Peerless Peptides

Tesamorelin

Synthetic 44-amino-acid GHRH 1-44 analog with N-terminal trans-3-hexenoyl modification

Tesamorelin is a synthetic 44-amino-acid analog of growth hormone-releasing hormone (GHRH 1-44) bearing a trans-3-hexenoyl moiety on the α-amine of N-terminal Tyr1. The hexenoyl cap blocks dipeptidyl peptidase IV cleavage while preserving the pulsatile GHRH-receptor signaling mode of native GHRH. Tesamorelin is the active drug substance in Egrifta (Theratechnologies, NDA 022505), approved by the FDA on November 10, 2010 for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. Egrifta WR (F8) was approved March 25, 2025; tesamorelin was reclassified as a biologic under the BPCIA on March 23, 2020.

Available for laboratory research use only.

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Biochemical Profile

CAS Number
218949-48-5
Molecular Formula
C221H366N72O67S
Molecular Weight
5135.86 g/mol
Purity
≥98% (HPLC-UV (220 nm))
PubChem CID
16137828
Amino Acid Sequence
trans-3-hexenoyl-Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-Arg-Gly-Ala-Arg-Ala-Arg-Leu-NH2

Receptor Targets, Pharmacokinetics, and Regulatory Context

Tesamorelin is a synthetic 44-amino-acid analog of human growth hormone-releasing hormone (GHRH; somatocrinin; somatoliberin) carrying a single structural distinction from the native parent peptide: a trans-3-hexenoic acid moiety amide-coupled to the α-amine of N-terminal Tyr1. Native GHRH 1-44 is encoded by the GHRH gene at chromosome 20q11.23 (UniProt P01286) and circulates with a plasma half-life of approximately 7 minutes, dominated by N-terminal cleavage at the Tyr1-Ala2 bond by dipeptidyl peptidase IV (DPP-IV)[1]. The trans-3-hexenoyl cap sterically blocks DPP-IV access to the substrate cleavage site while preserving the full 44-amino-acid sequence and the GHRH-receptor binding affinity of the native parent. Subcutaneous tesamorelin in healthy adults displays a plasma half-life of approximately 26-38 minutes per the FDA Clinical Pharmacology Review for NDA 022505[2].

The GHRH receptor (GHRH-R) is a class B G-protein-coupled receptor expressed on anterior pituitary somatotrophs. Receptor binding activates Gαs/cAMP/PKA signaling, with downstream activation of GH gene transcription and exocytosis of pre-formed growth hormone from secretory granules. Tesamorelin's modestly extended half-life is sufficient to block DPP-IV-mediated inactivation without converting the signaling mode from pulsatile to sustained. This pharmacokinetic profile distinguishes tesamorelin from CJC-1295 with DAC, which adds covalent serum-albumin conjugation via a maleimide-Lys30 group and produces a ~6-8 day half-life that converts pulsatile GHRH-R signaling into sustained signaling[3].

The Phase 3 clinical trials supporting the November 10, 2010 FDA approval of Egrifta (Falutz et al. 2007 N Engl J Med; Falutz et al. 2010 J Clin Endocrinol Metab pooled analysis, total pooled n = 816) reported sustained IGF-1 elevation and reduction of visceral adipose tissue over 26-52 weeks in HIV-infected adults with lipodystrophy[4][5][6]. The mechanistic interpretation in the published clinical literature attributes the visceral-adipose-tissue effect to growth-hormone-mediated lipolysis on visceral adipocytes, with relative sparing of the subcutaneous adipose depot.

The regulatory channel for tesamorelin is structurally distinct from every other peptide circulating in the laboratory research supply. The molecule was reclassified as a biologic under the Biologics Price Competition and Innovation Act of 2009 on March 23, 2020, which closes the 503A bulks-list compounding pathway available to BPC-157, TB-500, GHK-Cu, and other unapproved drug substances. Three FDA-approved formulations exist: original Egrifta (F1, approved November 10, 2010), Egrifta SV (F4, approved 2019, reduced reconstitution volume), and Egrifta WR (F8, approved March 25, 2025, weekly reconstitution and reduced administration volume relative to F4). F8 patent protection in the United States extends through 2033.

