Best Peptides for Hormone Optimization

Educational content only — not medical advice. Consult a licensed healthcare provider before starting, changing, or stopping any peptide protocol.

Overview

Hormone optimization peptides are the largest category in the peptide space and the one with the most real human pharmacology behind it. They occupy a middle ground between doing nothing and full exogenous hormone replacement: they act upstream, at the hypothalamus and pituitary, rather than replacing the hormone the gland produces.

The three axes that matter here:

• HPA — hypothalamic-pituitary-adrenal (stress, cortisol, DHEA)
• HPG — hypothalamic-pituitary-gonadal (LH, FSH, testosterone, estrogen)
• HPT — hypothalamic-pituitary-thyroid, which peptides rarely target

Because these compounds act on release rather than substituting for the product, the negative-feedback loop stays intact. That is the genuine mechanistic argument for them, and it is a real one.

It is worth separating, at the top, what is established from what is convention. Established with human trial data: the GHRH + GHRP synergy (PMID 2108187), CJC-1295 pharmacokinetics (PMID 16352683), ipamorelin's selectivity (PMID 9849822), tesamorelin's visceral fat effect (PMID 20554713), MK-677's body composition and glucose data at the 1-year primary endpoint of a 2-year trial (PMID 18981485), and bremelanotide's phase 3 results (PMID 31599840). Convention without trial support: gonadorelin for testicular preservation on TRT, peptide PCT protocols, and most of the specific dosing and cycling schedules that circulate.

This hub covers the growth hormone axis, HPG axis maintenance, and sexual and reproductive function. Whether you are researching the best peptides for hormones, a TRT peptide stack, growth hormone peptides for anti-aging, or peptides for libido, this is the map.

The Hormone Peptide Universe

The Growth Hormone Axis: A Short Primer

GH is released in pulses from the anterior pituitary, largely at night in association with slow-wave sleep. The age-related decline is real and quantified: in 149 healthy men, deep slow-wave sleep fell from about 18.9% of the night at ages 16–25 to about 3.4% by midlife, with a parallel decline in GH (PMID 10938176). More precisely on the GH–sleep coupling: a sleep-onset-associated pulse is generally the major or only daily episode of active GH secretion in normal men, the amount of SW sleep and the amount of concomitant GH secretion are linearly related, and both decline exponentially with the same chronology (PMID 10984255).

The specific claim that "by 40 you make roughly half the GH you did at 20" has been removed from this page — the decline is well documented but that ratio was not sourced, and the citable figures above are more useful anyway.

Two receptor families drive GH release:

1. The GHRH receptor, activated by growth hormone-releasing hormone. Sermorelin, tesamorelin, and CJC-1295 act here.
2. GHS-R1a, the ghrelin receptor. Ipamorelin, GHRP-2/-6, hexarelin, and MK-677 act here.

GH's main downstream output is hepatic IGF-1, which is what bloodwork measures, because GH pulses are too brief to catch reliably on a single draw.

Why pulsatility matters — and the evidence for it

This is not just a theoretical preference. In healthy volunteers, 200 µg of GHRH given as four 50 µg episodic boluses across the evening significantly increased stage 4 slow-wave sleep and REM sleep versus placebo, while the same total dose given as a continuous infusion produced no significant sleep effect (PMID 8772566). Same drug, same total exposure, different result depending on whether it was pulsed.

That is the strongest available argument for pulsatile dosing patterns and for preferring short-acting compounds. It also cuts against the long-acting forms: CJC-1295 with DAC has an estimated half-life of 5.8 to 8.1 days and keeps IGF-I above baseline for up to 28 days after multiple doses (PMID 16352683) — which is the opposite of pulsatile.

• GH Secretagogue Protocol for the mechanism overview
• GH Peptide Stacking Guide for combination protocols

GHRH Analogs: Sermorelin, Tesamorelin, CJC-1295

That last row is the single most under-acknowledged fact in this category. The community prefers the no-DAC form on pulsatility grounds — a preference the GHRH sleep data supports in principle (PMID 8772566) — but the compound with the published human pharmacology is the DAC form.

