Tesamorelin is a synthetic version of growth hormone-releasing hormone (GHRH), the hypothalamic hormone that tells the pituitary gland to release growth hormone (GH). It is sold by Theratechnologies as Egrifta and is the only drug in the GHRH family with a current FDA approval: since 2010 it has been approved to reduce excess abdominal fat in adults with HIV-associated lipodystrophy (Drugs@FDA).
Unlike sermorelin, Mod GRF 1-29 and CJC-1295, which are built on the short 29-amino-acid fragment of GHRH, tesamorelin is the full-length 44-amino-acid hormone with one chemical cap added. Its evidence base is also different in kind: two phase 3 randomized trials with more than 800 patients, plus smaller controlled trials in liver fat, obesity and cognition. Even so, the label is explicit that it is not a weight-loss drug, and no trial has tested it for muscle gain or athletic performance in healthy people.
This page summarizes what the FDA label, the randomized trials and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Synthetic GHRH analog; full-length GHRH(1-44) with an N-terminal hexenoyl group |
| Other names | TH9507, tesamorelin acetate, Egrifta, Egrifta SV, Egrifta WR |
| Approval | FDA, November 10, 2010 (Theratechnologies); former NDA deemed a BLA (022505) in 2020 |
| Indication | Reduction of excess abdominal fat in HIV-infected adults with lipodystrophy |
| Labeled dose | Egrifta SV 1.4 mg or Egrifta WR 1.28 mg, subcutaneously into the abdomen once daily; the two are not interchangeable |
| Half-life (label) | About 8 minutes (SV) to 11 minutes (WR) after a subcutaneous dose in healthy adults |
| Molecular formula | C₂₂₁H₃₆₆N₇₂O₆₇S; molecular weight 5135.9 Da as the free base |
| EU status | Marketing application withdrawn in 2012 after a negative provisional CHMP opinion |
| US controlled status | Prescription drug; not a controlled substance |
| WADA status | Prohibited at all times under S2.2.4 (named as an example) |
What it is
Structure
The label describes tesamorelin as the complete 44-amino-acid sequence of human GHRH with a hexenoyl group (a six-carbon chain with a double bond at position 3) attached to the tyrosine at the start of the chain. It is supplied as the acetate salt, and its molecular weight as the free base is 5135.9 Da (Egrifta WR label; PubChem). Apart from that cap, the amino acids are the natural ones.
The cap solves the same problem the sermorelin page describes: the blood enzyme dipeptidyl peptidase IV (DPP-IV) clips the first two amino acids off natural GHRH and inactivates it. In the developer’s preclinical work, the hexenoyl group made the peptide resistant to DPP-IV, slowed its breakdown in rat, dog and human plasma, and prolonged its elimination compared with natural GHRH(1-44) (Ferdinandi et al., Basic Clin Pharmacol Toxicol 2007). The label states that in laboratory tests tesamorelin binds and activates human GHRH receptors with potency similar to the natural hormone.
How it compares with related peptides
| Peptide | Built on | How it resists DPP-IV | Status |
|---|---|---|---|
| Sermorelin | GHRH(1-29), unmodified | It does not | FDA-approved as Geref (pediatric); discontinued 2008 |
| Mod GRF 1-29 / CJC-1295 no DAC | GHRH(1-29) | Four amino acid substitutions | Never approved; no published human trials |
| CJC-1295 with DAC | GHRH(1-29) | Same substitutions plus an albumin-binding group | Never approved; early-phase studies only |
| Tesamorelin | GHRH(1-44), full length | Hexenoyl cap on the first amino acid | FDA-approved as Egrifta (2010) |
The sermorelin page covers the shared biology of the family in more depth. The practical point is that tesamorelin’s trial data belong to tesamorelin. They do not transfer to the 29-amino-acid analogs, which are different molecules with far less human data.
How it works in the body
Tesamorelin acts on GHRH receptors on the pituitary’s GH-producing cells (somatotrophs), which then release GH in their natural pulsatile pattern. GH drives the liver and other tissues to make IGF-1 (insulin-like growth factor 1). The label reports rises in IGF-1 and its carrier protein IGFBP-3, and no clinically significant changes in TSH, LH, ACTH or prolactin. Because it works through the pituitary, it is contraindicated when the hypothalamic-pituitary axis is disrupted, for example after pituitary surgery or head irradiation (Egrifta WR label).
