Ipamorelin

What it is

Ipamorelin is the cleanest growth-hormone secretagogue available. It is a five-amino-acid peptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) engineered by a chemistry team at Novo Nordisk in the mid-1990s. The development process was systematic: the team started with GHRP-1 and stripped pieces off one at a time while testing for GH release at each step. What remained was a pentapeptide as potent as the earlier secretagogues (GHRP-2, GHRP-6) for GH release — but without their cortisol, prolactin, and appetite baggage. The discovery was published in the European Journal of Endocrinology in 1998 [PMID 9849822].

It acts on a receptor called GHS-R1a — the growth hormone secretagogue receptor — which was discovered by Andrew Howard’s team at Merck Research Laboratories and published in Science in 1996 [PMID 8688086]. The natural endogenous ligand for that receptor, ghrelin, wasn’t identified until 1999. In other words: the receptor was characterized and the first synthetic agonists were developed before anyone knew what the body’s own key to that lock was.

Ipamorelin does not inject GH into you. It asks your pituitary to release the GH you already make, in the natural pulses your body is built around. That is a fundamentally different — and more physiologic — approach than exogenous HGH, which floods the system with a non-pulsatile signal your body never sees naturally. Secretagogues restore declining endogenous growth-hormone signaling rather than replace it.

It is most famous as half of the CJC-1295 + Ipamorelin blend (see CJC-1295 / Ipamorelin), where it supplies the ghrelin-pathway pulse while CJC-1295 supplies the GHRH-pathway baseline. But it stands on its own as a single agent too — and one practitioner’s recommendation is to learn it as a solo tool first (see Protocol below).

How it works

Your body releases growth hormone in pulses — roughly 6–10 times per day — with the largest pulse during deep sleep. Two upstream signals drive those pulses: GHRH (growth-hormone-releasing hormone: the lever Sermorelin and CJC-1295 pull) and ghrelin, the gut peptide better known as the “hunger hormone.” Ghrelin is also a powerful, independent GH stimulator working through its own receptor, GHS-R1a [PMID 8688086]. Somatostatin acts as the brake on each GH pulse — suppressing secretion between peaks. Ipamorelin is a selective mimic of ghrelin’s action at GHS-R1a on pituitary somatotroph cells, triggering a calcium-dependent signaling cascade that fires a GH pulse.

GH kinetics after subcutaneous injection: GH rises within 15–30 minutes, peaks around 40 minutes, and returns to baseline in approximately 3 hours. When injected before sleep, the peptide’s pulse stacks on top of the body’s largest natural overnight GH pulse — amplifying it rather than replacing it.

The defining feature is selectivity. The earlier ghrelin-mimics (GHRP-6, GHRP-2) also spiked cortisol and prolactin. Ipamorelin doesn’t. In pigs and rat pituitary cells, it released GH without touching cortisol, ACTH, prolactin, or thyroid even at more than 200 times the GH-effective dose. That selectivity is the entire engineering achievement — and the reason it has outlasted the earlier GHRPs as a long-term wellness tool.

Because it hits a different receptor than GHRH analogs, ipamorelin pairs naturally with one. Stimulate GHS-R1a and the GHRH receptor simultaneously and the pituitary — which expresses both — puts out a bigger pulse than either signal alone. Hataya et al. 2001 confirmed that a low dose of ghrelin stimulates GH release synergistically with GHRH in humans. Williams characterizes the combined practical pulse as “3 to 10 times larger than either compound alone” — that magnitude framing is his clinical-coach read, not a number from the Hataya paper, but the synergistic principle is real. That dual-receptor synergy is the entire rationale for the CJC + Ipamorelin blend.

Because ipamorelin amplifies the existing GH pulse rather than overriding the pulse generator, it preserves the body’s own somatostatin brake — meaning there is a physiologic ceiling on how far GH can rise, in a way that continuous exogenous HGH does not have.

What the research shows

Here is the full picture, every tier labeled, strongest findings first.

Selectivity & mechanism: the foundation. The original Raun 1998 work is the bedrock: ipamorelin releases GH cleanly and dose-dependently while leaving cortisol, prolactin, ACTH, and thyroid untouched [PMID 9849822]. This is the most-cited, best-replicated thing about the molecule.

