Understand the source comparison
Hexarelin Cardiac GH Receptor Activation: Mechanism Comparison
Hexarelin CD36 + GHSR1a Partially (20–30%) High (Kd ~10 nM) 35–40% at 80 µg/kg Phase II halted GHRP-2 GHSR1a only Yes (>80%) None detected 10–15% at equivalent dose Research-grade only Ipamorelin Yes (>90%) <10% at equivalent dose GHRP-6 Minimal 12–18% at equi
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- Hexarelin
- CD36 + GHSR1a
- Partially (20–30%)
- High (Kd ~10 nM)
- 35–40% at 80 µg/kg
- Phase II halted
- GHRP-2
- GHSR1a only
- Yes (>80%)
- None detected
- 10–15% at equivalent dose
- Research-grade only
- Ipamorelin
- Yes (>90%)
- <10% at equivalent dose
- GHRP-6
- Minimal
- 12–18% at equivalent dose
- JMV-1843 (hexarelin analog)
- CD36 only (GHSR1a-null)
- No
- High (Kd ~8 nM)
- 30–35% at 100 µg/kg
- Preclinical
- Hexarelin's dual-receptor profile is the key differentiator. Compounds with exclusive GHSR1a activity produce modest cardioprotection only when GH release is intact, and the effect disappears in hypophysectomized animals. CD36-selective analogs like JMV-1843 replicate most of hexarelin's cardiac benefits without stimulating GH, confirming the receptor's central role. This receptor specificity is why hexarelin is the only GH secretagogue with published cardioprotective data in GH receptor knockout models. The others require intact GH signaling to show any cardiac phenotype.