In 13 healthy men given 2 mg daily for 2 weeks, tesamorelin increased overnight GH, GH pulse size and basal GH secretion, and raised IGF-1 by a mean of 181 µg/L. Fasting glucose and insulin-stimulated glucose uptake (measured by a glucose clamp) did not change significantly (Stanley et al., JCEM 2011).
Pharmacokinetics
The peptide itself is gone from the blood within minutes. The GH and IGF-1 response is what lasts.
| Parameter | Finding (label) |
|---|---|
| Absolute bioavailability, subcutaneous | Under 4% (2 mg dose of the original formulation) |
| Time to peak | 0.15 h (about 9 minutes) |
| Volume of distribution | 4.8 ± 1.9 L/kg |
| Elimination half-life | 8 minutes (Egrifta SV 1.4 mg); 11 minutes (Egrifta WR 1.28 mg) |
| Exposure in HIV patients | AUC 34% higher than in healthy subjects; peak similar |
| Metabolism | No formal human metabolism studies |
| Renal, hepatic, pediatric, elderly | Not established |
Sources: Egrifta SV label; Egrifta WR label.
Approved medical use
Indication and formulations
Egrifta is indicated “for the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy,” a condition in which antiretroviral therapy is associated with abnormal fat distribution, including fat build-up inside the abdomen. The label lists three limitations of use (Egrifta WR label):
- long-term cardiovascular safety has not been established;
- it is not indicated for weight loss management, because its effect on weight is neutral;
- there are no data showing it improves adherence to antiretroviral therapy.
The pivotal trials used a 2 mg daily dose of the original 1 mg-per-vial product. The current formulations were approved on the basis of comparable exposure to that dose:
| Product | Vial strength | Labeled dose | Basis |
|---|---|---|---|
| Egrifta (original) | 1 mg | 2 mg once daily | Phase 3 trials |
| Egrifta SV | 2 mg | 1.4 mg once daily | Similar exposure to the 2 mg original dose |
| Egrifta WR | 11.6 mg (multi-day vial) | 1.28 mg once daily | Similar exposure to the 2 mg original dose |
The labels state that Egrifta SV and Egrifta WR are not substitutable, because their doses and preparation differ (Egrifta SV label; Egrifta WR label).
Regulatory history
- United States. FDA approved Egrifta on November 10, 2010. The application was deemed a biologics license application (BLA 022505) on March 23, 2020 (Drugs@FDA).
- European Union. Ferrer Internacional withdrew its EU marketing application in June 2012. At that point the CHMP (EMA’s human medicines committee) held the provisional view that Egrifta could not be approved. Its concerns: excess abdominal fat from lipodystrophy is hard to distinguish from obesity; the fat reduction had not been shown to give meaningful health benefits; the trial patients were heavier than typical European HIV patients; IGF-1 rose in many patients, a major safety concern given possible links to cancer and diabetic eye disease; and no long-term safety data were provided for a drug expected to be used long term (EMA, Egrifta withdrawal).
What the research shows
Visceral fat in HIV-associated lipodystrophy
Two multicenter, double-blind trials randomized 816 HIV patients on antiretroviral therapy who had excess abdominal fat. Patients received 2 mg tesamorelin or placebo daily (2:1) for 26 weeks. Visceral adipose tissue (VAT, the fat around the abdominal organs) was measured by CT at the L4–L5 level (Falutz et al., NEJM 2007; Falutz et al., JAIDS 2010). The label reports these 26-week results (Egrifta WR label):
| Outcome at 26 weeks | Study 1 (n = 410) | Study 2 (n = 396) |
|---|---|---|
| VAT, difference vs placebo | −31 cm² (95% CI −39 to −24) | −21 cm² (95% CI −29 to −12) |
| VAT, % difference vs placebo | −20% (95% CI −24 to −15) | −12% (95% CI −16 to −7) |
| IGF-1, difference vs placebo | +122 ng/mL (95% CI 101–141) | +105 ng/mL (95% CI 85–126) |
| Waist circumference, difference | −2 cm | −1 cm |
| Body weight, difference | −0.4 kg (95% CI −1.3 to 0.5) | +0.2 kg (95% CI −0.7 to 1.3) |
A pooled analysis of both trials found a 15.4% treatment effect on VAT, no significant change in abdominal subcutaneous fat (the fat under the skin), and reductions in triglycerides and the total-to-HDL cholesterol ratio. Patients also reported less distress about the appearance of their belly (Falutz et al., JCEM 2010).