Human pharmacokinetics. Intact ipamorelin and its active metabolites were confirmed in human urine after dosing — it is real, absorbed, and biologically present in people [PMID 26811125].

The human ileus trial. Beck et al. 2014 ran a multicenter, double-blind, placebo-controlled Phase 2 trial (n=114) testing IV ipamorelin for post-operative ileus. Time-to-first-meal was faster on ipamorelin (25.3 h vs 32.6 h) but the difference did not reach statistical significance (p=0.15), and the program was not advanced [PMID 25331030]. Read that finding as information, not a verdict: this was a single trial of an IV gut-motility indication, dosed by body weight — a completely different use, route, and dose from the subcutaneous GH-axis microdosing people actually run. It tells you almost nothing about ipamorelin for sleep, recovery, or body composition. What it does tell you is that ipamorelin was well tolerated in humans short-term.

Preclinical efficacy. The GH-axis benefit signal lives here:

• Counteracted glucocorticoid-induced bone and muscle loss in rats [PMID 11735244].
• Accelerated gut motility in rodent ileus models [PMID 19289567, 27186127].
• Blunted chemotherapy-induced weight loss in ferrets [PMID 39043357].

MK-677 comparison (insulin sensitivity). Nass et al. 2008 ran a 2-year double-blind, randomized, placebo-controlled trial of MK-677 (an oral, non-peptide ghrelin agonist targeting the same GHS-R1a receptor) in 65 healthy older adults. Fasting blood glucose increased an average of 5 mg/dL and insulin sensitivity declined significantly in the MK-677 group vs. placebo. Cortisol also increased. Fat-free mass rose but so did total body weight. This is the comparison document for choosing injectable pulsatile ipamorelin over oral continuous MK-677.

The body-composition story is mechanistic and animal-derived. The downstream logic (restored GH → IGF-1 → muscle protein synthesis, mitochondrial biogenesis, fat mobilization, better recovery) is built on GH/IGF-1 physiology, not yet on a positive human body-comp RCT of ipamorelin specifically. The mechanism is well-mapped, the selectivity is proven in the lab, the human safety looks clean short-term, and body-composition outcomes are extrapolated from GH biology plus the wide real-world use base.

Who it's for

The primary candidates:

• Anyone over 35 with slower recovery. Training hard, recovering more slowly than before, wanting better sleep, faster healing, and less soreness. This is the broadest and most common use case.
• Peri- and post-menopausal women (40s–50s). Williams calls this the single most important underserved application in the GH peptide space. Declining estrogen hits sleep, body composition, bone density, skin, and hair simultaneously — ipamorelin addresses several of those at once. The clean cortisol/prolactin profile matters even more for this cohort than for male users. Women who have never used a GH peptide can see meaningful quality-of-life benefit from ipamorelin alone, before or as a gateway to full HRT.
• Body composition optimization with training and nutrition dialed in — wanting a 6–12-month measurable arc of change in visceral fat and lean mass.
• GLP-1 users. Williams considers ipamorelin near-mandatory alongside GLP-1 therapy: it preserves lean mass, supports sleep, improves gut motility (partially offsetting GLP-1 GI side effects), and pulls blood sugar mildly upward vs. GLP-1’s lowering effect — creating a rough metabolic balance.
• Poor sleepers and longevity-minded individuals who want GH benefits without the cost or commitment of exogenous HGH.

Who should skip it or proceed carefully: Active cancer (GH/IGF-1 may promote tumor growth — talk with your doctor); pregnancy or breastfeeding; severe untreated sleep apnea (fix the apnea first); people with suboptimal thyroid or sex hormones who haven’t addressed those first (see Foundation below).

Real-world protocol

The doses and schedules here are for educational and informational purposes only. These peptides are sold for research use only and are not FDA-approved drugs. This is not medical advice. Consult a qualified physician before beginning any protocol.

Foundation first

GH peptides do not work well in a hormone vacuum. Thyroid and sex hormones must be addressed before starting. A man with low testosterone may get slightly better sleep from ipamorelin but essentially nothing in body composition — the increased GH/IGF-1 signal needs optimized testosterone to produce the synergistic anabolic effect on muscle. Same principle for thyroid: subclinical hypothyroidism significantly blunts GH-axis response. The foundation check: thyroid panel (TSH, free T4, free T3), sex hormones (total T, free T, estradiol for women), and fasting metabolic labs.

