Tesamorelin (Egrifta, TH9507)

Tesamorelin is a synthetic analog of growth hormone-releasing hormone (GHRH) developed by Theratechnologies. The molecule is a 44-amino-acid full-length GHRH peptide modified by attaching a trans-3-hexenoic acid moiety to the N-terminus — a structural change that protects against DPP-4 (dipeptidyl peptidase-4) cleavage and dramatically extends the molecule's plasma half-life relative to native GHRH (which has a half-life of minutes).^[1]

It was approved by the FDA in November 2010 as Egrifta for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy — a specific clinical syndrome of fat redistribution that develops in some HIV patients on antiretroviral therapy, characterized by visceral fat accumulation and peripheral fat loss. As of 2026, it remains the only FDA-approved GHRH analog and one of very few peptides in the broader GH-axis category to clear a Phase 3 regulatory pathway in the modern era.

How it differs from CJC-1295: Both are GHRH analogs, but with fundamentally different engineering strategies. CJC-1295 uses a Drug Affinity Complex (DAC) modification — a maleimide linker that conjugates to circulating albumin, extending half-life to 6-8 days. Tesamorelin uses a smaller trans-3-hexenoic acid modification that resists DPP-4 cleavage and allows once-daily dosing rather than weekly. The clinical implication: Tesamorelin produces a more physiologic pulsatile GH release pattern with daily administration, while CJC-1295 DAC produces sustained "bleed" elevation. Tesamorelin has Phase 3 evidence; CJC-1295 does not.

Tesamorelin binds the pituitary GHRH receptor (GHRH-R) on somatotroph cells, stimulating endogenous growth hormone (GH) release. This in turn elevates IGF-1 production in the liver and peripheral tissues. The result is a more physiologic GH/IGF-1 elevation pattern than exogenous GH administration — preserving pulsatility and downstream feedback regulation.

Key mechanistic features:

• Pulsatile GH release — Tesamorelin amplifies endogenous GH pulses rather than producing sustained pharmacologic elevation. Less suppression of natural axis function than recombinant GH.
• Visceral fat lipolysis — GH and IGF-1 preferentially mobilize visceral adipose tissue (VAT) over subcutaneous fat. The Phase 3 program demonstrated this selective effect — VAT decreased substantially while subcutaneous fat was largely preserved.
• Hepatic lipid metabolism — Increased fatty acid oxidation contributes to the NAFLD-relevant effects observed in HIV-positive populations with overlapping fatty liver disease.
• IGF-1 elevation — Plasma IGF-1 rises substantially with Tesamorelin therapy. The elevation is the desired effect but is also the principal safety consideration — IGF-1 elevation has theoretical implications for cancer-history populations.

The peer-reviewed literature on Tesamorelin is summarized below across two tiers: human research (the highest standard), and preclinical / emerging research (animal models and early-stage human work).

This table summarizes commonly discussed claims and how the published evidence weighs in. The aim is clarity — supported claims, claims that look promising but need more data, and claims that outrun the science.

FDA label: 2 mg subcutaneous injection daily. Refer to the product labeling and prescribing physician.

Tesamorelin is the only FDA-approved GHRH analog in clinical use — a genuine outlier in the growth-hormone-axis peptide space where most compounds have animal-model or small-clinical evidence at best. The Phase 3 dossier in HIV-associated lipodystrophy is substantial; the NAFLD evidence in HIV+ populations adds a second indication of credible interest; the broader visceral fat reduction effect motivates ongoing off-label exploration.

For users comparing it to CJC-1295, Ipamorelin, Sermorelin, GHRP-2/6, or Hexarelin: Tesamorelin has the strongest regulatory dossier and the cleanest Phase 3 evidence. Off-label use for body recomposition in healthy adults extends beyond the approved population without equivalent trial support — that's a defensible extrapolation given the mechanism, but it's not the same as the FDA-supported indication. The IGF-1 elevation concern that applies to all GH-axis peptides applies to Tesamorelin too — see our high-caution peptides article and peptide drug interactions article for the cancer-history and drug-interaction framework. For the broader GH-axis peptide comparison, see our Best GH Secretagogues 2026 evidence-based ranking.