Growth hormone axis

Tesamorelin

Name: Tesamorelin: What the Research Actually Shows
Creator: Peptide Health Lab

Also known as: Egrifta, GHRF(1-44) analog

Regulatory status: FDA approved
Evidence grade: Human RCT evidence

Last reviewed September 1, 2026 · 13 sources

What tesamorelin is and how it works

Tesamorelin is a synthetic analog of human growth-hormone-releasing hormone — the same hypothalamic signal that CJC-1295 and sermorelin imitate, and a different molecule from all of them. Where sermorelin is the first 29 amino acids of that hormone, tesamorelin is the full 44-residue sequence carrying a trans-3-hexenoyl group attached at the N-terminus. That modification protects the peptide from the enzyme that would otherwise clip it apart in circulation, and it is what turns a laboratory curiosity into a drug that survives a daily subcutaneous injection.^[4]

The pharmacology from there is unremarkable in the best sense. Tesamorelin binds the GHRH receptor on pituitary somatotropes, the pituitary releases growth hormone in its own pulsatile pattern, and the liver responds by making more IGF-1. In the first phase 3 trial, IGF-1 rose 81% on tesamorelin and fell 5% on placebo.^[1] Nothing about that mechanism is contested. What makes tesamorelin the most solidly evidenced compound in the growth-hormone-axis section of this library is not the mechanism but what happened next: somebody ran the trials.

The clinical problem it was built for is specific and worth understanding, because it explains everything about how the evidence should be read. Long-term antiretroviral therapy for HIV can produce a distinctive redistribution of body fat, in which visceral adipose tissue — the fat packed around the abdominal organs — accumulates while subcutaneous fat does not, and sometimes wastes. That visceral compartment is the one associated with metabolic dysregulation and cardiovascular risk. Growth hormone is lipolytic and preferentially mobilizes visceral fat, so a GHRH analog that raises endogenous growth hormone offered a way at that compartment without administering growth hormone itself.^[4] Every trial below tested that idea in that population.

What the research actually shows

Two phase 3 randomized placebo-controlled trials, with imaging endpoints. The registrational programme enrolled 412 and 404 adults with HIV on antiretroviral therapy who had abdominal fat accumulation, randomized them 2:1 to 2 mg of daily subcutaneous tesamorelin or placebo, and measured percent change in visceral adipose tissue on computed tomography as the primary endpoint. In the first, visceral adipose tissue fell 15.2% on tesamorelin and rose 5.0% on placebo; triglycerides fell 50 mg/dL and rose 9 mg/dL respectively; the total-to-HDL cholesterol ratio improved. Adverse events did not differ significantly between groups, though more patients on the drug withdrew because of one.^[1] The second reported a 10.9% reduction versus 0.6%, with improvements in waist circumference, waist-to-hip ratio, and both patient- and physician-rated body image, and no change in limb or abdominal subcutaneous fat.^[3]

The effect held for a year and reversed on withdrawal. The extension phases re-randomized participants at six months. Those who continued reached roughly an 18% reduction in visceral adipose tissue at 52 weeks with sustained triglyceride improvement; those switched to placebo reaccumulated the fat they had lost. The investigators wrote the conclusion plainly: the effects do not last beyond the duration of treatment.^[2]^[3]

Liver fat was measured separately, twice. An investigator-initiated randomized trial in 50 adults found that six months of tesamorelin reduced both visceral fat and liver fat measured by magnetic resonance spectroscopy, with a net treatment effect of −2.9% in the lipid-to-water percentage, while calling for further study of what that means clinically.^[7] A 61-person multicenter trial in people with HIV and non-alcoholic fatty liver disease then randomized 12 months of blinded treatment and reported a 37% relative reduction in hepatic fat fraction.^[9]

Independent synthesis reaches the same place. A 2026 meta-analysis of five randomized trials found significant reductions in visceral adipose tissue, hepatic fat percentage, waist circumference, and limb fat, and an increase in lean body mass of 1.42 kg — but no significant reduction in subcutaneous adipose tissue or body-mass index.^[10] A separate 2026 systematic review of four trials in 909 patients reported the same body-composition picture, modest lipid improvements, growth-hormone-related adverse effects, and higher discontinuation rates that did not reach statistical significance (RR 2.25, 95% CI 0.98–5.17, p = 0.06), and cautioned that data on long-term safety, optimal dosing, and durability remain limited.^[11] Correlative work has also linked the visceral fat reduction to an improved metabolic profile and to changes in inflammatory markers within the trial populations.^[6]^[5]

