Tesamorelin FDA Approved

What It Is

Tesamorelin is a synthetic analog of human growth-hormone-releasing hormone (hGHRH) consisting of the full native 44-amino-acid GHRH sequence with a trans-3-hexenoic acid moiety conjugated to the α-amino group of the N-terminal tyrosine residue. The N-terminal fatty-acid modification confers resistance to dipeptidyl peptidase-4 (DPP-4) cleavage — the primary mechanism of native GHRH degradation — while leaving the biologically active core intact. The drug was developed by Theratechnologies Inc. (Montreal) under the code TH9507 and is marketed in the US as Egrifta (and the 2019 reformulation Egrifta SV).

Tesamorelin is the only FDA-approved GHRH analog for an adult metabolic indication. The FDA granted approval on November 10, 2010, for the reduction of excess visceral adipose tissue (VAT) in HIV-infected adults with antiretroviral therapy-associated lipodystrophy. The approval was based on two Phase 3 placebo-controlled trials (Falutz 2007 NEJM, Falutz 2008 AIDS, Falutz 2010 JAIDS) showing consistent 15–18% VAT reduction over 26 weeks with daily 2 mg SC dosing, with improvements in triglycerides and other metabolic markers and a generally acceptable safety profile.

Unlike CJC-1295 (whose N-terminal protection relies on the D-Ala2 substitution) and Modified GRF (1-29) (a truncated 29-aa backbone), tesamorelin preserves the complete native hGHRH(1-44) sequence. This is the reason tesamorelin is often described as the "most native" GHRH analog — the receptor engagement is maximally physiologic; only the N-terminal fatty-acid protection group is non-native. Half-life remains short (~26 minutes in HIV-infected patients after SC administration), so the pharmacodynamic effect is pulsatile GH release rather than a sustained plateau.

Mechanism of Action

Tesamorelin's mechanism is straight GHRH receptor biology with an engineered protection group. It does not introduce any non-physiologic signaling.

• GHRH receptor (pituitary somatotropes) — Binds the Gαs-coupled GHRH receptor on anterior pituitary somatotropes. Drives cAMP-PKA signaling, which triggers GH synthesis and pulsatile release. Because the full native 44-amino-acid sequence is retained, tesamorelin is a full agonist at the receptor.
• DPP-4 resistance via N-terminal acylation — Native GHRH is cleaved by DPP-4 at the Tyr1-Ala2 bond within minutes. The trans-3-hexenoic acid conjugate on the α-amino group of Tyr1 sterically blocks DPP-4 access while preserving receptor binding. Half-life in healthy adults is ~26 minutes SC — long enough to drive a robust GH pulse, short enough to clear before the next daily dose.
• Endogenous pulsatile GH release — Tesamorelin does not override hypothalamic somatostatin tone. GH secretion is gated physiologically. Plasma GH typically peaks within 1–2 hours of SC injection, then returns toward baseline. Repeated once-daily dosing produces cumulative IGF-1 elevation over weeks without eliminating the natural pulsatile pattern.
• IGF-1 elevation (pharmacodynamic marker) — Sustained tesamorelin dosing raises mean IGF-1 levels by ~80–120% over baseline within weeks. The FDA label uses IGF-1 monitoring as the primary means of detecting supra-physiologic exposure (SDS > 3 triggers dose reduction or discontinuation).
• Visceral fat reduction (downstream of GH lipolysis) — The clinically validated effect. Elevated GH drives hormone-sensitive-lipase-mediated lipolysis, with a preferential effect on visceral rather than subcutaneous fat depots. This is likely related to higher β-adrenergic receptor density and greater lipolytic responsiveness of visceral adipocytes under GH stimulation. In HIV-lipodystrophy Phase 3 trials, VAT declined 15–18% over 26 weeks without a corresponding loss of subcutaneous fat.
• Liver fat (MASH/NAFLD context) — In the Stanley et al. 2019 Lancet HIV trial, tesamorelin reduced hepatic fat fraction by ~3.1% absolute (~37% relative) compared with placebo in HIV-infected adults with NAFLD, and reduced fibrosis progression markers. Mechanism: hepatic lipid clearance secondary to improved visceral/ectopic fat mobilization plus direct GH effects on hepatic DNL pathways.
• Cognition (Baker 2012) — In healthy older adults and adults with amnestic mild cognitive impairment, 20 weeks of 1 mg/day tesamorelin improved executive function and, to a lesser extent, verbal memory. Proposed mechanism: restoration of youth-range IGF-1 exposure to the CNS via GH-axis signaling and IGF-1 effects on hippocampal and prefrontal synaptic biology.
• Lipid profile — Triglycerides typically decrease 15–25% over 26 weeks; non-HDL cholesterol declines modestly; HDL may rise slightly. Consistent across the Falutz Phase 3 data and subsequent real-world analyses.