Choosing between them, honestly:

• Tesamorelin is the only one with rigorous human RCT data, and that data is specific: visceral fat, in HIV-associated lipodystrophy, with no effect on subcutaneous fat. Extending it to general body recomposition is an extrapolation. Its approval and compounding position are dated on our tracker as tesamorelin.
• Sermorelin is the most physiologic by half-life and has the longest clinical history, without modern outcome trials in the way it is now used.
• CJC-1295 no-DAC is the stacking workhorse by convention, not by published pharmacokinetics.
• CJC-1295 with DAC has the data and the least physiologic profile. Both facts are true.

Deeper dives: Sermorelin Protocol · Tesamorelin Protocol · CJC-1295 Protocol

GHRPs: Ipamorelin, GHRP-2, GHRP-6, Hexarelin, MK-677

The honest summary of this class: ipamorelin's clean reputation is earned in animal work, hexarelin's sleep cost is measured in humans, and MK-677's lean-mass benefit comes packaged with added limb fat and worse glucose handling at the same 1-year endpoint. The FDA position for the two of them is recorded with dates as ipamorelin and MK-677. The "hunger / cortisol / strength" ratings previously tabulated here without sources have been replaced with what the cited studies actually measured.

Deeper dives: Ipamorelin Protocol · GHRP-2 Protocol · GHRP-6 Protocol · Hexarelin Protocol · MK-677 Protocol

The Classic Synergy: GHRH + GHRP

This is the best-evidenced idea in the whole hub, and it is worth citing properly rather than asserting.

In 18 normal men, the synthetic hexapeptide GHRP (His-DTrp-Ala-Trp-DPhe-Lys-NH2) was given by intravenous bolus at 0.1, 0.3, and 1.0 µg/kg, alone and together with GHRH(1-44)-NH2 at 1.0 µg/kg. GHRP stimulated GH release dose-dependently and acted synergistically with GHRH — the combination exceeded what either produced alone. Specificity was assessed by measuring prolactin, LH, TSH and cortisol, and no adverse clinical effects or laboratory abnormalities were observed in response to GHRP (PMID 2108187).

Two caveats that matter for translating it. That was an acute intravenous study measuring GH peaks, not a subcutaneous protocol measuring body composition over months. And the GHRP tested was the parent hexapeptide, not ipamorelin — so the popular CJC-1295-plus-ipamorelin pairing inherits the synergy principle by analogy rather than by direct test.

The mechanistic explanation usually given — GHRH increases the response of somatotrophs while GHRPs increase the number responding by suppressing somatostatin — is a reasonable reading of the pharmacology and is not something the 1990 study set out to prove.

No dosing figures appear here. The canonical microgram-per-injection, two-to-three-times-daily pattern is community convention with no trial behind it, and it belongs in the protocol guide with that context attached.

Timing does have a rationale. Pre-bed dosing layers onto the sleep-associated GH pulse, which is the major daily secretory episode in normal men (PMID 10984255). And the fasted-dosing instruction has a real mechanistic basis — elevated glucose and insulin suppress GH release — though the specific "no calories for two hours before" window is convention rather than a studied interval.

Full detail: GH Peptide Stacking Guide

The Sexual & Reproductive Peptides

These act on the central nervous system and the melanocortin system rather than on testosterone or estrogen.

PT-141 (Bremelanotide) — The One With Phase 3 Data

Bremelanotide is a melanocortin receptor agonist acting centrally, FDA-approved as Vyleesi for hypoactive sexual desire disorder in premenopausal women, and used off-label in men.

What the trials showed. Two identical phase 3, randomized, double-blind, placebo-controlled multicentre trials (RECONNECT) randomized 1,267 premenopausal women with HSDD to bremelanotide 1.75 mg subcutaneously as needed or placebo for 24 weeks. Women on bremelanotide had statistically significant increases in sexual desire on the Female Sexual Function Index desire domain (0.30 in study 301, 0.42 in study 302, 0.35 integrated; all P ≤ .005) and significant reductions in desire-related distress (−0.33 integrated). More nausea and flushing occurred on drug, and most treatment-emergent adverse events were tolerability-related and mild to moderate (PMID 31599840).

Read those numbers honestly. They are statistically robust across two identical trials, and the effect sizes are small — a third of a point on a desire scale. That is a real drug with a real, modest effect, which is a different claim from the transformative one usually made for it. Prespecified subgroup analyses have been published separately (PMID 35230162), along with a phase 2b responder analysis (PMID 31277966).

Mechanistically it does not act on the vasculature the way PDE5 inhibitors do, which is the basis for using it when desire rather than mechanics is the limiting factor. The claim that it works specifically in psychogenic erectile dysfunction or post-SSRI sexual dysfunction has been removed — the phase 3 program studied premenopausal women with HSDD, not those populations.