Where the evidence is weak

Every participant in every trial had HIV. This is the central limitation and it is easy to skim past. Tesamorelin has never been studied in a randomized trial of people without HIV-associated fat redistribution — not in general obesity, not in metabolic syndrome, not in healthy adults who would like less abdominal fat. The condition treated is a specific iatrogenic pattern with a specific visceral-subcutaneous dissociation, and the drug's selectivity for the visceral compartment is what made it useful there. Nothing in the published record establishes what it does in a body that got its abdominal fat some other way.

It is not a weight-loss drug, and the trials say so. Body-mass index did not change significantly in meta-analysis; subcutaneous fat did not fall; lean mass rose. The approved labeling states directly that the drug is not indicated for weight-loss management and describes its effect as weight neutral.^[10]^[4] A compound that moves fat out of one compartment without changing the number on a scale is a poor fit for the goal most people bring to it.

No outcome trial exists. The entire evidence base rests on imaging and laboratory surrogates: square centimeters of visceral fat, hepatic fat fraction, triglycerides, IGF-1. The justification for caring about visceral adiposity is its association with cardiovascular events, and no trial has tested whether reducing it this way reduces those events. The labeling concedes the point under Limitations of Use, and independent reviewers repeat it.^[11]

The longest randomized exposure is twelve months. For a treatment whose benefit vanishes when it stops — which is to say, an indefinite one — that is a short record. Long-term safety data beyond a year come from clinical use rather than from controlled follow-up.^[2]

Raising IGF-1 is the mechanism, and IGF-1 exposure is not a neutral variable. Large prospective cohorts associate higher circulating IGF-1 with the risk of several cancers, most consistently prostate cancer.^[12]^[13] That work describes naturally varying IGF-1 in untreated people and is not a measured risk of this drug. It is the reason active malignancy is a labeled contraindication and the reason the malignancy question belongs in the prescribing conversation.

Predictors of response have been named, but not established. A pooled analysis of the two phase 3 trials, covering 543 patients on tesamorelin and 263 on placebo, concluded that people with baseline metabolic syndrome by NCEP criteria, triglycerides above 1.7 mmol/L, or white race were the most likely to see visceral fat fall at six months, and put the odds of reaching visceral adipose tissue below 140 cm² at 3.9 times placebo (95% CI 2.03–7.44). Nothing predicted the response at three months. Those conclusions are weaker than they sound: the analysis was post-hoc and exploratory, two of the three interaction p-values were borderline — 0.054 for metabolic syndrome and 0.063 for triglycerides, against 0.025 for race — and it was sponsored and conducted by the manufacturer and a commercial partner. It is a hypothesis about who responds, not a validated rule for choosing patients.^[8]

Legal and regulatory status

Tesamorelin is an FDA-approved drug, and its approval is narrower than the word "approved" usually suggests to a reader. The original biologics license application was approved in November 2010, and the currently marketed presentations carry a single indication: the reduction of excess abdominal fat in HIV-infected adult patients with lipodystrophy. At the time of the first review of the drug it was the first and only treatment carrying that indication.^[4]

The labeling attaches limitations to that indication that are unusual in their directness. Long-term cardiovascular safety has not been established. Continuation is to be reconsidered in patients who have not had a reduction in visceral adipose tissue. The drug is explicitly not indicated for weight-loss management, on the grounds that its effect is weight neutral. And there are no data supporting improved adherence to antiretroviral therapy in patients taking it. Those are the manufacturer's own statements in the approved labeling, and they narrow the claim considerably.

Two presentations are currently marketed under the same active ingredient. They carry different vial strengths, different reconstitution instructions, different diluents, different storage requirements after mixing, and different labeled daily doses — and the labeling states that they are not substitutable for one another. That is a pharmacy-level fact worth knowing exists, and it is resolved by the dispensed labeling rather than by any page on the internet.

Use of an approved drug outside its approved indication is off-label practice: lawful for a licensed prescriber exercising clinical judgment, and outside what the approval evaluated. That distinction matters here more than it does for most drugs, because the indication is scoped to one population with one condition, and the entire randomized evidence base was generated in that population. Off-label use of tesamorelin for general abdominal fat is not use supported by the trials described above; it is use in a setting the trials never examined.

