Hexarelin

All three are ghrelin/GHS-R1a agonists, but hexarelin is more potent per microgram and adds a cardiac CD36 interaction the others lack. GHRP-6 (its parent peptide) drives noticeably more hunger, while Ipamorelin is the cleaner option for cortisol and prolactin. Hexarelin's trade-off is a stronger tendency toward desensitization with daily use.

Yes, and this is its main limitation. Rahim and Shalet dosed healthy elderly subjects twice daily for 16 weeks and saw the GH response decline significantly over time [3]. The good news is that the attenuation was partial and reversible: responsiveness returned after a treatment-free break. This is why research protocols favor intermittent dosing and defined cycles rather than continuous daily use.

Human studies used 1-2mcg/kg by intravenous or subcutaneous bolus, which translates to roughly 100mcg once or twice daily subcutaneously in practical research protocols. Intranasal and oral routes are active but need much larger doses for the same GH rise due to low bioavailability [1]. Subcutaneous injection is the standard research route.

Plasma half-life is about 55 minutes. GH typically peaks near 30 minutes after a dose and returns to baseline within roughly 4 hours. Rodent pharmacokinetic work reported a comparable intravenous half-life of around 76 minutes with rapid clearance [7].

It can produce mild, transient rises in ACTH, cortisol, and prolactin, more than a selective agent like Ipamorelin but generally modest at research doses. Notably, exogenous GH feedback does not suppress the GH response to hexarelin in normal men, which points to a mechanism acting above the usual somatostatin brake [8].

Hexarelin binds CD36 on cardiomyocytes and, in rodent models, raises coronary perfusion pressure and protects heart tissue from ischemia/reperfusion injury through interleukin-1 signaling [2,6]. These effects are GH-independent and genuinely interesting, but the evidence is preclinical. Hexarelin is not an established cardiac therapy in humans.