PT-141 Protocol

Melanotan II

A non-selective melanocortin agonist, originally developed in the context of skin pigmentation, with sexual side effects that drive much of its off-label use. It is not the same as PT-141: less selective, longer-acting, with a broader effect profile including pigmentation, appetite suppression and nausea.

No clinical trial of Melanotan II for any indication was located. The pigmentation concern is documented rather than theoretical: dermoscopic changes in melanocytic naevi have been reported during Melanotan II use (PMID 23052015). A compound that stimulates melanocytes and visibly changes existing moles is a compound that makes melanoma surveillance harder, which is the concrete version of the "theoretical melanoma concern" this page used to state. Anyone using it needs dermatological mole monitoring, and anyone with a history of atypical naevi or melanoma should not.

Melanotan II Protocol

Oxytocin — Where the Evidence Went Backwards

This section has been substantially rewritten, because the finding the whole "bonding peptide" framing rests on did not replicate.

The influential result was that intranasal oxytocin increased transfers made by investors in a trust game, interpreted as oxytocin increasing trust in strangers (PMID 15931222). A large double-blind, placebo-controlled registered replication with more than 95% power, which deliberately reproduced the original study's minimal-social-contact condition, found no effect of oxytocin on trusting behaviour (PMID 32514040). A subsequent registered report using pooled equivalence testing reached the same conclusion, titled "Absence of a meaningful effect of intranasal oxytocin on trusting behavior" (PMID 41880977).

So: the trust effect is, on current evidence, not there. That does not mean oxytocin does nothing — it is a real neuropeptide with real receptors — but the specific social-cognition claims that sell compounded intranasal oxytocin are built on a result that has now failed a high-powered replication twice. Effects reported by users are subtle, and the page previously described the social cognition literature as merely "controversial," which understated it.

Oxytocin Protocol

PT-141 vs Sildenafil

Plain summary: if the issue is desire rather than mechanics, PT-141 has the approval and the trial data, for a modest effect. If the issue is mechanics, PDE5 inhibitors are the far better-evidenced option. Use in men is off-label, and combining them is a decision for a physician — particularly given the blood pressure profile.

Gonadorelin & Kisspeptin: HPG Axis Maintenance

When a man starts testosterone replacement, the hypothalamus senses the exogenous androgen and reduces its GnRH signal; LH falls, and the testes lose their stimulus. That is the testicular shutdown behind TRT-associated infertility.

The legacy solution is hCG, which mimics LH and acts directly on the testes.

The popular modern alternative is gonadorelin, synthetic GnRH, on the reasoning that it acts one step upstream and prompts the pituitary to release its own LH and FSH. This is the part of the page that needs the most honesty, so here it is plainly: no published trial of gonadorelin for testicular preservation during TRT could be located. The mechanism is coherent and the practice is widespread, but it is practice, not evidence.

There is also a specific mechanistic question worth raising rather than glossing over. GnRH is secreted by a hypothalamic pulse generator, and gonadotropin release depends on that pulsatile pattern (PMID 30272161); continuous or non-physiologic GnRH receptor stimulation causes pituitary desensitization, which is the entire basis of GnRH agonist therapy in prostate cancer and precocious puberty. Gonadorelin has a very short half-life and is typically injected a few times a week. Whether a handful of brief weekly spikes meaningfully supports an axis that normally pulses every couple of hours is a fair question that the available literature does not answer.

Kisspeptin-10 acts further upstream still, on the GnRH neurons themselves, and kisspeptin signalling is an active research area in fertility and hypothalamic amenorrhoea (PMID 36103784). Its use in peptide protocols is newer and less studied than gonadorelin's.

Gonadorelin & Kisspeptin Protocol

Peptide PCT: Post-Cycle Recovery

Post-cycle therapy is used after suppressive androgen cycles to restart endogenous testosterone production. Traditional PCT relies on SERMs such as clomiphene or enclomiphene and on hCG, both of which have a clinical literature. Peptide-based PCT adds gonadorelin or kisspeptin as an upstream restart signal.

No trial of a gonadorelin-containing PCT protocol was located. The structural logic — keep the axis stimulated during clearance, then add a SERM once exogenous androgens have cleared, and monitor LH, FSH, total and free testosterone and estradiol on a schedule — is reasonable and is what practitioners do. The monitoring half of that is the part with actual clinical grounding.

