Tesamorelin
Stabilized GHRH analog · FDA-approved for HIV-associated visceral fat
Tesamorelin is a stabilized synthetic analog of growth-hormone-releasing hormone (GHRH) and, unusually for a research peptide, an FDA-approved drug: marketed as Egrifta, it is approved for the reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. Rather than supplying growth hormone directly, it stimulates the pituitary to make and release the body's own GH in its natural pulsatile pattern, which raises IGF-1 and selectively reduces visceral adipose tissue. In its pivotal Phase III trial, a daily subcutaneous dose cut visceral fat by about 15% and raised IGF-1 by roughly 80% over 26 weeks. The benefit depends on continued use — it reverses toward baseline within a few months of stopping. Tesamorelin is approved only for HIV-associated lipodystrophy (not for general fat loss, fatty liver, or anti-aging), and it is prohibited in sport at all times (WADA).
The short version
Tesamorelin is a lab-made copy of GHRH — the natural hormone that tells the pituitary gland to release growth hormone — modified so it survives longer than the natural version.
It is one of the few peptides in this catalog that is an actual approved medicine. The FDA approved it (brand name Egrifta) to reduce the deep abdominal fat that can build up in people with HIV. Instead of injecting growth hormone, it nudges the body to make more of its own — keeping the natural rhythm intact — which in turn lowers visceral belly fat.
In its main clinical trial, a daily injection reduced visceral fat by about 15% over six months. The catch: the effect is not permanent — when people stop, the fat comes back over the next few months, so it only works while you keep taking it.
It is approved only for HIV-associated fat accumulation — not for general weight loss, fatty liver, or anti-aging — and it is banned in competitive sport.
Molecular identity
Specs
- Molecular weight
- 5,135.9 g/mol
- Molecular formula
- C221H366N72O67S
- Monoisotopic mass
- 5,132.72 Da
- CAS / UNII
- 218949-48-5 · MQG94M5EEO
- Structure / class
- Synthetic GHRH (GRF 1-44) analog; N-terminal trans-3-hexenoyl groupPubChem CID 16137828
- Brand / approval
- Egrifta / Egrifta SV / Egrifta WR — FDA-approved (HIV lipodystrophy)FDA label (Egrifta SV)
- Molecular target
- GHRH receptor (GHRHR) on pituitary somatotrophsPMID 18057338
- Regulatory status
- FDA-approved (HIV lipodystrophy) · WADA S2 prohibitedFDA / WADA
Plain English
Mechanism
Tesamorelin binds and activates the GHRH receptor (the docking site for growth-hormone-releasing hormone) on the somatotroph cells (the growth-hormone-making cells) of the anterior pituitary — the front part of the hormone gland at the base of the brain. This stimulates both the synthesis and the pulsatile release (the natural come-and-go bursts) of the body's own growth hormone. The increased growth hormone in turn raises insulin-like growth factor 1 (IGF-1, the growth-hormone messenger that carries out most of its effects), and the net downstream effect is a selective reduction of visceral adipose tissue (the deep fat packed around the abdominal organs, which is more metabolically active than fat just under the skin).
The defining design point is that tesamorelin raises endogenous growth hormone (the body's own) rather than replacing it with exogenous hormone (an injected outside supply), so the body's natural feedback control and pulsatile rhythm remain in the loop. Structurally it is an analog (a close copy) of human GHRH (GRF 1-44) carrying an N-terminal trans-3-hexenoyl group (a small fatty tag added to one end of the chain); this modification is understood to stabilize the molecule against rapid enzymatic breakdown (being chopped up by the body's enzymes). The stabilization mechanism is described in secondary literature, while the GRF(1-44) analog identity and the hexenoyl modification are confirmed in the primary chemical record.
Why people reach for it
Potential benefits
Tesamorelin is the one GHRH analog in this catalog with a real FDA approval behind it — here's what draws people to it.
- Targets deep visceral belly fat — Its headline appeal and approved use: in its pivotal Phase III trial a daily dose cut visceral abdominal fat by about 15% over 26 weeks — the deep, metabolically active fat around the organs, not just fat under the skin.
