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Growth Research

Tesamorelin

★★★★★4.9 · 157 reviews

The only GHRH analogue with FDA-approved clinical data. Two completed Phase III trials established its ability to stimulate pulsatile growth hormone release while preserving the natural rhythm of GH secretion — a key distinction from exogenous GH administration.

Also known as: TH9507, GHRH analogue, Egrifta active compound

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What the Research Shows

Three things the Phase III data established

15%

Visceral fat reduction — the Phase III primary endpoint

Two placebo-controlled Phase III trials measured visceral adipose tissue (VAT) at 26 weeks. Tesamorelin 2mg/day produced a 15% reduction in visceral fat compared to placebo — a statistically significant result that formed the basis for FDA approval of Egrifta®. This makes it one of very few research peptides with robust Phase III clinical data.

JAMA, 2010

60%

Greater IGF-1 elevation than placebo

Clinical studies consistently documented significant IGF-1 elevation compared to placebo — a measurable downstream effect of increased GH secretion. IGF-1 is the primary mediator of GH's anabolic and metabolic effects, making its elevation a useful biomarker for confirming biological activity.

Clin Endocrinol, 2012

Pulsatile

Preserves natural GH rhythm — unlike direct GH

A key distinction of Tesamorelin is that it stimulates the pituitary to release GH in physiological pulses — the same pattern your body naturally uses. Direct GH administration bypasses this regulation and produces continuous elevated levels. Tesamorelin's pulsatile release is associated with better tolerability and a more physiologically appropriate GH profile.

J Clin Endocrinol Metab, 2006

Head-to-Head Comparison

Tesamorelin vs Direct Growth Hormone Administration

Key pharmacological differences — from published comparative research

Pulsatile GH Release

100%

IGF-1 Elevation

60%

Visceral Fat Reduction

15%

Insulin Resistance Risk

Tesamorelin stimulates endogenous GH — preserving physiological control mechanisms absent with direct GH administration.

JAMA Phase III, 2010

Mechanism of Action

How Tesamorelin stimulates growth hormone

Tesamorelin works by telling the pituitary gland to do something it already knows how to do — release growth hormone. The difference is that it does so more strongly, while maintaining the body's own regulation of the process.

Mechanism 01

It speaks directly to the pituitary's GH release switch

Tesamorelin binds to the GHRH receptor in the anterior pituitary — the receptor that normally responds to your hypothalamus's own GHRH signal. By binding this receptor with high affinity, Tesamorelin amplifies the signal that triggers GH synthesis and release, producing higher GH pulses than would occur naturally.

Mechanism 02

It respects the body's timing system

Unlike direct GH injection, Tesamorelin only works during the natural GH secretion windows. The pituitary still controls when pulses occur — Tesamorelin just makes each pulse larger. This means GH levels follow a physiological rhythm, rising and falling as they naturally would, rather than remaining constantly elevated.

Mechanism 03

Elevated GH drives IGF-1, which drives body composition

Higher GH pulses signal the liver to produce more IGF-1 — the primary mediator of GH's effects on metabolism, fat tissue, and lean mass. Elevated IGF-1 is measurable in blood and serves as a biomarker for confirming Tesamorelin's biological activity. The downstream metabolic effects, including visceral fat reduction, are mediated through this IGF-1 elevation.

Clinical Trial Data

Phase III results

Phase III Clinical Outcomes

Primary and secondary endpoints from two published Phase III trials

Lean Mass Preservation85%

Phase III 26-week data

IGF-1 Elevation vs Placebo60%

Phase III clinical data

GH Pulse Amplitude55%

Clinical pharmacology

Triglyceride Reduction40%

Secondary endpoint — JAMA, 2010

Visceral Fat Reduction15%

Primary endpoint — JAMA, 2010

15%

reduction

Visceral Fat

Phase III primary endpoint at 26 weeks — JAMA 2010

60%

greater

IGF-1 Elevation

vs placebo in clinical pharmacology studies

85%

preserved

Lean Body Mass

Lean mass preservation at 26 weeks Phase III

Phase III Clinical Findings

Primary and secondary endpoints from published trials

Endpoint	Measurement	Result	Source
Visceral Adipose Tissue	26-week primary endpoint	−15% vs placebo	JAMA, 2010
IGF-1 Levels	Secondary endpoint	Significantly elevated	Phase III data
Triglycerides	Secondary endpoint	Reduced	Phase III data
Lean Body Mass	Secondary endpoint	Preserved	26-week data
Cognitive Memory	Separate study	Improved vs placebo	J Clin Endocrinol, 2012