The effect lasted only as long as treatment. Patients who stayed on tesamorelin for a full year kept a VAT reduction of about 18%. Those re-randomized to placebo at week 26 regained visceral fat: in the label’s extension data, VAT rose by 22% and 16% over the next 26 weeks in the two studies (Falutz et al., AIDS 2008; Egrifta WR label).
Not everyone responds. In a post hoc analysis, patients with at least an 8% VAT reduction (defined in advance as responders) had better triglyceride and glucose results than non-responders (Stanley et al., Clin Infect Dis 2012). The label advises weighing whether to continue in patients whose visceral fat does not fall.
Lean mass and muscle
Lean body mass rose by 1.3 kg and 1.2 kg on tesamorelin over 26 weeks in the two phase 3 trials, versus a decrease of 0.2 kg and 0.03 kg on placebo. After switching to placebo, patients lost 1.8 kg and 1.7 kg of lean mass over the following 26 weeks (Egrifta WR label). Part of this change may reflect fluid, since fluid retention is a labeled effect; the label does not separate the two.
An exploratory CT re-analysis of the same trials, limited to tesamorelin responders (n = 193) and placebo patients (n = 148), found small increases in trunk muscle area (under 1.1 cm² per muscle group) and density, which suggests less fat inside the muscle (Adrian et al., J Frailty Aging 2019). A 2026 meta-analysis of five randomized trials in HIV estimated a lean-mass gain of 1.42 kg (95% CI 1.13–1.71) and a VAT reduction of 27.7 cm² (Badran et al., Obes Res Clin Pract 2026). No trial measured strength or performance as an outcome.
Liver fat
Tesamorelin has been studied for fatty liver in people with HIV, which is not a labeled use:
| Study | Design and n | Regimen | Main result |
|---|---|---|---|
| Stanley et al., JAMA 2014 | Double-blind RCT; 50 HIV patients with abdominal fat | 2 mg daily or placebo, 6 months | VAT −42 cm² vs placebo (95% CI −71 to −14); liver fat net −2.9% (lipid-to-water ratio) |
| Stanley et al., Lancet HIV 2019 | Double-blind multicenter RCT; 61 HIV patients with NAFLD (liver fat 5% or more) | 2 mg daily or placebo, 12 months | Liver fat fraction −4.1% absolute vs placebo (95% CI −7.6 to −0.7), a 37% relative reduction; 35% vs 4% fell under 5% liver fat |
In the 2014 trial, fasting glucose rose by 7 mg/dL more than placebo at 2 weeks, but the difference was not significant by 6 months. In the 2019 trial, glucose and HbA1c did not differ between groups at 12 months.
People without HIV
| Study | Population and n | Regimen | Main result |
|---|---|---|---|
| Makimura et al., JCEM 2012 | 60 abdominally obese adults with reduced GH secretion; double-blind RCT | 2 mg daily or placebo, 12 months | VAT −35 cm² vs placebo (95% CI −58 to −12); triglycerides, CRP and carotid wall thickness improved; no change in glucose or HbA1c |
| Clemmons et al., PLoS One 2017 | 53 adults with type 2 diabetes; placebo-controlled RCT | 1 or 2 mg daily or placebo, 12 weeks | No difference in insulin response, fasting glucose or HbA1c |
| Baker et al., Arch Neurol 2012 | 152 adults aged 55–87, 66 with mild cognitive impairment; double-blind RCT | 1 mg nightly or placebo, 20 weeks | Favorable effect on a cognition composite (P = .03), mainly executive function; IGF-1 +117%; body fat −7.4%; mild adverse events in 68% vs 36% |
| Ellis et al., J Infect Dis 2025 | 73 people with HIV, abdominal obesity and cognitive impairment; open-label RCT | Tesamorelin vs standard care, 6 months | No significant between-group difference in cognition; waist −2.7 cm vs standard care |
These are small, single trials, and none has led to an approved use outside HIV lipodystrophy. The cognition results in particular are mixed.