Peptides do not replace SERMs in PCT. The dose schedules previously listed here have been removed. Full framework: Peptide PCT Protocol

Protocol Structures

The stack table that used to occupy this section listed microgram and milligram doses for nine protocols. Those have been removed: apart from tesamorelin's 2 mg and bremelanotide's 1.75 mg, both of which are trial and label doses, none came from a published study.

Detailed stacks: AOD-9604 + Tesamorelin Stack · GH Peptide Stacking Guide · the full protocol library

Hormone Optimization vs Direct Replacement

The clinical pattern holds: peptides act on a gland that still works; hormones replace one that does not. What has been removed from this section is the implication that the peptide column wins on outcomes — for most rows, the peptide column wins on mechanism and loses on evidence.

WADA Status — Critical for Tested Athletes

Assume every GH-releasing compound in this hub is prohibited at all times.

The WADA Prohibited List includes growth hormone, its releasing factors and secretagogues — GHRH and its analogs, GHRPs and ghrelin mimetics — and IGF-1 and its analogs, under the peptide hormones, growth factors and related substances class. Agents affecting gonadotropin release, and hCG and LH in males, appear under hormone and metabolic modulators. Non-approved substances with no current human therapeutic approval are prohibited as a class.

Per-compound classifications have been removed from this page and replaced with a direct instruction: check the current list yourself. WADA republishes the Prohibited List annually, classifications and specific-substance status change, and a table on a hub page is exactly the wrong place to learn your eligibility from. The list is at wada-ama.org/en/prohibited-list, and your federation's medical liaison is the authority for your sport.

Two points worth keeping. Detection for this class increasingly relies on biomarker and longitudinal-profile approaches rather than on catching the parent compound, so "it clears quickly" is not a defence. And a compound being unapproved rather than a hormone does not make it permitted — the non-approved substances class exists precisely to cover that.

Bloodwork

A real hormone protocol is built on labs. Baseline first, then repeat on a schedule your clinician sets.

The "optimal range" column that used to appear here has been removed. Those figures were community-optimization targets presented as reference ranges, they differ from laboratory reference intervals, and none was sourced — publishing them next to a protocol on a YMYL page turns convention into a target. Bring the numbers to a clinician who can read them against your history and your assay's own reference interval.

IGF-1 is the dial for GH-axis protocols, and the reason not to push it above the age-adjusted range is that association: pooled individual participant data from 12 prospective studies, 3,700 prostate cancer cases and 5,200 controls, found high circulating IGF-I associated with moderately increased risk (PMID 18838726). Those studies measured endogenous IGF-I within the physiological range, which is a reason to stay inside it rather than a measurement of what happens outside it.

See the Bloodwork Checklist.

Side Effects & Safety

GH-axis peptides

• Fluid retention, carpal-tunnel-type tingling, numbness, joint discomfort. These are recognized effects of growth hormone excess and are the classic signal that exposure is too high.
• Glucose and insulin drift. Documented, not theoretical: fasting glucose rose about 5 mg/dL and insulin sensitivity fell by the 1-year primary endpoint of a 2-year trial of MK-677 25 mg daily (PMID 18981485). GH is counter-regulatory to insulin.
• Cortisol and prolactin elevation with the non-selective GHRPs — measured for GHRP-2 and GHRP-6 versus ipamorelin in swine (PMID 9849822) and for hexarelin in humans (PMID 15177700).
• Sleep disruption with hexarelin, which decreased stage 4 sleep and delta power in the same human study (PMID 15177700). Worth knowing if you are taking a GH peptide for sleep.
• IGF-1 and cancer. The prostate association above (PMID 18838726) is the reason most clinicians avoid these compounds in active or recent malignancy and keep IGF-1 within range.
• Injection site reactions and headache, commonly reported.

Sexual function peptides

• Bremelanotide. Nausea and flushing were significantly more common than placebo in the phase 3 trials, and most adverse events were tolerability-related and mild to moderate (PMID 31599840). Transient blood pressure elevation is described in the label, so uncontrolled hypertension and cardiovascular disease are the relevant cautions.
• Melanotan II. Nausea, flushing, appetite suppression, and pigmentary change — including documented dermoscopic changes in existing melanocytic naevi (PMID 23052015). Dermatological monitoring is not optional, and prior atypical naevi or melanoma should rule it out.
• Oxytocin. Generally well tolerated in research use. The relevant caveat is efficacy rather than safety: the trust finding failed a high-powered registered replication (PMID 32514040).

