Is tesamorelin an approved medicine?

Yes, in the United States, as Egrifta, for reduction of excess abdominal fat in people with HIV-associated lipodystrophy. The authorisation is specific to that indication and to the authorised product — not to material supplied as a research reagent.

What did the tesamorelin trials measure?

Visceral adipose tissue, measured on imaging, over 26 weeks, against placebo. Two multicentre randomised double-blind trials reported reductions, alongside elevation of IGF-1.

How is tesamorelin different from sermorelin?

Both act at the GHRH receptor. Tesamorelin carries a chemical modification that slows its breakdown, and it has a large randomised trial programme behind it; sermorelin is the unmodified fragment and its clinical literature is paediatric.

Because the compound is doing what it was designed to do — stimulating pituitary growth hormone release, and IGF-1 is the downstream marker of that. The rise confirms engagement of the axis; it is not itself an outcome.

Research guides

Tesamorelin (Egrifta): what the research says

An approved medicine in the US with one of the largest trial programmes here. Every efficacy trial was in HIV-associated visceral fat, and that limits it.

Available in the catalogue

Supplied as research material. Sizes and pricing are on the product page. Availability is not a statement about what a compound does.

TESAMORELIN
Growth Hormone

Tesamorelin is an authorised medicine in the United States, sold as Egrifta. That fact should be stated at the top of any description of it, and so should the second fact that qualifies it: the authorisation covers one indication in one patient population, and that is also where essentially all the evidence comes from.

What the molecule is

A stabilised analogue of growth hormone-releasing hormone, carrying a trans-3-hexenoyl group that slows its enzymatic breakdown. It has been published as TH9507.

The trial programme

The pivotal work was conducted in people with HIV-associated abdominal fat accumulation, with visceral adipose tissue as the measured endpoint. Two multicentre randomised double-blind placebo-controlled trials, later pooled, reported reductions in visceral adipose tissue against placebo over 26 weeks, alongside elevation of IGF-1. Subsequent published analyses examined associated changes in metabolic profile, liver enzymes and the composition rather than merely the quantity of fat.

By the standards of this catalogue that is an unusually strong evidence base: randomised, placebo-controlled, multicentre, several hundred participants, and independently followed up in later cohorts.

What it is evidence about

It is evidence about visceral adipose tissue in a population with a specific metabolic complication of HIV and its treatment. It is not evidence about body composition in people without that condition, and the endpoint measured was a fat compartment on a scan rather than a health outcome. The distinction is not pedantry — it is the difference between what the trials tested and what the compound is usually described as doing.

The IGF-1 elevation reported in those trials is worth reading carefully too. It confirms the mechanism is engaging the axis as intended; it is not by itself a benefit.

What studies reported

Each entry states what a study examined and the model it used. Nothing below describes an outcome for a person.

Everything below is drawn from published research, and each entry names the model the study used. Approval status varies by compound and by country, and nothing described here is supplied as a medicine or for use in a person.

Falutz et al. (2007)New England Journal of Medicine · 357(23):2359–70
Reported reduction in visceral adipose tissue over 26 weeks against placebo, with elevation of IGF-1, in patients with HIV-associated abdominal fat accumulation.
human, randomised double-blind placebo-controlled, 412 participants Source
Falutz et al. (2010)Journal of Clinical Endocrinology & Metabolism · 95(9):4291–304
Pooled efficacy and safety analysis across two multicentre double-blind placebo-controlled trials, with extension data.
human, pooled analysis of two phase 3 trials Source
Stanley et al. (2012)Clinical Infectious Diseases · 54(11):1642–51
Reported that reduction in visceral adiposity was associated with an improved metabolic profile in the trial population.
human, analysis of randomised trial data Source
Fourman et al. (2017)AIDS · 31(16):2253–9
Examined liver enzymes alongside visceral fat reduction, reporting an association between the two in this population.
human, analysis of randomised trial data Source
Lake et al. (2021)AIDS · 35(9):1395–402
Reported changes in fat quality that were independent of changes in fat quantity, examining what the compound alters beyond the volume endpoint the pivotal trials measured.
human Source

Adverse and null findings reported

No dedicated safety study has been published for this compound. That is not a finding that none exists — it means the question has not been asked in print, and the gaps below say so.

What the research does not establish

An absence cannot be cited, so these are stated plainly. They are the part of the picture that silence would otherwise hide.

The `adverse` list is empty here for an unusual reason: the safety data exists but sits inside the pooled trial analysis cited above rather than in separate publications. That is a limitation of how this article cites, not a claim that no adverse events were recorded — a compound with an authorised label has a documented adverse effect profile, and the label rather than this page is where it is stated in full.
Every efficacy trial was conducted in people with HIV-associated visceral fat accumulation. No randomised trial has tested the compound in people without that condition, so nothing published supports reading the results across.
The measured endpoint was visceral adipose tissue on imaging over 26 weeks. Longer-term outcomes, and whether the change persists after stopping, are not established by the pivotal programme.
The compound raises IGF-1, and the long-term consequences of sustained IGF-1 elevation are an open question in the endocrine literature generally rather than one this trial programme answered.
It is an authorised medicine in the United States and is supplied here as a research reagent. Material supplied for laboratory use is not the authorised product and carries none of its regulatory guarantees.

Common questions

Is tesamorelin an approved medicine?: Yes, in the United States, as Egrifta, for reduction of excess abdominal fat in people with HIV-associated lipodystrophy. The authorisation is specific to that indication and to the authorised product — not to material supplied as a research reagent.
What did the tesamorelin trials measure?: Visceral adipose tissue, measured on imaging, over 26 weeks, against placebo. Two multicentre randomised double-blind trials reported reductions, alongside elevation of IGF-1.
Does the trial evidence apply to people without HIV?: No published randomised trial has tested that. The entire pivotal programme was conducted in people with HIV-associated abdominal fat accumulation, and reading the results across to anyone else is an assumption rather than a finding.
How is tesamorelin different from sermorelin?: Both act at the GHRH receptor. Tesamorelin carries a chemical modification that slows its breakdown, and it has a large randomised trial programme behind it; sermorelin is the unmodified fragment and its clinical literature is paediatric.
Why does IGF-1 rise?: Because the compound is doing what it was designed to do — stimulating pituitary growth hormone release, and IGF-1 is the downstream marker of that. The rise confirms engagement of the axis; it is not itself an outcome.

Compounds covered

The reference page for each compound this article discusses.

Tesamorelin

Sermorelin (GHRH 1-29): what the research says
A former prescription medicine sold as Geref. The clinical evidence is in children with growth hormone deficiency, and it does not transfer to healthy adults.
CJC-1295 (Mod GRF 1-29): what the research says
The best-known CJC-1295 human trial studied the DAC form, not the no-DAC form sold as Mod GRF 1-29. Why the two have very different pharmacokinetics.
IGF-1 LR3 (Long R3 IGF-1): what the research says
An analogue engineered to evade the binding proteins that regulate natural IGF-1 — which is exactly why it is a cell-culture reagent, and why that matters.

About this article

Everything reported here comes from published research, and each finding names the model the study used — cell culture, rat, or human. Findings in one model do not transfer to another, most of the work described is preclinical, and none of it is a claim that a compound is safe or effective for any purpose. Nothing on this page describes doses, routes of administration, or use in a person.

Approval status varies by compound and by country. A few of the substances described are the active ingredient of medicines authorised in the EU; most have no marketing authorisation anywhere and have never been assessed by a regulator. Neither is supplied as a medicine here. All material supplied by ASSAY is sold for in-vitro laboratory research only, and is not a drug, food, cosmetic or medical device, and not for human or veterinary use.

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