Tesamorelin is the only GHRH analogue that went through approval as a medicine. The FDA authorised it in 2010 under the name Egrifta, for reducing excess abdominal fat in adults with HIV and lipodystrophy. The mechanism is the same as in the rest of the group: the peptide prompts the pituitary to release the body’s own growth hormone, which raises IGF-1 and reduces visceral fat. In trials visceral fat fell by about 15 per cent against placebo, but the effect disappeared after the drug was stopped. Outside that single indication tesamorelin is not a medicine, and in sport it is banned all year round.
How is tesamorelin built?
Tesamorelin is a synthetic GHRH analogue of 44 amino acids, that is, the full GRF 1-44 sequence. It differs from natural GHRH by a modification at the start of the chain: the tyrosine residue at the N-terminus is joined to a trans-3-hexenoic acid group. That attached group works like a stopper, protecting the start of the peptide from the enzyme dipeptidyl peptidase-4. As a result tesamorelin persists longer than the natural hormone. Under laboratory conditions its half-life is given as 3 to 8 hours, against about half an hour for human GRF.
How does tesamorelin work?
Tesamorelin starts up your own growth hormone axis rather than supplying the hormone from outside. The peptide stimulates GHRH receptors on pituitary cells, which leads to synthesis and release of growth hormone in a rhythm close to natural pulses. Growth hormone then acts on many tissues, among them liver cells, where it drives production of IGF-1. IGF-1 mediates part of the effects, including glucose uptake, suppression of cell death and fat breakdown. The net result is a fall in visceral fat, the kind that surrounds the organs of the abdomen. This whole pathway, shared by GHRH analogues, is described in the article on growth hormone peptides.
What did the research on tesamorelin confirm?
Approval rested on phase 3 trials in people with HIV and lipodystrophy. The main findings from those trials:
- The FDA decision was based on two phase 3 trials covering 816 people in total.
- In one of the large trials, in 412 people, visceral fat fell by an average of 15 per cent on tesamorelin and rose by 5 per cent on placebo.
- The improvement held only during treatment; after it stopped, visceral fat returned.
- The approved dose is 2 mg subcutaneously once daily. A newer form, Egrifta WR, authorised in 2025, simplifies preparation of the solution to once a week.
All of this data comes from one population: adults with HIV and excess visceral fat. Tesamorelin has no authorisation for weight loss, for building muscle or for slowing ageing.
Why is it the only approved GHRH analogue?
Approval of a medicine depends not on the molecule itself but on a complete set of human trials and on a company answerable for the preparation. Sermorelin also held approval, as Geref, but the manufacturer withdrew it for commercial reasons; the difference between sermorelin and Mod GRF 1-29 is taken apart in a separate article. CJC-1295 and Mod GRF 1-29 never went through full phase 3 trials in a defined indication. Tesamorelin is the exception because one company ran the entire approval programme for a clearly defined group of patients and kept the preparation on the market. That is the difference between a medicine and a research substance: not the structure of the peptide, but the evidence and the responsibility for the product.
What limitations and adverse effects does tesamorelin have?
Tesamorelin raises IGF-1, which is why monitoring it during treatment is advised. Raised IGF-1 is linked to a risk of glucose intolerance and diabetes, and to a theoretical risk of stimulating the growth of an existing tumour. For that reason the medicine is contraindicated in active malignant disease and in pregnancy. Common adverse effects include injection site reactions, joint pain, muscle pain and peripheral oedema. This is a medicine run under a doctor’s supervision, with monitoring tests, not a preparation for an experiment of one’s own.
What is the status of tesamorelin in the shop and in sport?
Tesamorelin is a prescription medicine. A vial labelled tesamorelin in a reagent shop is not the same thing as approved Egrifta in terms of quality control and purity. Buying such a vial, you are buying a substance intended for laboratory research, not a medicinal product. On the WADA prohibited list tesamorelin is named explicitly, under section S2.2.4 covering growth hormone releasing hormone and its analogues. The ban applies all year. More on the legal categories is in the article on the legal status of peptides and on the legal warning page.
Frequently asked questions
What is tesamorelin approved for?
For reducing excess abdominal fat in adults with HIV and lipodystrophy. The FDA authorised it in 2010 as Egrifta. That is its only approved indication.
How does tesamorelin reduce fat?
It prompts the pituitary to release the body’s own growth hormone, which raises IGF-1 and increases the breakdown of visceral fat. In one large trial visceral fat fell by about 15 per cent against placebo.
Does the effect hold after stopping?
No. In the trials visceral fat returned once tesamorelin was stopped.
Can tesamorelin be used in sport?
No. Tesamorelin is on the WADA prohibited list under section S2.2.4 as a GHRH analogue and is banned all year, in and out of competition.
Where this information comes from
The 44 amino acid sequence, the trans-3-hexenoic acid group at the N-terminus and the half-life of 3 to 8 hours come from the published chemistry of tesamorelin. The 2010 approval, the indication, the two phase 3 trials in 816 people, the 15 per cent fall in visceral fat against a 5 per cent rise on placebo in the trial of 412 people, the return of fat after stopping, the 2 mg daily dose, the contraindications and the common adverse effects come from the Egrifta prescribing information and the FDA approval record; the Egrifta WR form dates from 2025. The section S2.2.4 listing comes from the WADA prohibited list. These sources were checked on 6 September 2026.