Start with ipamorelin alone first

Use ipamorelin by itself for 4–8 weeks before adding CJC-1295. A significant number of people experience adverse reactions specifically to CJC (injection-site redness, hives, headaches) and — if they started with the pre-blended vial — they attribute the whole experience to ipamorelin and abandon the protocol entirely. Starting solo lets you confirm your own tolerance, get the early sleep/recovery benefits quickly (building commitment and confidence), and then layer in CJC as a separate variable at a low dose. If CJC causes a problem, you can remove it without losing what ipamorelin is already delivering.

Dosing tiers

Tier 1 — General optimization / sleep / longevity / anti-aging:

• Ipamorelin: 100–200 mcg, once daily, pre-bed
• Optional CJC-1295 no-DAC add-on (after tolerance confirmed): 100 mcg alongside
• Most people running ipamorelin for sleep, recovery, and longevity never need more than this

Tier 2 — Performance and body composition:

• Ipamorelin: 200–300 mcg per dose, 2–3× daily
• Optional CJC-1295 no-DAC: Pair at a 1:1 ratio (equal mcg) or 3:1 (ipamorelin:CJC, e.g. 300:100 mcg)
• Pre-bed is always the most important dose. For multiple daily doses: pair with fasted training windows (inject ~60 minutes pre-training, eat right before training to let the pulse land; or inject immediately post-training and wait ~60 minutes before eating)

Dose ceiling: ~300 mcg per dose. Beyond that, no additional GH response — only faster desensitization. 500 mcg per dose is wasted product and accelerated receptor downregulation.

CJC no-DAC vs. with-DAC — where practitioners differ: Williams is explicit about preferring no-DAC: the DAC version extends half-life to 5–8 days and creates persistent GHRH-pathway stimulation, which flattens the natural pulsatile GH pattern — the same “tonic exposure” problem associated with continuous HGH injections. One practitioner (the other practitioner in the KB) preferred the DAC version for more consistent IGF-1 elevation. Both views are represented; the no-DAC daily blend is what Alyve stocks and is what most protocols run.

Timing rules:

• Dose at least 90 minutes after your last meal
• Avoid eating for 30–60 minutes after injecting (carbs and fat blunt the GH pulse)
• If on a GLP-1 drug that slows gastric emptying, give 60–90 minutes post-meal — the 2-hour standard rule is insufficient but 4 hours isn’t necessary
• Space multiple daily doses at least 3 hours apart so each lands on a clean receptor baseline

Schedule and cycling

Weekly cadence: 5 days on, 2 days off. The two off-days meaningfully help receptor reset and allow longer cumulative cycles than 7 days/week.

Cycle length: 8 weeks on, 4 weeks off — or 12 weeks on, 4 weeks off. Both are valid. Most users notice diminishing returns in the 8–12-week window. The off-cycle option: rotate to a GHRH-class peptide (sermorelin, tesamorelin, CJC), which hits a different receptor and allows full GHS-R1a recovery.

Why cycling matters: The ghrelin receptor desensitizes with sustained high-amplitude stimulation. Unlike GLP-1s (where dose escalation can partially recapture effect), the ipamorelin-GHS-R1a relationship hits a genuine floor — the same dose starts producing a smaller GH pulse, and going higher doesn’t help. Cycling resets the receptor and prevents dose creep.

Reconstitution

Mix with bacteriostatic water. Williams recommends 2 mL water per vial; the one practitioner/cheat-sheet convention in the KB uses 3 mL for a 10 mg vial. Both are fine — what matters is the concentration you calculate from it. Always label the vial with the water volume you added so future dosing math is unambiguous.

Vial size	Water added	Concentration	150 mcg dose	300 mcg dose
5 mg	2 mL	2,500 mcg/mL	6 units (0.06 mL)	12 units (0.12 mL)
10 mg	2 mL	5,000 mcg/mL	3 units (0.03 mL)	6 units (0.06 mL)
10 mg	3 mL	3,333 mcg/mL	4.5 units (0.045 mL)	9 units (0.09 mL)

Technique: inject bacteriostatic water slowly down the vial wall (not into the puck directly), let dissolve with gentle swirl, refrigerate. Rotate injection sites. Ipamorelin has minimal injection-site reactions — notably less than CJC, which causes redness or hives in roughly 30% of users. If you’re mixing both in one syringe and reactions develop, CJC is the likely culprit.

