Fat Loss

Tesamorelin

Also known as: Egrifta, TH9507

RouteSubcutaneous

UK StatusTesamorelin occupies a complex legal position in the UK. Despite FDA approval in the United States for HIV-associated lipodystrophy, it is not currently licensed by the MHRA as a prescription medicine in Britain, meaning it cannot be legally prescribed or used for therapeutic purposes. **Current Regulatory Status** Tesamorelin remains an unlicensed medicine in the UK. The MHRA does not currently approve tesamorelin for any therapeutic indication. Healthcare professionals cannot legally prescribe it through standard NHS or private prescription channels. **Research Access** Several UK-based suppliers offer tesamorelin explicitly "for research purposes only." Purchase and possession for legitimate research remains legal under current regulations, though human consumption outside authorised clinical research settings is not permitted. The MHRA has increased scrutiny of peptide suppliers since 2020, particularly those implying human use in marketing materials. **Important Disclaimer** This information is for educational purposes only. Tesamorelin is not approved for therapeutic use in the UK, and individuals should not attempt to use it for medical purposes outside of proper clinical supervision. Always consult qualified medical professionals before considering any peptide therapy. **International Considerations** Personal importation for research purposes may be permissible in small quantities, though Brexit has complicated EU sourcing routes. Larger quantities may attract regulatory attention and require appropriate documentation demonstrating legitimate research use. The regulatory landscape continues evolving, with enforcement focusing primarily on commercial suppliers rather than individual researchers. Our comprehensive [UK peptide legality guide](/learn/uk-peptide-legality) provides detailed guidance on navigating these complex regulations safely and legally.

Overview

Tesamorelin is a synthetic growth hormone-releasing hormone (GHRH) analogue that has shown promise in clinical trials for treating HIV-associated lipodystrophy. Originally developed by Canadian firm Theratechnologies as TH9507, this 44-amino acid peptide received FDA approval in 2010 under the brand name Egrifta, though it remains unlicensed by the MHRA in the UK.

Research suggests that tesamorelin differs from other growth hormone secretagogues like [Sermorelin](/peptides/sermorelin) or [CJC-1295](/peptides/cjc-1295) due to its potential selectivity for visceral fat reduction. Unlike direct growth hormone administration, studies indicate that tesamorelin may preserve natural pulsatile GH release patterns whilst potentially targeting abdominal fat accumulation—a property that clinical trials have demonstrated to be particularly beneficial for HIV patients suffering from lipodystrophy syndrome.

The peptide's key innovation lies in its structural modification: a trans-3-hexenoic acid group attached to the N-terminus of GHRH(1-29). Research suggests this modification may extend tesamorelin's half-life from minutes (typical of native GHRH) to 26-38 minutes, potentially making it clinically viable whilst maintaining selectivity and reducing side effects compared to direct GH therapy.

Clinical evidence is strongest for HIV-associated lipodystrophy, where one Phase III trial showed a 15.2% reduction in visceral adipose tissue over 26 weeks (Falutz et al., 2010, The Lancet). However, the peptide's mechanism—stimulating natural GH release and subsequent IGF-1 production—has sparked research interest in broader applications including age-related body composition changes and [metabolic health](/learn/peptide-metabolism).

Researchers value tesamorelin for its demonstrated ability to reduce visceral fat in specific populations without the broader side effect profile of growth hormone therapy. The peptide works through the hypothalamic-pituitary axis, maintaining natural feedback loops whilst delivering targeted benefits. For those researching tesamorelin, understanding proper [reconstitution](/learn/reconstitution-guide), [injection techniques](/learn/injection-guide), [growth hormone](/peptides/growth-hormone) relationships, and UK legal requirements through our [legality guide](/learn/uk-peptide-legality) is essential.

Mechanism of Action

Tesamorelin functions as a synthetic analogue of growth hormone-releasing hormone, binding specifically to GHRH receptors on somatotroph cells in the anterior pituitary gland. This targeted approach allows for precise stimulation of the body's natural growth hormone production pathways.

Upon binding to GHRH receptors (G-protein coupled receptors), tesamorelin triggers a well-characterised cascade: adenylyl cyclase activation increases cyclic adenosine monophosphate (cAMP) levels, which activates protein kinase A (PKA). This phosphorylates CREB (cAMP response element-binding protein), ultimately enhancing growth hormone gene transcription and triggering GH synthesis and release.

The released growth hormone then travels to the liver and peripheral tissues, binding to growth hormone receptors and stimulating IGF-1 production—the primary mediator of GH's effects. This includes enhanced lipolysis (particularly in visceral fat deposits), increased protein synthesis, and improved glucose metabolism.

Studies indicate that tesamorelin's effectiveness lies in what it doesn't disrupt. Unlike exogenous growth hormone, it preserves natural pulsatile release patterns and maintains feedback mechanisms. The hypothalamus can still regulate the system, preventing the desensitisation common with direct hormone replacement.

The peptide's structural modification—that trans-3-hexenoic acid group—protects it from rapid degradation by dipeptidyl peptidase-4 (DPP-4), extending its activity window. This is crucial because native GHRH has a half-life measured in minutes, whilst tesamorelin remains active for 26-38 minutes.

Research suggests that tesamorelin shows relative selectivity for visceral adipose tissue reduction compared to other GHRH analogues like [Sermorelin](/peptides/sermorelin). The exact mechanism behind this selectivity isn't fully understood but likely relates to tissue-specific receptor sensitivity and local IGF-1 production patterns. This targeted action explains why clinical trials have shown tesamorelin to be particularly effective for HIV lipodystrophy, where visceral fat accumulation is the primary concern.