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GHRP-26 residues (approx.)AAWFKEach bubble = one amino acid. Size = residue mass. Color = chemical class.Uses closest standard amino acids for non-standard residues.Also known as: pralmorelin, GHRP Kaken 100, KP-102
A 38% drop in GH response after just five days of continuous use. That single data point from Ghigo et al. [1] tells you everything about GHRP-2: it hits hard and fast, but the pituitary adapts quickly. GHRP-2 (pralmorelin) is a synthetic hexapeptide that binds GHS-R1a, the ghrelin receptor, to trigger a potent growth hormone pulse. Japan approved it in 2004 as a one-time diagnostic agent for GH deficiency testing. No therapeutic approval exists anywhere. Athletes and anti-aging users favor it for the strongest per-injection GH spike among commonly available GHRPs, paired with a GHRH peptide and strict cycling to outrun desensitization.
A 38% decline in peak GH response from day one to day five. That finding from a Ghigo et al. study of healthy adults dosed at 100 mcg/day subcutaneous [1] shaped how experienced users run GHRP-2 today. GHRP-2, also called pralmorelin (CAS 158861-67-7), is a synthetic hexapeptide growth hormone secretagogue. It binds GHS-R1a on pituitary somatotrophs, mimicking ghrelin to trigger a rapid, dose-dependent GH pulse. Compared to GHRP-6, it produces a stronger GH spike per unit dose with less appetite stimulation and lower cortisol and prolactin elevation. Compared to ipamorelin, the GH output is higher but comes with mild hormonal side effects that ipamorelin avoids. The practical community protocol runs 100 to 200 mcg subcutaneous two to three times daily on an empty stomach, co-injected with CJC-1295 (no DAC) for complementary GHRH + GHRP stimulation. That combination produces two to three times the GH pulse of either peptide alone, according to consistent user reports across hundreds of Reddit threads. Cycling is mandatory: 5 days on, 2 days off within each week, plus 8 weeks on, 4 weeks off for the gross cycle. Japan's PMDA approved GHRP-2 (brand name GHRP Kaken 100) in 2004 as a single-dose IV diagnostic agent for GH deficiency. No country has approved it therapeutically. Over 200 PubMed papers cover its pharmacology, but most are mechanistic or short-term. No long-term therapeutic RCT exists for the doses the community uses. The evidence base is strong on mechanism and acute pharmacology; it's thin on multi-month safety at 100 to 300 mcg SC daily.
GHRP-2 (pralmorelin) binds the growth hormone secretagogue receptor GHS-R1a, a G-protein coupled receptor on pituitary somatotrophs and hypothalamic neurons. GHS-R1a is the same receptor that ghrelin, the endogenous hunger hormone, activates. Binding triggers phospholipase C and protein kinase C signaling. That depolarizes somatotrophs and opens voltage-gated calcium channels, producing a rapid GH pulse within 15 to 30 minutes of injection. The mechanism also works upstream: GHRP-2 stimulates hypothalamic GHRH neurons and suppresses somatostatin tone, creating a dual push-pull effect on GH release. The cortisol and prolactin elevation users notice comes from partial activation of ACTH-releasing pathways at the pituitary. Popovic et al. confirmed this is transient, returning to baseline within two to three hours post-injection [2]. The effect is milder than hexarelin and substantially milder than GHRP-6. One pharmacological detail matters for protocol design. GHS-R1a undergoes beta-arrestin-mediated receptor internalization with chronic agonist exposure. That is the molecular basis for the 38% GH attenuation Ghigo documented over five continuous days [1]. Receptor density recovers during off periods, which is why the 5-on/2-off weekly schedule preserves response. The elimination half-life is short (0.55 hours per Yen et al. Phase I pediatric PK)[3], so the compound clears quickly once injections stop.
Well-studied second-generation GHRP. GHS-R1a binding mechanism and acute GH pulse confirmed across multiple human studies. Approved in Japan as a single-dose diagnostic agent (100 mcg IV, 2004 PMDA). No therapeutic RCT exists for the bodybuilding/anti-aging dosing range (100-300 mcg SC 2-3× daily). Published data documents rapid receptor desensitization: 38% GH attenuation from day 1 to day 5 at 100 mcg/day SC [1]. Mild, transient cortisol and prolactin elevation confirmed [2]. 200+ PubMed papers; most are mechanistic or short-term pharmacological studies, not therapeutic trials.
