Hexarelin Dosage & Cycle: Why It Gets Stacked With Ipamorelin
Hexarelin is a growth-hormone-releasing hexapeptide developed by the same research group behind GHRP-6, and it's unusual among GH secretagogues for hitting a second receptor entirely: CD36, a scavenger receptor on heart tissue tied to cardioprotection in animal models, independent of its GH-releasing effect. Its human evidence is real and specific: a 12-person multi-route dose-response trial and a completed 16-week chronic-dosing study that measured exactly how fast its GH-releasing effect fades with daily use, and that the fade fully reverses after stopping. That reversible fade is also why vendor and bodybuilding protocols almost universally pair it with a non-desensitizing secretagogue like Ipamorelin rather than running it alone.
Reviewed by the PepGuard team · Last reviewed Jul 28, 2026
Synthetic growth-hormone-releasing hexapeptide (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2), a dual agonist of the ghrelin receptor (GHS-R1a) and the CD36 scavenger receptor · also referred to as Examorelin, HEXA
Photo: Alexander Mass / UnsplashA GH secretagogue that also binds heart tissue.
Like GHRP-6 and ipamorelin, hexarelin triggers a growth hormone pulse by activating the ghrelin receptor (GHS-R1a). What sets it apart is a second target: CD36, a scavenger receptor found on heart tissue. In animal models of ischemia-reperfusion injury, hexarelin activates CD36 to protect cardiomyocytes through a pathway that's completely independent of its GH-releasing effect. That dual mechanism is real and mechanistically distinct, but it's also where the evidence for each half of hexarelin's reputation diverges sharply, see below.
What's been measured, acutely and over 16 weeks.
| What's cited | Range |
|---|---|
| Acute IV dose-response (Ghigo et al. 1994, n=12) | 1-2 mcg/kg; GH response roughly double that of an equal GHRH dose |
| Acute subcutaneous dose (same trial) | 1.5-3 mcg/kg; ~77% bioavailability relative to IV |
| Acute intranasal / oral dose (same trial, markedly lower bioavailability) | 20 mcg/kg intranasal (4.8% bioavailability); 20-40 mg oral (0.3% bioavailability) |
| Chronic dosing trial (Rahim et al. 1998, 16 weeks, subcutaneous, twice daily) | 1.5 mcg/kg per dose; GH response (AUC) fell from 19.1 to 10.5 mcg/L·h by week 16, fully reversed 4 weeks after stopping |
| Commonly cited cycling protocol (vendor/community, built around the tachyphylaxis finding above) | 100-200 mcg, 1-3 times daily, cycled 4-8 weeks on / 4 weeks off |
The two doses with real human trial data behind them measure very different things: an acute dose-response study establishing how much hexarelin triggers a GH pulse by different routes, and a chronic 16-week study measuring how much of that effect survives daily dosing over time. Neither is a bodybuilding protocol. The cycling patterns below are vendor and community conventions built directly around the chronic study's central finding, that the GH response fades with continuous use, not a clinically validated regimen.
Why Ipamorelin, specifically.
A completed 16-week human trial gave hexarelin twice daily and tracked the GH response the entire time. It fell from an AUC of 19.1 to 10.5 mcg/L·h by week 16, roughly a 45% drop, then fully recovered 4 weeks after stopping. That's a documented, reversible loss of effect from continuous use, not a guess.
That specific finding is the actual reason vendor and community protocols almost never run hexarelin alone long-term. Ipamorelin activates the same ghrelin receptor but is more selective and doesn't show the same rapid desensitization pattern, and it produces less of the cortisol and prolactin rise that hexarelin's lower receptor selectivity causes. Stacking the two, or cycling hexarelin on and off, is a direct response to a real trial result, even though the specific stacking and cycling schedules themselves haven't been tested in a trial.
Less selective than newer secretagogues, and it shows.
| Signal | Frequency | Context |
|---|---|---|
| Transient rise in cortisol and prolactin | commonly reported | Documented across the human PK studies cited on this page. Hexarelin is less receptor-selective than newer secretagogues like ipamorelin, which is the specific mechanistic reason it produces more of this than they do. |
| Increased hunger | commonly reported | Consistent with ghrelin-receptor agonism generally, not unique to hexarelin. |
| Progressive loss of GH-releasing effect with continuous daily use (tachyphylaxis) | commonly reported | Directly measured in the 16-week human trial: GH response (AUC) fell by roughly 45% by week 16 of twice-daily dosing, then fully recovered 4 weeks after stopping. |
| Cardiac effects in humans | unknown / not studied | Hexarelin's CD36-mediated cardioprotection is established in animal ischemia-reperfusion models. No completed human cardiac-outcome trial exists, despite hexarelin briefly reaching Phase II development for cardiac-related indications. |
| Long-term safety of repeated on/off cycling protocols | unknown / not studied | The only long-duration human trial ran 16 continuous weeks. No study has tested the on/off cycling patterns vendors recommend specifically to work around tachyphylaxis. |
Not FDA-approved. Reached Phase II development for GH-deficiency diagnosis before being discontinued. Not found on any current FDA 503A compounding list.
No hexarelin product has ever been approved by the FDA. It was developed and studied through Phase II clinical trials, primarily as a diagnostic tool for growth hormone deficiency, with its CD36-mediated cardioprotective mechanism explored separately, but it was never advanced to an approved product or marketed drug. We checked directly against FDA's current 503A Category 1, Category 2, and withdrawn-nomination documents and could not find hexarelin listed on any of them, unlike its close chemical relative GHRP-2, which the FDA does restrict. The public record doesn't explain that gap, so treat hexarelin's absence from these lists as a regulatory blind spot, not a clean bill of health.
See the GHRP-2 report for the FDA’s specific safety finding on that compound, and the one country where a member of this peptide family is actually an approved drug.
Every claim above, traced back.
Two primary human trials (acute multi-route dosing and 16-week chronic dosing), the CD36 mechanism paper and a cardiovascular review, and current FDA compounding records. Click through and check them yourself.
Hexarelin questions, answered.
No. It reached Phase II development, mainly as a diagnostic tool for growth hormone deficiency, but was never approved or marketed. It doesn't appear on any of FDA's current 503A compounding lists at all, unlike its close chemical relative GHRP-2, which the FDA does restrict, a gap the public record doesn't explain. See our GHRP-2 report for that compound's own regulatory story.
Because a real 16-week human trial measured what happens if you don't: the GH response fell by roughly 45% by week 16 of twice-daily dosing. The same trial found that effect fully reversed 4 weeks after stopping, which is the direct evidence behind the on/off cycling protocols vendors recommend, even though those specific cycling schedules haven't themselves been tested in a trial.
It's a direct response to hexarelin's documented tachyphylaxis. Ipamorelin is a more receptor-selective secretagogue that doesn't show the same rapid desensitization pattern, and produces less of the cortisol and prolactin rise that hexarelin's lower selectivity causes. Pairing the two is a community workaround for hexarelin's specific, trial-documented weakness, not an arbitrary combination.
There's a real, distinct mechanism behind that claim: hexarelin binds CD36, a receptor on heart tissue, independent of its GH-releasing effect, and this has been shown to protect against ischemia-reperfusion injury in animal models. No completed human trial has tested cardiac outcomes in people, so the cardioprotective claim is real at the mechanism level and unproven at the human-outcome level.
Keep researching.
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