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Hexarelin6 residues (approx.)HAWFKEach bubble = one amino acid. Size = residue mass. Color = chemical class.Uses closest standard amino acids for non-standard residues.Also known as: Examorelin, HEX, EP-23905
Six amino acids produce the largest growth hormone pulse of any secretagogue ever tested in humans. Hexarelin (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2) is a synthetic growth hormone releasing peptide that hits both the pituitary GHS-R1a receptor and a separate cardiac CD36 receptor, giving it a dual action profile no other GHRP shares. It reached Phase II clinical trials for GH deficiency and congestive heart failure in the 1990s before development stopped. The tradeoff is real: hexarelin raises cortisol and prolactin more than GHRP-2 or GHRP-6, and receptor desensitization limits continuous use to roughly four weeks. Experienced users run it in short, intense cycles stacked with a GHRH for maximum output.
The strongest GH pulse any secretagogue can produce from a single subcutaneous injection. That claim isn't marketing; Ghigo and colleagues confirmed it in a controlled dose-response study across multiple routes of administration [1]. Hexarelin is a synthetic hexapeptide GHS-R1a agonist, sometimes listed under CAS 140703-51-1, that mimics ghrelin at both the pituitary and hypothalamus to trigger growth hormone release. What makes hexarelin different from ipamorelin, GHRP-2, or GHRP-6 is the CD36 scavenger receptor. Bodart and colleagues identified this second binding site on cardiomyocytes in 1999 [2]. Through CD36, hexarelin produces anti-fibrotic cardiac effects and preserves cell contractility during ischemia, completely independent of the GH axis. No other GHRP has this dual receptor profile. The practical reality is a 4-week ceiling. Hexarelin's high GHS-R1a binding affinity drives receptor downregulation faster than any other peptide in this class. Community protocols converge on 4 weeks on, 2 to 4 weeks off, with many users adding 5-on/2-off weekly cycling within each block to slow desensitization further. The typical stack pairs 100 to 200 mcg hexarelin with 100 mcg CJC-1295 (no DAC) co-injected subcutaneously at bedtime. About 311 PubMed papers cover hexarelin. Most are mechanistic or short-term pharmacological work, not long-term therapeutic trials. It reached Phase II for adult GH deficiency and heart failure before development was abandoned, likely because desensitization made chronic dosing impractical. It was never submitted for FDA approval and remains a research-only compound. Community experience across dozens of Reddit threads tracks closely with the published pharmacology; the 100 to 200 mcg per injection dosing range is where most users land.
Hexarelin binds GHS-R1a at the anterior pituitary with higher affinity than any other growth hormone releasing peptide. That binding triggers a calcium-dependent signaling cascade in somatotroph cells, producing a GH pulse within 30 minutes of subcutaneous injection. Unlike ipamorelin, which is selective for GHS-R1a, hexarelin also activates ACTH release from the pituitary. This cross-reactivity explains the cortisol and prolactin elevations that Popovic and colleagues documented at doses equivalent to GHRP-2 [3]. The second receptor is what sets hexarelin apart. Bodart's group identified CD36, a scavenger receptor expressed on cardiomyocytes, as a direct hexarelin binding target [2]. Through CD36, hexarelin reduces cardiac fibrosis, preserves cell shortening during ischemia-reperfusion injury, and regulates intracellular calcium handling. A 2018 mouse study confirmed that hexarelin treatment preserves myocardial function and reduces fibrosis after acute myocardial infarction [4]. These cardiac effects operate entirely independently of GH release. Plasma half-life runs approximately 55 to 70 minutes after subcutaneous injection, with GH peak occurring around 30 minutes post-dose. Oral bioavailability is only about 0.3%, making subcutaneous injection the only practical route. The short half-life means each injection produces a discrete GH pulse rather than sustained elevation; that pulsatile pattern mimics natural physiology better than continuous GH administration.
Most potent GHS-R1a agonist of any GHRP in human studies: confirmed in dose-response trials [1]. Reached Phase II clinical trials for adult GH deficiency and congestive heart failure (1990s); development discontinued, likely due to desensitization limiting long-term utility. Never FDA-approved. CD36-mediated cardioprotective mechanism confirmed in vitro and in rodent models (28321024)[2], not validated in human clinical endpoints. Cortisol and prolactin elevation more pronounced than GHRP-2 or GHRP-6 [3]. ~311 PubMed papers; the majority are mechanistic or short-term pharmacological studies, not therapeutic RCTs.