Timeline of expected results

One of the more practical additions from the Williams masterclass — a week-by-week expectations framework:

Window	What to expect
Week 1	Deeper, more restorative sleep; vivid dreams are common and a sign the peptide is working
Weeks 2–3	Better recovery from training; reduced day-to-day soreness
Weeks 6–8	IGF-1 climbing into the upper third of your age-adjusted range on labs; body composition beginning to shift
Weeks 8–12	Visible body composition changes with adequate training and protein intake
Months 6–12	Compounded effect through multiple cycles: sustained sleep quality, modest fat loss, lean mass support, fewer injuries (better collagen signaling), improved skin and hair

The most common reason people quit early is expecting a transformation in the first month. GH peptides are a long-arc tool — the compounding value comes from cycling through it multiple times across a year, not from a single 4-week run.

Stacking

What pairs well

• CJC-1295 no-DAC: The primary pairing. Dual-receptor synergy (ghrelin + GHRH pathways simultaneously) → a larger combined GH pulse than either alone. Use the start-alone-first rule above before adding.
• Tesamorelin + ipamorelin: Williams describes this as the strongest GH-axis peptide stack available — more powerful than CJC + ipamorelin. Tesamorelin is FDA-approved for visceral fat and sits on the GHRH side. Trade-off: some water retention and bloat. Reserve for situations where visceral fat or maximum GH-axis response is the explicit goal.
• BPC-157 + TB-500 (the Wolverine stack): BPC and TB-500 upregulate growth hormone receptor sensitivity — the cells become more responsive to the IGF-1 signal that ipamorelin generates downstream. The GH stack provides the systemic IGF-1 signal; the healing peptides drive local angiogenesis and tissue repair. Standard stack for injury rehabilitation.
• SS-31: Pairs well with essentially all peptides for mitochondrial health support. Better mitochondrial function improves downstream utilization of the GH/IGF-1 signal.
• GLP-1 receptor agonists (Retatrutide, Semaglutide, Tirzepatide): Near-mandatory pairing in Williams’s view. GLP-1 drives fat loss while risking lean mass erosion; ipamorelin counteracts muscle wasting, supports sleep, provides gut motility benefit (offsetting GLP-1 GI slowing), and mildly raises blood sugar — creating a rough net-neutral glucose effect while preserving GH-axis benefits. On GLP-1s, the standard “90-minute post-meal” pre-bed timing window may not be long enough; see Timing rules above.
• TRT / HRT / estrogen / progesterone: All compatible. Foundation hormones must be optimized first — they are what the GH-axis benefit is built on.

What does NOT stack with ipamorelin

• GHRP-2, GHRP-6, hexarellin, MK-677: All target the same GHS-R1a receptor. Stacking any of these with ipamorelin is redundant — two different keys in the same lock simultaneously. Net effect: faster receptor desensitization, no additive GH benefit.
• Somatostatin analogs: Directly block GH release at the pituitary — they cancel out what ipamorelin triggers.

MK-677 comparison

MK-677 (ibutamoren) is an oral, non-peptide ghrelin-receptor agonist targeting the same GHS-R1a receptor as ipamorelin. It’s often considered as an alternative — particularly by people who want to avoid injections.

Feature	Ipamorelin (injectable)	MK-677 (oral)
Signal type	Clean, pulsatile GH release	Continuous around-the-clock stimulation
Hunger effect	Minimal and transient	Strong and sustained
Water retention	Mild	Significant
Insulin sensitivity	Minimal documented effect at therapeutic doses	2-year RCT: measurable decline
Blood glucose	Modest potential rise	Fasting glucose rose avg 5 mg/dL in 2-yr trial
Cortisol	Flat at therapeutic doses [PMID 9849822]	Elevated significantly in 2-yr trial [PMID 18981485]
Pulse preservation	Yes — amplifies natural pulses	No — tonic stimulation flattens pulse pattern
Administration	Subcutaneous injection	Oral pill

The 2-year MK-677 trial (Nass et al. 2008) is the clearest human comparison document: 65 healthy older adults (60–81 yrs), double-blind, placebo-controlled, 2 years. MK-677 increased fat-free mass (+1.1 kg) and GH/IGF-1 levels but also increased total body weight (+2.7 kg), significantly worsened insulin sensitivity, raised fasting glucose by 5 mg/dL, and elevated cortisol. The injectable pulsatile approach avoids the continuous tonic stimulation problem and the metabolic trade-offs that come with it.

