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Tesamorelin — research-grade lyophilized peptide vial from Peptide.Express, ≥99% HPLC purity
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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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Tesamorelin complete research guide

In-depth research overview, mechanism of action, and study applications.

Showing CoA for 5mg
Certificate Details
Purity≥99%
Methodology
HPLCLC-MS/MS
CAS Number218949-48-5
Molecular FormulaC221H366N72O67S
Molecular Weight5135.9 g/mol
SequenceStabilized 44-amino-acid GHRH analog (trans-3-hexenoyl-modified)

This Certificate of Analysis was issued by an independent third-party laboratory. Peptide.Express does not conduct in-house testing. Results are provided as-is from the testing facility and confirm batch identity, purity, and analytical methodology. For questions about specific CoA results, contact [email protected].

≥99% by HPLCLC-MS/MS VerifiedCoA Every BatchIn-Vitro Research Use Only

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)

FeatureTesamorelinCJC-1295 (No DAC)
IdentityStabilized full-length GHRH analogModified GRF(1-29), also called Mod GRF 1-29
Amino acid count4429
Molecular formulaC221H366N72O67SC152H252N44O42
Molecular weight5,135.9 Da3,367.9 Da
CAS number218949-48-5863288-34-0
Structural modificationTrans-3-hexenoyl group at the N-terminusFour amino acid substitutions (positions 2, 8, 15, 27)
Receptor targetGHRH-RGHRH-R
Second messengercAMP-PKAcAMP-PKA
Approximate plasma half-lifeTens of minutes (per FDA label)Approximately 30 minutes
FDA statusApproved as Egrifta for HIV-associated lipodystrophyNot approved for any indication
Human clinical dataPhase 3 program publishedNone published for the No DAC form
WADA statusProhibited at all timesProhibited 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 comparison

Tesamorelin Technical Specifications

Technical specifications for Tesamorelin, including molecular data, purity standard, testing methods and storage requirements.
Compound NameTesamorelin
Brand Name (approved form)Egrifta
Common SynonymsTH9507, tesamorelin acetate, GHRH(1-44) analog
ClassificationSynthetic growth hormone-releasing hormone (GHRH) analog
Receptor TargetGHRH-R (growth hormone-releasing hormone receptor)
CAS Number218949-48-5
Molecular FormulaC221H366N72O67S
Molecular Weight5,135.9 Da
Amino Acid Count44
Sequence NoteStabilized 44-amino-acid GHRH analog, trans-3-hexenoyl-modified at the N-terminus
Purity≥99% by HPLC
Purity ConfirmationLC-MS/MS molecular weight verification
Endotoxin TestingLAL (Limulus Amebocyte Lysate) method
Physical FormLyophilized powder
AppearanceWhite to off-white powder
ReconstitutionBacteriostatic 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 Life24 months from manufacture (lyophilized)
Testing MethodsHPLC, LC-MS/MS, LAL Endotoxin
DocumentationCertificate of Analysis (CoA) per batch
FDA StatusApproved as Egrifta for HIV-associated lipodystrophy; research material sold here is not a drug product
WADA StatusProhibited at all times (growth hormone releasing factors)
Intended UseIn-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.

  1. Bring the vial to room temperature before opening. Cold glass draws condensation onto the septum.
  2. 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.
  3. Swab the septum with alcohol and allow 30 seconds to dry.
  4. 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.
  5. Swirl gently for 60–90 seconds. Do not shake and do not vortex.
  6. Confirm the solution is clear and colorless with no visible particulate. Discard if cloudy or if a precipitate forms.
  7. Label the vial with the reconstitution date and the resulting concentration in mg/mL.
  8. 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?

Tesamorelin is studied as a GHRH-R agonist in somatotropic axis research — GH pulsatility, hepatic IGF-1 output, and adipose depot selectivity are the usual endpoints. Its published human dataset in HIV-associated lipodystrophy makes it a reference compound when investigators need a GHRH analog with a known clinical profile. Sold for in-vitro laboratory research use only.

Is tesamorelin a growth hormone?

No. Tesamorelin is a growth hormone-releasing hormone analog, which puts it one step upstream. It signals the pituitary to release the growth hormone the body already makes, rather than supplying GH from outside. The distinction matters mechanistically: recombinant GH suppresses endogenous production through negative feedback, while a GHRH analog works through that feedback loop instead of around it.

Is tesamorelin FDA approved?