Body composition and performance in healthy people
No controlled trial has tested tesamorelin for fat loss, muscle gain or athletic performance in healthy, active people. A 2026 review of GH-axis peptides rated tesamorelin as the best-studied member of its class, but cautioned that its trial data should not be extrapolated to hypertrophy or athletic uses. It also noted that some of the key safety precautions, such as IGF-1 thresholds and fluid retention, come mainly from the prescribing information rather than peer-reviewed trials (Dominikowski et al., Front Endocrinol 2026).
On “tesamorelin is a fat burner.” Tesamorelin reduced visceral fat by roughly 10–20% in selected HIV patients, but body weight did not change, abdominal subcutaneous fat did not change significantly, and the fat returned within months of stopping. The FDA label states outright that it is not indicated for weight loss management.
Side effects and risks
Common adverse reactions
The label pools the 26-week placebo-controlled phase of the trials (543 on tesamorelin, 263 on placebo) (Egrifta WR label):
| Adverse reaction | Tesamorelin | Placebo |
|---|---|---|
| Injection site reaction | 17% | 6% |
| Arthralgia (joint pain) | 13% | 11% |
| Pain in extremity | 6% | 5% |
| Myalgia (muscle pain) | 6% | 2% |
| Peripheral edema | 6% | 2% |
| Paresthesia (tingling) | 5% | 2% |
| Hypoesthesia (numbness) | 4% | 2% |
| Rash | 4% | 2% |
| Carpal tunnel syndrome | 1% | 0% |
In the first trial, adverse event rates did not differ significantly between groups, but more tesamorelin patients withdrew because of an adverse event (Falutz et al., NEJM 2007).
Labeled warnings
- Elevated IGF-1. After 26 weeks, 47% of patients had IGF-1 above 2 standard deviation scores (SDS) and 36% above 3 SDS. The long-term effect of high IGF-1 is unknown. The label calls for IGF-1 monitoring and suggests considering stopping if it stays elevated (for example over 3 SDS), particularly if the fat response is weak.
- Cancer. Because GH is a growth factor, tesamorelin is contraindicated in active malignancy. Previous cancer should be inactive and fully treated before starting, and treatment should stop if cancer recurs.
- Fluid retention. Edema, joint pain and carpal tunnel syndrome are attributed to GH-driven fluid retention and are transient or resolve after stopping.
- Glucose intolerance. HbA1c of 6.5% or higher developed in 5% on tesamorelin vs 1% on placebo (hazard ratio 3.3, CI 1.4–9.6). Glucose should be checked before and during treatment. People with diabetes should be monitored for new or worsening retinopathy.
- Hypersensitivity. Reactions such as itching, flushing, hives and rash occurred in 4% of treated patients.
- Critical illness. Pharmacologic GH has been linked to increased mortality in acutely critically ill patients, so stopping should be considered in that setting.
Source: Egrifta WR label.
Antibodies
Anti-tesamorelin antibodies developed in about half of trial patients (50% at 26 weeks, 47% at 52 weeks), and about 60% of those also cross-reacted with the body’s own GHRH. Neutralizing antibodies were found in 10% of patients against tesamorelin and 5% against natural GHRH at week 52. Antibody status did not change the fat or IGF-1 response (Egrifta WR label).
Interactions
- Glucocorticoids. GH inhibits the enzyme that activates cortisone (11β-HSD1). People on glucocorticoid replacement for adrenal insufficiency may need higher maintenance or stress doses after starting tesamorelin.
- Drugs cleared by CYP450 liver enzymes. GH may change the clearance of drugs such as corticosteroids, sex steroids, anticonvulsants and cyclosporine. In formal studies, tesamorelin changed simvastatin and ritonavir exposure by 15% or less.
Source: Egrifta WR label.
Who should not use it
The label contraindicates tesamorelin in:
- disruption of the hypothalamic-pituitary axis (hypophysectomy, hypopituitarism, pituitary tumor or surgery, head irradiation or head trauma);
- active malignancy;
- known hypersensitivity to tesamorelin or its excipients;
- pregnancy. In rats, exposure during organogenesis caused hydrocephaly in offspring at about two times the clinical exposure.
It is not approved for children. In children with open growth plates it may cause excessive linear growth. There is no information on use in people over 65.
Legal status and use outside medicine
- United States. Tesamorelin is a prescription biologic. It is not named in the DEA’s anabolic steroid schedule (21 CFR 1308.13).
- Europe. No EU marketing authorization exists; the application was withdrawn in 2012 (EMA).