It is prescription-only. Legitimate access runs through a licensed prescriber who evaluates whether it is appropriate and monitors the response. Peptide Health Lab does not sell peptides and does not tell anyone where to obtain anything. Athletes in tested sport should note that growth-hormone-releasing hormone analogs as a class are prohibited at all times under the World Anti-Doping Agency's hormone and metabolic modulator provisions, and should confirm the current year's list rather than rely on a static page.

Questions to bring to a provider

Because real evidence exists here, the useful questions are about fit and duration rather than about whether the drug does anything:

Does the fat pattern in question actually resemble the visceral accumulation the trials enrolled, and what imaging or measurement would establish that rather than assume it?^[1]
Given that visceral fat reaccumulated in everyone who stopped, what is the plan for the long run?^[2]
What is the intended endpoint — a measured change in visceral or hepatic fat, or a change in how something feels — and how will it be assessed?^[9]
What baseline and follow-up monitoring makes sense for glucose, given the transient early rise reported at two weeks in one trial?^[7]
Does a personal or family history of malignancy change the calculus, given both the labeled contraindication in active malignancy and the cohort associations between circulating IGF-1 and cancer risk?^[13]
If the goal is weight loss rather than visceral fat specifically, is this the right drug at all, given that the trials found no change in body-mass index?^[10]
Which presentation is being dispensed, and what are its specific storage and in-use instructions?^[4]

A clinician who says "the evidence is strong, and it is strong for a population and an endpoint that may not be yours" is reading the literature correctly.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Reduction of visceral adipose tissue in HIV-associated lipodystrophy

Human RCT evidence human RCT · review

This is the claim the drug was approved on, and it is well supported. In a 412-patient randomized placebo-controlled trial, visceral adipose tissue fell 15.2% on tesamorelin and rose 5.0% on placebo over 26 weeks. A second 404-patient trial reported a 10.9% reduction versus a 0.6% reduction, sustained at roughly 18% in those who continued for 12 months. A 2026 meta-analysis of five randomized trials confirms significant reductions in visceral adipose tissue, trunk fat, hepatic fat percentage, and waist circumference, with an increase in lean body mass.

[1] [3] [2] [10]

Reduction of liver fat in people with HIV

Human RCT evidence human RCT

Two randomized trials measured it directly. In 50 adults at a single center, tesamorelin reduced liver fat by magnetic resonance spectroscopy alongside visceral fat over 6 months. A 61-person multicenter trial in people with HIV and non-alcoholic fatty liver disease reported a 37% relative reduction in hepatic fat fraction at 12 months. Both are small, both were conducted in people with HIV, and the investigators of the earlier one explicitly called for further study of the clinical importance of the finding.

[7] [9]

Improvement in the lipid profile

Human RCT evidence human RCT · review

In the first phase 3 trial, triglycerides fell by 50 mg/dL on tesamorelin and rose by 9 mg/dL on placebo, and the total-to-HDL cholesterol ratio improved. Meta-analysis across trials finds the lipid benefit real but modest, with a mean total cholesterol difference of about 0.16 mmol/L. These are laboratory values, not events.

[1] [11]

Durability of any benefit after treatment ends

Human RCT evidence human RCT

Randomized evidence exists and it is negative. Participants switched from tesamorelin to placebo in the extension phase reaccumulated visceral fat, and the investigators concluded that the effects do not persist beyond the treatment period. This is one of the few claims in this library where the absence of a lasting benefit has actually been tested rather than assumed.

[2] [3]

Weight loss, or fat loss, in people without HIV-associated lipodystrophy

Anecdotal reports only review

No published randomized trial has enrolled this population. Every trial above recruited adults with HIV on antiretroviral therapy who had excess abdominal fat, a specific and unusual pattern of fat redistribution. The approved labeling states that the drug is not indicated for weight loss management and describes it as weight neutral, and the trials bear that out: body-mass index did not change significantly in meta-analysis, and neither did subcutaneous adipose tissue. Applying a visceral-fat result from this population to general weight loss is not supported by anything published.

