Tesamorelin
TH9507 · Egrifta · Egrifta SV · trans-3-hexenoyl-GHRH(1-44)
Last updated
At a glance
Overview
Why Tesamorelin Earned Its Niche#
Tesamorelin is the one peptide with human clinical trial data showing it actually reduces visceral fat — not theoretically, not in rats, but measured by MRI in multi-center phase 3 trials. A stabilized 44-amino-acid GHRH analog, it drives pulsatile endogenous GH release from the pituitary and preferentially mobilizes visceral adipose tissue (VAT) and liver fat while leaving subcutaneous fat largely alone. That specificity is why it occupies a slot nothing else really fills.
In the bodybuilding and looksmaxxing community, tesamorelin has become the go-to tool for two very specific jobs: reducing the distended "GH gut" seen in long-term AAS/HGH/insulin users, and cutting hepatic fat in guys with stubborn NAFLD markers. It's not a hypertrophy driver and not a strength compound — it's a recomposition and metabolic-health peptide that happens to sit on the GH axis.
"After 26 weeks, patients who received tesamorelin had a greater reduction in visceral adipose tissue than those who received placebo (−15.2% vs. 5.0%; P<0.001), with no significant loss of subcutaneous adipose tissue." — Falutz et al., NEJM (2007)
The rest of this page covers what tesamorelin actually does mechanistically, how to dose it (1–2 mg SC daily, why 2 mg is the practical ceiling, AM fasted vs. pre-bed timing), how it stacks — particularly with ipamorelin for GHRH+GHRP synergy — what to expect on a 20–26 week VAT protocol, the glucose and IGF-1 monitoring cadence that keeps you out of trouble, and how it compares to running exogenous HGH directly.
How Tesamorelin works
GHRH Receptor Binding and Pulsatile GH Release#
Tesamorelin is a stabilized 44-amino-acid analog of endogenous growth hormone-releasing hormone (GHRH). The N-terminal trans-3-hexenoic acid modification protects the peptide from DPP-IV cleavage, extending its plasma half-life from ~7 minutes (native GHRH) to roughly 26–38 minutes — long enough to drive a meaningful GH pulse from a single SubQ shot.
Once in circulation, it binds the GHRH receptor (GHRH-R) on anterior pituitary somatotrophs — a Gs-coupled GPCR. Activation raises intracellular cAMP, triggering release of stored GH in a pulsatile, physiological pattern that mimics the body's own nocturnal surges. This is the critical distinction from exogenous rhGH: tesamorelin works upstream of the pituitary, so GH release remains pulsatile and subject to normal somatostatin negative feedback. That's why IGF-1 typically rises into the upper-normal range rather than the supra-physiological levels seen with pharmacological HGH dosing — and why tesamorelin carries less of the water retention, carpal tunnel, and insulin resistance burden of higher-dose rhGH.
"Following a single subcutaneous dose, Tmax was achieved within 10–15 min and the terminal half-life ranged from 26 to 38 min in animal models, supporting once-daily human dosing." — Ferdinandi ES, Brazeau P, High K, et al., Basic & Clinical Pharmacology & Toxicology (2007)
Downstream IGF-1 Elevation and Lipolysis#
The GH pulse triggers hepatic IGF-1 production, which plateaus after ~2 weeks of daily dosing. But the body-composition effects of tesamorelin are driven primarily by GH itself, not IGF-1. GH directly activates hormone-sensitive lipase (HSL) in adipocytes and suppresses lipoprotein lipase activity, producing potent lipolysis — especially in visceral depots, which are more GH-responsive than subcutaneous fat due to higher GH receptor density.
This is why the signature effect is preferential visceral fat reduction with relative sparing of subcutaneous fat, and why the waist-to-hip ratio shifts favorably even when total weight loss is modest.
"After 26 weeks, patients who received tesamorelin had a greater reduction in visceral adipose tissue than those who received placebo (−15.2% vs. 5.0%; P<0.001), with no significant loss of subcutaneous adipose tissue." — Falutz J, Allas S, Blot K, et al., New England Journal of Medicine (2007)
Hepatic Fat Mobilization#
Tesamorelin's effect on the liver is one of the most clinically validated uses of any GH-axis peptide. GH pulses mobilize intrahepatic triglycerides by stimulating hepatic lipid oxidation and reducing de novo lipogenesis. In NAFLD trials, 12 months of tesamorelin produced a meaningful reduction in liver fat fraction with a substantial minority of patients achieving outright resolution of fatty liver.
