Side-by-side · Research reference
CJC-1295 (no DAC)vsHGH Fragment 176-191
Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.
APhase 1HUMAN-REVIEWED15/51 cited
BAnimal-StrongHUMAN-REVIEWED28/59 cited
CJC-1295 (no DAC)
Short-acting GHRH · No DAC variant
SQ · Pre-sleep · 1–2×/day
HGH Fragment 176-191
GH Fragment · Pre-Clinical
SQ · IP (animal) · Oral (tested)
01Mechanism of Action
Parameter
CJC-1295 (no DAC)
HGH Fragment 176-191
Primary target
Pituitary GHRH receptorTeichman 2006
Beta-3 adrenergic receptors on adipocytesHeffernan 2001
Pathway
GHRH-R → Gαs → cAMP → PKA → GH vesicle exocytosisTeichman 2006
Fragment → β3-AR upregulation → Enhanced lipolytic sensitivityHeffernan 2001
Downstream effect
Pulsatile GH release matching physiological pattern; subsequent IGF-1 elevationIonescu 2006
Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation
Feedback intact?
Yes — short pulse preserves somatostatin negative feedbackIonescu 2006
N/A — does not interact with GH/IGF-1 axis
Origin
Modified human GRF 1-29 with four substitutions (D-Ala²/Gln⁸/Ala¹⁵/Leu²⁷) for protease resistanceTeichman 2006
Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191)Cox 2015
Antibody development
Not reported in short-term studies
Not reported in available studies
02Dosage Protocols
Parameter
CJC-1295 (no DAC)
HGH Fragment 176-191
Frequency
1–2× daily (pre-sleep ± morning)
Once daily (animal models)
Lower / starter dose
50 mcg per dose
—
Evidence basis
Phase 1 (CJC-1295 with DAC); analog dataTeichman 2006Ionescu 2006
No-DAC variant is less studied directly; PK extrapolated from native GHRH.
Animal studies only
Duration
8–12 weeks on / 4 off (anecdotal)
—
Reconstitution
Bacteriostatic water
—
Timing
Pre-sleep + fasted preferred
—
Half-life
~30 minIonescu 2006
Short pulse vs CJC-1295-DAC (~8 days). Choose no-DAC for pulsatile, DAC for sustained.
—
Animal dose (IP)
—
Not specified (14-day chronic administration)Heffernan 2001
Obese mice, daily IP injection.
Human equivalent dose
—
Not established — no published human RCTs
Detection window
—
50 pg/mL LOD in urine; stable metabolite extends detectionCox 2015
WADA-banned; anti-doping testing available.
Oral bioavailability
—
Demonstrated efficacy in animal oral administrationNg 2000
Potential for oral therapeutic development.
03Metabolic / Fat Loss Evidence
Parameter
CJC-1295 (no DAC)
HGH Fragment 176-191
Weight gain reduction
—
50% reduction vs control (15.8 ± 0.6 g vs 35.6 ± 0.8 g)Ng 2000
Obese Zucker rats, 19 days oral administration.
Body fat reduction
—
Significant decrease in body weight and body fat in obese mice (14 days)Heffernan 2001
Lipolytic activity
—
Increased adipose tissue lipolytic activityNg 2000
Direct measurement in treated animals.
Insulin sensitivity
—
No adverse effect — euglycemic clamp confirmedNg 2000
Contrasts with intact hGH diabetogenic effects.
IGF-1 impact
—
No elevation — fragment does not activate GH/IGF-1 axis
Beta-3 AR dependency
—
Effect abolished in β3-AR knockout miceHeffernan 2001
Confirms β3-AR as primary mechanism.
Human evidence
—
None published — pre-clinical only
04Side Effects & Safety
Parameter
CJC-1295 (no DAC)
HGH Fragment 176-191
Injection site reaction
Erythema, mild pruritus
—
Flushing / headache
Common transient effect
—
Cortisol elevation
Minimal at standard doses
—
Prolactin elevation
Minimal
—
Glucose intolerance
Possible at high cumulative doses
—
IGF-1 elevation
Dose-dependent; monitor with chronic use
—
Cancer risk
Contraindicated in active malignancy (GH/IGF-1 axis)
—
Pregnancy / OB
Avoid
—
Human safety data
—
Not available — no published human trials
Metabolic profile
—
Six metabolites identified; CRSVEGSCG most stableCox 2015
Detection window implications for doping control.
Absolute Contraindications
CJC-1295 (no DAC)
- ·Active malignancy or cancer history
- ·Pregnancy / breastfeeding
- ·Disrupted hypothalamic-pituitary axis
HGH Fragment 176-191
- ·Competitive athletes (WADA-banned)Cox 2015
Relative Contraindications
CJC-1295 (no DAC)
- ·Untreated diabetes
- ·Severe insulin resistance
HGH Fragment 176-191
- ·Absence of human safety data — experimental use only
05Administration Protocol
Parameter
CJC-1295 (no DAC)
HGH Fragment 176-191
1. Reconstitution
Add 2 mL bacteriostatic water to 2 mg vial → 1 mg/mL = 100 mcg per 0.1 mL. Roll gently.
Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.
2. Injection site
Subcutaneous, abdomen or thigh. Rotate sites.
Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.
3. Timing
Pre-sleep preferred. Often combined with ipamorelin in the same syringe.
Animal protocols: 14–19 days. Human duration not established — no published trials.
4. Storage
Lyophilised: room temp, protected from light. Reconstituted: refrigerate 2–8 °C, use within 30 days.
Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.
5. Needle
29–31G, 4–8 mm insulin syringe.
Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG.Cox 2015
06Stack Synergy
CJC-1295 (no DAC)
+ Ipamorelin
StrongCJC-1295 (no DAC) and ipamorelin are the canonical "GHRH + GHRP" dual-axis stack at physiological timing. Both peak within 30 min and clear within 2 hours, producing a sharp, high-amplitude GH pulse closely resembling natural physiology. Preferred over the CJC-1295-DAC + ipamorelin stack when pulsatility (vs sustained elevation) is the goal.
- CJC-1295 (no DAC)
- 100 mcg SQ · pre-sleep
- Ipamorelin
- 200–300 mcg SQ · same injection
- Primary benefit
- Pulsatile GH stimulation, recovery, body composition
HGH Fragment 176-191
— no documented stacks