Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/Tesamorelin
Growth Hormone & Anabolic Support
TH9507 · Egrifta® · trans-3-hexenoyl-GRF(1-44)
A stabilised growth-hormone-releasing hormone analogue and the only FDA-approved drug that specifically targets visceral adipose tissue — approved for one narrow indication and used far outside it.
Tesamorelin is the outlier on this site: an actually approved drug. It is a synthetic analogue of growth-hormone-releasing hormone, stabilised against enzymatic degradation by a trans-3-hexenoyl group at the N-terminus, and it was approved by the FDA in 2010 as Egrifta for the reduction of excess visceral abdominal fat in HIV-infected patients with lipodystrophy.
The pivotal data is unusually clean for anything in this field. In the phase 3 programme, daily 2 mg tesamorelin reduced visceral adipose tissue by roughly 15–18% over 26 weeks against placebo, with improvements in triglycerides — and, importantly, with subcutaneous fat largely preserved.[1][2] That visceral selectivity is the property that makes it interesting well beyond its licensed indication.
Because it acts on the pituitary rather than replacing growth hormone directly, tesamorelin preserves the pulsatile architecture of GH secretion and remains subject to somatostatin negative feedback — a meaningfully different safety profile from exogenous HGH. It is also the mechanism that requires it to be dosed daily, and requires a functioning pituitary to work at all.
Tesamorelin has a label, a boxed set of contraindications, defined monitoring requirements and post-marketing surveillance. Almost nothing else on this site does. Where the study tier here says something, it is backed by regulatory-grade evidence — which makes the gap to the grey-market tier all the more visible.
GHRH receptor agonism at the pituitary. Tesamorelin binds the GHRH receptor on somatotrophs, stimulating synthesis and pulsatile release of endogenous growth hormone. Because the stimulus is upstream, the resulting GH profile retains its natural pulsatility and remains subject to somatostatin-mediated negative feedback — the body can still say no.
Downstream IGF-1. GH acts on the liver to raise IGF-1, which mediates most anabolic effects. IGF-1 is the practical monitoring marker: it integrates GH exposure over time in a way that spot GH measurements cannot, and it is what the label directs clinicians to watch.
Visceral adipose selectivity. Visceral adipocytes are more lipolytically responsive to GH than subcutaneous adipocytes, with higher GH receptor density and greater sensitivity to GH-driven lipolysis. This is why the effect concentrates on visceral fat and largely spares subcutaneous fat — the finding that distinguishes tesamorelin from general weight-loss pharmacology.
Hepatic fat reduction. Follows from the same lipolytic mechanism plus reduced visceral fat flux to the portal circulation — the basis of the NAFLD/MASLD trial work.
Counter-regulatory glucose effect. GH is counter-regulatory to insulin. Raising GH raises insulin resistance, and this is a documented, label-level effect rather than a theoretical one.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Two phase 3 randomised placebo-controlled trials in HIV-associated abdominal fat accumulation reported significant CT-measured visceral adipose reduction on 2 mg daily, with subcutaneous fat preserved.
Significant reductions in triglycerides and improvements in the cholesterol:HDL ratio accompanied visceral fat loss in the pivotal trials.
Randomised trial work in people with HIV and hepatic steatosis reported reduced liver fat and attenuated fibrosis progression with tesamorelin.
Consistent, dose-related IGF-1 elevation confirming pituitary GH stimulation — the pharmacodynamic marker used throughout the programme.
Unlike exogenous GH administration, GHRH-analogue stimulation retains physiological pulse architecture and negative feedback control.
Visceral fat returns after tesamorelin is stopped — established in the extension studies. Any benefit is contingent on continued use.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The mechanism is not HIV-specific, and the entire off-label interest rests on this. Trials in general obesity and in metabolic syndrome are limited; the approval is narrow for regulatory reasons, not because the mechanism is thought to be indication-specific.
GHRH administration has been studied in cognition, with some reported benefit in older adults and in MCI. Interesting, small, and not a tesamorelin approval.
The rationale for pairing tesamorelin with incretin-driven weight loss. GH is nitrogen-sparing in principle; the specific combination has not been studied.
Extrapolated from GH axis physiology and slow-wave sleep association. Not a trial endpoint.
