Research guide

Tesamorelin (TH9507): GHRH-Analogue Research Guide

Tesamorelin is human growth hormone-releasing hormone with one deliberate change made to it. That change is the entire compound, and nineteen years of published trials are built on it. This guide sets out what that literature has examined, with an identifier for every study named.

Identifiers

Common name
Tesamorelin
Development code
TH9507
Compound class
Synthetic analogue of human growth hormone-releasing hormone, GHRH(1–44)
Structural modification
Trans-3-hexenoyl group added at Tyr1 of hGRF(1–44)NH₂ (Ferdinandi et al., 2007)
Receptor target
Pituitary GHRH receptor
Molecular formula
C₂₂₁H₃₆₆N₇₂O₆₇S (PubChem CID 16137828)
Molecular weight
≈5,136 g/mol (PubChem CID 16137828)
Originator
Theratechnologies Inc.
Regulatory status
The material supplied here is not approved. A separately manufactured tesamorelin product holds a United States approval from 2010 for one clinical indication — see Regulatory status
Supplied by Prime Peptides UAE as
20mg research pen — Tesamorelin product page

What tesamorelin is

Growth hormone-releasing hormone is the signal the hypothalamus sends to the pituitary to release growth hormone. In the bloodstream it does not last: an enzyme called dipeptidyl aminopeptidase-IV cuts it near one end, and the intact molecule is short-lived.

Tesamorelin is that hormone with a single group — a trans-3-hexenoyl moiety — attached at the first residue, Tyr1. Ferdinandi and colleagues characterised the compound in Basic & Clinical Pharmacology & Toxicology in 2007 (PMID 17214611), describing it in the paper’s own terms as “minimally modified”, and reporting that the modification renders the peptide resistant to dipeptidyl aminopeptidase-IV deactivation, slows its degradation in rat, dog and human plasma, and prolongs its plasma elimination kinetics compared with the unmodified hormone. In pigs, rats and dogs, the same paper reports elevated plasma growth hormone and insulin-like growth factor-1.

That is the whole design. One group, added at one position, to defeat one enzyme. Everything below is a study of what a releasing hormone that survives longer in circulation does to the pituitary’s own release pattern.

One naming trap, because it causes avoidable confusion in this literature. Older papers — including the 2007 New England Journal of Medicine trial — call the endogenous peptide growth hormone-releasing factor (GRF). Newer papers call it growth hormone-releasing hormone (GHRH). Same molecule, two conventions, and both appear across the citations below.

GHRH analogue, secretagogue, or growth hormone itself

These three get conflated constantly and they are not the same class of thing.

  • Growth hormone is the hormone itself. Supplying it externally bypasses the pituitary entirely.
  • A GHRH analogue is a structural variant of the releasing hormone, acting at the pituitary GHRH receptor. Tesamorelin is in this class.
  • A growth hormone secretagogue prompts release through a different receptor — the growth hormone secretagogue receptor — not the GHRH receptor. Ipamorelin is the commonly cited example.

The distinction is mechanistic, not a ranking, and it is why a compound’s class label carries real information about which literature applies to it. Compounds pairing a GHRH analogue with a secretagogue are covered in the CJC-1295 and ipamorelin research guide. Terms of this kind are collected in the research peptide terminology glossary.

What the published literature has examined

One qualifier belongs at the top rather than buried at the bottom.

Almost every human trial on this compound was conducted in people living with HIV who had abdominal fat accumulation associated with their condition or their antiretroviral regimen. That is not incidental context. It is the population the entire evidence base describes, and it is the single most important thing to know before reading any entry below. The entries are chronological, 2007 to 2026, and magnitudes are deliberately omitted throughout.

Preclinical pharmacology, 2007

Ferdinandi and colleagues, Basic & Clinical Pharmacology & Toxicology (PMID 17214611). Non-clinical pharmacology of TH9507: structure, resistance to enzymatic deactivation, plasma stability across three species, and elimination kinetics. This is the correct citation for any statement about what tesamorelin is structurally.

Multicentre randomised trial, 2007

Falutz and colleagues, New England Journal of Medicine (PMID 18057338). A multicentre, randomised, placebo-controlled trial in 412 participants living with HIV who had abdominal fat accumulation, over 26 weeks, with visceral adipose tissue, lipid measures and insulin-like growth factor-1 as endpoints. The reduction in visceral adipose tissue versus placebo was statistically significant. This is the trial most subsequent work builds on.

Long-term extension, 2008

Falutz and colleagues, AIDS (PMID 18690162). A randomised controlled extension examining tolerability and endpoint durability across 52 weeks in the same population, including whether observed changes persisted after the study period ended. They did not. That finding is one of the most frequently omitted points in secondary commentary on this compound, which is a good reason to put it in the third entry rather than a footnote.

