Source comparison
CJC-1295 no DAC & Ipamorelin History: Comparison
Mechanism of Action GHRH receptor agonist; increases cAMP and GH transcription GHS-R1a agonist; mobilizes intracellular calcium and amplifies GH burst amplitude Dual-pathway activation: priming (GHRH) + trigger (ghrelin mimetic) The combination exploits comple
This comparison does not assign a generated winner or score.
- Mechanism of Action
- GHRH receptor agonist; increases cAMP and GH transcription
- GHS-R1a agonist; mobilizes intracellular calcium and amplifies GH burst amplitude
- Dual-pathway activation: priming (GHRH) + trigger (ghrelin mimetic)
- The combination exploits complementary signaling for amplified GH release. Not merely additive
- Half-Life
- ~30 minutes (DPP-IV resistant but no albumin binding)
- ~2 hours (longer than GHRH, shorter than with DAC)
- N/A. Both clear within 4–6 hours post-injection
- Short half-lives preserve pulsatile dynamics and reduce tonic receptor occupancy
- Typical Research Dose
- 100–200 mcg per injection, 1–3× weekly
- 200–300 mcg per injection, 1–3× weekly
- 100 mcg CJC + 200 mcg Ipamorelin, 2–3× weekly
- Combined doses are lower than monotherapy equivalents due to synergy
- Off-Target Effects
- Minimal; no cortisol or prolactin elevation
- Minimal; designed specifically to avoid ACTH and prolactin pathways
- Minimal when dosed appropriately
- Ipamorelin's selectivity profile was the breakthrough that enabled clean combination protocols
- Year Introduced
- ~2008 (derived from CJC-1295 with DAC, 2005)
- 1998 (commercial synthesis); widespread research use post-2004
- ~2012–2015 as a deliberate combination strategy
- Ipamorelin predates CJC-1295 by seven years. Their convergence was retrospective, not planned
- IGF-1 Elevation (Monotherapy)
- 30–50% increase from baseline in human studies
- 25–40% increase from baseline in human studies
- 50–80% increase in observational case series
- The combined protocol achieves IGF-1 elevation comparable to low-dose rhGH but with preserved pulsatility