"Tesamorelin led to a 37% relative reduction in liver fat fraction compared with placebo after 12 months (p=0.02), with 35% of tesamorelin-treated patients achieving resolution of NAFLD." — Stanley TL, Fourman LT, Feldpausch MN, et al., The Lancet HIV (2019)
For users running years of heavy orals, insulin, and HGH — the classic "GH gut" population — this is the mechanistic basis for adding tesamorelin to a cleanup protocol.
Metabolic Profile Shift#
Beyond raw fat loss, the GH pulse drives a favorable shift in circulating lipids and adipokines. Visceral fat is metabolically active tissue that secretes pro-inflammatory cytokines and suppresses adiponectin; reducing it produces knock-on improvements independent of weight change.
"VAT responders to tesamorelin exhibited significant improvements in triglyceride levels, adiponectin, and HDL cholesterol, demonstrating a beneficial shift in metabolic profile with treatment." — Stanley TL, Falutz J, Mamputu JC, et al., Clinical Infectious Diseases (2012)
The trade-off — and it's real — is that GH is counter-regulatory to insulin. Expect fasting glucose to rise modestly during a cycle. This is the main reason to cap dosing at 2 mg/day and monitor HbA1c at week 12.
"Improvements in visceral adipose tissue and triglyceride concentrations were observed, although glucose homeostasis was modestly impaired, with a mean increase in fasting glucose of 0.30 mmol/L at week 26." — Falutz J, Mamputu JC, Potvin D, et al., JAIDS (2010)
Preserved Pulsatility and Timing#
Because tesamorelin relies on endogenous somatotroph output, postprandial somatostatin and elevated free fatty acids blunt the GH response. This is why experienced users inject AM fasted or pre-bed on an empty stomach — the same rule that applies to every GHRH analog. Eating a meal 30 minutes after the shot measurably reduces the downstream GH pulse.
Pre-bed dosing stacks the tesamorelin-driven pulse on top of the natural slow-wave sleep GH surge, amplifying total nightly GH exposure. AM fasted dosing is the cleaner slot for users who do fasted cardio or want the lipolytic window to overlap with morning training. Both work; select the slot that fits the individual's schedule and avoid eating within the 30-minute window after injection.
Protocol
| Level | Dose | Frequency | Notes |
|---|---|---|---|
| Low | 1–1.4 mg | Once daily | Documented entry-level range |
| Mid | 1.4–2 mg | Once daily | Most commonly studied range |
| High | 2–2 mg | Once daily | SubQ injection into the abdomen, AM fasted or pre-bed. Postprandial FFA and somatostatin blunt the GH pulse — inject on an empty stomach. Higher doses above 2 mg/day are not supported by evidence and worsen glucose and IGF-1 without adding VAT loss. |
Cycle length & outcomes
Documented cycle
12–26 weeks
Plateau after
26 wks
Cycle Length & Structure#
Tesamorelin is a slow-burn recomposition tool, not a blast compound. The clinical trials that established its VAT and liver-fat effects ran for 26 weeks minimum, and MRI-measurable visceral-fat loss doesn't meaningfully show up until around week 12. Running a 4- or 6-week "trial" of tesamorelin is a waste of vials — the pharmacology rewards patience.
"After 26 weeks, patients who received tesamorelin had a greater reduction in visceral adipose tissue than those who received placebo (−15.2% vs. 5.0%; P<0.001), with no significant loss of subcutaneous adipose tissue." — Falutz et al., NEJM (2007)
No loading phase is required. No taper is required on cessation — tesamorelin works upstream at the pituitary and doesn't suppress the HPG axis or create rebound endocrine issues. What does happen on discontinuation is that VAT gradually creeps back toward baseline over ~6 months unless diet and training hold the line.