GH-driven collagen synthesis is documented in GH-deficiency literature. Translation to healthy adults on a GHRH analogue is inferred.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The characteristic report — waist reduction disproportionate to total weight change, matching the visceral-selectivity mechanism. Among the more mechanistically consistent anecdotal claims on this site.
Reported with evening fasted dosing, in line with the physiological nocturnal GH pulse.
Reported over longer courses. Uncontrolled.
Classic GH-excess effects, reported by users who escalate beyond the labelled 2 mg. These are documented adverse effects, not novelties.
Community practice enforces a two-hour fasted window before evening dosing on the grounds that insulin blunts GH release. This is physiologically real — insulin suppresses GH secretion.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The most frequent adverse event in the pivotal trials — erythema, pruritus, pain and rash. Prominent enough to drive discontinuations.
A documented, label-level effect. GH is counter-regulatory to insulin; the label directs monitoring of glucose status, and this is the most clinically significant metabolic downside.
The characteristic GH-excess adverse-event cluster, reported at meaningful rates and generally dose- and duration-related.
Including rash and urticaria; the label carries a hypersensitivity contraindication.
The label contraindicates use in active malignancy and requires evaluation of pre-existing malignancy status, on the standard basis that GH/IGF-1 signalling is mitogenic.
Including after pituitary surgery, hypophysectomy, head irradiation or head trauma — the drug requires an intact axis to work and its use is contraindicated where that axis is disrupted.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The general concern attached to any sustained GH/IGF-1 elevation. Approved use is monitored with IGF-1 levels for exactly this reason; unmonitored off-label use is not.
Not a documented tesamorelin outcome at labelled dose, but the theoretical endpoint of sustained GH excess.
A documented insulin-resistance effect in an unmonitored user with unrecognised impaired glucose tolerance is the most likely real-world harm from off-label use.
Stacking a GH secretagogue with retatrutide pushes hepatic glucose output in the same direction from two mechanisms. Rarely acknowledged in community stacks.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common community complaint, typically early and often settling.
Reported at higher doses; a recognised GH-excess effect.
Consistent with trial findings.
Reported by users who test. Directly consistent with the labelled effect.
Frequently reported with evening dosing.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The labelled dose is 2 mg daily by subcutaneous abdominal injection, with site rotation. This is the dose the entire efficacy and safety dataset was generated at.
Trials used continuous daily dosing over 26 weeks with a 26-week extension. There is no cycled dosing in the approved regimen.
The label directs periodic IGF-1 monitoring, with dose interruption or discontinuation for persistent significant elevation.
| Setting | Dose | Duration | Key outcome |
|---|---|---|---|
| Phase 3 (HIV lipodystrophy) | 2 mg daily SC | 26 weeks | −15 to −18% visceral adipose tissue |
| Phase 3 extension | 2 mg daily SC | +26 weeks | Effect maintained; reverses off-drug |
| NAFLD trial | 2 mg daily SC | 12 months | Reduced hepatic fat, attenuated fibrosis |
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Aligns exogenous GHRH stimulus with the physiological nocturnal GH pulse and avoids insulin-mediated suppression of GH release. Physiologically coherent; trials did not mandate timing to this degree.
The argument is that the approved population had a specific pathology and lower doses may suffice elsewhere. No dose-ranging data supports any particular alternative.
Community rationale for 4-vial-on / 4-week-off patterns. The approved regimen is continuous, so this practice is not derived from the evidence base.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Half the labelled dose, taken two hours fasted before sleep — the figure specified in the Gold Standard protocol.
Users pursuing the trial-magnitude visceral fat effect generally use the approved dose.
The cycling pattern in the Gold Standard protocol. Not derived from any trial regimen.
The GHRH + ghrelin-mimetic pairing, on the argument that the two act through separate pituitary mechanisms.
| Community use | Dose | Timing | Cycle |
|---|---|---|---|
| Gold Standard Protocol | 1 mg | Nightly, 2 h fasted | 4 vials on, 4 weeks off |
| Label-equivalent | 2 mg | Nightly | Continuous or cycled |
| With ipamorelin | 1–2 mg | Nightly, fasted | Per stack |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
GHRH analogues and GH secretagogue receptor agonists act on distinct pituitary receptors and produce a greater GH response together than either alone. This is well characterised in endocrine physiology — though not as a tesamorelin + ipamorelin product.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Direct application of the two-receptor co-stimulation principle. The most mechanistically grounded stack on this site — and still not a studied combination product.
