Tesamorelin: what the research literature shows

What it is

Origin and names

GHRH is a peptide made in the hypothalamus. It acts on the somatotroph cells of the pituitary gland, where it stimulates the synthesis and pulsatile release of growth hormone (GH).⁷ Drug labels and older papers call it growth hormone-releasing factor, or GRF.⁷¹⁰

Tesamorelin is a GHRH analogue that Theratechnologies of Montréal developed under the code TH9507.³⁴

Sequence and chemistry

The molecule contains all 44 amino acids of human GHRH and ends in a C-terminal amide.¹ A hexenoyl group, a six-carbon chain with one double bond, is attached to the tyrosine at the N-terminus.⁷ The medicine is the acetate salt; PubChem gives the free peptide the formula C221H366N72O67S and a weight of 5136 g/mol.⁷¹¹

Cell study The added group answers a known weakness of the natural hormone. A 1989 study at the University of Cincinnati showed that plasma cuts GHRH between residues 2 and 3, and identified the enzyme as dipeptidyl peptidase IV (DPP-IV).² Theratechnologies later reported that TH9507 resisted DPP-IV and broke down more slowly than natural GHRH in rat, dog and human plasma.³

Cell study The rest of the sequence is unchanged, so tesamorelin still contains two residues that are weak points in the natural hormone. Researchers at Hoffmann-La Roche reported that, in water, the asparagine at position 8 of human GHRH(1-44) rearranges to aspartate forms and the methionine at position 27 oxidizes, and that both changes greatly reduce biological activity.¹⁰ The guide to how peptides degrade explains these reactions.

The receptor

Cell study A 2020 cryo-electron microscopy study solved the structure of the human GHRH receptor bound to GHRH and to its stimulatory G protein.¹² The hormone sits in the receptor as a helix, and its N-terminus makes a broad set of specific contacts with the receptor.¹² Tesamorelin modifies that end of the molecule, and the FDA label states that, in vitro, it binds and stimulates human GRF receptors with a potency similar to the natural hormone’s.⁷ The overview of growth hormone secretagogues compares other routes to the same pituitary cell.

How it is studied

Three kinds of study recur:

• Preclinical pharmacology. Plasma stability, hormone responses in pigs, rats and dogs, and toxicity studies of up to four months.³
• Human hormone studies. Blood is sampled frequently overnight to measure GH pulses.¹³
• Randomized trials. Participants receive tesamorelin or placebo under double-blind conditions, and the primary measure is the change in visceral adipose tissue (VAT) on a CT scan.⁴¹⁴

What the literature reports

Preclinical pharmacology

Animal study In pigs, rats and dogs, repeated administration of TH9507 produced marked rises in plasma GH and insulin-like growth factor 1 (IGF-1).³ In toxicity studies, dogs showed reversible liver and kidney findings and anemia, which the authors attributed to sustained exposure to GH and IGF-1 above physiological levels.³

Growth hormone pulses and IGF-1

Human study In a Boston study, 13 healthy men received tesamorelin for two weeks and were sampled overnight at baseline, at the end of treatment and two weeks after it stopped.¹³ Mean overnight GH, the area of GH pulses, basal GH secretion and IGF-1 all rose, and insulin-stimulated glucose uptake did not change significantly.¹³

Human study The Canadian monograph reports mean elimination half-lives of 26 minutes in healthy subjects and 38 minutes in patients with HIV.¹ The label for a later US formulation gives 8 minutes in healthy subjects, and states that no clinically significant changes were seen in other pituitary hormones in clinical trials.⁷

The pivotal trials

Human study Three placebo-controlled trials came before the authorization, all in adults with HIV who had accumulated abdominal fat.¹⁴¹⁵¹⁶ The last two were phase 3.⁴

Human study In the first phase 3 trial, triglycerides also fell, IGF-1 rose by 81%, and glycemic measures did not differ significantly between groups.¹⁶ Adverse events did not differ significantly overall, but more participants in the tesamorelin group withdrew because of one.¹⁶

Human study Both trials ran a further 26 weeks. Participants who stayed on tesamorelin kept a VAT reduction of about 18% at 52 weeks, and those switched to placebo regained the fat.⁵¹⁴ A pooled analysis of 806 participants put the effect on VAT at 26 weeks at −15.4% relative to placebo.⁴

Human study Product labels read the glucose data more cautiously than the trial abstracts do. Across the phase 3 trials, mean HbA1c, a marker of average blood glucose, was higher at week 26 with tesamorelin than with placebo, and more participants reached an HbA1c in the diabetic range, with a hazard ratio of 3.3.¹ Among participants treated for 26 weeks, 47% had an IGF-1 standard deviation score above 2, a level Health Canada’s reviewers describe as above the normal range.⁷⁹

Later investigational work

Human study In a single-centre trial of 50 adults with HIV, VAT and liver fat fell with tesamorelin relative to placebo over six months, and the authors called the study preliminary.¹⁷ A two-centre trial then followed 61 people with HIV and fatty liver for 12 months: hepatic fat fraction fell by 4.1 percentage points more with tesamorelin than with placebo.¹⁸