Ghigo et al. 1994 (PMID 8126144): dose-response and route comparison in healthy men; established SC efficacy and dose ceiling. Bodart et al. 1999 (PMID 10532947): identified CD36 as the cardiac hexarelin receptor independent of GHS-R1a. Popovic et al. 1995 (PMID 9285939): confirmed cortisol/ACTH/prolactin elevation greater than GHRP-2 at equivalent doses.
No long-term therapeutic RCT for SC dosing. Desensitization mechanism documented in animals; formal human desensitization kinetics unpublished. Oral bioavailability ~0.3% (clinical trial data): not a practical route. SC bioavailability not formally quantified in humans (estimated 60-70% from mechanistic extrapolation). All cardioprotective data from animal models or in vitro: no human clinical endpoints confirmed.
Highly respected but niche and considered an advanced GHRP. Strong consensus on it producing the largest GH pulse of any GHRP ("nothing else touches it for raw GH output") but most experienced users ultimately migrate to ipamorelin for long-term use due to cleaner hormonal profile and no desensitization. Hexarelin is reserved for short, intense cycles where maximum GH output is the priority. CD36 cardioprotective mechanism is frequently cited as a unique differentiator.
Science and community agree on GHS-R1a mechanism, strongest GH pulse among GHRPs, cortisol/prolactin elevation, and the principle of receptor desensitization requiring cycling. Community has independently converged on 4-week on/off cycling and the CJC-1295 no DAC stack: both mechanistically justified. Community SC dosing (100-300 mcg) extrapolates beyond any published clinical therapeutic RCT; 300 mcg 2×/day exceeds clinical dose-response ceiling.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Daily |
| Moderate | 200mcg | 2x Daily |
| Aggressive | 300mcg | 2x Daily |
Stack hexarelin with a GHRH, not another GHRP. The single most common mistake is pairing it with ipamorelin or GHRP-2. Both hit the same GHS-R1a receptor. You're wasting one compound. The correct partner is CJC-1295 (no DAC) or sermorelin, co-injected simultaneously. Reconstitution math for a 5mg vial: add 2 mL bacteriostatic water. That gives you 2,500 mcg/mL. On a U-100 insulin syringe, 4 units equals 100 mcg, 8 units equals 200 mcg, 12 units equals 300 mcg. For a 2mg vial with 2 mL BAC water, you get 1,000 mcg/mL; 10 units equals 100 mcg. Fasting compliance matters more with hexarelin than most peptides. Carbohydrates and fats raise somatostatin, which blunts the GH pulse considerably. No food 30 minutes before or after injection at minimum. Two hours post-meal is better. If your IGF-1 isn't moving after 4 weeks, check your fasting window before blaming the product. Refrigerate reconstituted vials and use within 3 to 4 weeks.
Hexarelin desensitizes GHS receptors with continuous use. Cycle 4 weeks on, 2-4 weeks off to maintain GH responsiveness. Some protocols use 5 days on, 2 days off within each on-cycle week.
Hexarelin has the highest GHS-R1a binding affinity of any GHRP. This high-affinity binding drives GHS-R1a downregulation and β-arrestin-mediated receptor internalization faster than any other peptide in this class. Desensitization of the GH pulse is the primary documented failure mode with continuous hexarelin use: onset typically within 4-6 weeks of daily dosing, with the community converging on a strict 4-week on / 2-4 week off protocol as the standard cycling approach. The 5-on/2-off within each week is a secondary mitigation strategy layered on top of the 4-week gross cycle. No long-term human receptor density data exists; the cycling rationale is mechanistically sound but the specific off-period duration is community convention rather than clinically validated.
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Expected: Sleep quality improvement within weeks 1-2; recovery improvement by weeks 2-3; modest body composition changes (reduced abdominal fat, improved muscle fullness) by end of 4-week cycle
Monitor: Baseline IGF-1 before starting; recheck at week 4. Fasting glucose at baseline.
For a 5mg vial, slowly inject 2 mL bacteriostatic water down the inside wall of the vial. Do not shake. Swirl gently until the powder dissolves completely. This gives you 2,500 mcg per mL.
Draw your dose using a U-100 insulin syringe (29-31 gauge, 0.5 inch needle). For 100 mcg, draw to the 4-unit mark. For 200 mcg, draw to 8 units. For 300 mcg, draw to 12 units.
Choose your injection site: abdomen (2 inches from the navel) or the fatty tissue on the outer thigh. Rotate sites with each injection.
Pinch a fold of skin, insert the needle at a 45-degree angle, inject slowly, hold for 5 seconds, then withdraw.