What the Research Shows

Tesamorelin has the deepest human evidence base of any GHRH-class compound. The HIV-lipodystrophy Phase 3 program enrolled over 800 patients, and subsequent academic trials have extended the efficacy story to liver fat, cognition, and non-HIV metabolic contexts.

• Phase 3 — Falutz 2007 NEJM — 412 HIV-infected adults (86% male) with abdominal fat accumulation randomized 2:1 to tesamorelin 2 mg SC daily or placebo for 26 weeks. Primary endpoint (% change in VAT by CT): –15.2% tesamorelin vs +5.0% placebo (between-group difference −20.2%, p < 0.001). Triglycerides declined −50 mg/dL more than placebo. IGF-1 rose ~81%. Glycemic measures preserved (N Engl J Med 357:2359-2370).
• Phase 3 — Falutz 2008 AIDS (extension) — 6-month extension of original trial. 154 patients on tesamorelin for 52 weeks; sustained VAT reduction in treatment-continued group, reversion toward baseline in tesamorelin-to-placebo crossover group. No new safety signals (AIDS 22:1719-1728).
• Phase 3 — Falutz 2010 JAIDS (pooled) — Pooled analysis of the two pivotal trials (~816 patients). Confirmed 15–18% VAT reduction, 22% triglyceride reduction, improvements in patient-rated abdominal distress and clinician-rated belly profile. Adverse event rates numerically similar to placebo.
• Metabolic responder analysis — Stanley 2012 CID — Among tesamorelin-treated patients, those achieving ≥8% VAT reduction (responders) had significantly improved triglycerides, adiponectin, and preserved glucose homeostasis over 52 weeks, whereas non-responders had worsened glucose. Clinically useful pharmacodynamic rule: if VAT hasn't dropped by 8% at week 26, glycemic benefit is unlikely and discontinuation is reasonable (Clin Infect Dis 54:1642-1651).
• Liver fat — Stanley 2014 JAMA — Randomized trial of tesamorelin vs placebo in HIV-infected adults with abdominal fat accumulation. Liver fat by MR spectroscopy declined significantly with tesamorelin, independent of VAT reduction. First signal that tesamorelin's hepatic effect is not fully explained by visceral-fat mobilization alone.
• NAFLD histology — Stanley 2019 Lancet HIV — 61 HIV-infected adults with hepatic fat fraction ≥5% by proton MRS, randomized to tesamorelin 2 mg SC daily or placebo for 12 months. Primary endpoint (absolute reduction in HFF): −4.1% tesamorelin vs +0.9% placebo (between-group difference −4.9%, p = 0.006). Secondary liver-biopsy analysis showed less fibrosis progression and less NAFLD Activity Score worsening with tesamorelin. Direct histologic evidence of hepatic benefit (Lancet HIV 6:e821-e830).
• Cognition — Baker 2012 Arch Neurol — 20-week placebo-controlled trial of tesamorelin 1 mg SC nightly in 76 healthy older adults and 61 adults with amnestic MCI. Tesamorelin improved executive function in both groups and attenuated the expected cognitive decline in the MCI cohort. Effects persisted partially after washout (Arch Neurol 69:1420-1429).
• Inflammatory markers — Stanley 2011 — Reductions in hsCRP and select inflammatory markers correlated with VAT reduction in tesamorelin responders; non-responders showed no inflammatory improvement.
• Liver enzymes — Fourman 2017 — VAT responders on tesamorelin had improvements in ALT and AST concordant with hepatic-fat reduction.
• Post-marketing LiverTox assessment — Pooled analysis of 816 HIV-infected patients treated for up to 52 weeks found no signal for clinically apparent hepatotoxicity. No DILI cases were attributed to tesamorelin in the NIDDK drug-induced liver injury network prospective cohort (2004–2013).