Human study Outside HIV, in 60 adults with abdominal obesity and reduced GH secretion, VAT, triglycerides and C-reactive protein fell with tesamorelin relative to placebo over 12 months, with no change in glucose measures.¹⁹

Human study Two trials looked at cognition. In Seattle, 152 adults aged 55 to 87, 66 of them with mild cognitive impairment, were assigned to tesamorelin or placebo for 20 weeks; the authors reported a favourable effect on cognitive test scores, and adverse events were reported by 68% of the tesamorelin group and 36% of the placebo group.²⁰ A later open-label trial in 73 people with HIV and abdominal obesity found no significant difference from standard care in neurocognitive performance, and its authors called it underpowered.²¹

Review A 2026 meta-analysis of four randomized trials with 909 participants found reductions in VAT, waist circumference and trunk fat, together with GH-related adverse effects, and advised caution because data on long-term safety and durability are limited.⁸

On 8 October 2026 ClinicalTrials.gov listed 24 studies with tesamorelin as an intervention, three of them recruiting.²²

Human evidence

Human study Tesamorelin has been tested in randomized human trials, and that evidence answers a narrow question. Placebo-controlled trials in more than 800 adults with HIV and excess abdominal fat found a reduction in visceral fat on CT that lasted as long as treatment did, for up to 52 weeks.⁴⁵ The endpoints reported were fat, lipids, hormone levels and body image, not clinical events such as heart attacks.¹⁶ The FDA label states that long-term cardiovascular safety has not been established.⁷

Outside that population the studies are smaller, and none of the uses they explore appears on the labels cited here.¹⁹²⁰²³ The authorization rests on trials of the manufacturer’s formulated product.⁷ Nothing in this literature describes what an unformulated research material does in a person.

Regulatory status

The Canadian and US statements were checked against each authority’s own pages on 8 October 2026; the anti-doping line comes from a 2021 paper.

• United States. The FDA’s approved-drug data list tesamorelin acetate under application BLA022505, first approved on 10 November 2010.⁶ The current labels for two presentations, Egrifta SV and Egrifta WR, give one indication: the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy.⁷²³ They say the medicine is not indicated for weight loss management, and they contraindicate it in pregnancy and in active malignancy.⁷²³
• Canada. Health Canada issued a Notice of Compliance, its marketing authorization, for Egrifta on 29 April 2014.⁹ The product monograph gives the indication as excess visceral adipose tissue, assessed by waist circumference and confirmed by CT scan, in treatment-experienced adult HIV-infected patients with lipodystrophy.¹ One strength was first marketed in Canada on 23 June 2015; the manufacturer later discontinued sale, and the Drug Product Database shows it as cancelled post-market from 30 September 2022.⁹²⁴ The other strength was cancelled in 2023 without having been marketed, and a database search for tesamorelin returned those two products and no others.⁹²⁵
• Sport. Anti-doping chemists in London state that GHRH and its synthetic analogues are prohibited by the World Anti-Doping Agency, and their method detects tesamorelin.²⁶
• Research material. Both authorizations were issued to Theratechnologies for Egrifta and do not cover tesamorelin from another source.⁶⁹ In an advisory dated 9 April 2026, Health Canada said that unauthorized drug products have not been assessed for safety, efficacy and quality, and that a research-use-only label does not make a product legal or exempt it from regulatory requirements.²⁷

Horizon Peptides supplies tesamorelin for laboratory research use only.

In the laboratory

Horizon lists tesamorelin as a lyophilized powder in vials; see the tesamorelin vial.

Two checks are commonly used to characterize a peptide: a purity trace by HPLC and a mass spectrum, here one consistent with the formula C221H366N72O67S.¹¹ The mass separates tesamorelin from unmodified GHRH(1-44) amide, which PubChem lists at 5040 g/mol, 96 mass units lighter.²⁸ The guide to analytical methods for peptides explains both checks, and batch documents are published on the Lab Results page when they exist.

The Canadian monograph describes tesamorelin acetate as a white to off-white powder that is soluble in water and in dilute acetic acid and very slightly soluble in phosphate-buffered saline at pH 7.2.¹

Storage statements on drug labels belong to their formulations. The original Canadian product, formulated with mannitol, was labelled for refrigerated storage at 2 to 8 °C and protection from light.¹ A later US formulation that adds histidine, sucrose and polysorbate 20 is labelled for storage at controlled room temperature.⁷ Neither condition can be assumed for a vial of peptide without those excipients. The peptide storage guide gives the general rules.

For cell-culture work, 1 mg of peptide in 1 mL is about 0.195 mmol/L at this molecular weight. The true figure is usually lower, because peptide powders also contain counter-ions and water; for the drug substance, the FDA label gives about seven acetate molecules for each peptide molecule.⁷