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Tesamorelin is a synthetic analogue of growth hormone-releasing hormone (GHRH). It consists of the full 44-amino-acid sequence of human GHRH with a hexenoyl group attached to the tyrosine at its N-terminus. Under the brand name Egrifta it is approved by the US FDA for one indication: reducing excess abdominal fat in adults with HIV who have lipodystrophy.1 Tesamorelin sold as a research chemical is not Egrifta and is supplied for laboratory research only.
This article covers the molecule itself, how a GHRH analogue works, what the clinical trials behind Egrifta and later studies reported, and how tesamorelin is treated in sport.
| Property | Detail |
|---|---|
| Class | Growth hormone-releasing factor (GHRF/GHRH) analogue1 |
| Other names | TH9507; Egrifta (brand)2 |
| Sequence (one-letter) | (E)-hex-3-enoyl-YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL-NH2: human GHRH(1-44) amide3 with the N-terminal hexenoyl group described in the FDA label1 |
| Molecular formula | C221H366N72O67S (PubChem; free base)2 |
| Molar mass | 5136 g/mol (PubChem); the FDA label gives 5135.9 Da as free base2,1 |
| CAS number | 218949-48-5 (PubChem)2 |
| Origin | Synthetic peptide; approved product developed by Theratechnologies4 |
| Approved product | Egrifta (FDA, first approved 10 November 2010); current US labels cover EGRIFTA SV and EGRIFTA WR4,1 |
| WADA 2026 | Named under S2.2.4 (growth hormone releasing factors); prohibited at all times5 |
Growth hormone-releasing hormone is a hypothalamic peptide that acts on somatotroph cells in the anterior pituitary. It stimulates the synthesis and pulsatile release of the body's own growth hormone (GH). GH in turn acts on many tissues, and some of its effects are mediated by insulin-like growth factor 1 (IGF-1) produced in the liver and elsewhere. According to the FDA label, tesamorelin binds and stimulates human GHRH receptors in vitro with potency similar to the endogenous hormone.1
The distinction from growth hormone itself matters to researchers. Tesamorelin does not replace GH. It acts one step upstream, on the pituitary, so its downstream effects depend on an intact hypothalamic-pituitary axis. The FDA label accordingly lists disruption of that axis among its contraindications.1 Trials therefore track serum IGF-1 as a pharmacodynamic marker: in the first phase 3 trial, IGF-1 rose by 81% with tesamorelin and fell by 5% with placebo.6
The N-terminal hexenoyl group is the only change from the human sequence, and trial reports describe tesamorelin as a "stabilized" GHRH analogue.7
The FDA first approved Egrifta on 10 November 2010. The application, originally a new drug application, was deemed a biologics licence application (BLA 022505) in March 2020.4 The current labels, for the EGRIFTA SV and EGRIFTA WR formulations, state a single indication: reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy.1 The label also sets limits that are worth knowing when reading the literature:
The label's warnings cover increased IGF-1 (the effects of prolonged elevation are unknown), fluid retention, glucose intolerance, hypersensitivity reactions and a caution about pre-existing malignancy.1 None of this approval extends to research-grade material. Tesamorelin supplied for laboratory research is a reagent, not the FDA-approved product.
The pivotal evidence comes from people with HIV on antiretroviral therapy who had accumulated abdominal (visceral) fat. In the first phase 3 trial, published in the New England Journal of Medicine in 2007, 412 patients were randomised to daily subcutaneous tesamorelin or placebo for 26 weeks. Visceral adipose tissue, measured by CT, fell by 15.2% with tesamorelin and rose by 5.0% with placebo. Triglycerides and the total-to-HDL cholesterol ratio also improved, with no significant differences in glycaemic measures. Overall adverse-event rates did not differ significantly between groups, although more tesamorelin patients withdrew because of an adverse event.6 A pooled analysis of two phase 3 trials (806 patients) reported a placebo-adjusted treatment effect of −15.4% in visceral fat at 26 weeks. Abdominal subcutaneous fat did not change significantly (treatment effect −0.6%), a pattern the authors described as preservation of subcutaneous fat. At week 26, tesamorelin patients were re-randomised to continue or switch to placebo, and in those who continued to 52 weeks the visceral-fat reduction was maintained. The authors reported no clinically meaningful changes in glucose parameters at 26 or 52 weeks.8
Two smaller trials led by a Massachusetts General Hospital group looked at liver fat in people with HIV. A 50-patient, 6-month trial, published in JAMA in 2014, reported reductions in both visceral fat and liver fat versus placebo. Fasting glucose rose slightly in the tesamorelin group at 2 weeks, but the difference from placebo was not significant across the 6 months.9 A 61-patient, 12-month trial in people with HIV and non-alcoholic fatty liver disease followed in 2019. It reported an absolute reduction in hepatic fat fraction of 4.1 percentage points versus placebo (a 37% relative reduction). At 12 months, 35% of the tesamorelin group and 4% of the placebo group had a hepatic fat fraction below 5%.10 The authors called for longer studies of liver histology.
Growth hormone use is associated with insulin resistance, so glucose has been a primary safety endpoint in several tesamorelin trials.7,10 A 12-week randomised trial in 53 people with type 2 diabetes found no significant differences between tesamorelin and placebo in insulin response, fasting glucose or HbA1c.7 That trial was sponsored by Theratechnologies.
