Tesamorelin is a synthetic 44-residue growth-hormone-releasing factor analog with an N-terminal trans-3-hexenoyl modification that improves resistance to enzymatic cleavage. It activates the GHRH receptor upstream of endogenous growth-hormone and IGF-1 signaling. Apex Laboratory supplies Tesamorelin as a research-grade chemical reagent for in-vitro and preclinical research, distinct from the EGRIFTA SV and EGRIFTA WR pharmaceutical formulations.
Tesamorelin is most useful as a research entity when three records remain separate: the exact 44-residue analog, GHRH-receptor signaling in defined models, and evidence from finished pharmaceutical formulations. The same molecule appears in all three, but formulation, manufacturing controls, indications, and regulatory status do not transfer between them.
This guide follows FDA’s March 2025 EGRIFTA WR label and the current BLA 022505 product history, and carries no clinical-use, administration, reconstitution, storage, or human-dose instructions. The growth-hormone-axis research hub owns family navigation; this page owns the Tesamorelin entity.
- Tesamorelin retains the full 44-residue human GHRF sequence and adds an N-terminal trans-3-hexenoyl group.
- GHRHR activation signals through Gs and cAMP upstream of endogenous GH and IGF-1.
- Visceral-adipose and liver-fat findings belong to named study populations and finished formulations.
- EGRIFTA WR and EGRIFTA SV are separate, non-substitutable FDA-approved formulations under BLA 022505.
- A research reagent is not EGRIFTA, is not a pharmaceutical, and carries no approved indication.
Tesamorelin Technical Identity
FDA’s current EGRIFTA WR description identifies Tesamorelin as a synthetic analog of human growth-hormone-releasing factor. The peptide contains the complete 44-amino-acid human GRF sequence plus a trans-3-hexenoyl moiety attached to the N-terminal tyrosine. FDA reports a free-base-equivalent molecular weight of 5135.9 Da and the tesamorelin acetate formula C221H366N72O67S · xC2H4O2, where x is approximately seven.
| Identity field | Recorded value | Record basis |
|---|---|---|
| Research designation | TH9507 | Preclinical and early clinical literature |
| CAS registry number | 218949-48-5 | PubChem CID 16137828 (DrugBank, EPA DSSTox) |
| Molecular formula, peptide free base | C221H366N72O67S | PubChem; FDA product description |
| Molecular formula, acetate salt | C221H366N72O67S · xC2H4O2, x approximately 7 | FDA EGRIFTA WR and SV descriptions |
| Molecular weight | 5135.9 Da, free-base equivalent | FDA EGRIFTA WR and SV descriptions |
| Backbone | Complete 44-residue human GRF sequence, C-terminal leucine amide | FDA description; UniProt P01286 residues 32-75 |
| Sequence, one-letter | YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL-NH2 | UniProt P01286 somatoliberin chain |
| Modification site | trans-3-hexenoyl moiety on Tyr1 of Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr | TH9507 non-clinical report[1]; FDA description |
| Relation to Sermorelin | The GHRH(1-29) N-terminal fragment of the same parent sequence | Same UniProt chain |
“Free-base equivalent” is an analytical basis, not a statement that every sample is the free base. Tesamorelin acetate carries variable acetate association, so a laboratory record should say whether formula, mass, concentration, and reference standard are expressed for the peptide, the acetate salt, or a finished formulation. An unexplained basis can hide a real mismatch.
The trans-3-hexenoyl group is the defining design feature, since native GHRH is cleaved rapidly by dipeptidyl peptidase-4 at its N-terminus. The modification does not make every tesamorelin-containing material interchangeable; salt, formulation, excipients, process, and lot still matter.
GHRH-Receptor Signaling
Tesamorelin acts upstream at the growth-hormone-releasing hormone receptor (GHRHR), a class B G-protein-coupled receptor expressed on pituitary somatotrophs. Receptor activation couples through Gs to adenylyl cyclase and increases intracellular cyclic AMP. That signal supports endogenous growth-hormone release, followed by downstream IGF-1 responses.
Two in-vitro records make that pathway concrete. In cells co-expressing cloned GHRH and GH-secretagogue receptors, activating the GH-secretagogue receptor alone produced no cAMP response, while co-activating both receptors produced a cAMP response approximately 2-fold that of GHRH-receptor activation alone; the potentiation was dose-dependent for both GHRH and the co-applied ghrelin or synthetic secretagogue, and selective for the GHRH receptor.[2] A separate study of human GHRHR found that the PDZ domain of PICK1 and the last four C-terminal receptor residues were both prerequisites for their interaction, and that the interaction changed the kinetics of receptor cell-surface expression and the intensity of the cAMP signal after ligand stimulation.[3] Both are transfected-cell results, not human dosing data, and neither tested tesamorelin.
