Tesamorelin
approvedAlso known as: Egrifta, TH9507
**Mechanism of Action** Tesamorelin is a synthetic stabilized analog of growth hormone-releasing hormone (GHRH), designed to restore endogenous growth hormone (GH) secretion. By binding to GHRH receptors on pituitary somatotrophs, it stimulates pulsatile GH release, subsequently elevating insulin-like growth factor 1 (IGF-1) levels. This activation of the GH/IGF-1 axis promotes lipolysis and reduces visceral adipose tissue (VAT) accumulation, particularly in patients with HIV-associated lipodystrophy, where GH deficiency is common. Unlike recombinant GH, tesamorelin preserves the physiological pulsatility of GH secretion, potentially reducing off-target metabolic effects. **Key Research Findings** Clinical trials (e.g., Phase III studies) demonstrate that tesamorelin (2 mg/day subcutaneous) significantly reduces VAT by 15–20% over 26 weeks in HIV patients with lipodystrophy, with sustained effects during long-term use. Improvements in triglycerides and total cholesterol are observed, though no significant changes in subcutaneous fat or lean body mass occur. Adverse effects include arthralgias, injection-site reactions, and transient increases in IGF-1; long-term safety data show no increased risk of glucose intolerance or malignancy. PubMed-indexed studies (n=90) confirm its efficacy in VAT reduction, with ongoing research exploring off-label applications in non-HIV metabolic disorders. **Clinical Relevance** Tesamorelin is FDA-approved (Egrifta) for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. It is the only pharmacologic agent specifically indicated for this condition, addressing a significant unmet need in HIV management. Its use requires monitoring of IGF-1, glucose, and pituitary function. Off-label applications (e.g., aging-related sarcopenia, obesity) remain investigational due to limited evidence and potential risks. For research purposes only — not medical advice.
Key data
C221H366N72O67SResearch & studies
MASLD is highly prevalent among PWH and is a major contributor to liver-related and cardiovascular morbidity and mortality.; MASLD-HIV follows a more aggressive clinical course than MASLD in HIV-negative individuals.; HIV-specific factors such as altered body composition, chronic immune activation, enhanced gut permeability, and antiretroviral therapy exacerbate disease progression.; Dedicated studies of GLP-1 receptor agonists and tesamorelin show promise in MASLD-HIV, but a critical gap remains in evaluating MASLD therapies specifically among PWH.
Tesamorelin reduced waist circumference more than standard of care (median difference -2.7 cm, P = .015).; Neurocognitive performance improvement trended in the tesamorelin group (mean change 0.146, P = .060) but between-group difference was not significant (P = .673).; IGF-1 levels increased with tesamorelin but did not correlate with cognitive changes or waist circumference reduction.; The study was limited by insufficient power and lack of placebo arm, suggesting no clear cognitive benefit from short-term abdominal obesity reduction with tesamorelin.
Tesamorelin led to significant declines in visceral fat (median -25 vs. 14 cm², P=0.001).; Hepatic fat fraction decreased significantly with tesamorelin (-4.2% vs. -0.5%, P=0.01).; Trunk-to-appendicular fat ratio improved with tesamorelin (-0.1 vs. 0.0, P=0.03).; Tesamorelin was well tolerated with similar adverse events, including hyperglycemia, between groups.
Tesamorelin reduced visceral adipose tissue and waist circumference in both dorsocervical fat groups among responders.; Changes in VAT (P = 0.657) and waist circumference (P = 0.093) did not statistically differ between groups.; Tesamorelin was equally effective regardless of the presence of dorsocervical fat.; Tesamorelin should be considered for treating excess visceral adipose tissue irrespective of dorsocervical fat.
NASH affects an estimated 35 million people globally and is the most common chronic liver condition in Western populations, with the therapy market projected to reach $27.2 B in 2029.; No FDA-approved therapies exist specifically for NASH; only Zydus Cadila's Saroglitazar was approved (2020) for NASH in India.; Obeticholic acid, Cenicriviroc, Aramchol, Resmetirom, Dapagliflozin, and Semaglutide are in advanced Phase 3 trials, while Belapectin, MSDC-0602K, Lanifibranor, Efruxifermin, and Tesamorelin are expected to start Phase 3 soon.; Given NASH's complex pathophysiology, the authors predict drug combinations with different mechanisms of action targeting each disease stage will likely be required, making a single therapy unlikely.
Tesamorelin increased VAT density by +6.2 HU and SAT density by +4.0 HU over 26 weeks, versus +0.3 HU for both in placebo.; Improvements in fat density persisted after controlling for baseline fat density and changes in fat area.; Tesamorelin improves fat quality (density) independently of its effects on fat quantity reduction.
Tesamorelin increased hepatic expression of hallmark gene sets involved in oxidative phosphorylation.; Tesamorelin decreased hepatic expression of gene sets contributing to inflammation, tissue repair, and cell division.; Tesamorelin reciprocally up- and downregulated curated gene sets associated with favorable and poor hepatocellular carcinoma prognosis.; Changes in hepatic expression correlated with improved fibrosis-related gene score among tesamorelin-treated participants.
Frequently asked questions
What is Tesamorelin?
**Mechanism of Action** Tesamorelin is a synthetic stabilized analog of growth hormone-releasing hormone (GHRH), designed to restore endogenous growth hormone (GH) secretion. By binding to GHRH receptors on pituitary somatotrophs, it stimulates pulsatile GH release, subsequently elevating insulin-like growth factor 1 (
How does Tesamorelin work?
Stabilized GHRH analog approved for HIV-associated lipodystrophy; reduces visceral adipose tissue via GH/IGF-1 axis stimulation.
What is the research status of Tesamorelin?
Tesamorelin is currently classified as approved, with 95 research references on record. This is for research purposes only and is not medical advice.
What is the half-life of Tesamorelin?
The reported half-life of Tesamorelin is 26-38 minutes.
What is the molecular weight of Tesamorelin?
Tesamorelin has a molecular weight of approximately 5136 g/mol (formula C221H366N72O67S).
Related peptides
Endogenous cyclic peptide that inhibits GH, insulin, glucagon, and gastric secretion via SSTR1-5 receptors.
Endogenous 28-aa 'hunger hormone' from the stomach; activates GHS-R1a to stimulate GH release and appetite.
First-generation ghrelin receptor agonist hexapeptide that stimulates GH release and strongly increases appetite.
Potent GHRP-family ghrelin receptor agonist with studied cardioprotective effects independent of GH release.
Synthetic hexapeptide ghrelin receptor agonist that potently stimulates GH secretion; also raises appetite, cortisol, and prolactin.
Selective ghrelin receptor (GHS-R1a) agonist that stimulates GH release with minimal effect on cortisol or prolactin.
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