The molecule sold for laboratory research is nominally the same drug substance described above. The cGMP-manufacturing chain-of-custody, identity/purity/potency testing standards, and post-administration surveillance available to FDA-approved Egrifta are not features of the research-supply channel. The published clinical-trial evidence base described in the research applications below was generated in defined patient populations using FDA-approved Egrifta and is not interchangeable with off-label use of compounded or research-grade tesamorelin.

Research Applications

HIV-Associated Lipodystrophy (the FDA-Approved Indication)

The FDA-approved indication for Egrifta is reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. Two identically-designed Phase 3 randomized double-blind placebo-controlled multicenter trials supported NDA 022505. The Falutz 2007 N Engl J Med trial (NCT00123253, n = 412 HIV-infected adults randomized 2:1 to tesamorelin or placebo subcutaneously, 26-week primary phase plus 26-week extension) reported the primary endpoint of visceral adipose tissue change by CT as -15.2% with tesamorelin vs +5.0% with placebo[4]. IGF-1 rose 81% from baseline on tesamorelin vs -5% on placebo; triglycerides decreased on tesamorelin and rose modestly on placebo over the 26-week primary phase.

The Falutz 2010 J Clin Endocrinol Metab pooled analysis of NCT00123253 plus the confirmatory NCT00435136 (combined n = 816 HIV-infected adults) reported sustained 15-18% visceral adipose tissue reduction over 52 weeks, with no liver-related serious adverse events and broadly stable glucose parameters[5]. The Adrian 2012 Clin Infect Dis post hoc analysis examined the association between visceral adiposity reduction and the metabolic profile in the Phase 3 study population[7]. The two Phase 3 trials, the pooled analysis, and the 52-week safety extension constitute the regulatory evidence base the FDA reviewed in approving Egrifta on November 10, 2010.

Hepatic Steatosis and NAFLD in HIV (the Grinspoon Program)

The Massachusetts General Hospital research program led by Steven K. Grinspoon has run a sustained academic investigation of tesamorelin in HIV-associated nonalcoholic fatty liver disease (NAFLD) extending beyond the FDA-approved indication. Stanley et al. 2014 JAMA (n = 50 HIV-infected adults, 28 tesamorelin vs 22 placebo, 6 months) reported a -2.9% net effect favoring tesamorelin on hepatic lipid-to-water percentage by magnetic resonance spectroscopy, alongside the expected visceral adipose tissue reduction[8].

The Stanley 2019 Lancet HIV trial (NCT02196831, n = 61 HIV-infected adults with hepatic fat fraction ≥5%, 12-month double-blind phase plus 6-month open-label extension) is the largest published Phase 2/3 investigation of tesamorelin in HIV-NAFLD[9]. The primary endpoint of hepatic fat fraction by 1H-MR spectroscopy was -4.1% absolute (-37% relative) on tesamorelin vs placebo; 35% of tesamorelin recipients achieved hepatic fat fraction below 5% vs 4% on placebo. The pre-specified analysis of fibrosis progression by liver biopsy reported 10.5% on tesamorelin vs 37.5% on placebo. Mechanistic follow-up by Fourman et al. characterized hepatic transcriptomic signatures and a targeted proteomic profile downstream of GHRH-R agonism in the Stanley 2019 cohort[10][11].

Cognition in Mild Cognitive Impairment and Aging

Baker et al. 2012 Arch Neurol (n = 152 adults aged 55-87; 137 completers comprising 76 healthy and 61 mild cognitive impairment subjects; 20 weeks of tesamorelin 1 mg subcutaneous daily 30 minutes before bedtime vs placebo) examined cognitive outcomes in a single-center Phase 2 trial[12]. The published report described executive-function results in both the healthy-aging and MCI groups, with separate verbal-memory analyses in the MCI subgroup at elevated risk of progression to Alzheimer-type dementia. The trial was conducted at the University of Washington with collaborating centers.

The cognition signal in Baker 2012 is a preliminary single-center Phase 2 finding. The mechanism is mechanistically plausible given the independent literature on the GH/IGF-1 axis in aging-brain biology, but Phase 3 replication has not been reported. A separate Phase 2 trial in HIV-infected aging adults (NCT02572323, UC San Diego) extended this investigation in a different population[13]. The published cognition data do not constitute regulatory-grade evidence for cognitive-enhancement claims outside the studied populations and trial protocols.