Two independent routes to visceral adipose reduction. The counter-consideration nobody raises: both push glucose handling in an unfavourable direction.
GH-driven collagen synthesis alongside BPC-157/TB-500 repair signalling. Speculative.
Insulin suppresses GH release. Eating before an evening dose works directly against the mechanism — the reason the fasted window exists.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The standard community GH stack.
The most common reason tesamorelin appears in a metabolic stack.
Practical community rule derived from the insulin-GH relationship.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
2 mg subcutaneously once daily, with defined reconstitution instructions, site rotation, IGF-1 monitoring, glucose monitoring, and contraindications including active malignancy, pregnancy and disrupted pituitary axis.
26-week randomised placebo-controlled treatment with CT-measured visceral adipose tissue as primary endpoint, plus a 26-week extension characterising maintenance and reversal.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Dose to an IGF-1 level within the age-adjusted reference range rather than to a fixed milligram figure. This is what the labelled monitoring requirement implies, and it is the single most useful thing an off-label user could adopt.
Given the documented insulin-resistance effect, HbA1c and fasting glucose before and during use is the minimum defensible monitoring.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
1 mg nightly, two hours fasted, sleep after dosing; run for four vials then break for four weeks before restarting. Reproduced as circulated.
Placed in the structural repair and anabolic rebuild quarter alongside GH-axis compounds rather than in the opening metabolic phase.
Tesamorelin is the only compound in the growth-hormone section of this library with an approval, and the only one whose effect on visceral fat was demonstrated rather than asserted. That makes it the reference point the others should be read against — and it makes the gap between its evidence and its off-label use unusually easy to see.
Tesamorelin is approved for one thing: reduction of excess visceral adipose tissue in HIV-associated lipodystrophy. Every other use on this page is extrapolation from that indication. It is a prescription medicine, and visceral fat re-accumulates when it is stopped — the effect is maintained by continued treatment, not banked.
Pathophysiology
Long-term antiretroviral therapy in some people produces redistribution of fat toward visceral depots, with the metabolic consequences that follow from visceral adiposity specifically.
Mechanistic rationale
Randomised trials reported significant reductions in visceral adipose tissue measured by CT, without the loss of subcutaneous fat that would worsen the appearance problem. This is the evidence base every other claim about this compound is borrowed from, and it is worth knowing that it was generated in a specific population with a specific cause of visceral accumulation.
Community reports
Patients describe waist reduction as the visible change. Discontinuation reverses it, which is consistently reported and is exactly what the trials predicted.
Components carrying the argument: Stabilised GHRH analogue → pulsatile GH → lipolysis
Pathophysiology
Visceral adipose tissue is metabolically active, drains to the portal circulation, and is independently associated with insulin resistance and cardiovascular risk in a way subcutaneous fat is not.
Mechanistic rationale
The mechanism — GH-driven lipolysis with a preference for visceral depots — does not depend on HIV, so the extrapolation is more reasonable than most in this library. What has not been shown is that reducing visceral fat pharmacologically in an otherwise healthy person changes any outcome, as opposed to changing a measurement.
Community reports
The dominant off-label use, generally in men in midlife. Waist reduction is commonly reported; nobody is measuring visceral fat by CT, which is what the trials measured and what distinguishes this from ordinary weight loss.
Components carrying the argument: GH-driven lipolysis
Pathophysiology
Hepatic steatosis progresses through steatohepatitis to fibrosis, and it is the fibrosis that determines outcome. Reducing liver fat is necessary but is not the same as changing the disease trajectory.
Mechanistic rationale
Randomised trial work in HIV-associated fatty liver reported reduced hepatic fat fraction and, in some analyses, less fibrosis progression. That is a real and specific finding. It is not equivalent to the steatohepatitis resolution data that the incretins and resmetirom have generated, and it was again generated in a specific population.
