Side-by-side · Research reference
CJC-1295 (no DAC)vsFollistatin-344
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
BHuman-MechanisticHUMAN-REVIEWED4/58 cited
CJC-1295 (no DAC)
Short-acting GHRH · No DAC variant
SQ · Pre-sleep · 1–2×/day
Follistatin-344
Myostatin/Activin Antagonist · Research Use
15–25%FST/MSTN ratio ↑
344 AACirculating isoform
ResearchPhase status
Research · No approved protocol
01Mechanism of Action
Parameter
CJC-1295 (no DAC)
Follistatin-344
Pathway
GHRH-R → Gαs → cAMP → PKA → GH vesicle exocytosisTeichman 2006
FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism
Downstream effect
Pulsatile GH release matching physiological pattern; subsequent IGF-1 elevationIonescu 2006
Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026
Feedback intact?
Yes — short pulse preserves somatostatin negative feedbackIonescu 2006
Yes — indirect antagonist, preserves endogenous regulation
Origin
Modified human GRF 1-29 with four substitutions (D-Ala²/Gln⁸/Ala¹⁵/Leu²⁷) for protease resistanceTeichman 2006
Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)
Antibody development
Not reported in short-term studies
Not documented in available trials (endogenous protein)
02Dosage Protocols
Parameter
CJC-1295 (no DAC)
Follistatin-344
Frequency
1–2× daily (pre-sleep ± morning)
—
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.
Human observational / biomarker studies
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.
Not established
Circulating isoform; lacks tissue-binding domain of FST-315.
Clinical protocol
—
None — no approved dosing regimen
Follistatin-344 measured as endogenous biomarker, not administered exogenously in cited trials.
Research context
—
Endogenous modulation via exercise + nutrition
Resistance training + EAA intake elevated FST/MSTN ratio by 15–25% in 12-week RCT (older women).
03Metabolic / Fat Loss Evidence
Parameter
CJC-1295 (no DAC)
Follistatin-344
Primary target
—
Muscle mass preservation, not direct lipolysis
Indirect fat effect
—
Increased lean mass → elevated resting metabolic rate
Not primary mechanism. Muscle-sparing during deficit.
Clinical evidence
—
Lorcaserin trial (6 mo) showed no MAFI axis changes during fat lossRamirez-Cisneros 2026
Suggests follistatin not primary driver of fat loss in weight-reduction interventions.
GLP-1RA studies
—
Liraglutide (35 days) — no significant MAFI axis modulation despite fat/lean changes
04Side Effects & Safety
Parameter
CJC-1295 (no DAC)
Follistatin-344
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
—
Clinical safety data
—
None — no human exogenous administration trials in literature
Theoretical risks
—
Excessive myostatin inhibition → muscle overgrowth, impaired glucose tolerance
Based on myostatin-null animal models and clinical myostatin inhibitor trials.
Endogenous elevation (exercise)
—
No adverse effects reported in 12-week resistance + EAA trials
Cancer risk (theoretical)
—
Myostatin inhibition may promote tumor growth in malignancy (preclinical data)
Regulatory status
—
Not approved for human use — research peptide only
Absolute Contraindications
CJC-1295 (no DAC)
- ·Active malignancy or cancer history
- ·Pregnancy / breastfeeding
- ·Disrupted hypothalamic-pituitary axis
Follistatin-344
- ·Active malignancy
- ·No approved protocol — research use only
Relative Contraindications
CJC-1295 (no DAC)
- ·Untreated diabetes
- ·Severe insulin resistance
Follistatin-344
- ·Insulin resistance / Type 2 diabetes (monitor glucose)
- ·Pregnancy / lactation (unknown safety profile)
05Administration Protocol
Parameter
CJC-1295 (no DAC)
Follistatin-344
1. Reconstitution
Add 2 mL bacteriostatic water to 2 mg vial → 1 mg/mL = 100 mcg per 0.1 mL. Roll gently.
Follistatin-344 is not approved for human administration. All cited studies measure endogenous serum follistatin as a biomarker, not as an exogenous therapeutic agent.
2. Injection site
Subcutaneous, abdomen or thigh. Rotate sites.
Resistance exercise combined with essential amino acid (EAA) supplementation elevated the follistatin/myostatin ratio by 15–25% in 12-week randomized trials. Protein intake (1.2–1.5 g/kg/day) synergizes with training to upregulate endogenous follistatin.
3. Timing
Pre-sleep preferred. Often combined with ipamorelin in the same syringe.
Serum follistatin and follistatin/myostatin ratio are used diagnostically in sarcopenia screening and as biomarkers of muscle anabolic balance in clinical trials.
4. Storage
Lyophilised: room temp, protected from light. Reconstituted: refrigerate 2–8 °C, use within 30 days.
Gene therapy and recombinant follistatin delivery are under preclinical investigation for muscular dystrophy and sarcopenia. No human safety or efficacy data for exogenous FST-344 administration.
5. Needle
29–31G, 4–8 mm insulin syringe.
—
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
Follistatin-344
+ BPC-157
Multi-pathwayFollistatin-344 (myostatin antagonist) and BPC-157 (tissue repair peptide) address complementary pathways in muscle recovery. FST-344 promotes muscle protein synthesis by disinhibiting myostatin signaling, while BPC-157 accelerates healing of tendons, ligaments, and microtears via angiogenesis and collagen synthesis. Combined, they may support both hypertrophy and structural repair during high-volume training or injury recovery.
- Follistatin-344
- No approved protocol — endogenous modulation via resistance exercise + EAA
- BPC-157
- 250–500 mcg SQ · twice daily · near injury site or systemic
- Duration
- 4–8 weeks
- Primary benefit
- Muscle hypertrophy + accelerated soft tissue repair
+ TB-500
ModerateTB-500 (thymosin beta-4 fragment) promotes cell migration, angiogenesis, and anti-inflammatory signaling in muscle and connective tissue. Follistatin-344's anabolic signaling may synergize with TB-500's regenerative effects during muscle damage or overtraining, particularly in older adults where both myostatin inhibition and tissue repair are rate-limiting.
- Follistatin-344
- Endogenous upregulation (resistance training + protein)
- TB-500
- 2–5 mg SQ · twice weekly · loading phase 4 weeks, then maintenance
- Frequency
- Twice weekly TB-500, daily training stimulus for FST
- Primary benefit
- Enhanced recovery, reduced inflammation, muscle growth support