Tesamorelin — Molecular Weight, Formula, Sequence & Half-Life Reference

01What is Tesamorelin?

Tesamorelin is a synthetic analog of human growth hormone-releasing factor, GRF(1-44), modified by attaching a trans-3-hexenoyl group to the N-terminal tyrosine and amidating the C-terminus. Those two changes protect the peptide from dipeptidyl peptidase-4 cleavage while preserving GHRH-receptor agonism, so the compound stimulates endogenous, pulsatile growth hormone release rather than supplying growth hormone directly.

It is approved in the United States for, in the label's own words, “the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy”. The word most reference sources add here — visceral — does not appear in the FDA indication, even though visceral adipose tissue is what the pivotal trials measured. That is a narrow indication in a specific population, and it is the only claim the approval supports; the compound's presence on an approved-drug list should not be read as validation of the broader body-composition uses it is discussed alongside.

One inconsistency deserves a flag for anyone doing pharmacokinetic comparisons: three FDA labels for the same active moiety in different formulations report three different healthy-subject elimination half-lives — approximately 26, 8 and 11 minutes. The discrepancy is real and is not explained within the labels themselves, which is why this record gives a range rather than a single figure.

02Molecular information

03Amino acid sequence

Structural modifications

Two modifications relative to the free 44-mer. (1) N-terminal acylation: a trans-3-hexenoyl group (C6 chain, E-configured double bond at position 3) is attached via an amide bond to the alpha-amino group of Tyr1. The FDA label describes this as 'a hexenoyl moiety, a C6 chain with a double bond at position 3, attached to the tyrosine residue at the N-terminal part of the molecule' [1]; PubChem's synonym '(3E)-hex-3-enoylsomatoliberin' confirms the E (trans) geometry. (2) C-terminal alpha-amidation of Leu44 (Leu-NH2), which reproduces the amidation present on native human GHRH(1-44) (UniProt P01286, MOD_RES 'Leucine amide'). No disulfide bonds (the single cysteine-free sequence contains one Met but no Cys), no cyclisation, no non-natural residues, no PEGylation, no DAC/albumin-binding moiety. The full descriptor is trans-3-hexenoyl-hGRF(1-44)-NH2.

04Pharmacokinetic information

Half-life context

All values below are human, subcutaneous, from FDA prescribing information. Original EGRIFTA (1 mg/vial formulation, 2 mg dose): mean elimination t1/2 26 minutes in healthy subjects and 38 minutes in HIV-infected patients; volume of distribution 9.4 ± 3.1 L/kg (healthy) and 10.5 ± 6.1 L/kg (HIV-infected) [2]. EGRIFTA SV (2 mg/vial formulation, 1.4 mg dose): mean elimination t1/2 8 minutes in healthy subjects; Cmax 2956.1 pg/mL (CV 47%); AUC0-inf 889.1 pg·h/mL (CV 57%); Vd 4.8 ± 1.9 L/kg [3]. EGRIFTA WR (11.6 mg/vial F8 formulation, 1.28 mg dose): mean elimination t1/2 11 minutes in healthy subjects; Cmax 3831 pg/mL (CV 40%); AUC0-inf 1172 pg·h/mL (CV 48%); Vd 4.8 ± 1.9 L/kg [1]. Median Tmax is 0.15 h across all three labels; absolute subcutaneous bioavailability is less than 4% [1][2][3]. The labels note no formal human metabolism studies have been performed [2]. Critically, plasma half-life of the peptide is not the duration of pharmacodynamic effect: tesamorelin acts by triggering endogenous pulsatile GH release, and the downstream IGF-1 response persists far beyond peptide clearance — clinical trials dosed once daily and measured visceral fat change over 26–52 weeks [4][5]. Vendor claims of a single fixed half-life for tesamorelin conflict with the label data and should be disregarded.

05Research focus

Primary research areas

• HIV-associated lipodystrophy and visceral adipose tissue
• GHRH-receptor agonism and pulsatile GH/IGF-1 axis
• hepatic steatosis and NAFLD in people with HIV
• body composition and ectopic fat distribution
• glucose tolerance and metabolic safety signals

Research context

Tesamorelin is a synthetic analogue of human growth hormone-releasing factor consisting of the complete 44-residue GHRH(1-44) amide sequence carrying a trans-3-hexenoyl group amide-linked to the N-terminal tyrosine [1]. It is an agonist at the pituitary GHRH receptor and acts by amplifying endogenous pulsatile growth hormone secretion rather than by supplying exogenous GH, with a downstream rise in IGF-1 [2]. Of the three compounds in this reference set, tesamorelin is the only one with substantial, regulator-reviewed human evidence.