Lab tracking

Objective markers:

• IGF-1: The primary proxy for GH-axis response. With ipamorelin alone, most users land in the 250–280 range; reaching 350–400 is uncommon but possible with strong responders. Supraphysiologic warning zone: sustained levels above ~500 (very rare with ipamorelin alone at therapeutic doses). A useful side-note from Williams: if prolactin has risen significantly on what should be ipamorelin, that’s evidence you may have a contaminated product — authentic ipamorelin leaves prolactin flat. Check IGF-1 at baseline and at weeks 6–8.
• Fasting glucose, A1C, fasting insulin: GH peptides can modestly raise blood sugar — track these, especially for anyone with metabolic risk factors.
• Prolactin: Both a safety check and a product quality indicator (see above).
• Full metabolic panel and lipids
• Full thyroid panel (TSH, free T4, free T3): Critical to confirm the foundation is sound before attributing results (or non-results) to the peptide.

Monitoring tools: Wearable sleep trackers (Oura, Garmin, WHOOP) for the sleep signal. Grip strength as a lean-mass proxy. DEXA scan for body composition at baseline and every 6 months if tracking composition seriously.

Troubleshooting

“I don’t feel anything”

• Baseline IGF-1 may already be naturally in the 250–300 range — some people sit there without any intervention; ipamorelin won’t move them noticeably
• Dose too low — start at 100 mcg and work up to 300 mcg before concluding it’s ineffective
• Not enough time — GH peptides are a 6–12-week cumulative arc; don’t evaluate at week 2–3
• Source quality — check prolactin; if it has risen, the product may not be ipamorelin (authentic ipamorelin leaves prolactin flat)
• Underlying blunting factor: untreated thyroid issues, low testosterone, chronic stress, or poor sleep hygiene all significantly reduce GH peptide response

“I feel worse or more tired”

• If using the CJC blend, isolate: switch to ipamorelin alone and see if symptoms resolve — CJC is the more likely culprit for adverse reactions
• Check thyroid labs; subclinical hypothyroidism can be worsened by GH-axis perturbation
• Run a full lab panel at the 8-week mark

When to discontinue:

• IGF-1 significantly and persistently elevated above 500 (very unlikely with ipamorelin alone)
• Fasting glucose trending consistently upward without a lifestyle explanation
• Persistent numbness or tingling (sign of IGF-1/GH excess — reduce dose first, then consider stopping)
• Active cancer diagnosis

Side effects & management

Ipamorelin is one of the better-tolerated peptides in this category, and the Beck 2014 RCT backs that up — adverse events were actually slightly lower on ipamorelin than on placebo [PMID 25331030].

What users report:

• A brief hunger spike shortly after injection — expected ghrelin-mimic effect; usually mild and fades within an hour. Minimal compared to GHRP-6 or MK-677.
• Transient flushing, mild headache, occasional lightheadedness — often within the first few minutes post-injection, typically resolves quickly.
• Mild water retention — Williams notes ipamorelin produces the least water retention of any GH peptide in his experience; dial back dose if it appears.
• Vivid dreams — expected and a sign the sleep-stage amplification is working.
• Injection-site irritation — rare with ipamorelin; roughly 30% of CJC users experience it, so ipamorelin is notably cleaner in this regard.

Most of these resolve in 30–60 minutes and are dose-related — smaller, well-timed doses minimize them.

Longer-term considerations: Anything that raises GH/IGF-1 warrants periodic monitoring. The sensible move is to keep IGF-1 elevation in the physiologic range and check it against your age-adjusted reference interval at 6-month intervals for long-term users. Secretagogues are safer than exogenous HGH precisely because they preserve pulsatility and the somatostatin brake — the body can’t be driven as far past its ceiling as raw injected GH can.

