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CJC-1295 (no DAC)

A short-acting, DPP-4-resistant GHRH analog that drives sharp, physiologic pulses of the body's own growth hormone.

CJC-1295 without DAC — universally sold as Mod GRF 1-29 — is a synthetic analog of the first 29 amino acids of growth hormone-releasing hormone (GHRH) carrying four amino-acid substitutions that resist enzymatic breakdown. Unlike the albumin-bound DAC variant, it clears in roughly 30 minutes, producing a single discrete GH pulse that mirrors natural hypothalamic signaling rather than sustained elevation. It is almost always stacked with a ghrelin-receptor agonist such as ipamorelin, whose complementary pathway amplifies each GH pulse several-fold. It has no FDA approval and is sold as a research-use-only compound.

Mod GRF 1-29Modified GRF 1-29MOD-GRF 1-29CJC-1295 without DACCJC no DACTetrasubstituted GRF 1-29

Class

Synthetic tetrasubstituted GHRH(1-29) analog (short-acting)

Half-life

~30 minutes (no-DAC / Mod GRF 1-29); the DAC variant runs ~6–8 days via albumin binding

Routes

Subcutaneous

Category

Growth Hormone & Performance

Researched benefits

What it's studied for

Pulsatile GH release

Because it clears in ~30 minutes, each injection produces a sharp, transient GH pulse (roughly 2–5x baseline) that mimics the body's natural nocturnal burst, preserving somatotroph sensitivity and negative-feedback regulation rather than overriding them.

Strong synergy with ghrelin-receptor agonists

Combined with ipamorelin, hexarelin, or MK-677, the GHRH (Gs/cAMP/PKA) and ghrelin (Gq/PLC/IP₃/Ca²⁺) pathways converge on the same somatotrophs, producing a GH pulse 3–5x larger than either agent alone — the mechanistic basis for modern GH-secretagogue protocols.

Downstream IGF-1 elevation

Released GH drives hepatic IGF-1 production; multi-week dosing achieves roughly 1.5–2x baseline IGF-1 (less than the sustained DAC form because the pulse is transient), supporting protein synthesis and recovery.

Improved sleep and recovery

Sleep depth and architecture improvement is the most consistent subjective and community-reported benefit, often the earliest effect noticed, alongside enhanced recovery from exercise and injury.

Body composition support

Over 8–16 week cycles, users report lean-mass preservation and modest fat loss, particularly when paired with resistance training and adequate protein; effects are subtle rather than dramatic.

Lower desensitization risk vs DAC

Pulsatile exposure avoids the continuous GHRH-receptor stimulation of the DAC variant, which is associated with receptor desensitization and fluid retention; clinic protocols have largely shifted to the no-DAC form.

Mechanism

How it works

Mod GRF 1-29 acts through a single, well-characterized target: the GHRH receptor (GHRHR), a Class B1 G-protein-coupled receptor on anterior-pituitary somatotroph cells. Ligand binding activates Gs, elevating intracellular cAMP, which activates PKA and phosphorylates CREB; phospho-CREB upregulates GH-1 gene transcription and mobilizes preformed growth hormone from secretory granules, producing acute GH release within 15–30 minutes. The four amino-acid substitutions (notably D-Ala at position 2) confer resistance to DPP-4 degradation, giving it roughly 15-fold higher potency at the receptor than native GHRH.

The defining feature is pharmacokinetic. Native GHRH clears in under two minutes; Mod GRF 1-29 clears in about 30 minutes, versus ~8 days for the DAC variant. This short window produces a sharp, transient pulse that returns to baseline within 2–3 hours — a pattern nearly identical to the body's natural nocturnal GH burst. Pulsatile exposure preserves somatotroph sensitivity, keeps somatostatin (GHIH) negative feedback intact between pulses, and amplifies rather than replaces the natural circadian rhythm, which is why most clinicians prefer it over the sustained-release DAC form.

