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Approved source synthesisEvidence current through August 2026

Tesamorelin Research Overview

September 01, 2026 · 10–12 minutes

Tesamorelin is a synthetic analogue of the human growth hormone–releasing hormone sequence GHRH(1–44). A trans-3-hexenoic-acid modification at the N-terminus increases resistance to enzymatic degradation while preserving activity at the GHRH receptor.

Evidence boundary: This article reviews published and regulatory research involving the specific tesamorelin drug products, formulations, populations, and study conditions identified in the cited sources. Clinical findings for FDA-approved Egrifta products or other investigated formulations cannot be transferred automatically to another material bearing the tesamorelin name. Nothing here is a claim about an FDB research product, a recommendation for human use, or medical advice. First Due Biotech products are offered strictly for laboratory research use only and are not for human consumption.

What is tesamorelin?

Tesamorelin is a synthetic analogue of the human growth hormone–releasing hormone sequence GHRH(1–44). A trans-3-hexenoic-acid modification at the N-terminus increases resistance to enzymatic degradation while preserving activity at the GHRH receptor.

That receptor-level design distinguishes tesamorelin from compounds that act directly at the growth hormone receptor. In the investigated clinical products, GHRH-receptor activation stimulated pituitary growth hormone release and increased downstream insulin-like growth factor 1 (IGF-1). The pathway retains more of the pituitary axis than direct administration of growth hormone, although increased GH–IGF-1 signaling remains central to both the observed endpoints and the safety questions.

Tesamorelin has an unusual evidence profile within peptide research. It is not supported only by animal models or early mechanistic experiments: two replicated Phase 3 randomized trials established a specific human body-composition endpoint, leading to FDA approval of branded tesamorelin products for a narrowly defined indication. Separate research programs have examined liver fat, cognition, skeletal muscle, inflammatory markers, and metabolic physiology, with varying levels of support.

Why tesamorelin attracted scientific interest

HIV-associated lipodystrophy can include disproportionate accumulation of visceral adipose tissue (VAT), even when overall body weight or subcutaneous fat does not change in the same way. Researchers therefore investigated whether stimulating endogenous GH secretion could alter this specific fat compartment.

The clinical program focused on VAT measured by computed tomography rather than general weight loss. That distinction is essential. VAT is metabolically important, but a change in VAT is not interchangeable with a change in scale weight, a cardiovascular event, or an improvement in every consequence associated with abdominal adiposity.

Tesamorelin nevertheless provided a valuable research test of the GH–IGF-1 axis: could a stabilized GHRH analogue produce a reproducible, compartment-specific body-composition change in a defined human population?

The pivotal program reported that it could.

Research at a glance

Research area What the cited evidence reported Evidence assessment
HIV-associated VAT Two replicated Phase 3 randomized trials reported significant reductions in CT-measured VAT at 26 weeks Strong for the studied indication and endpoint
Continued treatment Extension data reported maintenance or additional VAT change through 52 weeks among continuing participants Moderate; attrition and one-year horizon
Withdrawal Randomized withdrawal data reported reaccumulation after the investigated treatment stopped Moderate evidence that the effect was not durable after discontinuation
Body weight Pivotal trials did not establish tesamorelin as a general weight-loss intervention Not supported as a weight-loss claim
Liver fat Randomized HIV-associated NAFLD research reported MRI-measured liver-fat reduction and exploratory histologic signals Promising investigational human evidence
Cognition An older-adult GHRH study reported a positive signal; an HIV neurocognitive trial did not confirm benefit Mixed and indirect
Muscle and function Imaging and secondary analyses reported body-composition signals without established strength or disability benefit Preliminary
Safety Controlled trials characterized common events, glucose questions, and frequent IGF-1 elevation; long-term event data remain limited Moderate short-term, limited long-term

The pivotal human evidence

Two multicenter, double-blind Phase 3 trials studied adults with HIV and excess abdominal fat. Each used a randomized placebo-controlled 26-week phase followed by an extension. The primary endpoint was percentage change in visceral adipose tissue measured by CT.

Across the two trials, investigators reported mean VAT changes of approximately −14% and −18% in groups assigned to the investigated tesamorelin product, compared with −2% and +2% in placebo groups. The corresponding between-group differences were approximately −12% and −20%. The results were replicated across the pivotal datasets and were supported by FDA reanalysis.