- Raise your own growth hormone, not inject it — It signals the pituitary to make and release the body's own GH in its natural pulsatile rhythm, which then raises IGF-1 — keeping the body's feedback control in the loop rather than overriding it.
- Backed by real human trial data — Unusually for a research peptide, it is FDA-approved (brand Egrifta) with two pivotal Phase III trials — the efficacy and safety figures come from human studies, not rodent extrapolation.
- Body-composition and recomposition support — The visceral-fat reduction plus an ~80% IGF-1 rise is what people reach for it for off-label — fat loss alongside lean-tissue support, where IGF-1 drives protein synthesis.
- The canonical bedtime partner for a GHRP — It pairs with a ghrelin-receptor peptide for a bigger combined pulse than either alone — most commonly Ipamorelin, the GHRH arm plus the selective GHRP arm.
Sources:FDA labelPMID 18057338PMID 20101189
What people reach for Tesamorelin for, drawn from its FDA-approved use (HIV-associated visceral fat) and how it's used off-label — not proven outcomes for unapproved uses or medical claims.
Implied timing
Best time to dose
Implied best time
Bedtime (empty stomach)
Most people inject Tesamorelin at bedtime on an empty stomach, ~2–3 hours after the last meal.
- Tesamorelin amplifies the body's own GH release, and the single largest natural GH pulse fires in early slow-wave (deep) sleep — a bedtime dose stacks the peptide's signal on top of that nocturnal surge rather than fighting it.
- Food is the reason for the empty stomach: both insulin (raised after eating) and somatostatin (GH's off-switch) blunt the pulse, so the dose goes ~2–3 hours clear of the last meal. Its existing dosing protocol already foregrounds this empty-stomach bedtime rule.
- Its half-life is very short (~8 min per the FDA label, peaking around 9 min), so the active signal is over quickly — which is also why resuming food after the injection is fine.
- This is reasoned from mechanism and convention; the registration trials simply specified a daily subcutaneous dose, not a fixed clock time.
No study establishes an ideal time of day for Tesamorelin — this is reasoned from its GHRH mechanism and how it's used. As a rule of thumb peptide dosing lands in the midday-to-evening window; for Tesamorelin the lean is bedtime, fasted.
Sources:FDA label
How to run it
Dosing & protocol
Tesamorelin is unique in this catalog: it has a real FDA label with human-trial doses, not just community extrapolation. The numbers below are anchored to the pivotal Phase III trials and the approved label (2 mg/day), with the honest caveat that those trials were specifically in HIV lipodystrophy — off-label body-composition use is community convention, not a studied indication. The critical timing insight for any GH-secretagogue, foregrounded here: inject at bedtime on an empty stomach.
FDA-approved only for HIV-associated lipodystrophy; off-label use for body composition and anti-aging is community and practitioner convention, not a studied indication. WADA S2 — prohibited at all times in sport.
Tiered dose ranges
The anchor dose is the Phase III trial and original Egrifta approval dose. Current branded products are reformulated bioequivalents.
- Approved / trial dose:
- 2 mg once daily SC — the dose used in both pivotal Phase III trials (visceral fat −15%, IGF-1 +81% over 26 weeks). This is the anchor for every efficacy figure on this page.
- Current branded formulations:
- Egrifta SV 1.4 mg/day and Egrifta WR 1.28 mg/day are reformulated bioequivalents of the 2 mg dose — not a clinical dose reduction. Community off-label use typically mirrors the original 2 mg or Egrifta SV's 1.4 mg.
- Conservative off-label start:
- 1 mg once daily — some practitioners start lower when the goal is body composition rather than lipodystrophy, to assess tolerance and glucose response before escalating.
Subcutaneous administration
The single most important timing decision for any GH-secretagogue: bedtime on an empty stomach.
- Time of day — the key insight:
- Inject at bedtime, approximately 2–3 hours after the last meal. Both insulin (elevated after eating) and somatostatin (the brain's own GH-off switch, also raised by food-driven signaling) blunt the GH pulse. An empty-stomach bedtime injection rides the body's natural nocturnal GH surge rather than fighting two brakes simultaneously.
- Food window:
- Do not eat for 2–3 hours before injection. Resuming food after is fine — the ~8-minute half-life means the active signal is already complete by the time a post-injection snack would raise insulin.