On cancer risk, stated plainly: A meta-analysis found higher circulating IGF-1 associated with moderately increased risk of prostate and premenopausal breast cancer]. This is different from and exists alongside the finding that GH replacement in GH-deficient adults was associated with reduced cancer risk (RR 0.69) in a 9-study meta-analysis and no clear excess cancer risk in the large SAGhE European cohort. Both sides of this literature are real and worth holding simultaneously. The conservative move: avoid use with active cancer, monitor IGF-1 rather than leaving it to run unchecked, and integrate this into the full picture of how you manage metabolic health. Rick decides; this is the full landscape.

Frequently asked questions

Is it legal? Not freely compoundable — on the FDA 503A Category 2 list. Regulatory timeline: 2023 FDA restricted compounding status → 2024 lawsuit partially restored access → 2024–2025 the PCAB (Pharmacy Compounding Advisory Committee) voted against recommending it for the official compounding list → 2026 FDA scheduled further advisory meetings on ipamorelin and a batch of related peptides. The direction is toward eventual Category 1 re-listing, but this is ongoing. Everything sold today is research-use-only.

Will it make me gain weight? Small possible bump from water retention or lean mass increase. Not fat accumulation. Net body-composition direction is favorable with adequate training and protein.

Can it be taken orally or as a nasal spray? No — not bioavailable via those routes at therapeutic doses. The closest oral analog is MK-777, a small-molecule ghrelin agonist (distinct from MK-677).

Will it show up on a drug test? Ipamorelin is banned by WADA. Detection in urine is possible — treat it as positive for sport-ban purposes even if detection isn’t guaranteed on every test protocol.

Will stopping cause a crash or withdrawal? No addiction mechanism; no pituitary suppression from the peptide class. Baseline GH production resumes. Goes back to whatever your natural baseline was.

Can ipamorelin and CJC be mixed in the same syringe? Yes. Pre-blended vials exist; or draw both into one syringe if using separate vials for ratio control. If injection-site reactions develop with the combination, CJC is the more likely culprit.

Regulatory status

Ipamorelin is not FDA-approved. It originated as a Novo Nordisk investigational compound, studied through Phase 2, and not carried further commercially. In 2023 it was placed on the FDA’s 503A Category 2 bulk-substances list, restricting compounding-pharmacy access. The 2024 FDA lawsuit resulted in partial access being temporarily restored; the PCAB voted in 2024–2025 against recommending it for the official compounding list; and in 2026 the FDA scheduled further advisory meetings on ipamorelin alongside a group of related peptides. It is prohibited by WADA in sport. Everything sold today is research-use-only.

The Alyve product

Alyve lists Ipamorelin standalone at $34.00–$64.99 (5 mg / 10 mg), currently showing out of stock.

The route that is in stock and verified is the CJC-1295 + Ipamorelin Blend (5 mg / 5 mg), $68.00 (on sale from $78.00), tested at 99.90% purity by Freedom Diagnostics Testing (HPLC-UV purity + LC-MS identity, lot CJI583). That is genuinely high-purity, identity-confirmed product. The blend is covered fully in CJC-1295 / Ipamorelin.

Offer: Use coupon OHM-15 for 15% off — Alyve’s pricing is very competitive, and buying 3 vials of any given peptide in one purchase gets you over 30% off retail. (Full disclosure: OHM-15 also attributes the sale to me — I’d rather tell you than hide it.)

Technical & analytical reference (chemistry & QC)

Molecular identity verified against PubChem (2026-06-21). Analytical-method detail below is compiled from a third-party technical reference (PeptideBiologix) and tagged where the underlying figure is uncited.