Used alone, Mod GRF 1-29 produces a measurable but modest GH rise (~2–3x baseline), so it is almost always stacked with a ghrelin-receptor (GHS-R1a) agonist such as ipamorelin. The two pathways engage the same somatotrophs through distinct second messengers — GHRH via Gs/cAMP/PKA and ghrelin via Gq/PLC/IP₃/calcium — and dual activation yields a GH pulse 3–5x larger than either agent alone. Released GH then binds hepatic GH receptors (JAK2/STAT5), inducing IGF-1 expression that rises with a 1–3 day lag under chronic dosing.

Notably, Mod GRF 1-29 does not bind the ghrelin receptor, does not meaningfully raise cortisol, prolactin, or ACTH at therapeutic doses, and does not bypass endogenous feedback. High somatostatin tone — as occurs after a carbohydrate meal or during hyperglycemia — blunts the GH response by 30–70%, which is why fasted-state administration (2+ hours after carbohydrate) is the single most important dosing detail.

Dosing protocols

Dosing & administration

Dosing reflects protocols reported in research and community literature for educational purposes. It is not medical advice or a recommendation. Most peptides here are not approved for human use.

Reconstitution

Supplied as lyophilized powder, typically 2 mg or 5 mg per vial. Reconstitute with bacteriostatic water (0.9% benzyl alcohol) for multi-day stability. A standard 2 mg vial + 2 mL BAC water yields 1 mg/mL (1000 mcg/mL), so on a U-100 insulin syringe 10 units = 0.1 mL = 100 mcg. Alternatively 2 mg + 1 mL BAC gives 2000 mcg/mL (5 units = 100 mcg), useful for a smaller combined draw with ipamorelin. Inject slowly down the inner glass wall, swirl gently (never shake), and refrigerate at 2–8°C; use reconstituted solution within about 28 days and do not freeze it.

Beginner

Dose
100 mcg (add 100–200 mcg ipamorelin from week 3)
Frequency
Once daily, pre-bed (isolate tolerance for weeks 1–2, then add ipamorelin)
Timing
Fasted, 2+ hours after dinner
Duration
12-week cycle
Route
Subcutaneous

First cycle to establish tolerance and confirm sourcing. Track injection-site reaction, flushing, sleep, and any numbness/tingling. Confirm baseline IGF-1, fasting glucose, and HbA1c before starting.

Intermediate

Dose
100 mcg + 200 mcg ipamorelin (combined injection)
Frequency
Twice daily (AM fasted + pre-bed)
Timing
Fasted state, 2+ hours post-meal, consistent day-to-day
Duration
Months 3–12, continuous with monitoring
Route
Subcutaneous

Standard maintenance after a successful first cycle. Do not escalate single-dose above 100 mcg (receptor-saturated); ipamorelin ceiling ~300 mcg/dose. Monitor IGF-1 quarterly, keeping it upper-normal for age rather than supraphysiologic.

Advanced

Dose
100 mcg + 200–300 mcg ipamorelin per dose; do not exceed 400 mcg total Mod GRF daily
Frequency
2–3x daily (AM fasted, optional pre-workout, pre-bed)
Timing
Fasted before each dose; pre-workout 30–60 min before training
Duration
12+ months with monitoring; e.g. 12 weeks on / 4 weeks off quarterly
Route
Subcutaneous

For established users with 12+ months of uneventful use. Target IGF-1 ~75th percentile for age; titrate in 25% steps at 8-week intervals. Do not stack with exogenous rhGH, IGF-1 LR3, or MGF simultaneously, and do not chase ever-higher IGF-1.

  • Fasted administration is essential: postprandial somatostatin blunts the GH pulse by 30–70%. Inject at least 2 hours after the last carbohydrate meal and before eating afterward.
  • Standard dose is 100 mcg per injection; increasing per-dose beyond ~100 mcg does not meaningfully increase the GH pulse (receptor saturation) but adds side effects. Frequency, not dose size, scales the total effect.
  • Almost always dosed alongside a ghrelin-receptor agonist (usually ipamorelin) in the same syringe — reconstitute each peptide separately, then draw both into one insulin syringe.
  • Weight-based dosing is roughly 1–2 mcg/kg per injection, but a flat 100 mcg suits most individuals.
  • Subcutaneous only (IM offers no PK advantage); rotate sites on the lower abdomen, thigh, or upper arm using a 29–31G insulin needle.
  • Continuous daily use is reasonable for 6–12 months with monitoring; some clinicians run 5-days-on / 2-off or take a 4–6 week annual break to preserve pulsatile physiology.
  • Monitor IGF-1 (and IGFBP-3), fasting glucose, and HbA1c; keep IGF-1 upper-normal for age. Stop for any new malignancy diagnosis, new diabetic retinopathy, or pregnancy planning.