Human Data

Summary of the human evidence base:

• Phase 1 PK/PD (Koutkia et al. 2004 JAMA) — Early randomized placebo-controlled GHRH work in HIV-infected men with lipodystrophy established the GH-axis response and motivated the TH9507 development program (JAMA 292:210-218).
• Phase 2 — Falutz 2005 AIDS — Dose-ranging study (1, 2 mg daily) established the 2 mg dose selection (AIDS 19:1279-1287).
• Phase 3 registration trials — NCT00123253 (26-week + extension), NCT00435136 (6-month). Combined enrollment ~800 HIV-infected adults with abdominal fat accumulation. Consistent VAT and triglyceride effects.
• Liver-fat / NAFLD trials — NCT01263717 (Stanley 2014 JAMA), NCT02196831 (Stanley 2019 Lancet HIV NAFLD histology).
• Cognition trial — NCT00675506 (Baker 2012 Arch Neurol, N = 137).
• Pharmacokinetics — Tmax ~0.15 h SC; half-life 26 min in HIV-infected patients, ~38 min in healthy adults; steady-state IGF-1 reached at ~2 weeks; exposure roughly linear with dose across 1–2 mg range.
• Long-term (52 week) extension data — Multiple Theratechnologies-sponsored extensions plus the Stanley 2012 / 2019 academic trials provide ~12 months of continuous-use safety data in HIV cohorts.

Dosing from the Literature

Dosing below reflects FDA-approved prescribing plus published off-label practice. Tesamorelin is prescription-only in the United States.

Reconstitution & Storage

The branded product (Egrifta SV) is supplied as a lyophilized powder in a single-dose vial with a separate diluent (sterile water for injection). Compounded or research-chemical tesamorelin exists in some jurisdictions but is subject to the same FDA bulk-substance constraints as other peptides at publication.

• Reconstitution — Inject diluent slowly down the inside wall of the vial at a 45° angle. Swirl gently — do not shake. Solution should be clear and colorless. Use immediately or refrigerate.
• Storage — Egrifta SV unreconstituted vials: refrigerate 2–8°C. Reconstituted solution must be used immediately (label recommends single-use; practice-based use extends somewhat with refrigeration). Compounded vials typically labeled for 30-day refrigerated use after reconstitution; defer to compounder directives.
• Injection site — Abdomen, at least 2 inches away from the navel. Rotate sites weekly to minimize injection-site reactions and lipohypertrophy. Avoid scarred, bruised, or irritated skin.
• Needle — 29G–31G ½-inch insulin syringe for compounded vials. Egrifta SV is supplied with manufacturer needles.
• Inspection — Discard if solution shows cloudiness, particles, color change, or unusual odor.

→ Use the Kalios Dosing Calculator for exact syringe units on compounded vials

Side Effects & Risks

Tesamorelin's FDA label includes a defined adverse event profile derived from the Phase 3 program. Safety data extends across ~816 patients treated up to 52 weeks.

• Injection site reactions (most common) — Erythema (~25%), pruritus, pain, bruising, urticaria, hemorrhage, rash. Usually mild and self-limited. Rotate sites.
• Arthralgia and myalgia — Joint pain and muscle pain reported in 10–15% of patients, typically mild-to-moderate. May reflect GH-related water retention in connective tissues. Usually dose-related and tolerates with time.
• Peripheral edema — Classic GH-related effect. Mild fluid retention in extremities, sometimes with transient carpal tunnel–type symptoms. Usually resolves with continued dosing or dose reduction.
• Paresthesias / hypoesthesias — Tingling, numbness, or altered sensation. Again, GH-related nerve and tissue fluid dynamics. Evaluate if persistent.
• Hyperglycemia / glucose intolerance — GH is counter-regulatory to insulin. Tesamorelin can worsen fasting glucose, especially in non-responders or patients with baseline insulin resistance. Monitor HbA1c at baseline and during therapy. Stanley 2012 showed that responders (≥8% VAT reduction) preserve glucose homeostasis, while non-responders worsen — making the 6-month VAT-response decision pharmacologically important.
• IGF-1 elevation — Sustained use elevates mean IGF-1 by ~80%. FDA label mandates dose reduction or discontinuation if IGF-1 SDS exceeds 3 on two consecutive measurements.
• Pancreatitis — Rare reports in the post-marketing period; causality not established. Evaluate abdominal pain.
• Hypersensitivity — Urticaria, pruritus, rash, flushing, and rare anaphylaxis reported. Discontinue if hypersensitivity suspected.
• Fluid retention / weight gain — Classic GH class effect. Most patients gain 1–2 kg of body weight early, offset by fat mass reduction over time.
• Contraindications — Pregnancy (category X — may cause fetal harm), active malignancy, disruption of the hypothalamic-pituitary axis (pituitary surgery, head trauma, radiation, hypopituitarism), and known hypersensitivity to tesamorelin or mannitol. Use caution in critical illness.
• Discontinuation effect reversal — VAT benefit reverses within ~6 months of discontinuation. Tesamorelin is a maintenance therapy, not a curative one. Patients should understand this before starting.
• Pediatric use — Not indicated and not recommended; closure of epiphyseal plates is induced by GH/IGF-1 elevation.