The studies also reported changes in waist circumference, trunk fat, and some lipid measures. Overall body weight changed much less, reinforcing the point that the principal finding was redistribution or reduction within a specific fat compartment—not generalized weight loss.

These trials form the strongest part of the tesamorelin evidence base because they combined:

  • Randomized, double-blind designs
  • Replication in two pivotal trials
  • An objective CT endpoint
  • A defined clinical population
  • Regulatory review of the underlying data

The evidence is strong for the studied endpoint in the studied population. It should not be generalized automatically to people without HIV-associated lipodystrophy or to a differently manufactured material.

What happened when treatment stopped?

The randomized-withdrawal portion of the program adds an important dimension. Participants who continued the investigated tesamorelin product generally maintained or extended their VAT changes. Participants reassigned to placebo showed reaccumulation toward baseline.

This finding makes the research record more complete. It suggests that the observed body-composition effect depended on continued pathway stimulation under the study conditions rather than producing a permanent change after withdrawal.

That does not erase the positive 26- and 52-week findings. It clarifies their duration and helps distinguish an on-treatment biological effect from a durable post-treatment modification.

VAT reduction is not the same as weight loss

Tesamorelin is sometimes discussed in general weight-management terms because its pivotal trials changed abdominal fat. The evidence does not support collapsing those concepts.

Visceral adipose tissue is located within the abdominal cavity around internal organs. Subcutaneous fat sits beneath the skin. Scale weight combines fat, lean tissue, fluid, bone, and other compartments. A study can therefore report a substantial percentage change in VAT without a comparable percentage change in total body weight.

The pivotal tesamorelin findings are scientifically meaningful precisely because they were compartment-specific. Presenting them as ordinary weight loss would make the evidence less accurate, not more impressive.

It is equally important not to turn VAT change into a cardiovascular-outcome claim. Lipids and selected biomarkers changed in parts of the program, but the trials were not powered to establish fewer heart attacks, strokes, or deaths.

Liver-fat research

A later randomized study examined adults with HIV and nonalcoholic fatty liver disease. Investigators reported a significant reduction in MRI-measured hepatic fat fraction after 12 months in the group assigned to the investigated tesamorelin formulation compared with placebo.

The study also included liver-biopsy and biomarker analyses. Exploratory results suggested less fibrosis progression in the investigated group, but the trial was small and was not a definitive antifibrotic outcomes study. The evidence supports serious scientific interest in hepatic fat and related pathways; it does not establish broad reversal of steatohepatitis, fibrosis, cirrhosis, or clinical liver events.

This research area is particularly notable because it moves beyond the original VAT endpoint while remaining connected to the same metabolic pathway. Ongoing and future studies can clarify whether imaging findings translate into consistent histologic or clinical outcomes.

Glucose metabolism and the GH–IGF-1 axis

Growth hormone signaling can oppose some insulin actions, making glucose metabolism a central safety and mechanistic question. In the pivotal tesamorelin program, average glycemic changes were generally modest, but glucose intolerance and diabetes-related events remained clinically relevant monitoring domains in the approved-product record.

Investigational studies in obesity and type 2 diabetes did not establish tesamorelin as a glucose-lowering intervention. The most accurate interpretation is that the clinical program demonstrated VAT effects without a large average deterioration in glucose measures, while individual susceptibility and longer-term risk still required attention.

IGF-1 increased as expected from the mechanism. A meaningful proportion of participants reached values above age-adjusted reference ranges. This confirms target-pathway activity, but it also underlies continuing questions about prolonged exposure, malignancy risk, and the appropriate interpretation of biomarker elevation.

Cognition, muscle, and other research areas

The cognition literature requires careful identity and population control. A study in older adults using a GHRH analogue reported favorable cognitive signals, but that evidence should not be treated as a direct tesamorelin result without confirming the exact investigated molecule and formulation. In a separate randomized HIV-associated neurocognitive study of tesamorelin, investigators did not report a convincing cognitive benefit.

Skeletal-muscle and physical-function research is similarly preliminary. Imaging and secondary analyses have examined lean tissue, muscle fat, and functional measures, but the evidence has not established improved strength, disability outcomes, or broad physical-performance benefit.