HPG axis peptides

Gonadorelin is described as well tolerated at typical doses, with injection site reactions and transient headache. The honest risk here is not a side effect but an efficacy gap: no trial supports its use for TRT-adjunct testicular preservation, so someone relying on it for fertility preservation may be relying on something that has not been shown to work. LH, FSH and a semen analysis are how you find out, and both belong in the plan from the start.

Kisspeptin has limited side effect data in research dosing.

Reconstitution & Storage

Most of these peptides ship lyophilized and are reconstituted with bacteriostatic water before use. The general handling principles: add the diluent slowly down the side of the vial rather than directly onto the powder, swirl rather than shake, refrigerate after reconstitution, do not freeze a reconstituted vial, protect from light, and keep unopened lyophilized vials frozen for long-term storage.

Specific stability windows have been moved to the dedicated guides rather than asserted here, because they vary by peptide, concentration, and diluent and the single figure that used to appear on this page covered all of them. See the Reconstitution Cheat Sheet and Storage & Handling Guide.

Working With a Provider

Hormone peptides are prescription compounds in the US, and provider quality matters more than peptide price. On price itself, our price-per-milligram index publishes dated figures for the GLP-1 medications and states plainly that no first-party survey exists yet for the research-market compounds — so treat a hormone-peptide quote as a quote, not a market rate.

Three provider tiers: TRT and men's health clinics, strongest on testosterone and HPG work; anti-aging and longevity clinics, deepest on GH peptides and IGF-1 management; and telehealth peptide services, most convenient with the widest quality range.

Questions to ask before committing:

• What does the baseline panel include, and does it include IGF-1? If not, walk away.
• What is the protocol when IGF-1 goes above the age-adjusted range?
• Which compounding pharmacy, and can I see a certificate of analysis?
• For TRT: what is the testicular preservation plan, and how will fertility be monitored — because the popular peptide answer has no trial behind it?
• Are there real consultations, or only intake forms?

See the Compounding Pharmacy Guide.

Cycling Strategy

The cycling table previously here assigned on- and off-week counts to twelve compounds. None of those numbers derives from a published study of these peptides, so the table has been removed.

What the literature does support:

• Pulsed beats continuous for GHRH, demonstrated directly: episodic boluses increased stage 4 and REM sleep where the same total dose by infusion did not (PMID 8772566).
• Washout is slower than people assume with the long-acting forms: IGF-I remained above baseline for up to 28 days after multiple CJC-1295 doses (PMID 16352683).
• Continuous use is not automatically harmful, but it is not free either: MK-677 was dosed continuously across a 2-year trial and, by its 1-year primary endpoint, had produced both the lean-mass gain and the insulin-sensitivity decline (PMID 18981485). That trial was also explicitly underpowered to evaluate functional endpoints.
• Tesamorelin's effect was maintained at 52 weeks in those who continued treatment (PMID 20554713). What happens to visceral fat after long-term discontinuation was not followed in that programme, so claims that it "will" fully return are not sourced.
• On-demand compounds are not cycled. Bremelanotide was studied as needed, not on a schedule (PMID 31599840).

The general rule that survives: cycle if you are chasing IGF-1 elevation, run continuously if you are maintaining an axis, and monitor either way. See Peptide Cycling Strategies.

Frequently Asked Questions: Hormone Peptides

What are the best peptides for hormones? It depends which axis, and the evidence differs sharply by compound. For visceral fat, tesamorelin has phase 3 data. For low desire in premenopausal women, bremelanotide has two phase 3 trials. For the GH axis, a GHRH analog plus a selective GHRP is the best-reasoned combination, resting on a 1990 human study showing GHRH and GHRP act synergistically. For TRT support, gonadorelin is the popular choice and has no supporting trial.

Are hormone optimization peptides safer than HGH or TRT? "Different" rather than "safer." Peptides preserve your own feedback loops, which is mechanistically gentler. They are also less studied for most of the uses described here, and one of the best-documented compounds in the class measurably reduced insulin sensitivity by its 1-year primary endpoint, without being powered to show a functional benefit. For diagnosed deficiency, replacement remains the standard of care.