Evidence

Research & clinical studies (4)

RCTJournal of Clinical Endocrinology and Metabolism · 2006

Effects of a single injection of CJC-1295, a long-acting growth hormone-releasing hormone analog, in healthy adults

In two randomized controlled trials a single injection of CJC-1295 produced 2- to 10-fold increases in serum GH and 1.5- to 3-fold increases in IGF-1 sustained for 6+ days, with acceptable safety and tolerability in healthy adults.

PMID 16352683
RCTJournal of Clinical Endocrinology and Metabolism · 1997

Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women

A 5-month randomized placebo-controlled trial (n=19) found nightly subcutaneous GHRH(1-29)-analog dosing significantly raised 12-hour integrated GH, IGF-I, and IGFBP-3, increased lean body mass in men, improved skin thickness in both sexes, and enhanced insulin sensitivity and well-being in men.

PMID 9141536
RCTJournal of Clinical Endocrinology and Metabolism · 1997

Effects of [norleucine27]growth hormone-releasing hormone (GHRH) (1-29)-NH2 administration on the immune system of aging men and women

A randomized controlled trial (n=19) found 4-month nightly GHRH-analog dosing raised GH and IGF-I while enhancing immune activation — B-cell numbers, T-cell receptor expression, and interleukin-2 responsiveness — in elderly men and women.

PMID 9360512
ReviewJBJS Rev · 2026

Injectable Peptides in Sports Medicine: A Structured Narrative Review of Evidence, Safety, and Antidoping Implications

Concluded CJC-1295, a growth-hormone-axis secretagogue, remains investigational with uncertain safety, product-quality concerns, and broad antidoping restrictions, lacking the reproducible clinical evidence seen in other peptide categories.

PMID 42160466

Combinations

Stacking & blends

CJC-1295 + Ipamorelin: GH Optimization

CJC-1295 (no DAC)Ipamorelin

Foundational, more physiologic GH release

Pairs a GHRH analog with a selective ghrelin-receptor agonist; CJC-1295 extends GHRH signaling while ipamorelin adds GH pulses via the ghrelin receptor with minimal cortisol or prolactin, producing synergistic pulses larger than either alone.

CJC-1295 + Ipamorelin + BPC-157: Recovery & GH

CJC-1295 (no DAC)IpamorelinBPC-157

Systemic anabolic support plus targeted tissue repair

Adds BPC-157's localized tendon, ligament, and gut healing to the GH-secretagogue synergy, popular with athletes seeking both systemic recovery and injury repair simultaneously.

CJC-1295 + Ipamorelin + GHRP-6: GH Secretagogue Max

CJC-1295 (no DAC)IpamorelinGHRP-6

Maximal endogenous GH output

An advanced triple-secretagogue stack: CJC-1295 extends GHRH signaling, ipamorelin gives a clean selective pulse, and GHRP-6 adds pulse amplitude plus appetite stimulation, for the highest attainable GH without exogenous HGH.

Hexarelin + Mod GRF 1-29: Anabolic GH Amplification

HexarelinMod GRF 1-29

Maximize GH secretion for muscle growth and fat loss

Hexarelin is a potent GHRP with additional cardioprotective receptor activity; combined with Mod GRF 1-29's pulsatile GHRH stimulation, the complementary receptor pathways drive robust GH release.

