Source comparison
CJC-1295 No DAC & Ipamorelin: Comparison Table
Primary Mechanism GHRH receptor agonist. Extends GH pulse duration and amplitude Ghrelin receptor agonist (GHS-R1a). Increases GH pulse frequency and intensity Complementary pathways. One extends pulse, one amplifies peak The combination mimics natural pulsati
This comparison does not assign a generated winner or score.
- Primary Mechanism
- GHRH receptor agonist. Extends GH pulse duration and amplitude
- Ghrelin receptor agonist (GHS-R1a). Increases GH pulse frequency and intensity
- Complementary pathways. One extends pulse, one amplifies peak
- The combination mimics natural pulsatility better than either alone
- Half-Life
- ~30 minutes (clears within 2–4 hours)
- ~2 hours (clears within 4–6 hours)
- Both short-acting. Preserves pulsatile pattern
- Short half-lives prevent receptor desensitization
- Cortisol Impact
- Minimal. GHRH pathway doesn't activate HPA axis
- None. Selective GHS-R1a binding avoids cortisol release
- No cortisol elevation when dosed correctly
- This selectivity is why ipamorelin replaced GHRP-2 in most protocols
- IGF-1 Elevation
- 20–40% above baseline (monotherapy)
- 15–30% above baseline (monotherapy)
- 30–60% above baseline (combination)
- Combination produces additive, not merely synergistic, IGF-1 response
- Typical Dosing
- 100–200 mcg per dose, 1–2x daily
- Both peptides same dose, same timing
- Dosing must preserve pulsatility. Continuous administration fails