[10] [4]

Cardiovascular or mortality benefit from the visceral fat reduction

Anecdotal reports only review

Nothing has tested it. The rationale for treating visceral adiposity in this population is its epidemiological association with cardiovascular risk, and the approved labeling states outright that long-term cardiovascular safety has not been established. No published trial has used a cardiovascular event, hospitalization, or death as an endpoint.

[4] [11]

Response is predictable from patient characteristics

Anecdotal reports only human observational

Partially, and on evidence too soft to act on. A pooled analysis of the two phase 3 trials (543 on tesamorelin, 263 on placebo) concluded that individuals with baseline metabolic syndrome by NCEP criteria, triglyceride levels above 1.7 mmol/L, or white race were most likely to see visceral fat fall over six months, and that the odds of reaching visceral adipose tissue below 140 cm² were 3.9 times greater on tesamorelin than on placebo (95% CI 2.03–7.44) after adjustment. No predictors were identified at three months. The caveats are what set the grade: this is a post-hoc exploratory analysis of trial data rather than a prospective test, two of the three interaction p-values were borderline (0.054 for metabolic syndrome and 0.063 for triglycerides, against 0.025 for race), the analysis was sponsored and conducted by parties with a commercial interest, and none of it amounts to a validated rule for selecting patients.

[8]

Claim area	Evidence & sources	What the research shows
Reduction of visceral adipose tissue in HIV-associated lipodystrophy	Human RCT evidence human RCT · review [1] [3] [2] [10]	This is the claim the drug was approved on, and it is well supported. In a 412-patient randomized placebo-controlled trial, visceral adipose tissue fell 15.2% on tesamorelin and rose 5.0% on placebo over 26 weeks. A second 404-patient trial reported a 10.9% reduction versus a 0.6% reduction, sustained at roughly 18% in those who continued for 12 months. A 2026 meta-analysis of five randomized trials confirms significant reductions in visceral adipose tissue, trunk fat, hepatic fat percentage, and waist circumference, with an increase in lean body mass.
Reduction of liver fat in people with HIV	Human RCT evidence human RCT [7] [9]	Two randomized trials measured it directly. In 50 adults at a single center, tesamorelin reduced liver fat by magnetic resonance spectroscopy alongside visceral fat over 6 months. A 61-person multicenter trial in people with HIV and non-alcoholic fatty liver disease reported a 37% relative reduction in hepatic fat fraction at 12 months. Both are small, both were conducted in people with HIV, and the investigators of the earlier one explicitly called for further study of the clinical importance of the finding.
Improvement in the lipid profile	Human RCT evidence human RCT · review [1] [11]	In the first phase 3 trial, triglycerides fell by 50 mg/dL on tesamorelin and rose by 9 mg/dL on placebo, and the total-to-HDL cholesterol ratio improved. Meta-analysis across trials finds the lipid benefit real but modest, with a mean total cholesterol difference of about 0.16 mmol/L. These are laboratory values, not events.
Durability of any benefit after treatment ends	Human RCT evidence human RCT [2] [3]	Randomized evidence exists and it is negative. Participants switched from tesamorelin to placebo in the extension phase reaccumulated visceral fat, and the investigators concluded that the effects do not persist beyond the treatment period. This is one of the few claims in this library where the absence of a lasting benefit has actually been tested rather than assumed.
Weight loss, or fat loss, in people without HIV-associated lipodystrophy	Anecdotal reports only review [10] [4]	No published randomized trial has enrolled this population. Every trial above recruited adults with HIV on antiretroviral therapy who had excess abdominal fat, a specific and unusual pattern of fat redistribution. The approved labeling states that the drug is not indicated for weight loss management and describes it as weight neutral, and the trials bear that out: body-mass index did not change significantly in meta-analysis, and neither did subcutaneous adipose tissue. Applying a visceral-fat result from this population to general weight loss is not supported by anything published.
Cardiovascular or mortality benefit from the visceral fat reduction	Anecdotal reports only review [4] [11]	Nothing has tested it. The rationale for treating visceral adiposity in this population is its epidemiological association with cardiovascular risk, and the approved labeling states outright that long-term cardiovascular safety has not been established. No published trial has used a cardiovascular event, hospitalization, or death as an endpoint.
Response is predictable from patient characteristics	Anecdotal reports only human observational [8]	Partially, and on evidence too soft to act on. A pooled analysis of the two phase 3 trials (543 on tesamorelin, 263 on placebo) concluded that individuals with baseline metabolic syndrome by NCEP criteria, triglyceride levels above 1.7 mmol/L, or white race were most likely to see visceral fat fall over six months, and that the odds of reaching visceral adipose tissue below 140 cm² were 3.9 times greater on tesamorelin than on placebo (95% CI 2.03–7.44) after adjustment. No predictors were identified at three months. The caveats are what set the grade: this is a post-hoc exploratory analysis of trial data rather than a prospective test, two of the three interaction p-values were borderline (0.054 for metabolic syndrome and 0.063 for triglycerides, against 0.025 for race), the analysis was sponsored and conducted by parties with a commercial interest, and none of it amounts to a validated rule for selecting patients.