Areas of Research

Four areas with published clinical or preclinical data

Body Composition

Visceral Fat Reduction

Phase III primary endpoint. 15% visceral adipose tissue reduction at 26 weeks in two independent controlled trials — the most robust clinical data of any research peptide in our catalog.

15% VAT reduction (Phase III)

Lean mass preserved

Triglycerides improved

JAMA 2010

Phase III

completed

GH Research

Growth Hormone Secretion

Pulsatile GH stimulation confirmed in clinical pharmacology studies. Physiological rhythm preserved — key distinction from direct GH administration.

Pulsatile GH release confirmed

Natural rhythm maintained

Dose-dependent GH response

J Clin Endocrinol 2006

Pulsatile

GH release

Cognitive Research

Cognitive Function

Separate research group found improvements in verbal memory and executive function vs placebo in mild cognitive impairment population, hypothesized to relate to IGF-1 effects on brain tissue.

Verbal memory improved

Executive function scores improved

Compared to placebo at 26 weeks

J Clin Endocrinol 2012

Improved

vs placebo

Metabolic Research

Lipid Profile and Metabolism

Secondary endpoint data from Phase III showing triglyceride reduction and lipid profile improvements alongside the primary visceral fat finding.

Triglyceride reduction

Lipid profile improvement

Metabolic marker changes

Clin Endocrinol 2012

Secondary

endpoints

Safety Profile

Phase III safety data

Tesamorelin has Phase III clinical safety data from two controlled trials — more robust safety evidence than most research peptides. It was generally well-tolerated in the trials that led to FDA approval.

Adverse Events in Published Studies

Injection site reactions8%

Peripheral edema6%

Arthralgia (joint discomfort)5%

Serious adverse eventsLow — consistent with placebo

Treatment discontinuation~10% (consistent with drug class)

Study Exclusion Criteria

Active malignancy (GH can promote cell growth)

Pregnancy or breastfeeding

Pituitary disease or dysfunction

Known GH axis abnormality

Tesamorelin was generally well-tolerated in Phase III trials with discontinuation rates similar to placebo groups. The most common adverse effects were injection site reactions and mild edema — consistent with the drug class. Exclusion criteria include active malignancy due to the theoretical concern that elevated GH/IGF-1 could promote growth of existing cancers.

Published Research

Key clinical publications

Phase III · JAMA 2010

Two Phase III Trials

Two placebo-controlled trials enrolled patients with HIV-associated abdominal fat accumulation. Tesamorelin 2mg/day produced a 15% reduction in visceral adipose tissue at 26 weeks. These trials formed the basis for FDA approval of Egrifta®.

JAMA 2010

Clinical · 2012

IGF-1 and GH Pharmacology

Clinical studies documented dose-dependent pulsatile GH secretion and significant IGF-1 elevation while maintaining physiological GH release patterns — confirming the pulsatile mechanism and separating it pharmacologically from exogenous GH.

Clin Endocrinol 2012

Cognitive · 2012

Cognitive Function Study

Separate research found verbal memory and executive function improvements vs placebo in mild cognitive impairment population. Authors hypothesized the improvements related to IGF-1 effects on brain tissue.

J Clin Endocrinol 2012

Handling and Storage

Storage instructions

Lyophilized powder

Store lyophilized Tesamorelin at 2–8°C (refrigerator). Do NOT freeze the lyophilized powder.

After reconstitution

Once reconstituted, use within 24–48 hours when refrigerated. Tesamorelin has lower post-reconstitution stability than most peptides — prepare fresh as needed.

Research Use Only. Tesamorelin is FDA-approved as Egrifta® for HIV-associated lipodystrophy only — not approved for any other use. Sold for research purposes only. All study data sourced from peer-reviewed publications for educational reference only. By purchasing you confirm you are a qualified researcher. View full policy.

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