Studies of inflammatory and cardiovascular-risk biomarkers have generated hypotheses and secondary signals. They do not establish prevention of clinical cardiovascular events.

These areas remain worthwhile because they test whether GH-axis effects extend beyond the original VAT endpoint. Their evidence should remain separate from the replicated pivotal result until stronger studies report.

Safety and tolerability in the reported studies

Controlled trials and regulatory reviews of the approved drug products reported adverse events including joint discomfort, extremity pain, peripheral edema, injection-site reactions, and hypersensitivity reactions. Glucose intolerance and elevated IGF-1 were important mechanistic and safety domains.

The available record is strongest over approximately six to twelve months. Important longer-term uncertainties include:

  • Cardiovascular clinical outcomes
  • Malignancy incidence under prolonged GH–IGF-1 stimulation
  • Long-term glucose outcomes in higher-risk populations
  • Use in older adults and underrepresented groups
  • Renal and hepatic impairment
  • Reproductive and developmental safety
  • Durability and safety beyond the principal trial horizons

Safety findings for FDA-reviewed Egrifta products also cannot establish the profile of a separately manufactured research material. Formulation, purity, aggregation, impurities, sterility, stability, and container systems can alter the evidence question.

Regulatory context

FDA approved the original Egrifta formulation in 2010 for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. A later formulation, Egrifta SV, received approval with a different presentation and concentration. The approved indication is specific; it is not a general approval for weight loss, obesity, fatty-liver treatment, cognitive enhancement, or muscle improvement.

European regulators reached a different conclusion during the original review history. The European application was withdrawn after concerns regarding the clinical relevance of the VAT endpoint, long-term safety, glucose effects, and IGF-1 elevation. That divergence is scientifically informative: regulators can agree that an endpoint changed while weighing its clinical meaning and uncertainty differently.

Approval of named Egrifta drug products does not mean every material called tesamorelin is an approved drug or equivalent to the reviewed products.

Why the tesamorelin evidence remains scientifically important

Tesamorelin provides a relatively rare peptide-research example in which a mechanistic concept progressed into replicated Phase 3 human findings and regulatory review. The pivotal program reported a reproducible change in CT-measured VAT, and withdrawal data strengthened the biological interpretation by showing reaccumulation after discontinuation.

The liver-fat program has added an encouraging investigational direction, while cognition, muscle, inflammation, and cardiovascular research illustrate both the breadth of interest and the importance of keeping secondary signals separate from established endpoints.

The most evidence-aligned position is specific and still positive: the investigated clinical tesamorelin products produced a replicated VAT signal in a defined population, while broader metabolic and tissue-related questions remain active areas of research. Maintaining that specificity protects the value of what the trials genuinely demonstrated.

Key takeaways

  • Tesamorelin is a stabilized GHRH(1–44) analogue investigated through the pituitary GH–IGF-1 axis.
  • Two replicated Phase 3 trials reported significant CT-measured VAT changes in adults with HIV-associated lipodystrophy.
  • Withdrawal data reported reaccumulation, indicating that the observed effect was not maintained after discontinuation under the studied conditions.
  • VAT change is not interchangeable with general weight loss or cardiovascular-event reduction.
  • Randomized liver research reported encouraging MRI-measured hepatic-fat findings, with histologic and long-term outcomes still developing.
  • Cognition, muscle, inflammation, and cardiovascular findings remain mixed, indirect, or preliminary.
  • The approved-product safety record characterizes common short-term events but leaves important long-term questions.
  • Clinical and regulatory findings for Egrifta products cannot be transferred automatically to FDB research material.