- Injection site:
- Abdomen (2–3 cm / ~1 inch from the navel), the love-handle area, or the outer thigh. Rotate sites at every injection — using one spot repeatedly causes local irritation and lipohypertrophy (fatty nodules under the skin).
- Measuring the dose:
- Drawn on a U-100 insulin syringe from the reconstituted vial. With the standard 10 mg vial + 2 mL BAC water mix (5,000 mcg/mL), 1,400 mcg = 28 IU; 2,000 mcg = 40 IU. The on-page calculator converts any vial size live.
Cycle & washout
Tesamorelin's approved clinical use is continuous — but off-label body-composition protocols typically cycle it.
- Standard cycle:
- 8–16 weeks of daily use. The Phase III data shows meaningful visceral-fat change by 26 weeks; community recomp cycles often run 12 weeks and then assess.
- Washout:
- 4–8 weeks off. IGF-1 and fasting glucose should both be checked during the washout — IGF-1 should normalize (persistent elevation is a reason to extend the break); glucose should return to personal baseline.
- Continuous use caveat:
- The Phase III extension data showed fat returns ~3 months after stopping — which is why the approved indication uses it continuously. Off-label cycles accept that trade-off and re-run as needed.
- Monitor:
- Fasting glucose + HbA1c before the cycle and at 8 weeks — the drug label flags ~5% glucose-intolerance incidence (vs 1% on placebo). IGF-1 at baseline + midpoint; consider dose reduction for persistent upper-range or above-range IGF-1.
Reconstitution at a glance
The on-page calculator does this live; the quick reference for the 10 mg vial + 2 mL BAC water default:
- Mixing:
- 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a U-100 (100-unit / 1 mL) insulin syringe: 1,000 mcg (1 mg) = 20 IU · 1,400 mcg = 28 IU · 2,000 mcg (2 mg) = 40 IU.
Substrate the signal needs
Nutritional cofactor precision
Tesamorelin raises GH by activating the GHRH receptor — but the GH pulse is shaped by two brakes (somatostatin and insulin) and has one well-documented side effect (transient blood-sugar elevation). The cofactors below address exactly those three levers: relieve the brakes, offset the glucose cost, supply the substrate for what GH then builds.
Reasoned from GH-axis physiology and the tesamorelin label's documented glucose effect — not a tesamorelin cofactor trial. Supplement doses are community convention, not tesamorelin-specific findings.
Amplify the pulse — relieve the somatostatin brake
Somatostatin is GH's principal off-switch. Supporting choline and nitric-oxide pathways takes pressure off that brake so the GHRH signal lands harder.
- Alpha-GPC (choline precursor):
- 300–600 mg taken ~30–60 minutes before the tesamorelin injection. Choline supports acetylcholine signaling, which is linked to somatostatin inhibition in animal studies — the working hypothesis is that a choline-replete brain generates a cleaner GH pulse. Time it earlier in the evening so it doesn't compete with sleep onset.
- L-Arginine:
- 3–6 g on an empty stomach ~30 min before injection. L-arginine stimulates GH release partly by suppressing somatostatin; it is one of the oldest and best-characterized GH cofactors in the literature. Best taken as a standalone evening supplement rather than with a protein meal (competing amino acids blunt the arginine effect).
Mitigate the cost — offset the glucose liability
Growth hormone transiently raises blood sugar (the tesamorelin label records ~5% glucose-intolerance incidence). These are the practical tools for running the GH signal without letting blood sugar creep.
- Berberine:
- 500 mg with each main meal (1,500 mg/day total). Berberine activates AMPK (the cell's fuel sensor), improving insulin sensitivity and lowering post-meal glucose — the same mechanism as metformin but food-derived. It is the most direct dietary tool for offsetting the GH-induced glucose effect. Space it away from supplements you want to absorb well (berberine inhibits some intestinal transporters).
- Alpha-lipoic acid (ALA):
- 600 mg once daily with a meal. ALA is a mitochondrial cofactor and glucose-disposal agent; it improves insulin-mediated glucose uptake and has antioxidant effects in vascular tissue. Pairs well with berberine — they act on overlapping but not identical insulin-signaling steps.