Best timing is 30 to 60 minutes before bed to amplify the natural nocturnal GH pulse. For twice-daily protocols, the morning dose should be on waking and fully fasted. Keep a minimum of 3 to 4 hours between injections.
If stacking with CJC-1295 (no DAC), draw both peptides into the same syringe and co-inject simultaneously. Do not pre-mix vials.
Store the reconstituted vial in the refrigerator at 2 to 8 degrees Celsius. Use within 3 to 4 weeks. Never freeze reconstituted solution.
Primary and near-universal stack. GHRH (CJC-1295 no DAC) + GHRP (hexarelin) activates dual pituitary receptor pathways, GHRHR + GHS-R1a, producing a synergistic GH pulse significantly larger than either alone. Co-injected simultaneously to capture the synergistic window.
100 mcg CJC-1295 (no DAC) co-injected with 100-200 mcg hexarelin SC, once or twice daily, fasted
Lower-cost alternative GHRH for the hexarelin stack. Shorter half-life than CJC-1295 (no DAC), otherwise similar synergistic mechanism via GHRHR activation. Preferred by users seeking lower cost or softer GHRH stimulus.
100-300 mcg sermorelin + 100-200 mcg hexarelin SC, co-injected, once or twice daily fasted
Concurrent tissue repair stack: separate mechanism from GH pathway. GH elevation from hexarelin complements BPC-157 angiogenic and healing signaling in injury recovery protocols. Often used in the intermediate/advanced cycle off-period or alongside.
Systemic recovery stack. TB-500 actin-binding and cell migration support combined with hexarelin GH-mediated anabolic signaling in injury and post-surgery recovery protocols.
Both hexarelin and ipamorelin bind the same GHS-R1a receptor. Co-administration provides no additive GH benefit and accelerates receptor desensitization. Choose one GHRP and stack it with a GHRH peptide instead: the most common hexarelin mistake per community consensus.
Do not combineSame GHS-R1a receptor. Hexarelin already has the highest binding affinity and cortisol/prolactin elevation of any GHRP: combining with GHRP-2 compounds these side effects with no additional GH benefit from dual GHS-R1a occupancy.
Do not combineSame GHS-R1a receptor. Stacking hexarelin + GHRP-6 is redundant. GHRP-6 adds intense hunger stimulation and cortisol burden with no additive GH benefit over hexarelin alone.
Do not combineCombining GH secretagogues with exogenous recombinant HGH saturates the GH/IGF-1 axis and suppresses endogenous pulsatility. Eliminates the primary rationale for secretagogue use. Dramatically increases IGF-1 overshoot risk.
Do not combinePricing updated 2026-04-09
Cortisol and prolactin elevation are the primary safety concerns with hexarelin, and they're more pronounced than with any other GHRP. Popovic's group confirmed this directly against GHRP-2 at equivalent doses [3]. At the beginner 100 mcg once daily dose, the cortisol bump is transient and typically returns to baseline within 2 to 3 hours post-injection. At the aggressive 300 mcg twice daily protocol, the cumulative cortisol burden becomes clinically meaningful. Users at that dose level report disrupted sleep, increased irritability, and changes in fat distribution that track with chronic cortisol elevation. Prolactin follows a similar dose-dependent pattern. At lower doses, the spike is brief and unlikely to produce symptoms. At higher doses and twice-daily frequency, prolactin can rise enough to affect libido and, in rare cases, produce early gynecomastia signs. Checking prolactin at baseline and at week 4 is standard practice for anyone running intermediate or advanced protocols. Some users add low-dose cabergoline during aggressive cycles, though clinical backing for that approach in this context is thin. GHS-R1a receptor desensitization is not a side effect in the traditional sense, but it is the most common reason hexarelin "stops working." High-affinity binding drives beta-arrestin-mediated receptor internalization faster than GHRP-2, GHRP-6, or ipamorelin. The community figured this out before any formal study characterized the kinetics in humans. Four weeks of continuous daily dosing is the practical limit; beyond that, GH pulse magnitude drops noticeably. Receptor density recovers over 2 to 4 weeks off. Water retention and mild edema are common GH-class effects. At higher doses, fluid accumulation in the carpal tunnel can produce hand tingling, numbness, or grip weakness. These are early carpal tunnel symptoms. If they persist beyond a few days at a reduced dose, stopping the cycle entirely and allowing 4 or more weeks for resolution is the right call. Appetite increase occurs through the ghrelin pathway. It's less intense than GHRP-6, but still present, especially at 200 mcg and above. This can actually disrupt the fasting window required for proper dosing if not managed. Shifting the bedtime dose to 3 or more hours after dinner helps. Post-injection flushing and tingling within 10 to 20 minutes is a GH flush effect and is harmless. It's actually a useful signal: when the flush stops appearing in later weeks, it often indicates desensitization has begun. Hexarelin has not been studied in pregnant or breastfeeding individuals. GH and IGF-1 elevation carry theoretical risks for fetal development and should be avoided entirely. Anyone with active malignancy, pituitary tumors, intracranial hypertension, or uncontrolled diabetes should not use hexarelin. GH elevation impairs glucose tolerance and may promote tumor growth through the IGF-1 axis. When to see a doctor: persistent carpal tunnel symptoms beyond one week, fasting glucose climbing above 125 mg/dL, any signs of prolactin elevation (libido changes, breast tissue changes), or edema that doesn't resolve with dose reduction.