Study map

Study records discussed

Published protocol and registry-only recordsSee approved evidence mapOngoing

BMJ Open

TES-STUDY-P001

Erlandson KM, et al. Tesamorelin as an Adjunct to Exercise for Improving Physical Function in HIV (TRIUMPH): a clinical trial protocol. BMJ Open. 2026;16:e120740. DOI: 10.1136/bmjopen-2026-120740. PMID: 42419889. NCT06554717. https://bmjopen.bmj

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

New England Journal of Medicine

TES-STUDY-P011

Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. New England Journal of Medicine. 2007. DOI: 10.1056/NEJMoa072375. PMID: 18057338. NCT00123253. https://pubmed.ncbi.nlm.nih.gov/1805733

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

AIDS

TES-STUDY-P012

Falutz J, Allas S, Mamputu J-C, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. AIDS. 2008. DOI: 10.1097/QAD.0b013e32830a5058. PMID: 18690162. https

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

Journal of Acquired Immune Deficiency Syndromes

TES-STUDY-P013

Falutz J, Potvin D, Mamputu J-C, et al. Effects of tesamorelin in HIV-infected patients with excess abdominal fat. Journal of Acquired Immune Deficiency Syndromes. 2010. DOI: 10.1097/QAI.0b013e3181cbdaff. PMID: 20101189. NCT00435136. https://pub

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

JAMA

TES-STUDY-P015

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. JAMA. 2014. DOI: 10.1001/jama.2014.8334. PMID: 25038357. NCT01263717. https://pmc.ncbi.nlm.nih.

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

Lancet HIV

TES-STUDY-P016

Stanley TL, Fourman LT, Feldpausch MN, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV. Lancet HIV. 2019. DOI: 10.1016/S2352-3018(19)30338-8. PMID: 31611038. NCT02196831. https://pmc.ncbi.nlm.nih.gov/articles/PMC6981288

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

Archives of Neurology

TES-STUDY-P017

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. Archives of Neurology. 2012. DOI: 10.1001/archneurol.2012.1970. PMID: 22

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

Journal of Infectious Diseases

TES-STUDY-P018

Ellis RJ, Vaida F, Hu K, et al. Effects of tesamorelin on neurocognitive impairment in abdominally obese persons with HIV. Journal of Infectious Diseases. 2025. DOI: 10.1093/infdis/jiaf012. PMID: 39813152. NCT02572323. https://pubmed.ncbi.nlm.ni

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

PLOS ONE

TES-STUDY-P019

Clemmons DR, Miller S, Mamputu J-C. Safety and metabolic effects of tesamorelin in patients with type 2 diabetes. PLOS ONE. 2017. DOI: 10.1371/journal.pone.0179538. PMID: 28617838. NCT01264497. https://pmc.ncbi.nlm.nih.gov/articles/PMC5472315/

View study
Human clinical and physiological evidenceSee approved evidence mapCompleted

Journal of Clinical Endocrinology & Metabolism

TES-STUDY-P027

Makimura H, Feldpausch MN, Rope AM, et al. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion. Journal of Clinical Endocrinology & Metabolism. 2012. DOI: 10.1210/jc.2012-2794. PMID: 230

View study

Permanent sources

Reference ledger

  1. P001Published protocol and registry-only records

    BMJ Open

    Erlandson KM, et al. Tesamorelin as an Adjunct to Exercise for Improving Physical Function in HIV (TRIUMPH): a clinical trial protocol. Erlandson KM, et al. Tesamorelin as an Adjunct to Exercise for Improving Physical Function in HIV (TRIUMPH): a clinical trial protocol. BMJ Open. 2026;16:e120740. DOI: 10.1136/bmjopen-2026-120740. PMID: 42419889. NCT06554717. https://bmjopen.bmj.com/content/16/7/e120740(2026). DOI: 10.1136/bmjopen-2026-120740

  2. P002Regulatory and authoritative sources

    EGRIFTA WR (tesamorelin) Prescribing Information

    U.S. Food and Drug Administration. U.S. Food and Drug Administration. EGRIFTA WR (tesamorelin) Prescribing Information. Revised March 2025. https://www.accessdata.fda.gov/drugsatfdadocs/label/2025/022505s020lbl.pdf(2025)

  3. P003Regulatory and authoritative sources

    Office Director Memorandum - Summary Basis for Regulatory Action, NDA 022505

    Rosebraugh CJ. Rosebraugh CJ. Office Director Memorandum - Summary Basis for Regulatory Action, NDA 022505. FDA; 2010. https://www.accessdata.fda.gov/drugsatfdadocs/nda/2010/022505Orig1s000ODMemo.pdf(2010)