Ghigo et al. 1997 (PMID 9820615): 38% GH attenuation day 1→5, 100 mcg/day SC in healthy adults; strongest clinical basis for cycling requirement. Yen et al. 1998 (PMID 9543135): Phase I pediatric PK; elimination t½ = 0.55 ± 0.14 h (IV). Popovic et al. 1995 (PMID 9285939): confirmed transient cortisol/prolactin elevation, returning to baseline by 2-3h.
No long-term therapeutic RCT. Japan approval limited to single-dose IV diagnostic use. SC bioavailability not formally established in humans. Rapid desensitization limits continuous use. No human data on multi-month SC dosing safety.
Effective and reliable GHRP with a strong GH pulse, but losing market share to ipamorelin due to cortisol/prolactin side effects and faster desensitization. Preferred when maximum GH output per injection is the goal. Widely considered the "middle ground" GHRP: cleaner than GHRP-6 (less hunger), stronger than ipamorelin (larger GH spike). Near-universally stacked with CJC-1295 (no DAC) or Sermorelin for synergistic GHRH + GHRP GH pulse.
Science and community agree on the GHS-R1a mechanism, acute GH pulse, and cortisol/prolactin side effects. Desensitization is clinically documented (PMID 9820615) and community has independently converged on 5-on/2-off cycling: strong alignment on this point. Community SC dosing (100-200 mcg 2-3× daily) is not supported by any therapeutic RCT; it is extrapolated from the Japan diagnostic dose and short-term research studies. Cycling rationale is science-supported in principle, but the 8-week on / 4-week off ratio is community convention, not a clinical protocol.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Daily |
| Moderate | 200mcg | 2x Daily |
| Aggressive | 200mcg | 3x Daily |
Reconstitution math for the standard 5 mg vial: add 2 mL bacteriostatic water. That gives you 2,500 mcg/mL. On a U-100 insulin syringe, 100 mcg equals 4 units. A 200 mcg dose is 8 units. One vial at 200 mcg twice daily lasts about 12.5 days. The fasting window is non-negotiable. Food raises somatostatin, which directly blunts the GH pulse. No food for 30 minutes before or after injection. Most beginners who report "GHRP-2 doesn't work" are eating too close to their injection. Stack it. Running GHRP-2 alone leaves GH output on the table. Co-inject with CJC-1295 (no DAC) at 100 mcg for the complementary pulse. Same syringe, same injection, same time. Store reconstituted vials refrigerated at 2 to 8 degrees Celsius and use within four weeks. Don't freeze reconstituted solution. Lyophilized powder is stable refrigerated for up to 12 months. The 5-on/2-off schedule is the one thing experienced users universally agree on. Start it from week one, not after you notice declining response.
Continuous use may reduce GH response over time due to receptor desensitization. Cycle 8 weeks on, 4 weeks off. Some users run 5 days on, 2 days off within each cycle week to preserve sensitivity.
GHRP-2 produces the fastest-documented receptor desensitization of commonly used GHRPs: 38% GH pulse attenuation from day 1 to day 5 of 100 mcg/day SC dosing in healthy men (PMID 9820615). This is caused by GHS-R1a downregulation and β-arrestin-mediated receptor internalization with chronic agonist exposure. The 5-day attenuation curve is the primary rationale for the within-week 5-on/2-off schedule used by experienced community members. The 8-week on / 4-week off gross cycle is a community convention, not clinically validated, but consistent with the principle of allowing receptor recycling. Antibody formation has been reported with long-term use of some GHRPs but is not the primary desensitization mechanism here.
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Expected: Improved sleep depth within weeks 1-2; mild recovery improvement by weeks 3-4; modest body composition changes (reduced abdominal fat, improved muscle fullness) by months 2-3
Monitor: Baseline IGF-1 before starting; recheck at week 4 and week 8. Fasting glucose at baseline.
Aim the stream at the glass wall, not directly into the powder. Let it dissolve; don't shake. This gives you 2,500 mcg/mL.
Draw your dose into a U-100 insulin syringe (29 or 31 gauge, half-inch needle). For 100 mcg, draw to the 4-unit mark. For 200 mcg, draw to the 8-unit mark. For 300 mcg, draw to the 12-unit mark.