Verify Hexarelin dosing and safety with a second opinion
Hexarelin is a 6-amino-acid synthetic peptide (MW ~888 Da): synthesis is relatively straightforward for established peptide manufacturers. No GMP requirement applies to "research use only" peptide vendors. The compound is genuine GH axis-active; underdosed or impure product produces a measurably blunted IGF-1 response (objectively testable). Pricing range ($14-35 for 2mg; $45-76 for 5mg) indicates moderate market competition with the typical quality variance seen in research peptide categories.
| Test | When | Target |
|---|---|---|
| IGF-1 | Baseline before starting; repeat at week 4 (end of on-cycle) | Age-adjusted normal range: not supraphysiological. Flag if above upper limit of normal. |
| Fasting glucose | Baseline; repeat at week 4; weekly if pre-diabetic | <100 mg/dL (normal); 100-125 mg/dL warrants dose reduction and closer monitoring |
| Prolactin | Baseline; repeat at week 4 if libido changes or gynecomastia signs emerge | Normal laboratory reference range for sex |
| AM cortisol | Baseline; repeat at week 4 if cortisol symptoms emerge (disrupted sleep, fat gain, irritability) | Normal AM cortisol range (approximately 6-23 mcg/dL at 8 AM) |
| Thyroid (TSH, fT3, fT4) | Baseline; repeat at week 12 of ongoing protocols if symptoms emerge | — |
Primary efficacy marker for sustained GH axis activation. Confirms product quality and dosing adequacy. Detects over-response requiring dose reduction. IGF-1 responds to consistent pulsing within 2-4 weeks.
GH release antagonizes insulin action. Hexarelin-induced cortisol co-elevation further impairs glucose tolerance at higher doses. Essential in any individual with insulin resistance history.
Hexarelin raises prolactin more than any other GHRP (PMID 9285939). Returns to baseline within 2-3h post-injection but at high frequency (2×/day) cumulative elevation may become symptomatic. Relevant especially at intermediate/advanced doses.
Hexarelin produces the strongest cortisol/ACTH elevation of any GHRP. At aggressive doses and 2× daily frequency, cumulative cortisol burden can become clinically relevant for fat distribution, sleep, and immune function.
GH accelerates T4-to-T3 conversion. Untreated hypothyroidism blunts GH response; GH axis activation can unmask subclinical hypothyroidism.
Initial GH pulse detectable within 30 minutes of first dose. Mild hunger increase and possible facial flushing. Sleep quality may begin to improve with evening dosing.
Consistent GH and IGF-1 elevation. Noticeable appetite increase. Mild water retention and potential tingling or numbness at higher doses.
Recovery benefits become apparent. Fat loss and improved sleep solidify. Cortisol and prolactin effects may be noticeable at aggressive doses.
Peak GH response before receptor desensitization sets in. Best body composition changes observed. Transition to off-cycle period recommended.
GHS receptor sensitivity resets over 2-4 weeks. Most body composition gains are retained. GH and IGF-1 gradually return toward baseline.
