Tesamorelin — Synthetic GHRH Analog | 44-Amino Acid Growth Hormone-Releasing Hormone Research Compound
Research-Grade Compound
Tesamorelin is a synthetic analog of growth hormone-releasing hormone (GHRH), built on the full 44-amino-acid GHRH sequence and stabilized by a trans-3-hexenoyl modification at the N-terminus. Molecular formula C221H366N72O67S, molecular weight 5,135.9 Da, CAS 218949-48-5. It is also catalogued as TH9507.
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In-depth research overview, mechanism of action, and study applications.
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What is Tesamorelin?
Tesamorelin is a synthetic analog of growth hormone-releasing hormone (GHRH), built on the full 44-amino-acid GHRH sequence and stabilized by a trans-3-hexenoyl modification at the N-terminus. Molecular formula C221H366N72O67S, molecular weight 5,135.9 Da, CAS 218949-48-5. It is also catalogued as TH9507.
The N-terminal modification is the whole design argument. Native GHRH is cleaved at the Ala2 position by dipeptidyl peptidase IV within minutes of entering circulation, which makes the unmodified hormone impractical as a research tool. Capping the N-terminus blocks that cleavage without changing how the molecule engages its receptor. What you get is a peptide that behaves like GHRH at GHRH-R but survives long enough in plasma to produce a measurable downstream response.
Tesamorelin is unusual in this catalog because it has a completed clinical record. The FDA approved it as Egrifta for the reduction of excess visceral abdominal fat in HIV-infected patients with lipodystrophy, and the phase 3 program behind that approval published human safety and pharmacodynamic data that almost no other growth hormone secretagogue can point to. That record is narrow, though. The trials enrolled a specific patient population with a specific metabolic phenotype, and the visceral fat effect reverses when administration stops — researchers reading across from those results to other models are extrapolating well past what was tested.
How Does Tesamorelin Work? Mechanism of Action
Tesamorelin binds GHRH-R, a class B G-protein-coupled receptor expressed on anterior pituitary somatotrophs. Receptor occupancy couples to Gs, activating adenylyl cyclase and raising intracellular cAMP. The cAMP-PKA cascade then does two things at once: it phosphorylates CREB to drive transcription of the GH1 gene, and it opens voltage-gated calcium channels, producing the calcium influx that triggers exocytosis of pre-formed growth hormone granules. Transcription and secretion move together, which is why GHRH-R agonism raises both the amount of GH available and the rate at which it leaves the cell.
Because the signal enters the axis at the hypothalamic level rather than the periphery, the counter-regulation stays intact. Rising GH stimulates hypothalamic somatostatin release, somatostatin suppresses further somatotroph firing, and the resulting output is pulsatile rather than flat. Exogenous human growth hormone bypasses that loop entirely and suppresses endogenous production through negative feedback. The pulsatility difference is the single most-cited reason researchers choose a GHRH analog over recombinant GH when the question involves physiological GH signaling rather than raw GH exposure.
Downstream, GH acts on hepatocytes to drive transcription of IGF-1 (insulin-like growth factor 1) through the JAK2-STAT5 pathway. Circulating IGF-1 is the mediator most closely tracked in tesamorelin research, and it rises reliably in the published human data. IGF-1 and GH together increase lipolytic tone in adipose tissue, with the effect reported preferentially in visceral rather than subcutaneous depots.
That visceral selectivity is documented but not fully explained. Visceral adipocytes carry a different receptor density and a different lipolytic responsiveness than subcutaneous adipocytes, and portal drainage puts them in a different metabolic position — but no single mechanism accounts for the size of the depot difference observed in trials. The 2021 Falutz analysis approached the question from another angle, reporting changes in fat *quality* that were independent of how much fat was lost, which suggests the compound is doing something to adipose tissue beyond volume reduction. Treat the depot selectivity as an observation with an incomplete mechanistic story rather than a settled pathway.
One practical pharmacokinetic note: tesamorelin clears quickly. The Egrifta prescribing information reports a plasma half-life measured in tens of minutes, far shorter than the IGF-1 response it produces. Researchers designing sampling schedules should not expect parent-compound concentration and downstream effect to track each other in time.