GHRH-Receptor Pharmacology and Body Composition Research

Tesamorelin has been characterized in the published preclinical and Phase 1 pharmacokinetic literature as a GHRH-receptor agonist with affinity comparable to native GHRH 1-44 per the FDA Clinical Pharmacology Review for NDA 022505[2]. Phase 1 studies in healthy adults established subcutaneous pharmacokinetics with a plasma half-life of approximately 26-38 minutes, dose-proportional growth-hormone excursions, and sustained IGF-1 elevation under repeated dosing.

The published Phase 3 evidence base (Falutz 2007 N Engl J Med; Falutz 2010 J Clin Endocrinol Metab pooled analysis) characterized the visceral-adipose-tissue effect as selective for the visceral depot, with relative preservation of the subcutaneous depot[4][5]. In the originating clinical-trial population (HIV-infected adults with lipodystrophy), this selectivity is the mechanistic anchor of the approved indication. Generalization of the visceral-selective effect to non-HIV general populations is not directly Phase 3 evidence-supported as of May 2026. The published Phase 3 NAFLD/NASH development program in non-HIV general populations was announced by Theratechnologies in September 2020 with a planned cohort of approximately 650 patients carrying fibrosis stage 2-3 and NAS ≥4, plus 50 people living with HIV; top-line readout is pending verification.

Sister GHRH-Analog Comparative Pharmacology

Tesamorelin sits within a family of GHRH analogs sharing GHRH-receptor agonism but differing in sequence length, structural modification, and pharmacokinetic profile. The Frohman and Jansson 1986 review of GHRH receptor biology established the receptor pharmacology framework[14]. Sermorelin (GHRH 1-29) is the unmodified N-terminal 29-residue active fragment; tesamorelin is the full GHRH 1-44 sequence with trans-3-hexenoyl on Tyr1; CJC-1295 with DAC is a GHRH 1-29 backbone with D-Ala2/Gln8/Ala15/Leu27 substitutions plus maleimide-Lys30 albumin-conjugation chemistry.

The three analogs span the GHRH-analog pharmacokinetic spectrum. Native GHRH 1-44 has a plasma half-life of approximately 7 minutes; sermorelin approximately 12 minutes; tesamorelin approximately 26-38 minutes (subcutaneous); CJC-1295 with DAC approximately 6-8 days via covalent serum-albumin conjugation. Crucially, the three preserved-pulsatility analogs (sermorelin, tesamorelin, no-DAC GHRH analogs) generate discrete pulsatile receptor activation cycles; CJC-1295 with DAC converts the signaling mode to sustained receptor occupancy. Cross-importing tesamorelin's FDA-approved-indication evidence base to CJC-1295 with DAC is not supported by the published pharmacology, because the two analogs operate in different signaling modes.

Approved-Drug Context and Replication

Tesamorelin's regulatory posture is structurally distinct from every other peptide in the research-supply channel. The FDA approval is narrow: reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. Broader off-label uses, including general body composition outside HIV-lipodystrophy, NAFLD/NASH outside HIV populations, anti-aging applications, and cognitive enhancement, are not FDA-approved. The published Phase 2/3 academic evidence base in HIV-NAFLD (Stanley 2019 Lancet HIV) is methodologically rigorous within its 61-patient HIV-NAFLD population, but generalization to non-HIV NAFLD/NASH awaits Phase 3 readout from the September 2020 announced Theratechnologies development program[9]. The single-center Phase 2 cognition signal (Baker 2012 Arch Neurol) has not been replicated at Phase 3 scale[12].

Tesamorelin was reclassified as a biologic under the BPCIA on March 23, 2020, which closes the 503A bulks-list compounding pathway. Patient-specific 503A compounding remains theoretically possible with a valid prescription. Tesamorelin is not on the July 23-24, 2026 FDA Pharmacy Compounding Advisory Committee docket and was not named in the 2020 Tailor Made Compounding plea agreement or the April 2026 Watkins indictment (D. Utah). The GHRH-receptor-on-cancer concern arising from SV1 splice variants documented on multiple cancer cell types by the Schally/Rekasi group represents an unresolved mechanistic question across all chronic GHRH-receptor agonist exposure outside the FDA-approved HIV-lipodystrophy surveillance population[15]. Egrifta WR (F8) carries US patent protection through 2033.