A 20-week randomised trial at the University of Washington enrolled 152 older adults, 66 of them with mild cognitive impairment. It reported a favourable effect of tesamorelin on a composite cognitive score (P=.03), driven mainly by executive function. IGF-1 rose by 117% but, according to the authors, stayed within the physiological range, and percentage body fat fell by 7.4%. Adverse events, mostly mild, were reported by 68% of the tesamorelin group and 36% of the placebo group.11 A later 6-month open-label phase 2 trial in 73 people with HIV and abdominal obesity found no significant between-group difference in neurocognitive performance. Its authors noted it was underpowered and had no placebo arm.12
The endpoints in the tesamorelin literature are imaging measures and blood markers, which is worth knowing when comparing studies. The phase 3 trials measured visceral adipose tissue as a cross-sectional area on computed tomography.6,8 The 2019 liver trial measured hepatic fat fraction by proton magnetic resonance spectroscopy, and its primary safety endpoint was glucose.10 The cognition trial combined a cognitive test battery with oral glucose tolerance testing and a DXA scan for body composition.11 Serum IGF-1 served as a pharmacodynamic marker throughout. None of these trials measured hard clinical outcomes such as cardiovascular events, which is consistent with the label's statement that long-term cardiovascular safety has not been established.1
| Study | Model | n | Length | Reported finding |
|---|---|---|---|---|
| Falutz 2007, NEJM | Phase 3 RCT, HIV with abdominal fat | 412 | 26 weeks | Visceral fat −15.2% vs +5.0% placebo6 |
| Falutz 2010, JCEM | Pooled phase 3 + extension | 806 | 26 + 26 weeks | Treatment effect −15.4%; maintained to 52 weeks with continued treatment8 |
| Stanley 2014, JAMA | RCT, HIV with abdominal fat | 50 | 6 months | Reductions in visceral and liver fat9 |
| Stanley 2019, Lancet HIV | RCT, HIV with NAFLD | 61 | 12 months | Hepatic fat fraction −4.1 points vs placebo10 |
| Clemmons 2017, PLoS One | RCT, type 2 diabetes | 53 | 12 weeks | No change in insulin response or glycaemic control7 |
| Baker 2012, Arch Neurol | RCT, older adults ± MCI | 152 | 20 weeks | Favourable composite cognition effect11 |
| Ellis 2025, J Infect Dis | Open-label phase 2, HIV | 73 | 6 months | No significant cognitive difference vs standard care12 |
These compounds are often searched together, but they fall into different pharmacological groups. WADA's 2026 Prohibited List groups growth hormone releasing factors under section S2.2.4 into three categories. The first is GHRH and its analogues, where it names CJC-1293, CJC-1295, sermorelin and tesamorelin. The second is growth hormone secretagogues and their mimetics, where it names ipamorelin, ibutamoren (MK-677), anamorelin and others. The third is GH-releasing peptides such as GHRP-2 and GHRP-6.5 Tesamorelin works through the GHRH receptor. Ipamorelin is a different kind of molecule: a five-residue peptide first described in 1998. In rat pituitary cell experiments using receptor antagonists, it stimulated growth hormone release through a GHRP-like receptor rather than the GHRH receptor.13 The two therefore reach the same pituitary cells by separate receptor pathways, consistent with WADA placing them in separate subgroups.
Yes. Tesamorelin is named in section S2.2.4 of the 2026 WADA Prohibited List. Substances in S2 are prohibited at all times, in and out of competition, and all are non-Specified.5 In Australia, the rules are administered by Sport Integrity Australia. For how the other peptides on this site are classified, see peptides and the WADA Prohibited List.
The research-grade tesamorelin sold by Titan Peptides is supplied as a lyophilised 5 mg vial for laboratory use. It is not Egrifta, has no therapeutic approval, and is not for human or veterinary use. For how Australian law treats research peptides, including the Poisons Standard and importation, read are research peptides legal in Australia? For bench handling, our guides cover storing lyophilised and reconstituted peptides and reconstitution with bacteriostatic or sterile water.
Read the current FDA prescribing information for the complete regulatory text.
Tesamorelin is a synthetic peptide analogue of human growth hormone-releasing hormone (GHRH). It contains the same 44 amino acids as human GHRH plus a hexenoyl group on the first tyrosine. It acts on GHRH receptors in the pituitary, which release the body's own growth hormone. The FDA-approved product is called Egrifta.
Yes, for one use. Egrifta (tesamorelin) was first approved by the FDA in November 2010 and is indicated for reducing excess abdominal fat in HIV-infected adults with lipodystrophy. The label states it is not indicated for weight-loss management and that long-term cardiovascular safety has not been established. Research-grade tesamorelin is not an approved product.
Tesamorelin is a peptide, not a steroid. It is a 44-amino-acid chain based on human growth hormone-releasing hormone, with a small hexenoyl group added at one end. Anabolic steroids are chemically unrelated molecules built on a four-ring sterol skeleton, and they are listed separately under S1 of the WADA Prohibited List.
Yes. The 2026 WADA Prohibited List names tesamorelin under section S2.2.4, growth hormone releasing factors, alongside CJC-1295 and sermorelin. Substances in section S2 are prohibited at all times, both in and out of competition, and are non-Specified substances. In Australia, anti-doping rules are administered by Sport Integrity Australia.
They act through different receptors. Tesamorelin is a GHRH analogue that works through the GHRH receptor on pituitary cells. Ipamorelin is a five-residue growth hormone secretagogue that, in laboratory studies, stimulated growth hormone release through a GHRP-like receptor. WADA lists the two in separate subgroups of section S2.2.4. Tesamorelin is also the active ingredient of an FDA-approved medicine, Egrifta.
Which peptides does the 2026 WADA Prohibited List name, in which section, and what does "not named" really mean? Includes GLP-1 drugs, retatrutide and Sport Integrity Australia.
What the TGA, the June 2026 Poisons Standard, the Therapeutic Goods Act and customs law actually say about peptides, "research use only" labels, importing and advertising in Australia.
A laboratory guide to storing lyophilised and reconstituted peptides: freezer temperatures, moisture, oxidation-prone residues, light, freeze–thaw cycles and adsorption to containers.