“Upstream” is a boundary: supplying a GHRHR agonist is not supplying growth hormone or IGF-1. The experimental system must contain the receptor and functional downstream machinery, and the endpoint should match the model. A cAMP assay, GH-release study, and peripheral IGF-1 measurement answer different questions, and receptor density, species, cell background, incubation time, and comparator can each move an apparent potency value.
Exposure, Half-Life, and Stability Data
Stability belongs to the modification; exposure belongs to a species, a formulation, and a dose. The TH9507 non-clinical program reported that adding the trans-3-hexenoyl moiety to Tyr1 made the peptide resistant to dipeptidyl aminopeptidase-IV and slowed its in-vitro degradation in rat, dog, and human plasma compared with unmodified hGRF(1-44)NH2. Plasma growth hormone and IGF-1 rose markedly in pigs, rats, and dogs after daily repeat intravenous or subcutaneous injection at doses up to 600 µg/kg, and subchronic toxicity studies ran up to 4 months in rats and dogs, where prolonged supraphysiological growth-hormone and IGF-1 exposure drove the reported adverse findings.[1]
| Record | Species or population | Dose and route | Reported exposure |
|---|---|---|---|
| TH9507 non-clinical program[1] | Dogs, toxicokinetic evaluation | Daily repeat intravenous or subcutaneous, up to 600 µg/kg | Apparent elimination half-life 21 to 45 minutes; exposure dose-related by both routes |
| EGRIFTA WR prescribing information[8] | Healthy adult subjects | Single 1.28 mg subcutaneous dose | Mean elimination half-life 11 minutes; mean Cmax 3831 pg/mL; mean AUC0-inf 1172 pg·h/mL |
| EGRIFTA SV prescribing information | Healthy adult subjects | Single 1.4 mg subcutaneous dose | Mean elimination half-life 8 minutes; mean Cmax 2956.1 pg/mL; mean AUC0-inf 889.1 pg·h/mL; median Tmax 0.15 h |
| Population PK/PD analysis (PMID 25895899) | 41 phase I subjects: healthy volunteers and HIV-infected patients | 1 or 2 mg subcutaneous daily for 14 consecutive days | Growth-hormone secretion modeled as episodic and finite in duration, driving IGF-1 sequentially; age, body weight, BMI, sex, race, and health status were not significantly associated with model parameters |
Canine toxicokinetics are not human pharmacokinetics, so the 21-to-45-minute range must travel with the word “dogs”. The 11-minute WR and 8-minute SV values are single-dose label figures for two finished products in healthy subjects.
Evidence Landmarks and Their Limits
The best-known Tesamorelin evidence comes from randomized studies in adults with HIV-associated lipodystrophy and excess abdominal fat. In the 2007 pivotal trial, 412 adults with HIV and abdominal fat accumulation received 2 mg of tesamorelin or placebo subcutaneously each day for 26 weeks. Visceral adipose tissue fell 15.2% under tesamorelin and rose 5.0% under placebo; IGF-I rose 81.0% versus a 5.0% decrease; triglycerides fell 50 mg/dL versus a 9 mg/dL rise; and the total-to-HDL cholesterol ratio fell 0.31 versus a 0.21 rise, with P<0.001 for each of those comparisons and no significant difference in glycemic measures (PMID 18057338).