Community reports
Cited frequently in longevity and metabolic-optimisation contexts, usually without the population caveat attached.
Components carrying the argument: Hepatic lipid mobilisation
Pathophysiology
IGF-1 is neurotrophic — it supports cerebral blood flow, neurogenesis, neurite outgrowth and synaptic complexity, and is protective against oxidative stress. Visceral adiposity and systemic inflammation are independently associated with cognitive impairment.
Mechanistic rationale
That reasoning was tested rather than merely asserted: a randomised trial examined tesamorelin for neurocognitive impairment in people with HIV and abdominal obesity. The existence of the trial is the point. Anyone citing tesamorelin for cognition should be citing what that trial found rather than the mechanism it was built on, and the mechanism was never the weak link — the translation was.
Community reports
Sharper thinking is commonly reported on GH-axis compounds. It is also what better sleep, more exercise and a new health project produce.
Components carrying the argument: IGF-1 as a neurotrophic mediator
Pathophysiology
Every consequence of raising GH applies here, because raising GH is the mechanism.
Mechanistic rationale
GH is diabetogenic, and glucose intolerance is a labelled concern for this compound specifically — which matters because the population using it off-label is frequently already metabolically compromised. Fluid retention, arthralgia and carpal tunnel symptoms are dose-related class effects. Discontinuation returns visceral fat. And it is contraindicated in active malignancy, in pituitary disease and in pregnancy.
Community reports
The rebound on stopping is the most consistently reported disappointment, and it is not a failure of the compound — it is what the label says happens.
Components carrying the argument: GH itself
| Use | Status | Population studied | The thing to know |
|---|---|---|---|
| HIV lipodystrophy | Approved | HIV, CT-measured VAT | The whole evidence base |
| General visceral fat | Off-label | — | Mechanism transfers; outcomes untested |
| Fatty liver | Off-label | HIV cohort | Not equivalent to MASH resolution data |
| Cognition | Off-label | HIV + abdominal obesity | A trial exists — cite it, not the mechanism |
| Glucose | — | — | Labelled concern — GH is diabetogenic |
| On stopping | — | — | Visceral fat returns |
For visceral adiposity: an energy deficit that can actually be maintained, resistance training to protect lean mass while it happens, sleep, and alcohol reduction — which matters disproportionately for the visceral depot specifically. The incretins now have the largest pharmacological effect on total and visceral fat, with cardiovascular outcome data behind them.
For fatty liver: 7–10% weight loss produces steatohepatitis resolution in a substantial fraction of people and remains the most effective intervention available. Alcohol reduction, treatment of coexisting diabetes, and resmetirom for biopsy-confirmed steatohepatitis with fibrosis. Statins are safe in fatty liver and under-prescribed in it.
For cognition: the unfashionable list is the evidenced one — treating midlife hypertension, correcting hearing loss, physical activity, sleep, glycaemic control, social and cognitive engagement, and not smoking.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
The approved product ships with a defined reconstitution procedure and supplied diluent. Grey-market tesamorelin is supplied lyophilised, commonly 5 or 10 mg per vial, reconstituted with bacteriostatic water. At 1 mg nightly a 10 mg vial is ten days — one of the faster-consumed vials in a typical stack.
Lyophilised: refrigerated per label for the approved product; −20 °C for long-term research storage. Reconstituted: 2–8 °C and used within the in-use period. The approved product has a defined in-use window; research material has none.
Approved product: 1 mg and 2 mg presentations. Research supply: commonly 5 mg and 10 mg vials.
GHRH analogues are more fragile than short repair peptides. Avoid agitation, temperature cycling and light exposure.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
FDA approved as Egrifta for reduction of excess visceral abdominal fat in HIV-infected patients with lipodystrophy. It is a prescription medicine with a full label, defined contraindications and post-marketing surveillance.
Everything outside that indication is off-label. Material sold as research-grade tesamorelin is not the approved product, is not manufactured under the same controls, and carries none of the label's monitoring infrastructure.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: the HIV neurocognitive impairment trial. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
GHRH analogues including tesamorelin are explicitly prohibited by WADA under S2 (peptide hormones, growth factors, related substances and mimetics), at all times, in and out of competition.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