- Monitoring note:
- Fasting glucose + HbA1c before starting and at 8 weeks — the drug label flags this specifically. Berberine + ALA are nutritional cushions, not substitutes for monitoring. If fasting glucose rises meaningfully from personal baseline, reassess the cycle.
Supply the substrate — feed the lean tissue GH builds
Tesamorelin raises IGF-1, which drives protein synthesis and tissue repair. These are the raw materials that determine how much of that anabolic signal converts to actual lean mass.
- Protein intake:
- 1.6–2.0 g per kilogram of body weight per day (0.73–0.91 g/lb). IGF-1 is a potent anabolic signal but it needs amino acids to build with. A high-protein diet is the single highest-leverage nutritional decision on a GH-secretagogue cycle — it determines whether the raised IGF-1 actually builds lean tissue rather than just transiently elevating a blood marker.
- ZMA before bed:
- Zinc 30 mg + magnesium glycinate 450 mg + B6 10.5 mg, taken ~30–60 min before the tesamorelin injection. Zinc is essential for IGF-1 signaling at the receptor level; magnesium supports slow-wave (deep) sleep, which is when the largest natural GH pulse occurs and where tesamorelin's bedtime timing stacks best. Take on an empty stomach — both minerals absorb poorly alongside food.
- Vitamin D:
- 2,000–5,000 IU daily, dosed to a serum 25(OH)D in the 50–80 ng/mL range. Vitamin D receptors are present on muscle and bone tissue; GH and IGF-1 work better when the vitamin-D axis is replete. Simple background maintenance — just make sure it's not a gap.
Combinations + timing
Stacking notes + timing windows
Tesamorelin drives the GHRH arm of the growth-hormone axis — it signals the pituitary via the GHRH receptor. The most powerful complementary partners hit the same GH-secreting cells via a completely different receptor (the ghrelin/GHS receptor), so both arms fire together for a bigger pulse than either alone. Pairing with another GHRH analog (sermorelin, CJC-1295) is redundant — it presses the same receptor twice — and that is explicitly noted below.
All tesamorelin clinical evidence is as monotherapy (the approved indication). Stack combinations are reasoned from receptor biology — complementary pathways, not the same lever twice. No head-to-head trials of any tesamorelin stack exist. Doses for stack partners are community convention.
Tesamorelin + Ipamorelin
The canonical GH-secretagogue stack. Tesamorelin drives the GHRH arm; Ipamorelin adds the ghrelin-receptor arm — two different receptors, one bigger pulse.
- Why it works:
- GH release is naturally triggered by two simultaneous signals: GHRH (from the hypothalamus, mimicked by tesamorelin) and ghrelin (from the stomach/hypothalamus, mimicked by ipamorelin at the GHS-R1a receptor). Tesamorelin alone fires one receptor; the combination recreates the physiological dual-signal the body uses for its largest pulses. Ipamorelin is chosen as the GHRP because it is highly GH-selective — it does not meaningfully raise cortisol or prolactin, unlike GHRP-2 or GHRP-6.
- The protocol:
- Tesamorelin 1–2 mg SC + ipamorelin 200–300 mcg SC, co-injected at bedtime on an empty stomach. Both are drawn into the same syringe (they are compatible in solution) or injected as two nearby subcutaneous pricks, rotated daily.
- Outcome:
- The combination users reach for when the goal is body composition — fat loss with lean-tissue preservation — or general GH optimization. The combined GH pulse is larger than either alone; monitor IGF-1 at 8 weeks and dial back if it trends above the upper normal range.
Tesamorelin + GHK-Cu
A recomposition + tissue-repair layer. Tesamorelin handles the metabolic side (visceral fat, IGF-1 elevation); GHK-Cu handles tissue remodeling and wound healing — different mechanisms, different targets.
- Why it works:
- GHK-Cu (copper peptide) upregulates collagen synthesis, activates TGF-β (the main tissue-remodeling signal), and has antioxidant-SOD-mimetic properties. It does not act on the GH/IGF-1 axis — it works directly at the tissue level. On a tesamorelin cycle, where IGF-1 is elevated and lean-tissue anabolism is running hot, adding GHK-Cu directs repair and remodeling to connective tissue and skin simultaneously. Different lever entirely.