Pinch skin at the abdomen, thigh, or upper arm. Insert at a 45-degree angle and inject slowly.
Minimum 30 minutes fasted before and 30 minutes fasted after. Food raises somatostatin and kills the GH pulse.
Best timing is before bed (to amplify the natural nocturnal GH surge) or first thing in the morning fasted. For twice-daily protocols, do both. For three times daily, add a post-workout injection (minimum 20 minutes after exercise, still fasted, at least 3 hours between injections).
If stacking with CJC-1295 (no DAC), draw 100 mcg of CJC into the same syringe before drawing your GHRP-2 dose. One injection covers both.
Refrigerate the reconstituted vial between uses.
100 mcg IV single bolus (Japan PMDA approved diagnostic dose)
IV is the only clinically validated administration route for pralmorelin. Japan diagnostic protocol: 100 mcg IV bolus for GH deficiency testing (GH stimulation test). Half-life 33 min IV. Not appropriate for repeated self-administration.
PMID 9390009 studied intranasal GHRP-2 in children with short stature; systemic bioavailability via intranasal route significantly lower than SC
Studied in pediatric short stature context only. Bioavailability substantially lower than SC. Community does not use this route; no practical dosing conversion validated.
Primary and near-universal stack. GHRH (CJC-1295 no DAC) + GHRP (GHRP-2) activates dual pituitary pathways, GHRHR + GHS-R1a, producing 2-3× the GH pulse of either alone. Co-injected simultaneously to capture the synergistic window.
100 mcg CJC-1295 (no DAC) + 100-200 mcg GHRP-2 SC, 2-3× daily, fasted
Lower-cost alternative GHRH for the GHRP-2 stack. Shorter half-life than CJC-1295 (no DAC), otherwise similar synergistic mechanism via GHRHR activation. Preferred by users seeking lower cost or softer GH stimulus.
100-300 mcg Sermorelin + 100-200 mcg GHRP-2 SC, 2× daily, fasted
Concurrent tissue repair stack (separate mechanism, not GH pathway). GH elevation from GHRP-2 complements BPC-157 angiogenic and healing signaling for injury recovery and connective tissue repair protocols.
Systemic recovery stack. TB-500 actin-binding and cell migration support + GH-mediated anabolic signaling combined in injury and post-surgery protocols.
Both GHRP-2 and ipamorelin bind the same GHS-R1a receptor. Stacking two GHRPs at the same receptor provides no additive GH benefit and accelerates receptor desensitization. Choose one GHRP and pair it with a GHRH peptide instead.
Same GHS-R1a receptor as GHRP-2. Hexarelin already produces the highest cortisol and prolactin elevation of any GHRP: combining with GHRP-2 compounds these side effects with no documented GH benefit from dual GHS-R1a stimulation.
Do not combineSame GHS-R1a receptor. Stacking GHRP-2 + GHRP-6 is redundant. GHRP-6 adds dramatically more hunger stimulation and cortisol burden without additive GH benefit over a single GHRP.
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 (axis preservation). Dramatically increases IGF-1 overshoot risk.