Days 1 to 3, Initial GH pulse. The GH spike hits within 30 minutes of your first subcutaneous injection, per pharmacokinetic data from Ghigo's 1994 study [1]. Most users notice a warmth and tingling sensation 10 to 20 minutes post-injection. That's the GH flush. Sleep quality often starts improving within the first 2 to 3 doses if you're dosing at bedtime. Mild appetite increase kicks in through the ghrelin pathway. Some users report facial flushing at higher starting doses. Cortisol and prolactin both elevate transiently but return to baseline within 2 to 3 hours. Weeks 1 to 2, GH and IGF-1 climbing. Consistent GH pulsing with each injection drives IGF-1 upward, measurable on bloodwork by week 2 to 4. Sleep quality improvement solidifies. Recovery between training sessions gets noticeably faster. Mild water retention is common. The appetite bump post-injection is manageable at beginner doses but more pronounced at 200 mcg twice daily. Tingling in extremities may appear at higher doses from GH-mediated fluid retention. Weeks 2 to 3, peak response window. This is where body composition changes start showing. GH-mediated lipolysis and IGF-1 anabolic signaling have been accumulating for two weeks. Reduced abdominal fat and improved muscle fullness become visible. Recovery from training is well established. If you're running continuous daily dosing without 5-on/2-off weekly breaks, the GH response per injection may already be diminishing. Cortisol and prolactin effects become more noticeable at the 300 mcg aggressive dose level. Week 4, desensitization threshold. Best body composition results of the cycle are typically visible at this point. The post-injection flush and tingling that was strong in weeks 1 to 2 starts fading. That's not tolerance in the casual sense; it's GHS-R1a receptor downregulation from high-affinity binding. The community strongly recommends transitioning to the off-cycle here. Extending beyond 4 weeks produces diminishing returns with the same side effect burden. Weeks 5 to 8, off-cycle recovery. Hexarelin clears plasma within hours of the last injection (half-life roughly 70 minutes). GHS-R1a receptor density recovers over 2 to 4 weeks off. The good news: body composition gains from the 4-week cycle are largely retained for 4 to 6 weeks post-cycle. Sleep quality may dip modestly compared to on-cycle. Appetite returns to baseline within days. Water retention resolves. IGF-1 gradually returns toward pre-cycle levels. Most users plan their next cycle after a full 4-week off period.
GH pulse detectable within 30 min of SC injection per PK data (PMID 8126144). GH promotes slow-wave sleep architecture. Cortisol and prolactin transient elevation returns to baseline within 2-3h post-injection.
Post-injection warmth and tingling within 10-20 min is common (GH flush effect). Sleep improvement often noticed within first 2-3 doses. Mild appetite increase. Some users report facial flushing at higher doses.
Consistent GH pulsing with each injection. IGF-1 begins rising, measurable by week 2-4. GH stimulates slow-wave sleep. Cortisol and prolactin elevation remains transient per injection (PMID 9285939).
Consistent sleep quality improvement with bedtime dosing. Recovery from training noticeably faster. Mild water retention. Appetite increase manageable. Users at 200 mcg 2×/day begin noticing recovery gains.
GH-mediated lipolysis and IGF-1 anabolic signaling accumulate. GHS-R1a desensitization beginning to develop with continuous daily use without 5-on/2-off cycling.
Body composition improvements become visible: reduced abdominal fat, improved muscle fullness. Recovery solidified. Users on continuous protocols (no weekly breaks) start noticing diminishing post-injection response. Cortisol/prolactin effects more noticeable at 300 mcg aggressive doses.
GHS-R1a receptor downregulation progresses with continuous use; peak GH pulse per injection declining. Best timepoint to transition to off-cycle to allow receptor recovery.
Best body composition changes of the cycle visible at week 4. Post-injection flush/tingling diminishing (sign of receptor desensitization). Community strongly recommends not extending beyond this point.
Short plasma half-life (~70 min) means compound clears within hours of last injection. GHS-R1a receptor density recovers over 2-4 weeks off.
Body composition gains (lean mass, reduced fat) largely retained for 4-6 weeks post-cycle. Sleep quality may decline modestly vs. on-cycle. Most users plan next cycle after 4 weeks off. IGF-1 returns toward baseline.
Source: Human plasma t½ ~55-70 min (Ghigo et al. 1994, PMID 8126144; rat IV t½ 75.9 min, PMID 10611139)
Loading the interactive decay curve.
Hexarelin has never received FDA approval for any indication. It reached Phase II clinical trials in the 1990s for GH deficiency and congestive heart failure, but development was discontinued before any regulatory submission. It is currently classified as a research-only compound in the United States. Hexarelin is not on the FDA 503A bulk drug substances list, which means US compounding pharmacies cannot legally prepare it for human use. It falls under Category 2 of FDA compounding oversight. RFK Jr. announced intent on February 27, 2026, to reclassify approximately 14 Category 2 peptides, but no formal Federal Register rulemaking had been published as of April 2026. The compound is available from research peptide vendors as a "for research use only" product. WADA prohibits all growth hormone releasing peptides, including hexarelin, under Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Athletes subject to anti-doping testing should not use this compound. This content is for informational purposes only. Hexarelin is not approved for human therapeutic use. Consult a qualified healthcare provider before considering any peptide protocol.
Peptide Schedule Research TeamReviewed Apr 20266 Citations