Safety

Side effects & considerations

Risk profileModerate

Commonly reported effects

Injection-site redness, swelling, or itchingFlushing and warmth (vasodilation) 15–30 minutes post-injectionWater retention and mild edema during the initial weeksTransient increase in hungerHeadache (often resolves with continued use)Vivid dreamsOccasional elevated heart rate / palpitations

Contraindications & cautions

  • Active malignancy of any type (GH/IGF-1 axis stimulation is theoretically pro-tumorigenic)
  • Active or prior diabetic retinopathy (IGF-1 promotes retinal neovascularization)
  • Pregnancy and lactation (no safety data)
  • Children with open growth plates (unintended longitudinal growth)
  • Critical illness requiring ICU care (exogenous GH increased mortality in the critically ill)
  • Active acromegaly or pituitary adenoma
  • Caution in poorly controlled type 2 diabetes, cancer history within 5 years, severe hypothyroidism, and obstructive sleep apnea

Because it works through endogenous feedback, Mod GRF 1-29 does not suppress the body's own GH production the way exogenous rhGH does, and the axis returns to baseline within days to weeks after stopping. Serious risks are tied to chronic supraphysiologic GH/IGF-1: carpal-tunnel-like symptoms, impaired glucose tolerance/insulin resistance, and theoretical acceleration of pre-existing malignancy. Routine monitoring of IGF-1, fasting glucose, and HbA1c is standard; glucocorticoids, somatostatin analogs, and high-dose oral estrogens blunt its effect, and it should not be combined with somatostatin analogs. Long-term human safety data is limited given development stopped at Phase 2.

FAQ

CJC-1295 (no DAC) — common questions

What's the difference between CJC-1295 no-DAC and CJC-1295 with DAC?

The no-DAC form (Mod GRF 1-29) has a ~30-minute half-life and produces sharp, pulsatile GH release similar to natural physiology. The DAC form adds a maleimide linker that binds serum albumin, extending the half-life to ~6–8 days and producing continuous, non-pulsatile GH elevation dosed roughly once weekly. Most clinicians now prefer the no-DAC version because pulsatile release preserves somatotroph sensitivity and endogenous feedback, whereas the DAC form carries higher risk of receptor desensitization and fluid retention.

Is CJC-1295 no-DAC the same as Mod GRF 1-29?

Yes. CJC-1295 without DAC and Mod GRF 1-29 are the same molecule — GHRH(1-29) with four amino-acid substitutions for stability. The dual naming persists in research-grade catalogs for historical reasons; buyers should not pay to 'stack' both names.

Why is it stacked with ipamorelin?

Alone it produces only a modest GH pulse (~2–3x baseline). Paired with a ghrelin-receptor agonist like ipamorelin, the two signaling pathways converge synergistically on pituitary somatotrophs, and the net GH pulse is 3–5x larger than either agent alone. Dosing it without a ghrelin-axis partner leaves efficacy on the table.

Do I have to inject on an empty stomach?

Yes — this is the single most important dosing detail. Postprandial somatostatin blunts the GH response by 30–70%. Inject in a fasted state, at least 2 hours after your last carbohydrate meal and before eating afterward. Pre-bed and pre-breakfast dosing work well because of that natural fasting window.

Is CJC-1295 FDA-approved or legal?

It is not FDA-approved for any indication and is not a controlled substance; clinical development was halted at Phase 2. It was removed from the FDA compoundable bulk substances (503A) list, limiting prescription availability, and is otherwise sold as a research-use-only chemical not intended for human use. WADA prohibits GH-releasing peptides at all times for competitive athletes.

Will it help me build muscle?

Modestly, and only alongside resistance training and adequate protein. GH and IGF-1 elevation support protein synthesis and recovery but do not replace mechanical stimulus. Expect better recovery, modest lean-mass preservation during fat loss, and some early 'fullness' from glycogen and water — not dramatic physique change on its own.

Will my body stop making its own growth hormone?

No. It stimulates the pituitary to release endogenous GH rather than replacing it, and negative feedback stays intact, so somatostatin can still suppress GH appropriately. When you stop, the axis returns to baseline within days to weeks — unlike exogenous rhGH, which suppresses endogenous production.

How soon will I notice effects?

Acute effects (flushing, vivid dreams, better sleep) usually within 1–2 weeks; energy and recovery by weeks 3–4; a measurable IGF-1 rise by weeks 4–6; and body-composition changes, if they happen, by month 2–3. If you feel nothing by weeks 6–8 with correct timing, re-check your vendor COA, reconstitution technique, and fasting window.

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