Tesamorelin

What it actually is

Tesamorelin is a synthetic copy of all 44 amino acids of human growth hormone-releasing hormone, with a trans-3-hexenoic acid group attached for stability. Theratechnologies developed it, and the FDA approved it in 2010 under the brand name Egrifta for reducing excess visceral abdominal fat in HIV-associated lipodystrophy. A reformulated version, Egrifta WR, was approved in March 2025.

It is the only FDA-approved medication specifically indicated for visceral adipose tissue reduction. That is the strongest regulatory standing of any injectable peptide in this library.

Secretagogue, not replacement

The distinction that matters most: tesamorelin does not give you growth hormone. It tells your pituitary to make its own.

It binds GHRH receptors on the anterior pituitary, triggering the normal cascade of GH synthesis and secretion. That GH then drives IGF-1 production in the liver, which mediates most of the downstream effects on body composition.

Because the signal enters upstream, two things stay intact. The pulsatile release pattern, meaning GH released in bursts with the biggest pulse during deep sleep, is preserved, which prevents receptor desensitisation. And the somatostatin feedback loop, the body's own brake on GH, keeps working. Injecting GH directly overrides both, which is where supraphysiological exposure and its side effect profile come from.

Why visceral fat specifically

Growth hormone activates hormone-sensitive lipase inside fat cells, which breaks stored triglycerides into free fatty acids. Visceral fat cells respond more strongly than subcutaneous ones because they carry a higher density of beta-adrenergic receptors and are more metabolically active.

That is why tesamorelin reduces the deep fat around your organs rather than the fat you can pinch, and why scale weight often barely moves. Fat is lost and lean mass is gained roughly in parallel. Waist circumference and DEXA are the measurements that show the change; the bathroom scale is not.

The trial numbers: 15–18% reduction in visceral adipose tissue over 26 weeks in Phase III, with 69% of treated patients achieving clinically significant reduction against 33% on placebo. Waist circumference fell around 2–3 cm. Stanley et al. showed significant hepatic fat reduction with improved liver enzymes, which is why it is relevant to fatty liver disease.

Friedman et al. found improved executive function and verbal memory in older adults with mild cognitive impairment over 20 weeks, an effect attributed to GH and IGF-1's neurotrophic properties.

Running it

There are two approved products and they are not interchangeable. EGRIFTA SV is a 2 mg vial reconstituted with sterile water and dosed at 1.4 mg, 0.35 mL, once daily, injected immediately with the remainder discarded. EGRIFTA WR is an 11.6 mg vial reconstituted with bacteriostatic water and dosed at 1.28 mg, 0.16 mL, once daily, with one vial covering seven days. The labels state explicitly that the two formulations are not substitutable.

The number people get wrong is the SV dose. The vial holds 2 mg; the dose is 1.4 mg. Drawing the vial dry delivers 43% more than the label, and doing it with bacteriostatic water uses a diluent the SV label does not permit. Off-label protocols use 1–2 mg once daily, which is a different thing again and has no label behind it. Injection goes into the abdomen with rotating sites, avoiding the navel.

Two implementation details do most of the work.

Timing. Bedtime, because the largest natural GH pulse occurs during deep sleep and tesamorelin amplifies that rhythm rather than fighting it.

Fasting. At least 2–3 hours after the last meal. Carbohydrates and fats trigger insulin, and insulin blunts the GH response. Taking tesamorelin after dinner is not a small compromise. It works against the mechanism.

Reconstitution, per label. SV: 2 mg vial with 0.5 mL of sterile water gives 4 mg/mL, putting the 1.4 mg dose at 35 units. WR: 11.6 mg vial with 1.3 mL of bacteriostatic water, dosed at 16 units for 1.28 mg. The label's own dose-and-volume pairing works out at 8 mg/mL rather than the 8.9 the vial arithmetic suggests, because the vial is overfilled.

Cycles run 8–12 weeks with reassessment, or 12–26 weeks in the Playbook protocol matching the trial duration. IGF-1, fasting glucose and a lipid panel at baseline and mid-cycle are the monitoring set.

What to expect, and when

Weeks 1–2 are adaptation, and mild joint stiffness or water retention here is a sign the GH axis is responding rather than a problem. Weeks 3–4 typically bring the first noticeable benefit, which is sleep quality. Visceral fat change is internal before it is visible; trials measured it at 12–26 weeks. This is not a fast compound and treating it like one leads people to quit at week four.

The discontinuation finding is important: in LIPO-011, patients switched to placebo at week 26 saw visceral fat return to baseline. Effects are maintained by continued use, not banked.

The honest cautions

Active cancer or a cancer history is a contraindication, because GH promotes cell proliferation. Pituitary pathology and diabetic retinopathy are the other two.

Blood glucose needs monitoring: GH raises it, and that interaction with insulin and sulfonylureas is the one to discuss with a prescriber. Corticosteroids run the other way, potentially reducing efficacy because cortisol suppresses the GH axis.

The stacking warning is explicit in the Playbook: do not combine tesamorelin with exogenous GH or other GH secretagogues without medical guidance. Stacking GH-axis compounds amplifies risk unpredictably.

Tesamorelin is a prescription compound. Claritide will track what you are prescribed and will never suggest a dose or a change.