Research Applications of Tesamorelin
Somatotropic Axis and GH Pulsatility Research
- GHRH-R agonism assays: pituitary somatotroph preparations measuring cAMP accumulation and calcium flux give the proximal receptor readout, upstream of any GH measurement.
- Pulsatile versus continuous GH modeling: tesamorelin preserves somatostatin counter-regulation, so it is used when the research design needs endogenous pulse architecture rather than a clamped GH level.
- IGF-1 dose-response characterization: hepatic IGF-1 output is the standard downstream endpoint and the most reproducible signal in the published human dataset.
Adipose Tissue and Lipid Metabolism Models
- Visceral versus subcutaneous depot comparison: the preferential visceral effect reported in the HIV lipodystrophy trials makes tesamorelin a reference compound for depot-selectivity studies.
- Hepatic lipid content: the 2021 fat-quality work moved the field toward measuring composition and hepatic fat rather than cross-sectional area alone.
- Glucose homeostasis interaction: GH is counter-regulatory to insulin, and the prescribing information documents changes in glucose parameters — any metabolic protocol using tesamorelin needs a glycemic arm.
Comparative Secretagogue Pharmacology
- GHRH analog series comparison: tesamorelin (44 residues, N-terminally modified), sermorelin (29 residues, unmodified) and CJC-1295 No DAC (29 residues, four substitutions) share a receptor and differ only in stability, which makes the set useful for isolating half-life effects.
- GHRH-R plus GHSR-1a co-stimulation: pairing a GHRH analog with a ghrelin-receptor agonist such as ipamorelin activates two independent second-messenger systems on the same cell.
- Analog versus recombinant GH: running a tesamorelin arm against a direct GH arm separates receptor-mediated pulsatile signaling from raw GH exposure.
Tesamorelin vs CJC-1295 (No DAC)
| Feature | Tesamorelin | CJC-1295 (No DAC) |
|---|---|---|
| Identity | Stabilized full-length GHRH analog | Modified GRF(1-29), also called Mod GRF 1-29 |
| Amino acid count | 44 | 29 |
| Molecular formula | C221H366N72O67S | C152H252N44O42 |
| Molecular weight | 5,135.9 Da | 3,367.9 Da |
| CAS number | 218949-48-5 | 863288-34-0 |
| Structural modification | Trans-3-hexenoyl group at the N-terminus | Four amino acid substitutions (positions 2, 8, 15, 27) |
| Receptor target | GHRH-R | GHRH-R |
| Second messenger | cAMP-PKA | cAMP-PKA |
| Approximate plasma half-life | Tens of minutes (per FDA label) | Approximately 30 minutes |
| FDA status | Approved as Egrifta for HIV-associated lipodystrophy | Not approved for any indication |
| Human clinical data | Phase 3 program published | None published for the No DAC form |
| WADA status | Prohibited at all times | Prohibited at all times |
Same receptor, same second messenger, different molecule. The choice between them is a choice about sequence length, stability engineering and evidence base — tesamorelin is the only one of the two with published human trial data, while CJC-1295 No DAC is the shorter, cheaper fragment studied when GHRH-R activation alone is the variable of interest.