Supportive Nutrition & Supplements

Tesamorelin's visceral-fat-reduction effect proceeds through lipolysis and hepatic lipid clearance that depend on substrate availability and systemic metabolic context. Most of the supportive-nutrition framework for tesamorelin overlaps with general GH-axis support; a few elements are particularly relevant given the indication and the typical patient profile (visceral adiposity, often with elevated triglycerides, liver fat, or metabolic syndrome).

• Protein intake — 1.6–2.2 g/kg bodyweight/day across 3–5 feedings. Preserves lean mass during the fat-mass mobilization tesamorelin drives. Leucine-rich sources (whey isolate, eggs, lean meat) support mTOR-mediated protein synthesis.
• Low-glycemic dietary pattern — Tesamorelin can worsen fasting glucose in non-responders. A moderate-carb, protein-forward pattern with an emphasis on fiber helps offset this. Particularly important for patients with baseline insulin resistance or HIV-lipodystrophy physiology.
• Fiber — 25–35 g/day. Supports glycemic control, lipid profile improvement, and gut-hepatic axis function. Psyllium 5–10 g/day is cheap and effective.
• Omega-3 fatty acids (EPA/DHA) — 2–3 g combined. Reinforces tesamorelin's triglyceride-lowering effect and supports hepatic lipid clearance. Among the best-fit supplements for patients on tesamorelin for NAFLD/MASH off-label use.
• Vitamin D (25-OH) — Target serum 40–60 ng/mL. Supports insulin sensitivity and muscle/bone maintenance during active fat mobilization.
• Magnesium — 300–400 mg glycinate or threonate daily. Cofactor role in glucose metabolism and sleep quality. Commonly suboptimal in metabolic-syndrome patients.
• Zinc — 15–25 mg elemental daily. IGF-1 bioactivity cofactor; supports protein synthesis.
• Choline + betaine (hepatic support) — Choline 500–2,000 mg/day, betaine 2–5 g/day. Support methylation and hepatic lipid export (VLDL packaging). Particularly relevant for off-label NAFLD/MASH use where liver-fat reduction is the goal. Evidence is modest but the downside is minimal.
• Creatine monohydrate — 3–5 g/day. Lean-mass preservation during weight-loss phases; no interaction with tesamorelin's mechanism.
• Resistance training — Not a supplement, but mandatory for lean-mass preservation during any GH-axis-driven fat-mobilization protocol. 2–4 sessions/week of progressive loading.
• Low-to-moderate alcohol — Chronic alcohol impairs liver fat resolution (directly counter to a core tesamorelin effect), worsens triglycerides, and disrupts sleep architecture (where native GH pulses occur). Patients on tesamorelin for MASH/NAFLD indications should minimize alcohol; even for VAT-focused use, cutting alcohol materially improves response.
• Things to avoid — Chronic high-fructose intake (direct driver of hepatic DNL and visceral fat accumulation), late-night high-volume meals (blunt nocturnal GH), chronic high-dose corticosteroids (directly antagonize GH axis), and sedentary lifestyle (negates most of the tesamorelin effect on body composition).

What to Expect — Timeline

The tesamorelin timeline is better characterized than any other GHRH-class compound because of the replicated Phase 3 VAT data from the Falutz and Stanley programs. Individual response varies, but the curve below reflects the trial-level average.