Do not combinePricing updated 2026-04-09
Receptor desensitization is the most clinically documented concern. Ghigo et al. showed a 38% drop in peak GH response from day one to day five at 100 mcg/day subcutaneous in healthy adults [1]. This is not a theoretical risk; it's measured and reproducible. Without cycling (5 days on, 2 days off minimum), the peptide loses a third of its effectiveness within a week. Users who skip cycling waste product and lose the GH output they're paying for. Cortisol elevation is real but transient. Popovic et al. [2] documented mild ACTH and cortisol spikes post-injection that return to baseline within two to three hours. At standard doses (100 to 200 mcg once or twice daily), this rarely causes symptoms. At three times daily advanced protocols, cumulative cortisol burden can become clinically relevant: watch for disrupted sleep, irritability, or stubborn fat gain around the midsection. Get an AM cortisol lab at week eight if running the advanced protocol. Prolactin elevation follows a similar pattern: mild, transient, dose-dependent. Symptomatic hyperprolactinemia (libido changes, gynecomastia) is uncommon at standard doses but warrants lab work if symptoms appear. The prolactin burden is lower than hexarelin but higher than ipamorelin. Appetite increase hits 20 to 30 minutes after injection. GHRP-2 mimics ghrelin at GHS-R1a, and ghrelin is the hunger hormone. The effect is significantly less intense than GHRP-6 but more pronounced than ipamorelin. For cutting protocols, this can be disruptive. Shifting the bedtime dose to three or more hours after dinner (still fasted) helps manage it. Water retention and mild edema are GH-class effects, not specific to GHRP-2. Expect some puffiness in the first two to four weeks that stabilizes. Injection-site reactions include transient tingling and dizziness lasting 5 to 15 minutes post-injection. These are common, benign, and tend to diminish over the first week. Carpal tunnel symptoms (hand tingling, grip weakness) signal excessive GH-mediated fluid retention. Reduce dose or frequency immediately. If symptoms persist beyond one week at a lower dose, discontinue for a minimum of four weeks. GH antagonizes insulin action, and GHRP-2's cortisol co-elevation compounds this effect. Monitor fasting glucose at baseline and at weeks four and eight. Pre-diabetic individuals should check weekly. A fasting glucose above 125 mg/dL warrants dose reduction and medical review. Contraindications: active cancer or history of malignancy (GH promotes cell proliferation), uncontrolled diabetes or diabetic retinopathy, pregnancy or breastfeeding, active pituitary tumors, and known hypersensitivity to pralmorelin. No human data exists on multi-month subcutaneous dosing safety at the doses the community uses.
Verify GHRP-2 dosing and safety with a second opinion
GHRP-2 is among the more affordable GH secretagogues (~$28-$46 per 5mg vial), which attracts budget vendors with variable quality standards. No GMP requirement applies to "research use only" peptide vendors. The peptide is a hexapeptide (MW ~817 Da): synthesis is straightforward and impurity profiles vary by vendor. Reconstituted peptide degrades faster than lyophilized powder; improper storage (not refrigerated, exposed to light) significantly reduces potency. No systematic vendor testing data for GHRP-2 specifically comparable to the Finnrick Analytics CJC-1295 dataset, but general research peptide quality concerns apply.
| Test | When | Target |
|---|---|---|
| IGF-1 | Baseline before starting; repeat at week 4 and week 8 | Age-adjusted normal range (not supraphysiological). Flag if above upper limit of normal. |
| Fasting glucose | Baseline; repeat at week 4 and week 8; weekly if pre-diabetic | <100 mg/dL (normal); 100-125 mg/dL warrants dose reduction and closer monitoring |
| Prolactin | Baseline; repeat at week 8 if symptoms emerge (libido changes, gynecomastia) | Normal laboratory reference range |
| AM cortisol | Baseline; repeat at week 8 if symptoms of cortisol excess emerge | Normal AM cortisol range (roughly 10-20 mcg/dL AM) |
| Thyroid (TSH, fT3, fT4) | Baseline; repeat at week 12 if symptoms emerge | — |
Primary efficacy marker for sustained GH axis activation. Confirms peptide quality and dosing adequacy. Detects over-response requiring dose/frequency reduction.
GH release antagonizes insulin action. GHRP-2 causes cortisol co-elevation which further impairs glucose tolerance. Essential monitoring in individuals with any insulin resistance.
GHRP-2 causes mild transient prolactin elevation (confirmed PMID 9285939). Returns to baseline within 2-3h post-injection. Symptomatic hyperprolactinemia is uncommon at standard doses but warrants investigation at higher frequencies.
GHRP-2 transiently elevates cortisol/ACTH via pituitary ACTH-releasing pathway. At high frequencies (3× daily), cumulative cortisol burden may become clinically relevant for fat distribution and immune function.
GH accelerates T4-to-T3 conversion. Untreated hypothyroidism blunts GH response; GH supplementation can unmask subclinical hypothyroidism.
Improved sleep depth and recovery. Moderate appetite increase becomes noticeable. Mild water retention may occur as GH pulses elevate.
Recovery between training sessions improves. Skin quality begins to improve. Energy levels and mood stabilize. GH-mediated fat oxidation starts.
Body composition shifts become visible: reduced abdominal fat, improved muscle fullness. Joint and connective tissue feel better.
Peak benefits for body composition and recovery. Hair and nail growth may accelerate. Sustained fat loss with preserved lean mass.