Read the full tesamorelin vs CJC-1295 comparisonTesamorelin Technical Specifications
| Compound Name | Tesamorelin |
|---|---|
| Brand Name (approved form) | Egrifta |
| Common Synonyms | TH9507, tesamorelin acetate, GHRH(1-44) analog |
| Classification | Synthetic growth hormone-releasing hormone (GHRH) analog |
| Receptor Target | GHRH-R (growth hormone-releasing hormone receptor) |
| CAS Number | 218949-48-5 |
| Molecular Formula | C221H366N72O67S |
| Molecular Weight | 5,135.9 Da |
| Amino Acid Count | 44 |
| Sequence Note | Stabilized 44-amino-acid GHRH analog, trans-3-hexenoyl-modified at the N-terminus |
| Purity | ≥99% by HPLC |
| Purity Confirmation | LC-MS/MS molecular weight verification |
| Endotoxin Testing | LAL (Limulus Amebocyte Lysate) method |
| Physical Form | Lyophilized powder |
| Appearance | White to off-white powder |
| Reconstitution | Bacteriostatic water or sterile 0.9% sodium chloride |
| Storage (lyophilized) | -20°C, desiccated, protected from light |
| Storage (reconstituted) | 2–8°C, use within 14–28 days |
| Shelf Life | 24 months from manufacture (lyophilized) |
| Testing Methods | HPLC, LC-MS/MS, LAL Endotoxin |
| Documentation | Certificate of Analysis (CoA) per batch |
| FDA Status | Approved as Egrifta for HIV-associated lipodystrophy; research material sold here is not a drug product |
| WADA Status | Prohibited at all times (growth hormone releasing factors) |
| Intended Use | In-vitro laboratory research only |
How to Reconstitute Tesamorelin for Research
Tesamorelin is a 5 kDa peptide and goes into solution more slowly than the small pentapeptide secretagogues. It is also more sensitive to mechanical shear than a short sequence — swirling gets it there, shaking damages it. If a vial still shows undissolved cake after 90 seconds, give it another minute at room temperature rather than increasing agitation.
- Bring the vial to room temperature before opening. Cold glass draws condensation onto the septum.
- Draw the calculated volume of bacteriostatic water. For a 5 mg vial, 2.5 mL yields 2 mg/mL; 1 mL yields 5 mg/mL. For a 10 mg vial, 2 mL yields 5 mg/mL.
- Swab the septum with alcohol and allow 30 seconds to dry.
- Angle the needle and inject the diluent slowly down the inner vial wall. Spraying diluent directly onto the lyophilized cake causes foaming, and foam at a peptide-air interface is a denaturation route.
- Swirl gently for 60–90 seconds. Do not shake and do not vortex.
- Confirm the solution is clear and colorless with no visible particulate. Discard if cloudy or if a precipitate forms.
- Label the vial with the reconstitution date and the resulting concentration in mg/mL.
- Store at 2–8°C and use within 14–28 days. Avoid repeated freeze-thaw cycles.
Diluent: bacteriostatic water for peptide reconstitution. Full protocol: step-by-step peptide reconstitution guide. Concentration maths: peptide reconstitution calculator.
Frequently Asked Questions — Tesamorelin
What is tesamorelin used for in research?
Is tesamorelin a growth hormone?
Is tesamorelin FDA approved?
What is the difference between tesamorelin and CJC-1295?
What is the difference between tesamorelin and HGH?
Does tesamorelin increase IGF-1?
Does tesamorelin affect blood glucose?
Why does tesamorelin affect visceral fat more than subcutaneous fat?
Can tesamorelin and ipamorelin be studied together?
Is tesamorelin the same as Egrifta?
What purity standard does Peptide.Express use for tesamorelin?
What testing does tesamorelin undergo before shipping?
How should tesamorelin be stored before and after reconstitution?
Where is the Certificate of Analysis for tesamorelin?
Research References
- Falutz J, et al. "Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV-infected patients with abdominal fat accumulation." AIDS, 2008. Read the tesamorelin long-term safety study on PubMed
- Falutz J, et al. "Tesamorelin Improves Fat Quality Independent of Changes in Fat Quantity." AIDS, 2021. Read the tesamorelin fat quality analysis on PMC
- LiverTox: Clinical and Research Information on Drug-Induced Liver Injury — Tesamorelin. National Institute of Diabetes and Digestive and Kidney Diseases, NIH Bookshelf. Read the LiverTox tesamorelin monograph on NCBI Bookshelf
- Egrifta (tesamorelin for injection) FDA prescribing information, 2024. The authoritative source for the approved indication, pharmacokinetic parameters and monitored laboratory values. Read the Egrifta FDA prescribing information (PDF)
All products are sold for in-vitro laboratory research use only. Not intended for human consumption, clinical use, or veterinary use. Peptide.Express makes no medical claims. Consult the published literature for research application guidance.