Pooled phase 3 analysis, 2010

Falutz and colleagues, Journal of Clinical Endocrinology & Metabolism (PMID 20554713). A pooled analysis of two multicentre, international, randomised, double-blind, placebo-controlled phase 3 trials — 806 participants on antiretroviral regimens with excess abdominal fat, across a 26-week main phase and a 26-week extension. This is the largest single body of tesamorelin data published. The pooled analysis reports a statistically significant reduction in visceral adipose tissue relative to placebo, and no significant change in the other abdominal fat compartment it measured. Both are stated here, because a synthesis that reports only the significant endpoint is not a synthesis.

Visceral and hepatic fat, 2014

Stanley and colleagues, JAMA (PMID 25038357). A double-blind, randomised, placebo-controlled trial in 50 adults living with HIV at Massachusetts General Hospital, examining visceral adipose tissue and liver fat over six months with glucose measures tracked. This is where the research question moved from visceral fat toward the liver.

Hepatic steatosis, 2019

Stanley and colleagues, Lancet HIV (PMID 31611038). A randomised, double-blind, multicentre trial in 61 participants living with HIV and non-alcoholic fatty liver disease defined by a hepatic fat fraction threshold. The authors concluded that longer studies with liver histology endpoints were needed — a limitation worth carrying forward rather than dropping.

Integrase-inhibitor regimens, 2024

Russo and colleagues, AIDS (PMID 38905488). A randomised, double-blind, placebo-controlled analysis of 38 participants on integrase strand transfer inhibitor regimens, drawn from the 61-participant parent study above, examining visceral and hepatic fat endpoints and adverse-event frequency. The most recent primary trial publication in the series.

The one study outside the metabolic literature, 2012

Baker and colleagues, Archives of Neurology (PMID 22869065). A randomised, double-blind, placebo-controlled trial in older adults, examining cognitive endpoints across 20 weeks with a 10-week washout. The paper describes the compound it administered as “a stabilized analog of human GHRH”. This is the principal published departure from the HIV-associated metabolic literature, and it is frequently miscited as a study of a generic GHRH analogue rather than of tesamorelin specifically.

Where the evidence has been synthesised

Badran and colleagues, Obesity Research and Clinical Practice, 2026 (PMID 41545261). A systematic review and meta-analysis pooling five randomised controlled trials across body-composition, hepatic-fat, metabolic and adverse-event endpoints in HIV-associated lipodystrophy. The synthesis reports endpoints on which no significant change was observed alongside those where change was reported — a meta-analysis is the right place to see the null findings next to the positive ones, and it is the reason a meta-analysis is a better entry point than any single trial.

Regulatory status

The material supplied here is not approved. It is not a medicine, and it is not approved by any regulator, in any jurisdiction, for any indication.

EGRIFTA, a tesamorelin product manufactured by Theratechnologies under United States FDA application 022505, was approved in November 2010 for the reduction of excess visceral abdominal fat in adults with HIV-associated lipodystrophy. That approval covers that product, under that application. It does not extend to material supplied under the same compound name by other parties, including the material supplied here.

What that fact does and does not mean. It is a real, verifiable regulatory record, and a research guide that omitted it would be a worse guide. But an approval granted in one jurisdiction, for one narrowly defined clinical indication, in one population, under one manufacturer’s application, establishes nothing whatsoever about a research material sold under the same compound name by anyone else. It says nothing about that material’s identity, purity, origin or suitability. Those questions are answered by a third-party lab report, not by another company’s regulatory file.

Registration status in the United Arab Emirates is a separate question and is not addressed here.

Prime Peptides UAE supplies tesamorelin as a research material only. It is not supplied as a medicine, and it is not the approved product described above.

What this literature does not establish

Published research attaches to a compound. It does not attach to a vial.

Four limits, because tesamorelin is the compound in this catalogue where the gap between “well studied” and “well studied in a way that generalises” is widest:

  1. The population is specific, and consistent. With one exception, every human trial above enrolled people living with HIV who had a defined pattern of abdominal fat accumulation. A finding in that population is not a general statement about anyone else.
  2. Durability was tested, and reported. The 2008 extension examined whether changes persisted after the study period ended and reported that they did not. Any summary omitting that is incomplete.
  3. The synthesis includes null findings. The 2026 meta-analysis reports endpoints with no significant change alongside those with change. Both belong in an honest reading.
  4. A published trial says nothing about a research material’s provenance. The document that speaks to a specific material is its lab report — how to read a peptide COA.

How Prime Peptides UAE documents tesamorelin

A third-party lab report is published for this product and is available in full, with the issuing laboratory’s verification key, on Testing and Quality — where the reports we hold are published, and the products we hold none for are named. Format, strength, AED price and current document status are on the Tesamorelin product page.

This guide is a summary of published research. It contains no amounts, no schedules, no preparation or handling information, and no medical advice.

For research purposes only. Not for human consumption.

Prime Peptides UAE supplies this compound as a laboratory research material. Full regulatory information: Product and Regulatory Information.

Common questions

What is tesamorelin?