Consider cycling off for 2-4 weeks to maintain pituitary sensitivity. Benefits plateau without periodic breaks.
Week 1-2: GH pulse onset, sleep and appetite changes. The GH spike hits within 15 to 30 minutes of subcutaneous injection. Most users notice improved sleep depth and vivid dreams within the first week of bedtime dosing. Appetite kicks up 20 to 30 minutes post-injection; it's less intense than GHRP-6 but noticeable. Transient tingling or dizziness for 5 to 15 minutes after injecting is common and harmless. Mild water retention starts building. Weeks 3-4: Desensitization window, cycling is non-negotiable. Without 5-on/2-off scheduling, peak GH response drops roughly 38% by day five [1]. Users on continuous protocols notice a weaker post-injection response around this time. Those running the cycling schedule report more sustained effects. Recovery improvements become consistent: less DOMS, better training performance. Water retention stabilizes at a mild to moderate level. Months 2-3: Body composition changes become visible. GH-mediated lipolysis and IGF-1 anabolic signaling accumulate over 8 to 12 weeks of consistent protocol adherence. Expect reduced abdominal fat, improved muscle fullness, and faster connective tissue recovery. Skin quality improves (elasticity, hydration). Hair and nail growth may speed up. Carpal tunnel symptoms can appear at higher dose frequencies; reduce dose immediately if tingling or grip weakness develops. Month 3+ (off cycle): The compound clears within hours of the last injection (elimination half-life approximately 33 minutes). GHS-R1a receptor density recovers during the four-week off period. Sleep quality, recovery, and body composition benefits hold for four to six weeks post-cycle in most reports. Some regression occurs over eight to ten weeks without the protocol. Most users restart after four weeks off.
GH pulse detectable within 15-30 min of IV injection (Japan diagnostic data); SC GH peak at 30-60 min. GH promotes slow-wave sleep architecture.
Improved sleep depth and vivid dreams reported within the first week with bedtime dosing. Moderate appetite increase within 20-30 min post-injection. Mild tingling or dizziness shortly after injection is common.
GH attenuation reaches ~38% by day 5 of continuous daily dosing per PMID 9820615. Peak GH response declines measurably without cycling breaks. 5-on/2-off schedule attenuates this decline.
Users on continuous protocols note weaker post-injection response by week 3-4. Those running 5-on/2-off report more sustained effect. Recovery improvements become consistent: reduced DOMS, better training performance.
GH-mediated lipolysis and anabolic IGF-1 signaling accumulate over 8-12 weeks with consistent protocol adherence.
Visible reduction in abdominal fat, improved muscle fullness, and faster joint/connective tissue recovery. Skin quality improvements (elasticity, hydration) noted. Hair and nail growth may accelerate.
Short elimination half-life (~33 min) means compound clears within hours of last injection. GHS-R1a receptor density should recover within the 4-week off period.
Benefits (sleep quality, recovery, body composition) largely retained for 4-6 weeks post-cycle. Some regression in body composition over 8-10 weeks without protocol. Most users restart after 4 weeks off.
Source: Phase I pediatric PK study (Yen et al. 1998, PMID 9543140); t½β = 0.55 ± 0.14 h
Loading the interactive decay curve.
GHRP-2 (pralmorelin) is classified as a research chemical in the United States. It has no FDA approval, no IND designation, and no accepted medical use under US law. Selling it for human consumption is not legal; vendors market it labeled "for research purposes only." Japan is the only country with a regulatory approval. The PMDA approved GHRP Kaken 100 (Kaken Pharmaceutical) in 2004 as a single-dose IV diagnostic agent for GH deficiency testing. The approved dose is 100 mcg IV bolus. It is not approved therapeutically in Japan or anywhere else. GHRP-2 is not on the FDA's 503A bulk drug substances list for compounding pharmacies (Category 2 under current FDA oversight). An announcement from HHS Secretary RFK Jr. on February 27, 2026, indicated intent to reclassify approximately 14 Category 2 peptides, but no formal Federal Register rule had been published as of April 2026. WADA prohibits all GH secretagogues under the S2 category (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Athletes subject to anti-doping testing should not use GHRP-2. This content is for informational and research purposes only. It does not constitute medical advice. Consult a licensed healthcare provider before using any peptide.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