• Week 1–2 (initiation) — Daily injection routine establishes. Most patients feel no systemic change. Transient mild injection-site reactions (erythema, pruritus) are the most common early finding. IGF-1 begins to rise from baseline.
• Week 2–4 — IGF-1 rises toward its new plateau (~+80% of baseline). Some patients report mild peripheral fluid retention or transient arthralgia during this window — usually self-limited. Sleep quality improvements are variable.
• Week 4–8 — Early VAT reduction becomes measurable on imaging but not yet visually obvious. Waist circumference begins to decrease in responders. Triglycerides start declining.
• Week 12 (3 months) — Mid-protocol checkpoint. Labs (IGF-1, fasting glucose, HbA1c, lipid panel, CMP) should be reviewed. In responders, VAT reduction is typically 6–10% at this timepoint — detectable on CT/MRI but often still below waist-tape sensitivity.
• Week 26 (6 months) — the key decision point — The Falutz Phase 3 primary endpoint and the Stanley 2012 responder analysis both converge on this timepoint. Responders (≥8% VAT reduction) show paralleling improvements in triglycerides, adiponectin, and glucose homeostasis. Non-responders (<8% VAT reduction) typically show worsening glucose without compensating metabolic benefit; discontinuation is reasonable at this point. Mean VAT reduction in responders by week 26: 15–18%.
• Week 26–52 (extension phase) — In patients continued on tesamorelin, VAT reduction is maintained and often modestly deepens. Liver fat reduction becomes measurable (~30–40% relative reduction in Stanley 2019 Lancet HIV by 12 months). The Falutz 2008 AIDS extension and Stanley 2019 Lancet HIV trial both show the 26-week effects persist with continued dosing.
• Post-discontinuation (months 1–6 off) — VAT benefit reverses within ~6 months of stopping tesamorelin. This is a maintenance medication, not a curative one. Patients should understand this at initiation.
• Non-responders — Approximately 20–40% of patients fall into Stanley's non-responder category. Predictors of non-response include higher baseline fasting glucose, more severe insulin resistance, and less aggressive lifestyle adherence. Non-response does not mean "no IGF-1 rise" — IGF-1 rises similarly in responders and non-responders. The difference is in downstream VAT mobilization.
• If you feel worse — Persistent severe arthralgia, carpal-tunnel symptoms not resolving with dose reduction, fasting glucose drift toward diabetic range, any new persistent mass, severe injection-site reactions. Stop and consult your prescriber. Tesamorelin dose reduction (from 2 mg to 1 mg) often resolves tolerability issues while preserving meaningful effect.

Quick Compare — Tesamorelin vs CJC-1295 DAC vs Modified GRF (1-29) vs Sermorelin

All four are GHRH-class compounds binding the same pituitary GHRH receptor. The differences are structural protection strategy, half-life, development stage, and — most consequentially — evidence quality.

Practical interpretation:

• Evidence quality — Tesamorelin is the evidence-backed GHRH-class compound. CJC-1295's published human dataset is two small Phase 1 trials and one halted Phase 2. If evidence depth matters (and for chronic use, it should), tesamorelin is the defensible choice.
• Indication specificity — Tesamorelin is the only GHRH analog with a registered FDA indication (visceral adiposity in HIV-lipodystrophy). All off-label uses extrapolate. CJC-1295 forms are entirely off-label and gray-market.
• Half-life and cadence trade-off — Once-daily tesamorelin vs once-weekly CJC-1295 DAC is a convenience question. For protocols that prioritize mimicking native pulsatile biology, tesamorelin's shorter half-life is more physiologic; for protocols that prioritize sustained GHRH tone, CJC-1295 DAC provides it at the cost of slower wash-out.
• Cost vs access — Branded tesamorelin is expensive and narrowly indicated; CJC-1295 is inexpensive and broadly available from peptide vendors. Cost is a real-world driver of the choice despite the evidence asymmetry.
• Wash-out — Tesamorelin clears within hours; CJC-1295 DAC takes 3–4 weeks. Relevant for pregnancy planning, pre-operative considerations, and anti-doping wash-out.
• Stacking — All four are commonly paired with ipamorelin or another GHS. The GHRH + GHS synergy is the same regardless of which GHRH is chosen.

→ See full CJC-1295 profile  •  → See full Sermorelin profile

Bloodwork & Monitoring

Monitoring guidelines are clearer for tesamorelin than for any other peptide on this site because it is FDA-approved. The label specifies IGF-1 as the primary biomarker.