  4. P004Regulatory and authoritative sources

    Medical Review, NDA 022505

    Mohamadi A. Mohamadi A. Medical Review, NDA 022505. FDA; 2010. https://www.accessdata.fda.gov/drugsatfdadocs/nda/2010/022505Orig1s000MedR.pdf(2010)

  5. P005Regulatory and authoritative sources

    Clinical Pharmacology Review, NDA 022505

    U.S. Food and Drug Administration. U.S. Food and Drug Administration. Clinical Pharmacology Review, NDA 022505. 2010. https://www.accessdata.fda.gov/drugsatfdadocs/nda/2010/022505Orig1s000ClinPharmR.pdf(2010)

  6. P006Regulatory and authoritative sources

    Pharmacology/Toxicology Review, NDA 022505

    U.S. Food and Drug Administration. U.S. Food and Drug Administration. Pharmacology/Toxicology Review, NDA 022505. 2010. https://www.accessdata.fda.gov/drugsatfdadocs/nda/2010/022505Orig1s000PharmR.pdf(2010)

  7. P007Regulatory and authoritative sources

    Statistical Review, NDA 022505

    U.S. Food and Drug Administration. U.S. Food and Drug Administration. Statistical Review, NDA 022505. 2010. https://www.accessdata.fda.gov/drugsatfdadocs/nda/2010/022505Orig1s000StatR.pdf(2010)

  8. P008Regulatory and authoritative sources

    Egrifta Approval Letter

    U.S. Food and Drug Administration. U.S. Food and Drug Administration. Egrifta Approval Letter. 10 November 2010. https://www.accessdata.fda.gov/drugsatfdadocs/appletter/2010/022505s000ltr.pdf(2010)

  9. P009Regulatory and authoritative sources

    Egrifta withdrawal record and withdrawal assessment report

    European Medicines Agency. European Medicines Agency. Egrifta withdrawal record and withdrawal assessment report. 2012. https://www.ema.europa.eu/en/medicines/human/EPAR/egrifta(2012)

  10. P010Regulatory and authoritative sources

    Summary Basis of Decision: Egrifta

    Health Canada. Health Canada. Summary Basis of Decision: Egrifta. https://dhpp.hpfb-dgpsa.ca/review-documents/resource/SBD00185

  11. P011Human clinical and physiological evidence

    New England Journal of Medicine

    Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. New England Journal of Medicine. 2007. DOI: 10.1056/NEJMoa072375. PMID: 18057338. NCT00123253. https://pubmed.ncbi.nlm.nih.gov/18057338/(2007). DOI: 10.1056/NEJMoa072375

  12. P012Human clinical and physiological evidence

    AIDS

    Falutz J, Allas S, Mamputu J-C, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. Falutz J, Allas S, Mamputu J-C, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. AIDS. 2008. DOI: 10.1097/QAD.0b013e32830a5058. PMID: 18690162. https://pubmed.ncbi.nlm.nih.gov/18690162/(2008). DOI: 10.1097/QAD.0b013e32830a5058

  13. P013Human clinical and physiological evidence

    Journal of Acquired Immune Deficiency Syndromes

    Falutz J, Potvin D, Mamputu J-C, et al. Effects of tesamorelin in HIV-infected patients with excess abdominal fat. Falutz J, Potvin D, Mamputu J-C, et al. Effects of tesamorelin in HIV-infected patients with excess abdominal fat. Journal of Acquired Immune Deficiency Syndromes. 2010. DOI: 10.1097/QAI.0b013e3181cbdaff. PMID: 20101189. NCT00435136. https://pubmed.ncbi.nlm.nih.gov/20101189/(2010). DOI: 10.1097/QAI.0b013e3181cbdaff

  14. P014Human clinical and physiological evidence

    Journal of Clinical Endocrinology & Metabolism

    Falutz J, Mamputu J-C, Potvin D, et al. Effects of tesamorelin in HIV-infected patients with excess abdominal fat: pooled analysis of two phase III trials. Falutz J, Mamputu J-C, Potvin D, et al. Effects of tesamorelin in HIV-infected patients with excess abdominal fat: pooled analysis of two phase III trials. Journal of Clinical Endocrinology & Metabolism. 2010. DOI: 10.1210/jc.2010-0490. PMID: 20554713. https://pubmed.ncbi.nlm.nih.gov/20554713/(2010). DOI: 10.1210/jc.2010-0490