A second randomized placebo-controlled trial with a safety extension followed 404 adults on antiretroviral therapy for 12 months, randomizing them 2:1 to 2 mg daily or placebo. Visceral adipose tissue fell 10.9%, about 21 cm2, against a 0.6% fall, about 1 cm2, under placebo at the 6-month efficacy endpoint (P<0.0001); the reduction reached roughly 18% at 12 months in participants who stayed on tesamorelin, and it was rapidly lost in those re-randomized to placebo. IGF-1 rose (P<0.001) with no observed change in glucose parameters.[4] The pooled analysis of two multicenter phase 3 trials and their extensions covered 806 participants, 543 on tesamorelin and 263 on placebo, and reported a visceral-adipose-tissue treatment effect of -15.4% at week 26 (-24 ± 41 versus 2 ± 35 cm2, P<0.001) with no comparable change in abdominal subcutaneous fat, treatment effects of -12.3% for triglycerides and -7.2% for the cholesterol-to-HDL ratio, a mean IGF-I change of 108 ± 112 versus -7 ± 64 ng/mL, and a maintained -17.5 ± 23.3% visceral-fat change at week 52 among those continuing.[5]
Later work examined liver and metabolic endpoints. Among phase 3 participants whose baseline ALT or AST exceeded 30 U/L, visceral-fat responders, defined a priori as achieving at least an 8% reduction, showed greater ALT change (-8.9 ± 22.6 versus 1.4 ± 34.7 U/L, P=0.004) and AST change (-3.8 ± 12.9 versus 0.4 ± 22.4 U/L, P=0.04) than non-responders over 26 weeks.[6] A 2019 randomized, double-blind, multicenter trial enrolled 61 people with HIV and a hepatic fat fraction of 5% or more; 30 received tesamorelin 2 mg daily and 30 received placebo for 12 months. Hepatic fat fraction fell with an absolute effect size of -4.1% (95% CI -7.6 to -0.7, p=0.018), a -37% relative reduction (95% CI -67 to -7, p=0.016), and 35% of the tesamorelin group versus 4% of the placebo group finished below a 5% hepatic fat fraction (p=0.0069), with no between-group difference in fasting glucose or glycated hemoglobin.[7] These findings are scientifically relevant to GH-axis, adipose-tissue, and liver research. They do not establish a general weight-loss claim, a universal liver outcome, or efficacy for an Apex research reagent.
Transfer limits recur across this base: participants were selected for specific HIV-associated body-composition phenotypes, the trials used controlled finished formulations, and visceral fat, body weight, liver fat, glucose markers, and IGF-1 are not interchangeable outcomes.
Additional reported findings
Each row keeps its model, population, and result together, so no figure travels without its study.
| Compound and exposure | Model, species, population | Endpoint | Reported result | PMID |
|---|---|---|---|---|
| Tesamorelin 2 mg subcutaneous daily | 26-week extension to 52 weeks; adults with HIV and central fat accumulation (273 tesamorelin, 137 placebo at entry) | Visceral-fat durability and reversibility | Visceral adipose tissue sustained at -18% over 52 weeks (P<0.001 versus baseline); triglycerides -51 mg/dL; visceral fat reaccumulated after discontinuation | 18690162 |
| Tesamorelin 2 mg subcutaneous daily | Per-protocol analysis of 402 phase 3 participants; responders defined a priori as at least 8% visceral-fat reduction | Lipids, adiponectin, glucose homeostasis | Responders versus non-responders at 52 weeks: triglycerides -0.8 ± 1.8 versus 0.0 ± 1.1 mmol/L (P=0.003), fasting glucose -1 ± 14 versus 8 ± 17 mg/dL (P<0.001), HbA1c 0.0 ± 0.3% versus 0.2 ± 0.5% (P=0.003) | 22495074 |
| Tesamorelin 2 mg daily for 12 months | 60 abdominally obese adults with reduced growth-hormone secretion; randomized, double-blind | Visceral fat, carotid intima-media thickness, IGF-I | Visceral-fat treatment effect -35 cm2 (95% CI -58 to -12, P=0.003); intima-media thickness -0.04 mm (P=0.02); IGF-I treatment effect +92 µg/L (95% CI +52 to +132, P<0.0001); no fasting or 2-hour glucose change | 23015655 |
| Tesamorelin 1 mg daily for 20 weeks | 152 adults aged 55 to 87, 66 of them with mild cognitive impairment; randomized, placebo-controlled | Axis engagement and body composition | IGF-1 rose 117% while remaining inside the physiological range (P<0.001) and body fat fell 7.4% (P<0.001); the cognitive endpoint is investigational and is not an approved use | 22869065 |
| Tesamorelin versus placebo, pooled | Meta-analysis of 5 randomized trials in adults with HIV-associated lipodystrophy; searched through July 2025 | Body composition, hepatic fat, adverse events | Pooled mean differences (95% CI, all P<0.001): visceral fat -27.71 cm2 (-38.37, -17.06); trunk fat -1.18 kg (-1.40, -0.96); hepatic fat -4.28% (-6.31, -2.24); waist circumference -1.61 cm (-2.28, -0.95); lean mass +1.42 kg (1.13, 1.71); arthralgia, myalgia, paresthesia and injection-site reactions | 41545261 |
EGRIFTA clinical studies establish evidence for specified finished formulations in labeled or studied populations. They do not establish that a separate lyophilized research reagent has the same release, exposure, sterility, safety, or clinical performance.