Typical protocol range in the research

Phase 3 randomized, double-blind, placebo-controlled trial in 412 adults with HIV and abdominal fat accumulation on antiretroviral therapy, over 26 weeks, with percent change in visceral adipose tissue on computed tomography as the primary endpoint

2 mg by daily subcutaneous injection [1]
Second phase 3 trial of the same design in 404 adults, with a re-randomized extension phase carrying treatment to 12 months

2 mg by daily subcutaneous injection for 6 months, then either continued or switched to placebo for a further 6 months [3] [2]
Investigator-initiated randomized trial of 50 adults with HIV and abdominal fat accumulation at a single academic center, with liver fat by magnetic resonance spectroscopy as a co-primary endpoint over 6 months

2 mg by daily subcutaneous injection [7]
Randomized, double-blind, multicenter trial in 61 people with HIV and non-alcoholic fatty liver disease, 12 months of blinded treatment followed by a 6-month open-label phase

2 mg once daily [9]

Every published trial of tesamorelin used 2 mg daily of the formulation available at the time, in adults with HIV and excess abdominal fat. The currently labeled doses are lower because the marketed formulations changed, not because a trial compared doses. No published trial has established a dose of tesamorelin in anyone without HIV-associated lipodystrophy, and the labeled schedules belong to the prescriber who dispensed them.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

Growth hormone class effects — arthralgia, myalgia, peripheral edema, paresthesia, and injection-site reactions

The dominant adverse-event category across the programme. A 2026 meta-analysis of five randomized trials identified arthralgia, myalgia, paresthesia, and injection-site erythema as the events associated with treatment. · Mostly the recognizable growth-hormone class profile rather than drug-specific toxicity, and mostly mild to moderate in the registrational trials, where treatment-emergent serious adverse events occurred in under 4% of patients over 26 weeks. Not negligible, though: more patients on tesamorelin than on placebo withdrew from the first phase 3 trial because of an adverse event, and a 2026 systematic review of four trials in 909 patients reported higher discontinuation rates alongside the growth-hormone-related effects — though that difference did not reach statistical significance (RR 2.25, 95% CI 0.98–5.17, p = 0.06).

[1] [4] [10] [11]
Loss of the entire effect when treatment stops

Observed in every study that stopped the drug · This is the finding that reframes what the drug is. In the 52-week extension, participants re-randomized from tesamorelin to placebo reaccumulated visceral fat, and the initial 6-month improvement was rapidly lost. The authors state plainly that the effects do not last beyond the duration of treatment. Whatever else tesamorelin is, it is not a course of treatment with a durable endpoint.

[2] [3]
Glucose and insulin — measured, and mostly reassuring, with one caveat

Prespecified safety endpoints in the registrational programme and in the liver-fat trials. No clinically significant change in glucose parameters was observed at 26 or 52 weeks. · Growth hormone opposes insulin action, so glycemia was watched closely here in a way it never has been for the unapproved compounds in this class, and the reassurance is real rather than assumed. The caveat is timing: in the single-center liver-fat trial, fasting glucose rose significantly in the tesamorelin group at 2 weeks before the difference resolved by 6 months. Existing diabetes or prediabetes remains a provider-discussion flag, and it is the prescriber who decides what monitoring accompanies treatment.

[2] [7] [10]
Elevation of IGF-1

Reported in every trial. IGF-1 rose by 81% in the first phase 3 trial versus a 5% decrease on placebo. · Raising IGF-1 is the drug's mechanism, not an off-target effect. Separately from anything tesamorelin does, large prospective cohort work links higher circulating IGF-1 to the risk of several cancers, most consistently prostate cancer. That association comes from people taking nothing and is not a demonstrated effect of this drug; the approved labeling nonetheless treats active malignancy as a contraindication, and a personal or family history of malignancy is a specific reason to raise this with the prescriber.