Can I run a TRT peptide stack? People do combine testosterone with gonadorelin for testicular preservation, sometimes with an aromatase inhibitor and a GH peptide pair. This is a provider-managed protocol, and one component deserves a flag: no published trial supports gonadorelin for that purpose. If fertility preservation is the goal, monitoring LH, FSH and a semen analysis is how you find out whether it is working rather than assuming.

How fast do growth hormone peptides work? Axis activity shows up quickly on labs — after a single CJC-1295 dose, IGF-I was elevated for nine to eleven days. Body composition is much slower: the two-year MK-677 trial measured a 1.1 kg fat-free mass difference over a year. Subjective reports of better sleep and recovery within a few weeks are user reports rather than trial endpoints.

What are the best peptides for libido? Bremelanotide is the only one here with randomized phase 3 evidence, and that evidence is in premenopausal women with hypoactive sexual desire disorder, with modest effect sizes. Use in men is off-label. Melanotan II has no clinical trial and carries a documented pigmentary concern. Oxytocin's social and bonding claims rest on a finding that failed replication.

Do I have to inject hormone peptides? Mostly yes, though MK-677 is oral and oxytocin is often compounded for intranasal use. Route matters more than convenience in some cases: the GHRH sleep data shows that how a compound is delivered over time changes whether it works at all.

Will GH peptides give me bigger pecs and a six-pack? No. The most direct test available is a meta-analysis of 11 placebo-controlled trials of growth hormone itself in 254 healthy young subjects: it increased lean body mass and decreased fat mass but did not improve muscle strength or maximum oxygen uptake. Expect a composition effect over months, not a physique transformation, and treat anyone promising otherwise accordingly.

Can women use hormone peptides? Bremelanotide has its strongest evidence in women, since the phase 3 programme studied premenopausal women with HSDD. The GH-axis peptides are used in women, and the trials behind them enrolled mixed or predominantly male populations, so sex-specific dosing guidance does not really exist. Gonadorelin is rarely used in women outside fertility contexts. Provider supervision matters more here, not less.

Will GH peptides cause diabetes? The relevant data point is specific rather than reassuring: at the 1-year primary endpoint of a 2-year trial of MK-677 25 mg daily, fasting glucose rose by about 5 mg/dL and insulin sensitivity decreased (PMID 18981485). That is not diabetes, and it is a measurable move in the wrong direction from the best-documented compound in the class. Anyone running a GH-axis protocol beyond a few months should be tracking fasting glucose, fasting insulin and HbA1c rather than assuming.

What happens when I stop? Slower than people expect for the long-acting compounds — IGF-I stayed above baseline for up to 28 days after multiple CJC-1295 doses. Tesamorelin's visceral fat reduction was maintained at 52 weeks in those who continued treatment; what happens long-term after stopping was not followed, so claims either way are unsourced. Bremelanotide has no carry-over by design. Composition changes persist to the extent that training and nutrition persist.

Featured Protocols on Peptides.NYC

Growth Hormone Axis

• Sermorelin Protocol — the shortest-acting GHRH analog
• Tesamorelin Protocol — the one with phase 3 visceral fat data
• CJC-1295 Protocol — DAC vs no-DAC, and which one the data covers
• Ipamorelin Protocol — the selective GHRP
• GHRP-2 Protocol · GHRP-6 Protocol
• Hexarelin Protocol — strong GH release, measured sleep cost
• MK-677 Protocol — oral, with the 1-year glucose data
• GH Secretagogue Protocol — mechanism and selection framework
• GH Peptide Stacking Guide — combination protocols

Sexual & Reproductive Function

• PT-141 Protocol — the phase 3 data in full
• Melanotan II Protocol — pigmentation, arousal, and the naevi concern
• Oxytocin Protocol — including the replication failure

HPG Axis & TRT Support

• Gonadorelin & Kisspeptin Protocol — the modern TRT adjunct, and its evidence gap
• Peptide PCT Protocol — post-cycle restart with SERMs and peptides

Supporting Guides

• AOD-9604 + Tesamorelin Stack
• Bloodwork Checklist · Peptide Cycling Strategies
• Reconstitution Cheat Sheet · Storage & Handling Guide
• Compounding Pharmacy Guide