EGRIFTA WR, EGRIFTA SV, and Product History
FDA’s Purple Book identifies BLA 022505 for tesamorelin and records the original U.S. approval date as November 10, 2010. The original 1 mg EGRIFTA presentation is discontinued. Current product records include EGRIFTA SV, a 2 mg-per-vial formulation, and EGRIFTA WR, an 11.6 mg-per-vial formulation approved under supplement BLA 022505/S-020 on March 25, 2025.
That history is one continuous application record with formulation-specific presentations, not proof that the products are interchangeable: the active molecule anchors the BLA, while each presentation has its own strength, excipients, preparation controls, storage conditions, and labeling. The current label, not a legacy summary or a discontinued package, is authoritative for WR facts.
The March 2025 EGRIFTA WR label indicates WR for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy; states that long-term cardiovascular safety has not been established; states that the product is not indicated for weight-loss management; and states, most importantly for evidence transfer, that EGRIFTA WR and EGRIFTA SV are not substitutable. This guide does not reproduce label procedures.
| Record | What it establishes | What it does not establish |
|---|---|---|
| EGRIFTA WR FDA label | Current 11.6 mg finished formulation, approved indication, warnings, and non-substitutability statement | Properties or approved status of EGRIFTA SV or a research reagent |
| EGRIFTA SV product record | Current 2 mg finished formulation under BLA 022505 | Interchangeability with WR or a separate chemical reagent |
| Apex research-material record | Declared analyte, lot, specifications, and current commercial documentation | FDA approval, clinical safety, efficacy, sterility, or pharmaceutical equivalence |
The required framing is direct: same molecule; categorically distinct regulatory frameworks. Apex Tesamorelin is a chemical reagent for lawful in-vitro and preclinical research. It is not EGRIFTA WR or EGRIFTA SV, is not a pharmaceutical, and is not for human or veterinary consumption. See research-grade versus pharmaceutical-grade peptides for the general framework.
Tesamorelin Versus Adjacent GHRH Analogs
Tesamorelin and Sermorelin both activate GHRHR, but they are not the same peptide: Sermorelin is the shorter receptor-active GHRH(1-29) fragment, while Tesamorelin keeps all 44 residues and adds its N-terminal acyl modification. CJC-1295 variants use different stabilization strategies and need their own identity records.
The Tesamorelin versus Sermorelin comparison owns the symmetric side-by-side framework. This entity guide does not transfer pharmacokinetics, formulation behavior, or trial results between analogs merely because they share a receptor. One dimension does belong here, because it is frequently blurred: regulatory status is not shared across the family, and it is not shared between a finished pharmaceutical and a research reagent.
Regulatory status, stated per compound
| Compound | Current regulatory status | Record basis |
|---|---|---|
| Tesamorelin as EGRIFTA WR and EGRIFTA SV | FDA-approved finished formulations under BLA 022505, sponsor Theratechnologies; original U.S. approval November 10, 2010; WR supplement S-020 approved March 25, 2025; the original 1 mg presentation is discontinued | FDA Purple Book and supplement approval letter[9][10] |
| Tesamorelin as an Apex research reagent | No FDA, EMA, NMPA, MHRA or other national marketing authorization anywhere in the world; not a drug, not an approved product, and not covered by the EGRIFTA approvals | Research-material record; no approval covers research reagents |
| Sermorelin | Historical U.S. approvals as Geref (NDA 19-863, December 1990) and Geref Diagnostic (NDA 20-443, September 26, 1997), both discontinued in 2008 for commercial rather than safety reasons; no current U.S. marketing authorization | FDA application history |
| CJC-1295 with DAC | No FDA, EMA, NMPA or other regulatory approval in any jurisdiction; investigational only | No approval record in any national register |
Verification of a Tesamorelin Research Material
Verification begins with the full identity record: tesamorelin versus tesamorelin acetate, the expected mass basis, lot, and analytical method. HPLC reports a chromatographic profile and area percentage under a stated method; mass spectrometry supports identity when the reported ion or deconvoluted mass matches the declared material. Neither alone establishes biological potency, aggregation state, sterility, clinical safety, or equivalence to EGRIFTA.
Numbers make that concrete. A deconvoluted mass is interpretable only against a declared basis: 5135.9 Da is the free-base equivalent, while the acetate salt carries about 7 acetate equivalents, roughly 420 Da more at that stoichiometry. Purity is likewise a per-lot, method-specific area percentage belonging to the current Certificate of Analysis and its stated HPLC method, not a fixed article-level figure.