- Sport. The WADA 2026 Prohibited List bans growth hormone releasing factors at all times under S2.2.4, naming GHRH and its analogues, “e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin.”
- Non-medical use. The 2026 review notes that tesamorelin is often promoted in fitness circles for body composition and “recovery,” uses that its trial data do not support (Dominikowski et al., 2026). Product obtained outside a pharmacy is not the FDA-approved product, and its identity and dose are not regulated.
Key takeaways
- Full-length GHRH, lightly modified. Tesamorelin is all 44 amino acids of natural GHRH plus a hexenoyl cap that blocks enzyme breakdown, unlike the 29-amino-acid analogs sermorelin and CJC-1295.
- The only approved drug in its family. FDA approved Egrifta in 2010 to reduce excess abdominal fat in adults with HIV-associated lipodystrophy; the EU application was withdrawn in 2012 over doubts about clinical benefit and IGF-1 safety.
- Visceral fat falls, weight does not. Phase 3 trials showed roughly 10–20% less visceral fat than placebo, with no change in body weight, and the fat came back after stopping.
- IGF-1 is the main lab to watch. About a third of patients exceeded 3 SDS for IGF-1, and the label adds warnings for glucose intolerance, fluid retention and cancer.
- No evidence for physique goals. No controlled trial tested tesamorelin for muscle, fat loss or performance in healthy people, and WADA bans it at all times.
Sources
- Theratechnologies Inc. Egrifta WR (tesamorelin) for injection, prescribing information. DailyMed.
- Theratechnologies Inc. Egrifta SV (tesamorelin) for injection, prescribing information. DailyMed.
- Food and Drug Administration. Drugs@FDA: Egrifta (tesamorelin acetate), BLA 022505, approved November 10, 2010. Drugs@FDA.
- European Medicines Agency. Egrifta: withdrawal of the marketing authorisation application. EMA.
- National Center for Biotechnology Information. Tesamorelin, PubChem CID 16137828. PubChem.
- Ferdinandi ES, Brazeau P, High K, et al. Non-clinical pharmacology and safety evaluation of TH9507, a human growth hormone-releasing factor analogue. Basic Clin Pharmacol Toxicol. 2007;100(1):49–58. PubMed.
- Stanley TL, Chen CY, Branch KL, et al. Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. J Clin Endocrinol Metab. 2011;96(1):150–158. PubMed.
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- Falutz J, Potvin D, Mamputu JC, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010;53(3):311–322. PubMed.
- Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010;95(9):4291–4304. PubMed.
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- Stanley TL, Falutz J, Marsolais C, et al. Reduction in visceral adiposity is associated with an improved metabolic profile in HIV-infected patients receiving tesamorelin. Clin Infect Dis. 2012;54(11):1642–1651. PubMed.
- Adrian S, Scherzinger A, Sanyal A, et al. The growth hormone releasing hormone analogue, tesamorelin, decreases muscle fat and increases muscle area in adults with HIV. J Frailty Aging. 2019;8(3):154–159. PubMed.
- Badran AS, Helal A, Shata KS, Ayesh H. Body composition, hepatic fat, metabolic, and safety outcomes of Tesamorelin, a GHRH analogue, in HIV-associated lipodystrophy: a meta-analysis of randomized controlled trials. Obes Res Clin Pract. 2026;20(1):2–12. PubMed.
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- Stanley TL, Fourman LT, Feldpausch MN, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial. Lancet HIV. 2019;6(12):e821–e830. PubMed.
- Makimura H, Feldpausch MN, Rope AM, et al. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion: a randomized controlled trial. J Clin Endocrinol Metab. 2012;97(12):4769–4779. PubMed.
- Clemmons DR, Miller S, Mamputu JC. Safety and metabolic effects of tesamorelin, a growth hormone-releasing factor analogue, in patients with type 2 diabetes: a randomized, placebo-controlled trial. PLoS One. 2017;12(6):e0179538. PubMed.
- Baker LD, Barsness SM, Borson S, et al. Effects of growth hormone–releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial. Arch Neurol. 2012;69(11):1420–1429. PubMed.
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- Drug Enforcement Administration. Schedule III controlled substances, 21 CFR 1308.13. 21 CFR 1308.13.
- World Anti-Doping Agency. 2026 Prohibited List, section S2.2.4 (growth hormone releasing factors), in effect 1 January 2026. WADA 2026 Prohibited List.