- The protocol:
- Tesamorelin 1–2 mg SC at bedtime (as above) + GHK-Cu 1–2 mg SC once daily (typically mornings, separate injection). GHK-Cu timing is not rigidly meal-dependent — morning dosing keeps the two injections cleanly separated.
- Outcome:
- Commonly combined for recomposition cycles where the goal is fat loss + skin/connective-tissue quality alongside lean-mass preservation. Popular in anti-aging protocols where visceral fat, skin, and joint health are all on the agenda.
Do NOT stack: Tesamorelin + Sermorelin or CJC-1295
Both sermorelin and CJC-1295 are also GHRH analogs. Stacking them with tesamorelin is pressing the same receptor twice — redundant at best, potentially dysregulatory.
- Why it's redundant:
- Sermorelin and CJC-1295 bind the same GHRH receptor as tesamorelin. Adding a second GHRH-class molecule does not open a new signaling pathway — it competes for the same receptor. There is no complementary mechanism; the two signals overlap entirely. The result is not a bigger combined pulse — it is receptor competition and no net gain.
- What to do instead:
- If tesamorelin's GHRH arm isn't enough alone, add a GHRP (ipamorelin, GHRP-2) which hits the ghrelin receptor — the genuinely complementary pathway. That is the combination that recreates the body's natural dual-signal physiology.
Reconstitution math
Reconstitution calculator
Reconstitution calculator
Calculated for a 1 mL U-100 insulin syringe (100 units/mL).
Units per dose
28
Draw to this mark on a U-100 syringe
- Volume per dose
- 0.28 mL
- Doses per vial
- 7
- Concentration
- 5 mg/mL
One vial lasts
- Daily
- 7 days
- Every other day
- 14 days
- 5×/week
- 10 days
Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.
From the studies
Side effects from research
Tesamorelin's FDA label carries no boxed warning (the FDA's strongest safety alert). The most common adverse reactions (side effects seen in more than 5% of patients and more frequent than placebo) are arthralgia (joint pain), injection-site reactions (erythema and pruritus — redness and itching where the needle goes in; these occurred in about 25% on tesamorelin versus 14% on placebo), pain in the extremities (arms and legs), peripheral edema (fluid-swelling in the limbs), and myalgia (muscle aches). Hypersensitivity reactions (allergic-type responses) occurred in roughly 4% of trial participants.
The label's key precautions reflect the growth-hormone mechanism: it can raise IGF-1 (the growth-hormone messenger; monitor, and consider stopping for persistent elevation), can impair glucose tolerance (the body's ability to manage blood sugar — about 5% vs 1% on placebo developed glucose intolerance), and can cause fluid retention (edema, joint pain, and carpal tunnel syndrome — wrist-nerve compression from swelling). It is contraindicated (must not be used) with disruption of the hypothalamic-pituitary axis (the brain–hormone-gland control circuit), active malignancy (current cancer), known hypersensitivity (allergy) to tesamorelin or mannitol (a sugar-alcohol used as a filler in the product), and in pregnancy. The pregnancy contraindication is informed in part by rat reproductive-toxicity data (hydrocephaly — fluid buildup in the brain — in offspring at 2–4× the clinical dose, an animal finding). There is a class-level caution about increased mortality (death rate) in critically ill patients carried over from growth-hormone data.
Sources:FDA label
As reported in literature
Research dosing ranges
These are the doses actually used in the published human trials and on the FDA label — the evidence the practical guidance above rests on, shown separately so the trial data is never mistaken for a casual figure. Because tesamorelin is an approved drug, this table is human data, not rodent: the "2 mg daily" figure that dominates the literature is the ORIGINAL formulation used in both pivotal Phase III trials (the randomized human studies behind approval) and the first Egrifta approval. The currently marketed products deliver a lower nominal milligram amount — Egrifta SV 1.4 mg and Egrifta WR 1.28 mg — because of reformulation and bioequivalence (delivering the same active exposure) changes, not a clinical dose reduction. All efficacy figures below come from the 2 mg trials.