Tesamorelin, development code TH9507, is a synthetic analogue of human growth hormone-releasing hormone, GHRH(1–44), modified by a trans-3-hexenoyl group at Tyr1. Ferdinandi and colleagues (Basic & Clinical Pharmacology & Toxicology, 2007, PMID 17214611) report that the modification confers resistance to dipeptidyl aminopeptidase-IV deactivation and prolongs plasma elimination kinetics.

Why does one small modification matter so much?

Because the enzyme it defeats is what limits the unmodified hormone. Dipeptidyl aminopeptidase-IV cleaves native GHRH near one end, and the intact peptide is short-lived in circulation. The 2007 pharmacology paper reports that the modified analogue resists that cleavage and degrades more slowly in rat, dog and human plasma. Every trial below is, one way or another, a study of what that longer survival does.

How does a GHRH analogue differ from a growth hormone secretagogue?

By receptor. A GHRH analogue such as tesamorelin acts at the pituitary GHRH receptor. A secretagogue such as ipamorelin acts at the growth hormone secretagogue receptor instead. Both are described in the literature as prompting endogenous release rather than supplying growth hormone externally, but they are separate compound classes with separate research bases.

What population was tesamorelin studied in?

Almost entirely in people living with HIV who had abdominal fat accumulation associated with the condition or with antiretroviral regimens — the 2007 NEJM trial (PMID 18057338), the 2010 pooled phase 3 analysis (PMID 20554713), the 2014 JAMA trial (PMID 25038357), the 2019 Lancet HIV trial (PMID 31611038) and the 2024 AIDS analysis (PMID 38905488). Baker and colleagues (Archives of Neurology, 2012, PMID 22869065) is the principal exception.

Is tesamorelin an approved medicine?

Not the material supplied here. Prime Peptides UAE supplies tesamorelin as a research material only, not as a medicine, and it is not approved by any authority. A separately manufactured tesamorelin product holds a United States approval granted in November 2010, for one clinical indication in one population under one manufacturer’s application; that approval does not extend to material supplied under the same compound name by other parties.

What does TH9507 refer to?

The development code used for tesamorelin in the preclinical and early clinical literature, including Ferdinandi and colleagues (2007) and the pooled phase 3 analysis (2010). Searching either term reaches the same compound.

Has the tesamorelin literature been systematically reviewed?

Yes. Badran and colleagues, Obesity Research and Clinical Practice, 2026 (PMID 41545261), pooling five randomised controlled trials across body-composition, hepatic-fat, metabolic and adverse-event endpoints. It reports both significant and non-significant findings.

References

All identifiers verified against PubMed and PubChem.

  1. Ferdinandi ES, et al. Basic & Clinical Pharmacology & Toxicology. 2007;100(1):49–58. Non-clinical pharmacology of TH9507: structure, enzymatic stability and elimination kinetics. PMID 17214611 · DOI 10.1111/j.1742-7843.2007.00008.x
  2. Falutz J, et al. New England Journal of Medicine. 2007;357(23):2359–2370. Multicentre randomised placebo-controlled trial, 412 participants, 26 weeks. PMID 18057338 · DOI 10.1056/NEJMoa072375
  3. Falutz J, et al. AIDS. 2008;22(14):1719–1728. Randomised controlled extension; tolerability and endpoint durability across 52 weeks. PMID 18690162 · DOI 10.1097/QAD.0b013e32830a5058
  4. Falutz J, et al. Journal of Clinical Endocrinology & Metabolism. 2010;95(9):4291–4304. Pooled analysis of two phase 3 trials, 806 participants. PMID 20554713 · DOI 10.1210/jc.2010-0490
  5. Baker LD, et al. Archives of Neurology. 2012;69(11):1420–1429. Randomised double-blind placebo-controlled trial in older adults; cognitive endpoints, 20 weeks plus 10-week washout. PMID 22869065 · DOI 10.1001/archneurol.2012.1970
  6. Stanley TL, et al. JAMA. 2014;312(4):380–389. Double-blind randomised placebo-controlled trial, 50 adults, visceral and hepatic fat over six months. PMID 25038357 · DOI 10.1001/jama.2014.8334
  7. Stanley TL, et al. Lancet HIV. 2019;6(12):e821–e830. Randomised double-blind multicentre trial, 61 participants. PMID 31611038 · DOI 10.1016/S2352-3018(19)30338-8
  8. Russo SC, et al. AIDS. 2024;38(12):1758–1764. Randomised double-blind placebo-controlled analysis, 38 participants on integrase strand transfer inhibitor regimens. PMID 38905488 · DOI 10.1097/QAD.0000000000003965
  9. Badran AS, et al. Obesity Research and Clinical Practice. 2026;20(1):2–12. Systematic review and meta-analysis of five randomised controlled trials. PMID 41545261 · DOI 10.1016/j.orcp.2026.01.002
  10. PubChem CID 16137828 — tesamorelin: molecular formula and molecular weight.
  11. US FDA application 022505 — original approval letter, November 2010, published at accessdata.fda.gov.