The pivotal evidence base is two multicentre, randomised, double-blind, placebo-controlled phase 3 trials in adults with HIV and excess abdominal fat. Falutz and colleagues reported in the New England Journal of Medicine that 2 mg daily subcutaneous tesamorelin over 26 weeks reduced visceral adipose tissue relative to placebo, with increases in IGF-1 [4]. On this basis the FDA approved EGRIFTA in 2010 for the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy [2]. Two reformulations carry the identical indication: EGRIFTA SV [3] and EGRIFTA WR (tesamorelin F8), approved in March 2025 with room-temperature storage and a hydroxypropyl-betadex-containing formulation [1].

Beyond the approved indication, Stanley et al. conducted a randomised, double-blind, multicentre trial of 61 participants with HIV and NAFLD; 2 mg daily tesamorelin for 12 months produced a greater reduction in hepatic fat fraction than placebo (absolute effect size -4.1%), with 35% versus 4% reaching a hepatic fat fraction below 5%. Glucose and HbA1c did not differ significantly between groups, and injection-site complaints were more frequent with tesamorelin [5]. This indication is not approved.

The labels are explicit about what remains unestablished: long-term cardiovascular safety has not been established, the drug is not indicated for weight-loss management and is described as weight-neutral, and there are no data supporting improved antiretroviral adherence [1]. Pharmacokinetics are consistently short and low-bioavailability across formulations [1][2][3].

06Research evidence and limitations

Regulatory status

FDA-approved prescription drug. EGRIFTA (tesamorelin for injection) was approved in the United States in 2010 for the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy [2]. Two subsequent formulations share the same indication: EGRIFTA SV [3] and EGRIFTA WR (tesamorelin F8), approved by FDA in March 2025 [1]. Marketing authorisation holder: Theratechnologies Inc. ATC code H01AC06. Labelled Limitations of Use state that long-term cardiovascular safety has not been established, that it is not indicated for weight-loss management, and that there are no data supporting improved antiretroviral adherence [1]. Tesamorelin does not appear on the FDA list of bulk drug substances that may present significant safety risks (the 503A Category 2 list) as of the 22 April 2026 revision of that page — but as an approved drug it is subject to the separate restrictions governing compounding of commercially available products. Approval status outside the United States differs by jurisdiction and should be verified locally; a European marketing authorisation was not confirmed during this research. Any use outside the approved HIV-lipodystrophy indication is off-label.

07Research material and sourcing notes

Reported research-use reconstitution information

From FDA-approved manufacturer instructions (regulatory source, laboratory-relevant handling only). EGRIFTA WR 11.6 mg vial: reconstitute with 1.3 mL of Bacteriostatic Water for Injection, USP, giving 8 mg/mL; swirl the vial in a circle to mix, do not shake [1]. EGRIFTA SV 2 mg vial: reconstitute with 0.5 mL Sterile Water for Injection, USP; mix by rolling the vial gently for 30 seconds, do not shake [3]. Original EGRIFTA 1 mg vial: reconstituted with 0.5 mL Sterile Water for Injection, USP, per vial [2]. Excipients differ by formulation and affect solubility behaviour: EGRIFTA WR contains 145 mg hydroxypropyl betadex (a cyclodextrin solubiliser) and 43.5 mg mannitol per vial [1]; the original 1 mg formulation contained 50 mg mannitol [2]. No pH value is stated in the retrieved labels. No dosing guidance is given here.

Reported storage and stability information

Manufacturer/FDA label sources. Lyophilised powder, EGRIFTA WR 11.6 mg vial: store at room temperature, 20°C to 25°C (68°F to 77°F), in the original box to protect from light; excursions permitted 15°C to 30°C [1]. EGRIFTA SV 2 mg vial: store at room temperature 20°C to 25°C; excursions permitted 15°C to 30°C [3]. Reconstituted EGRIFTA WR: one reconstituted vial is labelled for use over 7 consecutive days, discard unused solution after 7 days, do not freeze [1]. The older 1 mg/vial EGRIFTA presentation had different (refrigerated) storage requirements — verify against the specific formulation before citing. Research-grade lyophilised peptide from suppliers is typically stored at -20°C or below; that is supplier technical documentation, not label data.