[1] [12] [13]
Long-term cardiovascular safety, stated by the labeling as not established

Not established · The indication exists because visceral adiposity in this population is associated with cardiovascular risk, and yet no trial has tested whether reducing it with this drug reduces events. The approved labeling says so itself under Limitations of Use. The longest randomized exposure in the published programme is 12 months. That is a surrogate endpoint honestly labeled as one, which is more than most compounds in this library can say, and it is still a gap.

[4] [11]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage: Approved tesamorelin is supplied as a sterile lyophilized powder in a vial, manufactured under a real stability programme with an assigned expiry date. The current presentations differ from one another in how they are held before mixing, and the dispensed labeling is what states the temperature and the date for the specific vial in hand. That labeling comes from the prescription, not from this page, and it is the only stability information about tesamorelin that has a manufacturer standing behind it.
Reconstituted storage: The two approved presentations diverge sharply once mixed, which is the single most consequential storage fact about this drug. One is prepared and given immediately, with anything left over discarded. The other is prepared with a preserved diluent and held refrigerated for a labeled multi-day window before the vial is discarded. Neither in-use window is interchangeable with the other, and the labeling dispensed with the prescription is the source for which one applies.
Reconstitution diluent: The approved presentations are reconstituted with the diluent supplied in the package, and the two current presentations do not use the same one: one is supplied with sterile water for injection, the other with bacteriostatic water for injection. Substituting one for the other changes the in-use window, so the diluent is not an interchangeable detail here the way it is for a generic research peptide.
Reconstitution & handling: Approved labeling directs gentle mixing rather than shaking, and directs visual inspection of the reconstituted vial: it is used only if the solution is clear, colorless, and free of particulate matter. Beyond that, the preparation steps for an approved drug come from the labeling dispensed with the prescription and from the pharmacist, both of which are specific to the presentation. PHL publishes no volume or unit calculations, because those are dosing decisions and dosing decisions belong with a licensed clinician.
Handling notes: Because tesamorelin is an approved drug, a manufacturer stability programme, an expiry date, and a labeled in-use period exist for it. That is a categorical difference from the unapproved compounds elsewhere in this library. It also means the handling questions here have documented answers that a pharmacist can read off a label, which is where they belong.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

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Citations

13 sources · every identifier checked against PubMed

[1] Metabolic effects of a growth hormone-releasing factor in patients with HIV · New England Journal of Medicine, 2007. Human RCT
[2] Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation · AIDS, 2008. Human RCT
[3] 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 · Journal of Acquired Immune Deficiency Syndromes, 2010. Human RCT
[4] Tesamorelin: a review of its use in the management of HIV-associated lipodystrophy · Drugs, 2011. Review
[5] Effects of tesamorelin on inflammatory markers in HIV patients with excess abdominal fat: relationship with visceral adipose reduction · AIDS, 2011. Human RCT
[6] Reduction in visceral adiposity is associated with an improved metabolic profile in HIV-infected patients receiving tesamorelin · Clinical Infectious Diseases, 2012. Human RCT
[7] Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial · JAMA, 2014. Human RCT
[8] Predictors of treatment response to tesamorelin, a growth hormone-releasing factor analog, in HIV-infected patients with excess abdominal fat · PLoS One, 2015. Human observational study
[9] Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial · The Lancet HIV, 2019. Human RCT
[10] Body composition, hepatic fat, metabolic, and safety outcomes of tesamorelin, a GHRH analogue, in HIV-associated lipodystrophy: a meta-analysis of randomized controlled trials · Obesity Research & Clinical Practice, 2026. Review
[11] Efficacy and safety of tesamorelin in people living with HIV (PLWH) with lipodystrophy: a systematic review and meta-analysis · Journal of the International Association of Providers of AIDS Care, 2026. Review
[12] A meta-analysis of individual participant data reveals an association between circulating levels of IGF-I and prostate cancer risk · Cancer Research, 2016. Human observational study
[13] Circulating insulin-like growth factor-I concentrations and risk of 30 cancers: prospective analyses in UK Biobank · Cancer Research, 2020. Human observational study

Before you act on any of this

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