# Tesamorelin: The GHRH(1-44) Analogue Research Record, Cell by Cell > Tesamorelin is a synthetic GHRH(1-44) analogue that raises endogenous growth hormone and IGF-1. It cut visceral fat 15.2% in its pivotal HIV trial. A cited research digest. A cell-by-cell digest of the published record: the GHRH-receptor mechanism, the visceral-fat and IGF-1 figures, the pharmacokinetics, and the FDA-approved scope — every quantitative claim filed to its source. ## The short version Tesamorelin is a lab-made copy of the brain's own "make growth hormone" signal, GHRH (growth hormone-releasing hormone — the hypothalamic peptide that tells the pituitary gland to release growth hormone). Instead of injecting growth hormone directly, tesamorelin nudges the body to release its own. That extra growth hormone raises IGF-1 (a growth signal the liver makes when growth hormone rises) and, in studies, burns off deep belly fat. In its main human trial, it cut visceral fat (the fat packed around the organs) by 15.2% and pushed IGF-1 up 81.0% [1]. It is FDA-approved, but only for one HIV-related condition; everything else is off-label. ## What the tesamorelin literature actually shows Tesamorelin is a synthetic 44-amino-acid analogue of human growth hormone-releasing hormone, GHRH(1-44), carrying a trans-3-hexenoic acid group on its N-terminus. That single chemical addition blocks DPP-IV (dipeptidyl peptidase-IV — an enzyme that snips native GHRH apart within minutes), so the molecule survives in plasma long enough to act [8]. It is not growth hormone itself. It is a signal to the pituitary gland to make and release more of the body's own. The headline result comes from a 412-patient Phase 3 trial in HIV patients with abdominal fat accumulation: tesamorelin 2 mg/day reduced visceral adipose tissue by 15.2% while placebo rose 5.0%, dropped triglycerides by 50 mg/dL, and raised IGF-1 by 81.0% [1]. A 52-week extension held visceral fat down by roughly 18% with continued dosing, and the fat reaccumulated once the drug stopped [2]. A separate JAMA trial added a liver finding: a visceral-fat treatment effect of -42 cm2 and a net hepatic-fat reduction of -2.9% [3]. This is an unusually rectangular literature — discrete, quotable figures, each tied to a randomized trial. The site lays them out the way they were measured: one finding, one cell, one citation. Read the full [visceral-fat research](/research), the [pharmacokinetics of tesamorelin](/half-life), the [doses studied in the literature](/dosage), or the structural comparison [tesamorelin vs sermorelin](/vs-sermorelin). ## How Tesamorelin Stimulates Pulsatile Growth Hormone Tesamorelin binds the GHRH receptor (GHRH-R — a Gs-coupled receptor on the pituitary's growth-hormone-making cells, the somatotrophs). Binding switches on adenylyl cyclase, which raises cAMP, which activates PKA, which drives growth-hormone gene transcription and the release of stored hormone [4]. The released growth hormone then travels to the liver and triggers IGF-1 production, and growth hormone plus IGF-1 together break down fat (lipolysis), preferentially in the visceral compartment. The key word is *pulsatile*. The body releases growth hormone in natural bursts, not a steady stream. A population pharmacokinetic-pharmacodynamic model confirmed that tesamorelin stimulates growth hormone in this same episodic, burst-like pattern rather than flooding the system continuously [7]. That is why its metabolic profile differs from injected recombinant growth hormone — it amplifies an existing rhythm instead of overriding it. In 13 healthy men, two weeks of 2 mg/day raised mean overnight growth hormone and lifted IGF-1 by 181 ug/L, while fasting glucose and insulin-stimulated glucose uptake were unchanged [4]. The detailed cascade is on the [how tesamorelin works](/research) page. ## Is Tesamorelin FDA Approved? Yes — but narrowly. Tesamorelin is FDA-approved (NDA 022505, November 2010) to reduce excess abdominal fat in HIV-infected adults with lipodystrophy (a fat-redistribution complication of HIV and its therapy) [5]. That is the one approved indication. Every other use — general weight loss, cosmetic fat reduction, anti-aging, growth-hormone optimization, non-HIV fatty-liver disease — is **off-label and not FDA-approved** [15]. The distinction matters because the pivotal efficacy trials enrolled HIV-positive adults on antiretroviral therapy. Generalizing those results to other populations is mechanistically plausible but not established by large randomized trials. Research-grade tesamorelin supplied for laboratory work is not the approved finished drug product and carries no purity or potency oversight from that approval. Tesamorelin is also prohibited in sport under the WADA Prohibited List (category S2, peptide hormones and growth factors), in- and out-of-competition. ## Is Tesamorelin a Steroid? No. Tesamorelin is a peptide — a short chain of amino acids — not a steroid. Steroids are fat-soluble molecules built on a four-ring carbon skeleton; tesamorelin is a 44-residue analogue of a natural hormone. It does not act on steroid receptors. It works one step upstream of the growth-hormone axis, signaling the pituitary to release the body's own growth hormone, which in turn raises IGF-1 [4]. Mechanistically it has nothing in common with anabolic-androgenic steroids. ## What Is Tesamorelin Used For? Its single FDA-approved use is to reduce excess visceral abdominal fat in HIV-associated lipodystrophy [5]. In that setting it has been studied for selective visceral-fat reduction, triglyceride lowering, and reduction of liver fat in HIV-associated fatty-liver disease [1][3]. Researchers have also examined it mechanistically in healthy adults [4] and in a cognition study in older adults, and a 2026 review lists it among pharmacologic candidates under investigation for preserving lean body mass during weight loss [14]. All uses outside the HIV indication remain off-label and investigational [15]. --- tesamorelin catalogued cell by cell on a nine-panel reference board — every visceral-fat figure, the minutes-fast plasma clearance against the day-long IGF-1 effect, and the FDA-approved-only-for-HIV-lipodystrophy boundary filed to its study; a laboratory reference grid, not a clinic, a vendor, or a prescription.