Yes, as the drug product Egrifta, for the reduction of excess visceral abdominal fat in HIV-infected patients with lipodystrophy. That approval covers a manufactured pharmaceutical for a specific indication in a specific population — it does not extend to research-grade tesamorelin, and the material Peptide.Express supplies is sold strictly for in-vitro laboratory research.

What is the difference between tesamorelin and CJC-1295?

Both bind GHRH-R and both run through the cAMP-PKA cascade. The differences are structural: tesamorelin carries the complete 44-amino-acid GHRH sequence with a trans-3-hexenoyl cap at the N-terminus (5,135.9 Da), while CJC-1295 No DAC is a 29-residue GRF(1-29) fragment with four amino acid substitutions (3,367.9 Da). Tesamorelin has a published phase 3 clinical record; CJC-1295 No DAC does not.

What is the difference between tesamorelin and HGH?

HGH is the hormone itself. Tesamorelin causes the pituitary to release that hormone. Administering HGH directly produces a sustained, non-pulsatile elevation and suppresses the somatotroph output that would otherwise occur; tesamorelin preserves the somatostatin counter-regulation and the resulting pulse pattern. For research questions about physiological GH signaling, that architectural difference is usually the reason a GHRH analog is chosen.

Does tesamorelin increase IGF-1?

Yes — hepatic IGF-1 rises reliably in the published human data, and it is the standard downstream marker in tesamorelin research. IGF-1 is produced when GH activates JAK2-STAT5 signaling in hepatocytes.

Does tesamorelin affect blood glucose?

Growth hormone is counter-regulatory to insulin, so anything that raises GH has a plausible route to affecting glucose handling. The Egrifta prescribing information includes glucose parameters among the values monitored during treatment. Any metabolic research protocol using tesamorelin should include a glycemic arm rather than treating glucose as a passive variable.

Why does tesamorelin affect visceral fat more than subcutaneous fat?

Honestly, the mechanism is not settled. Visceral adipocytes differ from subcutaneous adipocytes in lipolytic responsiveness, receptor density and portal drainage, and all three probably contribute — but no single pathway accounts for the size of the depot difference reported in the trials. The 2021 Falutz analysis added a further wrinkle by showing changes in fat quality that were independent of changes in fat quantity. This is an open research question, not a solved one.

Can tesamorelin and ipamorelin be studied together?

The pharmacological rationale is straightforward: tesamorelin acts at GHRH-R through cAMP-PKA while ipamorelin acts at GHSR-1a through a calcium-mediated pathway, so the two signals are independent at the second-messenger level and converge on the same somatotroph. What does not exist is published combination pharmacokinetic data for this specific pairing. Investigators combining them are inferring from single-compound literature and from the broader GHRH-plus-GHRP co-administration work, and study designs should state that explicitly.

Is tesamorelin the same as Egrifta?

Egrifta is the brand name of the FDA-approved tesamorelin drug product. The active molecule is the same; the manufacturing, formulation, labeling and regulatory status are not. Research-grade tesamorelin is not a substitute for a drug product and is not sold as one.

What purity standard does Peptide.Express use for tesamorelin?

≥99% by reverse-phase HPLC, with LC-MS/MS confirming the 5,135.9 Da molecular weight. Mass confirmation matters more than usual for a peptide of this size, because truncation products from incomplete synthesis are the most common contaminant in long sequences and they can be difficult to resolve chromatographically.

What testing does tesamorelin undergo before shipping?

Reverse-phase HPLC for purity by area-under-curve, LC-MS/MS for molecular weight identity, LAL endotoxin testing, and visual QC for appearance and particulate. Testing is performed by an independent third-party laboratory and a batch-specific Certificate of Analysis is issued for each lot.

How should tesamorelin be stored before and after reconstitution?

Lyophilized: -20°C, desiccated, protected from light, stable for 24 months from manufacture. Reconstituted: 2–8°C, used within 14–28 days. Do not freeze the reconstituted solution — freeze-thaw cycling drives aggregation in peptides of this size faster than it does in short sequences.

Where is the Certificate of Analysis for tesamorelin?

On this page and in the Peptide.Express lab results library. Each CoA is batch-specific and lists the HPLC chromatogram and purity figure, LC-MS/MS mass confirmation, endotoxin result, testing laboratory and test date. The batch number printed on the vial label maps to a specific CoA.

Research References

  1. 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
  2. Falutz J, et al. "Tesamorelin Improves Fat Quality Independent of Changes in Fat Quantity." AIDS, 2021. Read the tesamorelin fat quality analysis on PMC
  3. 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
  4. 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.

Further Reading