  15. P015Human clinical and physiological evidence

    JAMA

    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. 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. JAMA. 2014. DOI: 10.1001/jama.2014.8334. PMID: 25038357. NCT01263717. https://pmc.ncbi.nlm.nih.gov/articles/PMC4363137/(2014). DOI: 10.1001/jama.2014.8334

  16. P016Human clinical and physiological evidence

    Lancet HIV

    Stanley TL, Fourman LT, Feldpausch MN, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV. Stanley TL, Fourman LT, Feldpausch MN, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV. Lancet HIV. 2019. DOI: 10.1016/S2352-3018(19)30338-8. PMID: 31611038. NCT02196831. https://pmc.ncbi.nlm.nih.gov/articles/PMC6981288/(2019). DOI: 10.1016/S2352-3018(19

  17. P017Human clinical and physiological evidence

    Archives of Neurology

    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. 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. Archives of Neurology. 2012. DOI: 10.1001/archneurol.2012.1970. PMID: 22869065. NCT00257712. https://pubmed.ncbi.nlm.nih.gov/22869065/(2012). DOI: 10.1001/archneurol.2012.1970

  18. P018Human clinical and physiological evidence

    Journal of Infectious Diseases

    Ellis RJ, Vaida F, Hu K, et al. Effects of tesamorelin on neurocognitive impairment in abdominally obese persons with HIV. Ellis RJ, Vaida F, Hu K, et al. Effects of tesamorelin on neurocognitive impairment in abdominally obese persons with HIV. Journal of Infectious Diseases. 2025. DOI: 10.1093/infdis/jiaf012. PMID: 39813152. NCT02572323. https://pubmed.ncbi.nlm.nih.gov/39813152/(2025). DOI: 10.1093/infdis/jiaf012

  19. P019Human clinical and physiological evidence

    PLOS ONE

    Clemmons DR, Miller S, Mamputu J-C. Safety and metabolic effects of tesamorelin in patients with type 2 diabetes. Clemmons DR, Miller S, Mamputu J-C. Safety and metabolic effects of tesamorelin in patients with type 2 diabetes. PLOS ONE. 2017. DOI: 10.1371/journal.pone.0179538. PMID: 28617838. NCT01264497. https://pmc.ncbi.nlm.nih.gov/articles/PMC5472315/(2017). DOI: 10.1371/journal.pone.0179538

  20. P020Secondary, post-hoc, mechanistic, and molecular evidence

    AIDS

    Stanley TL, Falutz J, Mamputu J-C, et al. Effects of tesamorelin on inflammatory and fibrinolytic markers in HIV. Stanley TL, Falutz J, Mamputu J-C, et al. Effects of tesamorelin on inflammatory and fibrinolytic markers in HIV. AIDS. 2011. DOI: 10.1097/QAD.0b013e328347f3f1. PMID: 21516030. https://pmc.ncbi.nlm.nih.gov/articles/PMC3673013/(2011). DOI: 10.1097/QAD.0b013e328347f3f1

  21. P021Secondary, post-hoc, mechanistic, and molecular evidence

    PLOS ONE

    Mangili A, Falutz J, Mamputu J-C, et al. Predictors of treatment response to tesamorelin in HIV-infected patients with excess abdominal fat. Mangili A, Falutz J, Mamputu J-C, et al. Predictors of treatment response to tesamorelin in HIV-infected patients with excess abdominal fat. PLOS ONE. 2015. DOI: 10.1371/journal.pone.0140358. PMID: 26457580. https://pmc.ncbi.nlm.nih.gov/articles/PMC4601733/(2015). DOI: 10.1371/journal.pone.0140358

  22. P022Secondary, post-hoc, mechanistic, and molecular evidence

    AIDS

    Fourman LT, Czerwonka N, Feldpausch MN, et al. Visceral fat reduction with tesamorelin is associated with improved liver enzymes in HIV. Fourman LT, Czerwonka N, Feldpausch MN, et al. Visceral fat reduction with tesamorelin is associated with improved liver enzymes in HIV. AIDS. 2017;31(16):2253-2259. DOI: 10.1097/QAD.0000000000001614. PMID: 28832410. https://pmc.ncbi.nlm.nih.gov/articles/PMC5633509/(2017). DOI: 10.1097/QAD.0000000000001614