Use the COA interpretation guide, HPLC guide, and mass-spectrometry guide to evaluate a current lot record.
Tesamorelin research-material record
The product page documents current availability and lot-specific records; it cannot transfer EGRIFTA evidence or FDA status to a research reagent. Confirm the current analyte declaration and lot documentation before relying on any specification.
Frequently Asked Questions About Tesamorelin
What is Tesamorelin?
Tesamorelin is a synthetic 44-residue analog of human growth-hormone-releasing factor. It carries a trans-3-hexenoyl group on its N-terminal tyrosine, a modification designed to improve resistance to enzymatic cleavage.
How does Tesamorelin signal?
Tesamorelin activates the GHRH receptor on pituitary somatotrophs. The receptor couples through Gs to adenylyl cyclase and cyclic AMP, supporting endogenous growth-hormone release and downstream IGF-1 signaling. The exact response depends on the model and measured endpoint.
How is Tesamorelin different from Sermorelin?
Sermorelin represents the shorter GHRH(1-29) receptor-active fragment. Tesamorelin retains the full 44-residue GHRF sequence and adds an N-terminal trans-3-hexenoyl modification. Shared receptor activity does not make their identity, stability, or evidence interchangeable.
What is EGRIFTA WR?
EGRIFTA WR is an FDA-approved 11.6 mg-per-vial tesamorelin finished formulation under BLA 022505. Its March 2025 label identifies a narrow indication in adults with HIV-associated lipodystrophy and states that it is not substitutable with EGRIFTA SV.
Is an Apex Tesamorelin reagent the same as EGRIFTA?
No. They share the tesamorelin active molecule, but EGRIFTA WR and EGRIFTA SV are FDA-approved finished pharmaceuticals with formulation-specific manufacturing, excipients, labeling, and controls. The Apex material is a research-only chemical reagent and is not a therapeutic equivalent.
What can HPLC and mass spectrometry verify?
HPLC can report a chromatographic profile under a stated method, while mass spectrometry can support mass identity with an interpretable result. Neither method alone establishes biological potency, aggregation state, sterility, clinical safety, efficacy, or equivalence to EGRIFTA.
What is the half-life of tesamorelin?
Half-life is formulation-specific and species-specific. Current FDA labels report a mean elimination half-life of 11 minutes in healthy subjects after a single 1.28 mg subcutaneous dose of EGRIFTA WR and 8 minutes after a single 1.4 mg dose of EGRIFTA SV. Preclinical TH9507 work reported an apparent elimination half-life of 21 to 45 minutes in dogs, which is a canine toxicokinetic value and not a human figure.
What did the pivotal visceral-fat trials report?
In the 2007 pivotal trial, 412 adults with HIV and abdominal fat accumulation received 2 mg of tesamorelin or placebo daily for 26 weeks; visceral adipose tissue fell 15.2% under tesamorelin and rose 5.0% under placebo, while IGF-I rose 81.0%. A pooled analysis of two phase 3 trials in 806 participants reported a 15.4% visceral-adipose-tissue treatment-effect reduction at week 26. Those results belong to that studied population and to finished pharmaceutical formulations.
References and Regulatory Sources
- Ferdinandi ES, et al. Non-clinical pharmacology and safety evaluation of TH9507, a human growth hormone-releasing factor analogue. Basic Clin Pharmacol Toxicol. 2007;100(1):49-58. PMID: 17214611.
- Cunha SR, et al. Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3′,5′-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology. 2002;143(12):4570-82. PMID: 12446584.
- Katsushima Y, et al. Interaction of PICK1 with C-terminus of growth hormone-releasing hormone receptor (GHRHR) modulates trafficking and signal transduction of human GHRHR. J Pharmacol Sci. 2013;122(3):193-204. PMID: 23823934.
- Falutz J, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010;53(3):311-22. PMID: 20101189.
- Falutz J, et al. 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. 2010;95(9):4291-304. PMID: 20554713.
- Fourman LT, et al. Visceral fat reduction with tesamorelin is associated with improved liver enzymes in HIV. AIDS. 2017;31(16):2253-2259. PMID: 28832410.
- Stanley TL, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial. Lancet HIV. 2019;6(12):e821-e830. PMID: 31611038.
- FDA. EGRIFTA WR prescribing information. Revised March 2025; current source check July 24, 2026.
- FDA. Supplement approval letter for EGRIFTA WR, BLA 022505/S-020. March 25, 2025.
- FDA Purple Book. Tesamorelin BLA 022505 product details. Current source check July 24, 2026.
