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Stabilized GHRH(1-44) analogue · trans-3-hexenoyl cap
A trans-3-hexenoyl-capped GHRH(1-44) analogue that resists the DPP-4 cleavage which clears native GHRH. Supplied as a lyophilized powder for research purposes only.
Launch Sale · Ends Nov 6
Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Take the full 44-residue human GHRH sequence, cap the N-terminus with a trans-3-hexenoyl group, and you get tesamorelin — a near-native analogue that resists the dipeptidyl peptidase-4 cleavage that ordinarily chews up GHRH in minutes. The lipid cap is the only departure from the natural hormone, and it is the part that buys the molecule time on the receptor.
Because it stays so close to native GHRH, it engages the same pituitary receptor and drives endogenous, pulsatile growth-hormone release rather than overriding the axis. That fidelity is what makes it a useful probe of the hypothalamic-pituitary feedback loop.
The work pairs a mechanism with measurable downstream endpoints. Upstream: GHRH-receptor engagement and DPP-4-resistant pharmacokinetics. Downstream: pulsatile GH secretion, IGF-1, and — in the most-cited trials — visceral and hepatic fat. Tesamorelin is studied as the case where preserving native feedback while extending half-life can be observed end to end.
The defining property is fidelity-plus-durability: tesamorelin reproduces the GHRH signal at the pituitary receptor but survives long enough in serum to be measurable, thanks to the hexenoyl cap that blocks DPP-4. Work reads the GH and IGF-1 output that follows, and watches whether normal feedback restraint stays intact.
The published evidence is unusually clinical for a research peptide. Falutz characterized its effect on visceral adipose tissue in HIV-associated lipodystrophy, and Stanley extended the question to hepatic fat — so the literature ties GHRH-receptor activation to downstream fat and IGF-1 endpoints rather than to binding alone.
Tesamorelin began as an exercise in minimal modification: keep human GHRH(1-44) intact, add a single N-terminal acyl group, and solve the one liability that made native GHRH impractical — its near-instant degradation by DPP-4. The hexenoyl cap did exactly that without remodeling the recognition sequence.
It was the first GHRH analogue to clear regulatory review, which is why its record skews toward human metabolic studies and why it serves as a reference point for stabilized-GHRH chemistry.
In vitro and animal studies
Tesamorelin is a synthetic analogue of human growth-hormone-releasing hormone, consisting of the full 44-residue GHRH sequence with a trans-3-hexenoic acid group attached at the N-terminus. That modification protects against dipeptidyl peptidase-4 cleavage, the principal route by which native GHRH is inactivated within minutes.
Unlike most compounds in this catalogue, tesamorelin's preclinical package was assembled to pharmaceutical regulatory standard, because it was developed as a drug and reached approval. The mechanism is straightforward GHRH receptor agonism on pituitary somatotrophs, producing GH release and downstream hepatic IGF-1 production, with the physiological pulsatility of the axis broadly preserved.
The specific preclinical and mechanistic interest concerned visceral adipose tissue. Visceral fat is metabolically distinct from subcutaneous fat and more responsive to GH-mediated lipolysis, which provided the rationale for the indication that tesamorelin was eventually approved for.
Human data, where it exists
Tesamorelin has the strongest regulatory standing of any growth hormone secretagogue in this catalogue. It completed phase 3 development and was approved by the FDA in 2010, marketed as Egrifta, for the reduction of excess visceral abdominal fat in HIV-infected patients with lipodystrophy. It has also been authorised in Canada.
The pivotal trials were randomised, double-blind and placebo-controlled, and reported statistically significant reductions in visceral adipose tissue measured by CT, along with changes in triglycerides. Effects reversed on discontinuation, indicating that continued administration was required to maintain them. Subsequent published work examined tesamorelin in non-alcoholic fatty liver disease in people with HIV, reporting reductions in liver fat.
That approval is specific: a defined indication, a defined population, defined dosing and prescribed monitoring. It is not a general endorsement of GHRH analogues, and it does not extend to research-grade material supplied outside that framework.
Common assertions, and what the record supports
Tesamorelin is frequently marketed by pointing at its FDA approval, and the approval is real. The unsupported step is the scope. What was demonstrated is reduction of visceral adipose tissue in HIV-associated lipodystrophy — a specific pathophysiology in a specific population, under supervision, with pharmaceutical-grade material.
Generalising that to fat loss in healthy people is not supported by the trial data. The trials did not study that population, and the mechanism's selectivity for visceral over subcutaneous fat means the effect people expect and the effect demonstrated are not the same effect.
A second claim treats the approval as a safety guarantee for any use. Approval means benefits outweighed risks for a defined indication under monitoring, with a label documenting contraindications. Those conditions do not travel with research material.
A third point worth noting: effects reversed after discontinuation in the trials.
Against the compounds it is most often confused with
Against CJC-1295 with DAC, both are GHRH analogues, but they sit at opposite ends of the development spectrum. Tesamorelin completed phase 3, holds approval, and has a published safety label. CJC-1295's development was discontinued after phase 1. Pharmacologically, tesamorelin preserves more of the physiological pulsatility of the axis, while the DAC construct is specifically engineered to produce a sustained plateau.
Against Modified GRF (1-29), the backbone differs — tesamorelin uses the full 44-residue sequence with an N-terminal modification, rather than the truncated 1-29 fragment with internal substitutions.
Against ipamorelin and GHRP-2, the difference is receptor system: GHRH receptor versus growth hormone secretagogue receptor. Tesamorelin does not stimulate appetite or raise cortisol as ghrelin-receptor agonists can, because it does not engage that receptor at all.
Adverse findings, toxicology gaps, material hazards
Because tesamorelin went through formal development, its adverse effect profile is documented in a regulatory label rather than inferred. Reported effects include arthralgia, injection site reactions, peripheral oedema, myalgia and paraesthesia. Hypersensitivity reactions were observed.
The metabolic consequences of GH axis stimulation apply: glucose intolerance and worsening insulin sensitivity are recognised concerns, and glucose monitoring is part of the approved use. Fluid retention and carpal tunnel symptoms follow from the same mechanism.
The label carries contraindications that exist for reasons relevant to the mechanism — active malignancy among them, reflecting the mitogenic concern attached to sustained IGF-1 elevation. Pregnancy is contraindicated. Disruption of the hypothalamic-pituitary axis is a further contraindication.
The existence of a documented safety profile makes tesamorelin better characterised than most of this shelf. It does not make it low risk, and none of the monitoring that accompanies approved use applies to research material.
Bench practice for this compound
Tesamorelin ships lyophilized and is a 44-residue peptide — longer than most on this shelf and correspondingly more prone to aggregation. Introduce bacteriostatic water slowly against the vial wall, never onto the cake, and allow it to dissolve with gentle swirling. Do not shake.
Store reconstituted material at 2–8 °C protected from light, observing the working window on this page. Keep unopened lyophilized vials frozen for long-term storage and avoid freeze-thaw cycling of solutions.
This summary describes published research. It is not a protocol, not a recommendation, and not a statement that this compound is safe or effective for any use. Not for human or animal use.
Falutz, J. et al. (2010). Effects of tesamorelin (TH9507), a growth hormone–releasing factor analogue, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension.
PubMedFalutz, J. et al. (2010). Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab 95(9):4291–4304.
PubMedStanley, T.L. et al. (2019). Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial. Lancet HIV 6(12):e821–e830.
PubMedEvery lot is tested for identity, purity, and net content.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%, on the lot you receive.
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