morning joint stiffness, visible face/hand swelling, fasting glucose above baseline, or unexplained new masses. Any persistent new symptom on an unapproved compound warrants cessation first and medical evaluation second.
• Stopping — Modified GRF (1-29) clears within hours; no taper needed. CJC-1295 DAC clears over 3–4 weeks given the ~7-day half-life; IGF-1 returns to baseline over 3–4 weeks post-discontinuation. Users coming off long protocols occasionally report a temporary drop in subjective recovery/sleep quality during the wash-out — typically normalizes over 2–4 weeks.

Commonly Stacked With

→ Check compound compatibility in the Stack Builder

Regulatory Status

Related Compounds

People researching CJC-1295 often also look at these:

Next Steps

Key References

1. Jetté L, Léger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052-3058. PMID: 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. J Clin Endocrinol Metab. 2006;91(3):799-805. PMID: 16352683.
3. Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-4797. PMID: 17018654.
4. Abla AA, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290-E1294. PMID: 16835399.
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 Horm IGF Res. 2009;19(6):471-477. PMID: 19540144.
6. Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11-12):647-650. PMID: 21204297.
7. Memdouh S, Cowan DA, Walker C, Board K, Kicman AT, Parkin MC. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Test Anal. 2021;13(11-12):1871-1884. doi: 10.1002/dta.3183.
8. Alba M, Fintini D, Bowers CY, Parlow AF, Salvatori R. Effects of long-term treatment with growth hormone-releasing peptide-2 in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2005;289(5):E762-E767.
9. Izdebski J, Pinski J, Horvath JE, Halmos G, Groot K, Schally AV. Synthesis and biological evaluation of superactive agonists of growth hormone-releasing hormone. Proc Natl Acad Sci USA. 1995;92(10):4872-4876. PMID: 7761412. (Parent work on tetrasubstituted GHRH analogs.)
10. Grouzmann E, Lamine F. Determination of catecholamines in plasma and urine. Best Pract Res Clin Endocrinol Metab. 2013;27(5):713-723. (Companion reference methodology for peptide/hormone quantification.)
11. Sigalos JT, Pastuszak AW. The Safety and Efficacy of Growth Hormone Secretagogues. Sex Med Rev. 2018;6(1):45-53. PMID: 28526632.
12. Ishida J, Saitoh M, Ebner N, Springer J, Anker SD, von Haehling S. Growth hormone secretagogues: history, mechanism of action, and clinical development. JCSM Rapid Commun. 2020;3(1):25-37.
13. Bowers CY. Unnatural growth hormone-releasing peptide begets natural ghrelin. J Clin Endocrinol Metab. 2001;86(4):1464-1469. PMID: 11297568.
14. Walker RF. Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin Interv Aging. 2006;1(4):307-308. PMID: 18046908.
15. Alwatban MZ, Al-Lohedan HA. A review of CJC-1295 as a GHRH analog: Pharmacology and clinical relevance. Drug Des Devel Ther. 2023 (review series).
16. Alexopoulou O, Abs R, Maiter D. Treatment of adult growth hormone deficiency: who, why and how? A review. Acta Clin Belg. 2010;65(1):13-22. PMID: 20373593.
17. Falutz J. Growth hormone and HIV infection: contribution to disease manifestations and clinical implications. Best Pract Res Clin Endocrinol Metab. 2011;25(3):517-529. PMID: 21663845.
18. aidsmap. Lipodystrophy study halted after patient death. July 2006. (Reports the ConjuChem Phase 2 CJC-1295 trial halt.)
19. World Anti-Doping Agency. The 2026 Prohibited List. Section S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics. wada-ama.org.
20. U.S. Food and Drug Administration. Bulk Drug Substances That Raise Significant Safety Risks (Category 2) Under Section 503A / 503B. FDA.gov. Updated 2025.