  23. P023Secondary, post-hoc, mechanistic, and molecular evidence

    Journal of Frailty & Aging

    Adrian S, Scherzinger A, Sanyal A, et al. The effects of tesamorelin on muscle density and area in adults with HIV. Adrian S, Scherzinger A, Sanyal A, et al. The effects of tesamorelin on muscle density and area in adults with HIV. Journal of Frailty & Aging. 2019. DOI: 10.14283/jfa.2018.45. PMID: 31237318. https://pmc.ncbi.nlm.nih.gov/articles/PMC6766405/(2019). DOI: 10.14283/jfa.2018.45

  24. P024Secondary, post-hoc, mechanistic, and molecular evidence

    AIDS

    Lake JE, La K, Erlandson KM, et al. Tesamorelin improves fat quality independent of changes in fat quantity. Lake JE, La K, Erlandson KM, et al. Tesamorelin improves fat quality independent of changes in fat quantity. AIDS. 2021;35(9):1395-1402. DOI: 10.1097/QAD.0000000000002897. PMID: 33756511. https://pmc.ncbi.nlm.nih.gov/articles/PMC8243807/(2021). DOI: 10.1097/QAD.0000000000002897

  25. P025Secondary, post-hoc, mechanistic, and molecular evidence

    Journal of Clinical and Translational Science

    Rahman F, McLaughlin T, Mesquita P, et al. Effect of tesamorelin in people with HIV with and without dorsocervical fat: Post hoc analysis of phase III double-blind placebo-controlled trial. Rahman F, McLaughlin T, Mesquita P, et al. Effect of tesamorelin in people with HIV with and without dorsocervical fat: Post hoc analysis of phase III double-blind placebo-controlled trial. Journal of Clinical and Translational Science. 2023;7(1):e40. DOI: 10.1017/cts.2022.515. PMID: 36845310. https://pmc.ncbi.nlm.nih.gov/articles/PMC9947601/(2023). DOI: 10.1017/cts.2022.515

  26. P026Secondary, post-hoc, mechanistic, and molecular evidence

    Clinical Pharmacokinetics

    González-Sales M, Barrière O, Tremblay P-O, et al. Population pharmacokinetics of tesamorelin. González-Sales M, Barrière O, Tremblay P-O, et al. Population pharmacokinetics of tesamorelin. Clinical Pharmacokinetics. 2015. DOI: 10.1007/s40262-014-0202-x. PMID: 25358450. https://pubmed.ncbi.nlm.nih.gov/25358450/(2015). DOI: 10.1007/s40262-014-0202-x

  27. P027Human clinical and physiological evidence

    Journal of Clinical Endocrinology & Metabolism

    Makimura H, Feldpausch MN, Rope AM, et al. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion. Makimura H, Feldpausch MN, Rope AM, et al. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion. Journal of Clinical Endocrinology & Metabolism. 2012. DOI: 10.1210/jc.2012-2794. PMID: 23015655. NCT00675506. https://pmc.ncbi.nlm.nih.gov/articles/PMC3513535/(2012). DOI: 10.1210/jc.2012-2794

  28. P028Secondary, post-hoc, mechanistic, and molecular evidence

    Journal of Clinical Endocrinology & Metabolism

    Makimura H, Murphy CA, Feldpausch MN, Grinspoon SK. The effects of tesamorelin on phosphocreatine recovery in obese subjects with reduced GH. Makimura H, Murphy CA, Feldpausch MN, Grinspoon SK. The effects of tesamorelin on phosphocreatine recovery in obese subjects with reduced GH. Journal of Clinical Endocrinology & Metabolism. 2014. DOI: 10.1210/jc.2013-3436. PMID: 24178787. NCT00675506. https://pmc.ncbi.nlm.nih.gov/articles/PMC3879673/(2014). DOI: 10.1210/jc.2013-3436