Related Hubs on Peptides.NYC

• Healing & Recovery Peptide Hub — BPC-157, TB-500, GHK-Cu
• Fat Loss Peptide Hub — GLP-1s, tesamorelin, AOD-9604
• Muscle & Performance Peptide Hub — the GH axis for body composition, and the IGF-1 evidence
• Cognitive Peptide Hub — Semax, Selank, Cerebrolysin
• Longevity Peptide Hub — Epitalon, GHK-Cu, and the IGF-1 trade-off
• Immune Peptide Hub — thymosin alpha-1, LL-37
• Sleep Peptide Hub — why pre-bed dosing is the convention

Disclaimer: This content is for educational purposes only and is not medical advice. Hormone optimization peptides are prescription or research compounds in the United States and are not FDA-approved for most uses described here; tesamorelin (Egrifta) and bremelanotide (Vyleesi) are approved for narrow, specific indications. Several claims common in this category are not supported by published trials, and this page flags them where that is the case. Hormone peptides act on complex endocrine systems and should be used only under the supervision of a qualified healthcare provider with appropriate baseline and follow-up bloodwork. Many of these compounds are prohibited under WADA and athletic governing-body rules — verify against the current Prohibited List. Discuss your full medical history, current medications, and goals with a licensed clinician before initiating any protocol. Peptides.NYC does not sell, prescribe, or recommend specific products.

Selected References

Every PMID linked above points to the PubMed record for that paper, so you can check the claim against the abstract yourself.

1. Bowers CY, Reynolds GA, Durham D, et al. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. Journal of Clinical Endocrinology and Metabolism. 1990. PMID 2108187 · doi:10.1210/jcem-70-4-975
2. Teichman SL, Neale A, Lawrence B, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. Journal of Clinical Endocrinology and Metabolism. 2006. PMID 16352683 · doi:10.1210/jc.2005-1536
3. Marshall L, Mölle M, Böschen G, et al. Greater efficacy of episodic than continuous growth hormone-releasing hormone (GHRH) administration in promoting slow-wave sleep (SWS). Journal of Clinical Endocrinology and Metabolism. 1996. PMID 8772566 · doi:10.1210/jcem.81.3.8772566
4. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology. 1998. PMID 9849822 · doi:10.1530/eje.0.1390552
5. Frieboes RM, Antonijevic IA, Held K, et al. Hexarelin decreases slow-wave sleep and stimulates the secretion of GH, ACTH, cortisol and prolactin during sleep in healthy volunteers. Psychoneuroendocrinology. 2004. PMID 15177700 · doi:10.1016/S0306-4530(03)00152-5
6. Nass R, Pezzoli SS, Oliveri MC, et al. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Annals of Internal Medicine. 2008. PMID 18981485 · doi:10.7326/0003-4819-149-9-200811040-00003
7. Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in HIV-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. Journal of Clinical Endocrinology and Metabolism. 2010. PMID 20554713 · doi:10.1210/jc.2010-0490
8. Hermansen K, Bengtsen M, Kjær M, et al. Impact of GH administration on athletic performance in healthy young adults: a systematic review and meta-analysis of placebo-controlled trials. Growth Hormone & IGF Research. 2017. PMID 28514721 · doi:10.1016/j.ghir.2017.05.005
9. Van Cauter E, Copinschi G. Interrelationships between growth hormone and sleep. Growth Hormone & IGF Research. 2000. PMID 10984255 · doi:10.1016/s1096-6374(00)80011-8
10. Van Cauter E, Leproult R, Plat L. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA. 2000. PMID 10938176 · doi:10.1001/jama.284.7.861
11. Roddam AW, Allen NE, Appleby P, et al. Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies. Annals of Internal Medicine. 2008. PMID 18838726 · doi:10.7326/0003-4819-149-7-200810070-00006
12. Kingsberg SA, Clayton AH, Portman D, et al. Bremelanotide for the treatment of hypoactive sexual desire disorder: two randomized phase 3 trials. Obstetrics and Gynecology. 2019. PMID 31599840 · doi:10.1097/AOG.0000000000003500
13. Simon JA, Kingsberg SA, Portman D, et al. Prespecified and integrated subgroup analyses from the RECONNECT phase 3 studies of bremelanotide. Journal of Women's Health. 2022. PMID 35230162 · doi:10.1089/jwh.2021.0225
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Inclusion here is not endorsement — reference 16 is listed alongside references 17 and 18 precisely because it did not replicate, and reference 8 because it is a null result for strength. Nothing on this page is medical advice.

Source: https://peptides.nyc/learn/goal/hormones