Field	Value
Molecular formula	C38H49N9O5 (PubChem CID 9831659)
Average MW	711.9 g/mol
CAS	170851-70-4
Sequence	Aib-His-D-2-Nal-D-Phe-Lys-NH2 (Aib = 2-methylalanine; D-2-Nal = D-3-(2-naphthyl)alanine; C-terminal amide)
HPLC purity criterion	RP-HPLC (C18 + 0.1% TFA), UV 220/280 nm, elutes ~12–18 min; ≥95% research-grade, ≥98% pharmaceutical
MS identity	ESI-MS (M+H)+ m/z 712.4 at 711.85 ± 0.5 Da; MS/MS for sequence confirmation
Counterion / net peptide	TFA/acetate counterions; peptide content ≥85% (corrected for TFA/water); net charge +2 at pH 7.4
Storage / reconstitution	Lyophilized −20 to −80°C (<2% loss / 24–36 mo); reconstitute with bacteriostatic water down vial wall, gentle swirl (never shake); reconstituted 2–8°C ~2–4 weeks (bacteriostatic) / 3–7 days (sterile)
Degradation / stability	Pathways = His oxidation, Asp isomerization; reconstituted solutions far less stable than lyophilized; limit freeze-thaw
Reported human PK	Terminal t½ ~2.0 ± 0.4 h; Tmax ~45 min SC; SC bioavailability ~85 ± 12%; GH peak 30–60 min
Selectivity (EC50)	GHS-R1a agonist, EC50 low nanomolar (~1–10 nM); releases GH without elevating cortisol, prolactin, ACTH or thyroid hormones at GH-effective doses

Primary-literature citation leads (PeptideBiologix; confirm before citing): PMID 9849822 (Raun 1998, first selective GHS — already cited), PMID 10373343 (Johansen 1999, longitudinal bone growth in rats), PMID 9733494 (Ankersen 1998, potent GHRP series from ipamorelin), PMID 11735230 (Andersen 2001, counters glucocorticoid bone loss), PMID 11185668 (Beck 2000, human PK/PD), PMID 10496658 (Gobburu 1999, human PK/PD modeling — already cited), PMID 11162489 (Lall 2001, GH-independent adiposity).

Sources

1. Raun K, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998. : 9849822
2. Beck DE, et al. Ghrelin mimetic ipamorelin for postoperative ileus — Phase 2 RCT. Int J Colorectal Dis. 2014. : 25331030
3. Andersen NB, et al. Ipamorelin counteracts glucocorticoid-induced bone/muscle loss (rat). Growth Horm IGF Res. 2001. : 11735244
4. Venkova K, et al. Ipamorelin in a rodent model of postoperative ileus. J Pharmacol Exp Ther. 2009. : 19289567
5. Greenwood-Van Meerveld B, et al. Ipamorelin on gastric dysmotility (rat). J Exp Pharmacol. 2012. : 27186127
6. Lu Z, et al. Anamorelin and ipamorelin inhibit cisplatin-induced weight loss in ferrets. Physiol Behav. 2024. : 39043357
7. Ferro P, et al. Structure-activity relationship for peptidic GH secretagogues (human excretion). Drug Test Anal. 2017. : 26811125
8. Hataya Y, et al. Low dose of ghrelin stimulates GH release synergistically with GHRH in humans. J Clin Endocrinol Metab. 2001. : 11549707
9. Gobburu JV, Agersø H, Jusko WJ, Ynddal L. Pharmacokinetic-pharmacodynamic modeling of ipamorelin in human volunteers. Pharm Res. 1999;16:1412–1416. : 10496658
10. Howard AD, Feighner SD, Cully DF, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release (GHS-R1a discovery). Science. 1996;273(5277):974–977. : 8688086
11. Nass R, et al. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults (MK-677 2-yr RCT; insulin sensitivity decline documented). Ann Intern Med. 2008. : 18981485
12. Renehan AG, et al. Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis (prostate OR 1.49; premenopausal breast OR 1.65). Lancet. 2004. : 15110491
13. Li Z, et al. GH replacement therapy reduces risk of cancer in adults with GH deficiency — meta-analysis (9 studies, 11,191 participants; RR 0.69). Oncotarget. 2016. : 27835910
14. Swerdlow AJ, et al. Cancer risks in patients treated with GH in childhood (SAGhE European cohort). J Clin Endocrinol Metab. 2017. : 28184422
15. Video digest — one practitioner CJC-1295/Ipamorelin Masterclass.
16. Video digest — one practitioner Ipamorelin Masterclass 2026.
17. Dosing/reconstitution cheat sheet (one practitioner).
18. Alyve COA summary (blend 99.90%, lot CJI583).
19. Alyve Peptides — Ipamorelin product page. / https://alyvepeptides.com/product/ipamorelin/

See also: CJC-1295, Sermorelin, CJC-1295 / Ipamorelin, Tesamorelin, Retatrutide, BPC-157, TB-500, SS-31 (Elamipretide).