Reconstitution & Storage

Recommended Diluent
Bacteriostatic water (0.9% benzyl alcohol) or sterile saline
Storage (lyophilized)
-20°C, dry, dark, sealed amber vial with desiccant
Storage (reconstituted)
2-8°C, use within 14 days
Shelf Life
24-36 months lyophilized

Research References

  1. [1] Frohman LA, Downs TR, Williams TC, Heimer EP, Pan YC, Felix AM. Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive product cleaved at the NH2 terminus. J Clin Invest. 1986;78(4):906-913. PMID:3093534
  2. [2] FDA Clinical Pharmacology Review for Egrifta (tesamorelin) NDA 022505. United States Food and Drug Administration; original approval November 10, 2010.
  3. [3] Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799-805. PMID:16352683
  4. [4] Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. N Engl J Med. 2007;357(23):2359-2370. PMID:18057338
  5. [5] Falutz J, Mamputu JC, Potvin D, 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):4291-4304. PMID:20554713
  6. [6] Falutz J, Potvin D, Mamputu JC, 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):311-322. PMID:20101189
  7. [7] Stanley TL, Falutz J, Marsolais C, et al. Reduction in visceral adiposity is associated with an improved metabolic profile in HIV-infected patients receiving tesamorelin. Clin Infect Dis. 2012;54(11):1642-1651. PMID:22495074
  8. [8] Stanley TL, Feldpausch MN, Oh J, et al. Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. JAMA. 2014;312(4):380-389. PMID:25038357
  9. [9] Stanley TL, Fourman LT, Feldpausch MN, 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
  10. [10] Fourman LT, Billingsley JM, Agyapong G, et al. Effects of tesamorelin on hepatic transcriptomic signatures in HIV-associated NAFLD. JCI Insight. 2020;5(16):e140134. PMID:32699192
  11. [11] Fourman LT, Stanley TL, Billingsley JM, et al. Delineating tesamorelin response pathways in HIV-associated NAFLD using a targeted proteomic and transcriptomic approach. Sci Rep. 2021;11(1):10485. PMID:34006942
  12. [12] Baker LD, Barsness SM, Borson S, et al. Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial. Arch Neurol. 2012;69(11):1420-1429. PMID:22869065
  13. [13] UC San Diego. Phase II Trial of Tesamorelin for Cognition in Aging HIV-Infected Persons. ClinicalTrials.gov Identifier: NCT02572323 (Phase 2, completed; verified 2026-05-19).
  14. [14] Frohman LA, Jansson JO. Growth hormone-releasing hormone. Endocr Rev. 1986;7(3):223-253. PMID:3530585
  15. [15] Rekasi Z, Czompoly T, Schally AV, Halmos G. Isolation and sequencing of cDNAs for splice variants of growth hormone-releasing hormone receptors from human cancers. Proc Natl Acad Sci U S A. 2000;97(19):10561-10566. PMID:10984544
  16. [16] Theratechnologies Inc. FDA approves Egrifta WR (tesamorelin F8), a weekly-reconstituted formulation for the treatment of excess abdominal fat in adults with HIV-associated lipodystrophy. Corporate news release; approval date March 25, 2025.
  17. [17] Hoffman AR, Kuntze JE, Baptista J, et al. Growth hormone (GH) replacement therapy in adult-onset GH deficiency: effects on body composition in men and women in a double-blind, randomized, placebo-controlled trial. J Clin Endocrinol Metab. 2004;89(5):2048-2056. PMID:15126519

Scientific Journal Author

Steven K. Grinspoon, MD

Chief, Metabolism Unit, Massachusetts General Hospital; Professor of Medicine, Harvard Medical School

Landmark Publications

  • Stanley TL, Feldpausch MN, Oh J, et al. Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. JAMA. 2014;312(4):380-389. (PMID 25038357)
  • Stanley TL, Fourman LT, Feldpausch MN, 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)
  • Fourman LT, Billingsley JM, Agyapong G, et al. Effects of tesamorelin on hepatic transcriptomic signatures in HIV-associated NAFLD. JCI Insight. 2020;5(16):e140134. (PMID 32699192)

Dr. Grinspoon is independently cited here as the principal investigator on the Massachusetts General Hospital tesamorelin academic research program in HIV-associated NAFLD and metabolic complications of HIV. There is no affiliation or commercial relationship between Dr. Grinspoon, Massachusetts General Hospital, Harvard Medical School, and Peerless Peptides.

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