• IGF-1 (age-adjusted, expressed as SDS) — Baseline, at 3 months, then every 6 months. Dose reduction or discontinuation if SDS > 3 on two consecutive draws. IGF-1 is the primary safety and efficacy biomarker for this class.
• Fasting glucose + HbA1c — Baseline, at 3 months, then every 6 months. Critical for risk stratification — non-responders have meaningful glucose worsening.
• Comprehensive metabolic panel (CMP) — Baseline and every 6 months. Liver enzymes, renal function, electrolytes.
• Lipid panel — Baseline and 3–6 months. Expect triglyceride reduction in responders.
• Waist circumference + imaging (VAT indication) — Baseline and every 6 months. Waist circumference as proxy; CT or MRI for definitive VAT measurement at the 6-month decision point. If <8% VAT reduction at 6 months, consider discontinuation per Stanley 2012.
• Body composition / DEXA — Optional but useful for fat/lean mass ratio tracking.
• Liver ultrasound or MRI-PDFF (NAFLD use) — Baseline and every 6–12 months if used for NAFLD/MASH indication.
• Cancer screening — Age-appropriate colonoscopy, mammography, prostate labs, skin exam. Contraindicated in active malignancy; theoretical concern with chronic IGF-1 elevation in patients with occult neoplasia.
• Thyroid panel (TSH + free T4) — Baseline and periodic; GH-axis activation can unmask central hypothyroidism.
• Cardiovascular monitoring — BP and resting HR periodically; GH-axis activation is neutral-to-modestly favorable for lipids but fluid retention can raise BP transiently.

Practical User Notes

• Why tesamorelin vs other GHRH analogs — The single strongest argument for tesamorelin over CJC-1295 (either form) is evidence quality. Tesamorelin has registered Phase 3 data in ~800 patients, replicated independent academic trials for liver fat and cognition, a post-marketing safety record, and a monitored IGF-1 endpoint. CJC-1295 has two small Phase 1 trials. If access and cost permit, tesamorelin is the more defensible GHRH-class choice.
• The 6-month rule — Stanley et al. (2012) demonstrated that patients with ≥8% VAT reduction at 26 weeks are "responders" who gain metabolic benefit; patients below that threshold are "non-responders" whose glucose drifts worse without compensating improvement. This is a practical decision rule: if VAT hasn't responded by 6 months, the metabolic risk-benefit flips, and continuation is difficult to justify.
• Timing of injection — The FDA label does not specify time of day; consistency matters more than clock time. Some clinicians follow the Baker 2012 cognition protocol and dose 30 minutes before bed to leverage nocturnal GH biology. Others dose in the morning for convenience. No head-to-head timing data exists.
• Fasting considerations — Unlike the ipamorelin / GHS community practice, tesamorelin's label does not require fasting. The drug is daily and produces cumulative IGF-1 elevation independent of the single-dose GH pulse window. Practically, most patients inject whenever fits their schedule.
• Abdominal injection is standard — Label-directed. Rotate sites across the abdomen weekly. Avoid the navel area (2-inch radius) and any scarred, bruised, or inflamed skin.
• Water retention management — Mild ankle/hand fluid retention in the first 4–8 weeks is expected. Most patients accommodate; if it persists or produces new carpal-tunnel-type symptoms, dose reduction is appropriate. Adequate hydration and sodium moderation help — not a treatment, but a comfort measure.
• Diabetes screening before initiation — Because non-responders may have glucose worsening, baseline HbA1c should be normal. Active or poorly controlled T2D is not a formal contraindication but is a reason to reconsider or combine with a glucose-lowering therapy.
• IGF-1 targeting — Aim for age-adjusted upper-quartile, not above the normal range. Most responders settle around the 75th–90th percentile. Elevated SDS > 3 triggers dose reduction per label.
• Cost — Branded Egrifta SV / Egrifta WR is expensive and historically insurance-difficult outside of HIV-lipodystrophy indication. For off-label users without insurance coverage, compounded supply (where legally accessible) has been the practical workaround — but the compounding landscape has shifted repeatedly since 2024; verify legality before assuming availability.
• Discontinuation — No taper needed pharmacologically. Plan for VAT reversion within ~6 months of stopping. This is not a curative protocol; it is a maintenance therapy. Patients should understand this before starting.
• What tesamorelin does NOT do — It is not a general weight-loss drug (it does not reduce subcutaneous fat meaningfully). It does not replace lifestyle intervention. It does not normalize glucose in non-responders. It is not effective as a one-shot aesthetic intervention for patients without elevated visceral adiposity.
• Red flags to stop — Persistent severe headache, new visual changes, new-onset diabetes-range glucose, persistent joint swelling that doesn't resolve with dose reduction, any new unexplained mass, or signs of hypersensitivity. Any persistent new symptom warrants cessation first and medical evaluation second.

