Hexarelin (Examorelin)
Hexarelin (examorelin) — evidence, the CD36 cardiac story & status

Class: peptide
Synonyms: Hexarelin
INN examorelin
developer code EP 23905
Function tags: GH secretagogue / ghrelin agonist
cardiac (CD36)
(studied:) GH deficiency, heart failure — research context
Overall evidence grade: B
WADA prohibited: yes
WADA note: Sport: WADA-prohibited at all times — Section S2.2 (GH secretagogues).
Last updated: 2026-07-11

In brief: Hexarelin (examorelin) is the most potent classic GHRP and the most distinctive — uniquely, alongside the ghrelin receptor it binds the cardiac CD36 receptor, producing direct cardioprotective effects independent of GH (documented even in GH-deficient models, and abolished in CD36-knockouts). It reached Phase 2 for both GH deficiency and heart failure but was never approved. The cardiac biology is genuinely interesting and legitimate — but it is preclinical/early, and the popular anti-aging use is untested in humans. Banned in sport.

## Identity a synthetic **hexapeptide** (6 amino acids, < 40 aa → peptide) derived from **GHRP-6** by a **D-2-methyltryptophan** substitution that boosts potency and metabolic stability. Uniquely among GHRPs, it engages **two** receptors: the ghrelin receptor **GHS-R1a** (for GH release) and the cardiac scavenger receptor **CD36**. ## Development & history - Developed in the **early 1990s by Romano Deghenghi** at **Europeptides** (Argenteuil, France) and **Mediolanum Farmaceutici** (Italy) — Deghenghi being a central figure in GHRP chemistry.
- Reached **Phase 2** clinical trials for **both** GH-deficiency (diagnosis/therapy) **and** congestive heart failure — but did **not advance to Phase 3** and was **never marketed.** ## Mechanism (as proposed) through **GHS-R1a** (the ghrelin receptor) on pituitary somatotrophs → GH release and downstream IGF-1 (like all GHRPs). Separately, through **CD36** on cardiomyocytes → activation of PI3K/Akt and ERK1/2 pro-survival signalling → protection from ischemic apoptosis, improved contractility and reduced fibrosis — **independent of GH.** This dual-receptor engagement is unique among GH secretagogues.

Evidence grades by outcome:
outcome: GH release
grade: B
base: Most potent GHRP (~10× GHRP-6); human PK
effect: Strong, sustained GH pulse
caveat: Real, potent pharmacology; GH response desensitises with continuous use
outcome: Cardioprotection (CD36, GH-independent)
grade: C
base: Preclinical (infarct ↓40–60%, LV function ↑, anti-fibrotic; CD36-KO abolishes it) + incomplete Phase 2
effect: Genuine, mechanistically distinct
caveat: Preclinical / early; Phase 2 didn't complete; not an established therapy
outcome: Metabolic / "fat-burning" (CD36 / adipocyte)
grade: C
base: Preclinical (Rodrigue-Way 2007)
effect: Mitochondrial biogenesis
caveat: Preclinical
outcome: Anti-aging / body composition (the popular use)
grade: F
base: None in humans
effect: Not demonstrated
caveat: Untested for these goals
outcome: Safety
base: Research + PK data
effect: Characterised (short-term)
caveat: Raises cortisol/prolactin; GH desensitisation; WADA-banned

Legal status:
region: INT
status: See note
note: - Everywhere — not approved for human therapeutic use (Phase 2 reached, never marketed). Research compound. Not FDA-approved, and reportedly not on the FDA Category-2 list (a slightly different position from GHRP-2/6).
- ⚠ Sport: WADA-prohibited at all times — Section S2.2 (GH secretagogues).

Cosmetic claims:

Note: Reference entry — not sold here. The most potent of the classic GHRPs and the most pharmacologically distinctive — the only one that also acts on a cardiac receptor, with effects independent of growth hormone. No dosing published here.

Sources:
Bodart V, Ong H, et al. CD36 mediates the cardiovascular action of growth-hormone-releasing peptides in the heart. Circ Res. 2002. (CD36 identification)
Locatelli V, Rossoni G, Deghenghi R, et al. Growth-hormone-independent cardioprotective effects of hexarelin in the rat. Endocrinology. 1999.
Rodrigue-Way A, et al. A GHRP promotes mitochondrial biogenesis and a fat-burning phenotype through CD36 in white adipocytes. Endocrinology. 2007.