  29. P029Human clinical and physiological evidence

    Journal of Clinical Endocrinology & Metabolism

    Stanley TL, Chen CY, Branch KL, Makimura H, Grinspoon SK. Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. Stanley TL, Chen CY, Branch KL, Makimura H, Grinspoon SK. Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. Journal of Clinical Endocrinology & Metabolism. 2011. DOI: 10.1210/jc.2010-1587. PMID: 20943777. NCT00850564. https://pmc.ncbi.nlm.nih.gov/articles/PMC3038486/(2011). DOI: 10.1210/jc.2010-1587

  30. P030Secondary, post-hoc, mechanistic, and molecular evidence

    JCI Insight

    Fourman LT, Billingsley JM, Agyapong G, et al. Hepatic transcriptomic analysis from the HIV-NAFLD trial. Fourman LT, Billingsley JM, Agyapong G, et al. Hepatic transcriptomic analysis from the HIV-NAFLD trial. JCI Insight. 2020. DOI: 10.1172/jci.insight.140134. PMID: 32701508. https://pmc.ncbi.nlm.nih.gov/articles/PMC7455119/(2020). DOI: 10.1172/jci.insight.140134

  31. P031Secondary, post-hoc, mechanistic, and molecular evidence

    Scientific Reports

    Fourman LT, Stanley TL, Billingsley JM, et al. Proteomic and transcriptomic analysis associated with tesamorelin. Fourman LT, Stanley TL, Billingsley JM, et al. Proteomic and transcriptomic analysis associated with tesamorelin. Scientific Reports. 2021. DOI: 10.1038/s41598-021-89966-y. PMID: 34006921. https://pmc.ncbi.nlm.nih.gov/articles/PMC8131688/(2021). DOI: 10.1038/s41598-021-89966-y

  32. P032Secondary, post-hoc, mechanistic, and molecular evidence

    Obesity Research & Clinical Practice

    Badran AS, Helal A, Shata KS, Ayesh H. Systematic review and meta-analysis of tesamorelin trials. Badran AS, Helal A, Shata KS, Ayesh H. Systematic review and meta-analysis of tesamorelin trials. Obesity Research & Clinical Practice. 2026. DOI: 10.1016/j.orcp.2026.01.002. PMID: 41545261. https://pubmed.ncbi.nlm.nih.gov/41545261/(2026). DOI: 10.1016/j.orcp.2026.01.002

  33. P033Published protocol and registry-only records

    ClinicalTrials.gov. NCT03375788. https://clinicaltrials.gov/study/NCT03375788

    ClinicalTrials.gov. NCT03375788. https://clinicaltrials.gov/study/NCT03375788

  34. P034Published protocol and registry-only records

    ClinicalTrials.gov. NCT03150511. https://clinicaltrials.gov/study/NCT03150511

    ClinicalTrials.gov. NCT03150511. https://clinicaltrials.gov/study/NCT03150511

  35. P035Published protocol and registry-only records

    ClinicalTrials.gov. NCT01591902. https://clinicaltrials.gov/study/NCT01591902

    ClinicalTrials.gov. NCT01591902. https://clinicaltrials.gov/study/NCT01591902

  36. P036Published protocol and registry-only records

    ClinicalTrials.gov. NCT01388920. https://clinicaltrials.gov/study/NCT01388920

    ClinicalTrials.gov. NCT01388920. https://clinicaltrials.gov/study/NCT01388920

  37. P037Published protocol and registry-only records

    ClinicalTrials.gov. NCT03226821. https://clinicaltrials.gov/study/NCT03226821

    ClinicalTrials.gov. NCT03226821. https://clinicaltrials.gov/study/NCT03226821

  38. P038Published protocol and registry-only records

    ClinicalTrials.gov. NCT01632592. https://clinicaltrials.gov/study/NCT01632592

    ClinicalTrials.gov. NCT01632592. https://clinicaltrials.gov/study/NCT01632592

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ghk-cu

GHK-Cu Research Overview

GHK-Cu is a copper-binding tripeptide complex built from glycine, histidine, and lysine. The peptide without copper is called GHK. When it coordinates copper, it becomes part of a dynamic chemical ...

Read overview
ghk-cu

GHK-Cu Research Overview

GHK-Cu is a copper-binding tripeptide complex built from glycine, histidine, and lysine. The peptide without copper is called GHK. When it coordinates copper, it becomes part of a dynamic chemical ...

Read overview