Source comparison
CJC-1295 No DAC Receptor Pharmacology: Mechanism Comparison
Native GHRH 1-29 Type 1 GHRH receptor (anterior pituitary) ~2 nM <7 minutes None (natural sequence) Direct GPCR activation → cAMP → PKA → vesicular exocytosis Rapid degradation by DPP-IV limits therapeutic use. Serves as endogenous baseline for comparison CJC-
This comparison does not assign a generated winner or score.
- Native GHRH 1-29
- Type 1 GHRH receptor (anterior pituitary)
- ~2 nM
- <7 minutes
- None (natural sequence)
- Direct GPCR activation → cAMP → PKA → vesicular exocytosis
- Rapid degradation by DPP-IV limits therapeutic use. Serves as endogenous baseline for comparison
- CJC-1295 No DAC (Modified GRF 1-29)
- ~3 nM
- ~30 minutes
- Asp2Ala, Gln8Glu, Ala15Leu, Leu27Asp (DPP-IV resistance)
- Same GPCR cascade as native GHRH but with extended receptor occupancy window
- Extended half-life allows sustained receptor engagement through physiological pulse. Preferred for mimicking natural GH dynamics
- CJC-1295 DAC
- ~4 nM
- 6–8 days
- Drug Affinity Complex (lysine linkage to albumin)
- Prolonged receptor activation due to albumin binding and slow peptide release
- Non-physiological continuous receptor stimulation. Does not replicate pulsatile GH secretion and may downregulate receptors over time
- Ipamorelin
- Ghrelin receptor (GHS-R1a) on somatotrophs and hypothalamus
- ~50 nM
- ~2 hours
- Synthetic ghrelin mimetic (non-peptide core)
- GHS-R1a activation → calcium signaling independent of GHRH receptor
- Works via separate receptor pathway. Synergistic when combined with GHRH agonists but does not engage GHRH receptor pharmacology