Identity and sourcing notes

Naming: 'tesamorelin' refers to the free base; the drug substance and most research material is the acetate salt, and TFA salts are also common in research-grade supply. A certificate of analysis should state the counter-ion and the peptide content (net peptide, free-base equivalent) separately from gross powder mass — a nominal '5 mg' vial of acetate salt contains meaningfully less peptide than 5 mg of free base. Identity should be confirmed by high-resolution mass spectrometry (expected average free-base mass ~5136 Da) plus RP-HPLC purity, and, for a 44-mer, by sequence confirmation rather than mass alone: the trans-3-hexenoyl N-terminal acyl group and the C-terminal amide are both easy to omit or mis-form in synthesis, and either omission shifts mass only modestly. Deletion sequences, des-amido, and Met27 oxidation products are the expected impurities and are the reason purity by HPLC alone is insufficient. Distinguish tesamorelin from sermorelin (GHRH 1-29 amide, unacylated) and from CJC-1295 variants, which are shorter modified GHRH analogues, not the full 1-44 sequence. Because tesamorelin is an FDA-approved drug, non-pharmaceutical supply is not equivalent to the approved product in identity, purity, sterility, or excipient composition. This is informational, not a purchasing recommendation.

08References and evidence

Primary sources

1. EGRIFTA WR (tesamorelin) for injection, for subcutaneous use — Full Prescribing InformationregulatoryTheratechnologies Inc. — US FDA / DailyMed, 2025
2. EGRIFTA (tesamorelin for injection) — original approved prescribing information, NDA 022505regulatoryTheratechnologies Inc. / US Food and Drug Administration — US FDA Drugs@FDA, 2010
3. EGRIFTA SV (tesamorelin for injection), for subcutaneous use — Full Prescribing InformationregulatoryTheratechnologies Inc. — US FDA / DailyMed
4. Metabolic effects of a growth hormone-releasing factor in patients with HIVclinical trialFalutz J, Allas S, Blot K, Potvin D, Kotler D, Somero M, Berger D, Brown S, Richmond G, Fessel J, Turner R, Grinspoon S — New England Journal of Medicine, 2007;357(23):2359-2370
5. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trialclinical trialStanley TL, Fourman LT, Feldpausch MN, Purdy J, Zheng I, Pan CS, Aepfelbacher J, Buckless C, Tsao A, Kellogg A, Branch K, Lee H, Liu CY, Corey KE, Chung RT, Torriani M, Kleiner DE, Hadigan CM, Grinspoon SK — The Lancet HIV, 2019;6(12):e821-e830

Chemical and molecular databases

• PubChem CID 16137828 (Tesamorelin) — formula C221H366N72O67S, computed MW 5136 g/mol, UNII MQG94M5EEO, synonym (3E)-hex-3-enoylsomatoliberin
• UniProt P01286 (SLIB_HUMAN, Somatoliberin/GHRH precursor) — mature 44-residue peptide, C-terminal leucine amide
• DrugBank DB08869 (Tesamorelin)
• ChEMBL/EMBL-EBI 'New Drug Approvals 2010 — Tesamorelin (Egrifta)' — gives sequence as trans-3-hexenoyl-YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL-NH2 (blog post, corroborative only)
• Wikipedia: Tesamorelin — CAS/UNII for free base and acetate salt (tertiary, corroborative only)

09Related compounds

• SermorelinThe truncated GHRH(1-29) amide fragment — the same receptor and mechanism as tesamorelin but without the 30-44 extension or the N-terminal acyl group.Reference page in preparation
• CJC-1295 (no DAC)Also a GHRH analogue (modified GHRH 1-29) that stabilises the peptide by amino-acid substitution rather than by N-terminal acylation, so it is the closest structural design comparator.Reference page in preparation
• CJC-1295 (with DAC)Same GHRH 1-29 backbone carrying a maleimide drug-affinity complex for albumin binding, representing the long-acting end of the GHRH-analogue design spectrum against tesamorelin's minutes-long plasma half-life.
• IpamorelinRaises GH through the ghrelin/GHS-R1a receptor rather than the GHRH receptor, making it the standard mechanistic contrast for how endogenous GH release is stimulated.
• MK-677 (Ibutamoren)An orally active non-peptide ghrelin-receptor agonist that raises GH and IGF-1 by a different receptor, frequently compared with tesamorelin in discussions of GH-axis modulation.Reference page in preparation

10Frequently asked questions