| Dose | Route | Model | Outcome | Sources: |
|---|---|---|---|---|
| 2 mg | SC daily | Human (pivotal Phase III, n=412) | Visceral fat −15.2% vs +5.0% placebo; IGF-1 +81% over 26 weeks | PMID 18057338 |
| 2 mg | SC daily | Human (Phase III + extension, n≈404) | Benefit reverses toward baseline ~3 months after discontinuation | PMID 20101189 |
| 1.4 mg / 1.28 mg | SC daily | Human (current FDA-approved Egrifta SV / WR) | Reformulated equivalents of the 2 mg trial dose | FDA label |
Labs before / during / after
Cofactor blood markers to track
The drug label defines the markers a clinician follows during tesamorelin treatment — these are label-directed monitoring points, not general wellness suggestions:
IGF-1 (the growth-hormone messenger) is monitored because tesamorelin works by raising growth hormone and IGF-1; the label advises watching for persistent elevations and considering discontinuation (stopping the drug) if they occur. Glucose status (fasting glucose and HbA1c — a blood marker of average blood sugar over the past few months) is followed because growth-hormone stimulation can impair glucose tolerance (the body's ability to keep blood sugar in check) — in the pivotal trials about 5% of treated patients developed glucose intolerance (a step toward higher blood sugar) versus 1% on placebo (the inactive comparison treatment).
Sources:FDA labelPMID 18057338
Quick answers
Frequently asked
What is tesamorelin approved for?
Its only FDA-approved indication is the reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. It is not approved for general weight loss, fatty-liver disease, anti-aging, or muscle building — those uses are off-label or investigational.
How is tesamorelin different from taking growth hormone?
It does not supply growth hormone directly. It is a GHRH analog that signals the pituitary to make and release the body's own growth hormone in its natural pulsatile rhythm, which then raises IGF-1. This keeps the body's normal feedback control in the loop rather than overriding it with an external hormone.
Why inject at bedtime on an empty stomach?
Two factors blunt the GH pulse: insulin (elevated after eating) and somatostatin (the hypothalamus's GH off-switch, also raised by food-driven signals). Injecting 2–3 hours after the last meal removes both brakes simultaneously, and bedtime timing places the injection immediately before the body's largest natural nocturnal GH surge — so tesamorelin rides that wave rather than fighting it.
What is tesamorelin's half-life?
About 8 minutes after subcutaneous injection, per the FDA label, with a peak around 9 minutes. The very short half-life is by design — a brief signal that triggers a pulse of growth-hormone release. A longer 26–38 minute figure circulates on peptide sites, but the label value of ~8 minutes is authoritative.
Does the effect last after you stop?
No. In the Phase III extension, patients switched from tesamorelin to placebo lost the visceral-fat benefit, with fat returning toward baseline within about three months. Maintaining the effect requires continued use.
Is the approved dose really 2 mg a day?
The 2 mg daily dose was the original formulation used in the pivotal trials and the first Egrifta approval. The currently marketed products are reformulated to deliver a lower nominal amount — Egrifta SV 1.4 mg and Egrifta WR 1.28 mg daily — which is a bioequivalence change, not a clinical dose reduction.
Is tesamorelin banned in sport?
Yes. WADA names tesamorelin explicitly among prohibited GHRH analogues (class S2), prohibited at all times — both in and out of competition. This page presents the drug label and research literature only and makes no therapeutic claims for non-approved uses.
Primary sources
References
- PubChem CID 16137828PubChem CID 16137828 (Tesamorelin)
- FDA labelFDA label / DailyMed — Egrifta SV (tesamorelin) prescribing information
- FDA labelFDA label — Egrifta WR (tesamorelin) 2025 prescribing information
- PMID 18057338Falutz et al., N Engl J Med 2007 (pivotal Phase III, VAT/IGF-1)
- PMID 20101189Falutz et al., J Acquir Immune Defic Syndr 2010 (Phase III + extension, discontinuation)
- NBK548730LiverTox (NIH) — Tesamorelin monograph (approval, mechanism, liver fat)
- WADAWADA Prohibited List (S2.2.4, GHRH analogues — tesamorelin named, prohibited at all times)
Research use only · Not medical advice · Updated 2026-06-01