Commonly Stacked With

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Regulatory Status

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Next Steps

Key References

1. Falutz J, Allas S, Blot K, Potvin D, Kotler D, Somero M, 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.
2. Falutz J, Allas S, Mamputu JC, Potvin D, Kotler D, Somero M, et al. Long-term safety and effects of tesamorelin, a growth hormone-releasing factor analogue, in HIV patients with abdominal fat accumulation. AIDS. 2008;22(14):1719-1728. PMID: 18690162.
3. Falutz J, Mamputu JC, Potvin D, Moyle G, Soulban G, Loughrey H, 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 Acquir Immune Defic Syndr. 2010;53(3):311-322. PMID: 20101189.
4. Falutz J, Allas S, Kotler D, Thompson M, Koutkia P, Albu J, et al. A placebo-controlled, dose-ranging study of a growth hormone releasing factor in HIV-infected patients with abdominal fat accumulation. AIDS. 2005;19(12):1279-1287. PMID: 16052083.
5. Koutkia P, Canavan B, Breu J, Torriani M, Kissko J, Grinspoon S. Growth hormone-releasing hormone in HIV-infected men with lipodystrophy: a randomized, controlled trial. JAMA. 2004;292(2):210-218. PMID: 15249570.
6. Stanley TL, Falutz J, Marsolais C, Morin J, Soulban G, Mamputu JC, 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.
7. Stanley TL, Feldpausch MN, Oh J, Branch KL, Lee H, Torriani M, Grinspoon SK. 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.
8. Stanley TL, Fourman LT, Feldpausch MN, Purdy J, Zheng I, Pan CS, 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.
9. Fourman LT, Czerwonka N, Feldpausch MN, Weiss J, Mamputu JC, Falutz J, et al. Visceral fat reduction with tesamorelin is associated with improved liver enzymes in HIV. AIDS. 2017;31(16):2253-2259. PMID: 28832410.
10. Stanley TL, Falutz J, Mamputu JC, Soulban G, Potvin D, Grinspoon SK. Effects of tesamorelin on inflammatory markers in HIV patients with excess abdominal fat: relationship with visceral adipose reduction. Clin Infect Dis. 2011;53(11):1150-1158. PMID: 22016502.
11. Baker LD, Barsness SM, Borson S, Merriam GR, Friedman SD, Craft S, Vitiello MV. 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.
12. Dhillon S. Tesamorelin: a review of its use in the management of HIV-associated lipodystrophy. Drugs. 2011;71(8):1071-1091. PMID: 21668043.
13. Spooner LM, Olin JL. Tesamorelin: a growth hormone-releasing factor analog for HIV-associated lipodystrophy. Ann Pharmacother. 2012;46(2):240-247. PMID: 22252983.
14. Bedimo R. Growth hormone and tesamorelin in the management of HIV-associated lipodystrophy. HIV AIDS (Auckl). 2011;3:69-79. PMID: 22096408.
15. Memdouh S, Cowan DA, Walker C, Board K, Kicman AT, Parkin MC. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Test Anal. 2021;13(11-12):1871-1884. doi: 10.1002/dta.3183.
16. U.S. Food and Drug Administration. Egrifta (tesamorelin for injection) Prescribing Information. Initial U.S. Approval: 2010. Latest revision 2024.
17. Theratechnologies Inc. Egrifta SV and Egrifta WR product information. theratech.com.
18. ClinicalTrials.gov. NCT00123253, NCT00435136 (Phase 3 registration); NCT01263717 (JAMA liver fat); NCT02196831 (Lancet HIV NAFLD); NCT00675506 (Arch Neurol cognition).
19. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Tesamorelin. National Institute of Diabetes and Digestive and Kidney Diseases. NBK548730.
20. World Anti-Doping Agency. The 2026 Prohibited List. Section S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics. wada-ama.org.