Dose Ladder by Goal#
| Goal | Cycle Length | Daily Dose |
|---|---|---|
| Beginner / tolerance assessment | 8–12 weeks | 1 mg SC AM fasted |
| Visceral fat reduction (flagship protocol) | 20–26 weeks | 2 mg SC AM fasted |
| NAFLD / hepatic fat reduction | 26–52 weeks | 2 mg SC daily |
| GH-gut reversal (ex-heavy AAS/slin users) | 16–20 weeks | 1.4–2 mg SC daily |
| Recomp + sleep / recovery (w/ ipamorelin) | 12–20 weeks | 1–2 mg SC + ipamorelin 200–300 mcg 2–3×/day |
| Longevity / maintenance | 12–16 weeks on, 8–12 off | 1 mg SC daily (or 5-on / 2-off) |
Doses above 2 mg/day are not supported by the evidence and worsen glucose and IGF-1 without adding VAT loss — the dose-response curve plateaus hard at 2 mg.
Onset & Expected Timeline#
- Weeks 1–2: IGF-1 rises and plateaus. Subjective effects are minimal — maybe deeper sleep, some water retention, occasional injection-site redness.
- Weeks 3–6: Water retention / mild edema / joint achiness peaks and usually settles. Some users notice improved skin quality and fasted training feel.
- Weeks 8–12: First measurable waist-circumference changes. Lipid panel starts shifting favorably.
- Weeks 13–26: The main event — 15–18% VAT reduction on imaging, 2–3 cm off the waist, meaningful hepatic fat reduction.
"Tesamorelin led to a 37% relative reduction in liver fat fraction compared with placebo after 12 months (p=0·02), with 35% of tesamorelin-treated patients achieving resolution of NAFLD." — Stanley et al., Lancet HIV (2019)
Bloodwork Cadence#
This is non-negotiable if you're running the full 2 mg protocol:
| Timing | Panel |
|---|---|
| Baseline | Fasting glucose, HbA1c, IGF-1, full lipid panel, waist circumference (DEXA/MRI if available) |
| Week 12 | Repeat fasting glucose, HbA1c, IGF-1 |
| End of cycle | Full repeat + anthropometrics |
Action thresholds:
- IGF-1 > 2× upper limit of normal → reduce dose to 1 mg or pause
- HbA1c rise > 0.4 → reduce dose, tighten carb timing, reassess at 4 weeks
- Fasting glucose drift of 10+ mg/dL → same
"Improvements in visceral adipose tissue and triglyceride concentrations were observed, although glucose homeostasis was modestly impaired, with a mean increase in fasting glucose of 0.30 mmol/L at week 26." — Falutz et al., JAIDS (2010)
GH is diabetogenic by design — this isn't a surprise, it's a known tradeoff, and it's manageable with monitoring and sensible carb handling.
On/Off Cycling#
Tesamorelin doesn't require PCT, doesn't aromatize, doesn't suppress testosterone, and doesn't need a taper. The practical question is whether to cycle off at all — and the consensus answer is yes, run 20–26 weeks on, then 8–12 weeks off before restarting. The rationale isn't rebound (there isn't one); it's long-term IGF-1 exposure. Sustained upper-normal IGF-1 over years carries a theoretical malignancy-promotion risk, and giving the axis periodic breaks is cheap insurance.
Users running it for NAFLD reversal will sometimes push continuous 12-month blocks — that matches the clinical trial design and is defensible when the indication is hepatic rather than cosmetic.
Timing Within the Day#
Inject fasted — postprandial FFA and somatostatin blunt the GH pulse, so injecting right after a meal is essentially wasting the dose. Two good slots:
- AM fasted, ~30–60 min before first meal: clean, predictable, pairs with fasted cardio
- Pre-bed, ≥2 hours after last meal: amplifies the natural nocturnal GH pulse, which is the largest endogenous pulse of the day
Pick one and stay consistent — swapping slots daily makes bloodwork interpretation messier without any upside.
Run the full 20–26 weeks, hit the bloodwork checkpoints, and tesamorelin will do exactly what it was approved to do. It's one of the few peptides in this space with hard clinical-trial evidence behind the marketing.
Body Transformation Preview
Lean Mass Gain
0.8 lbs
0.6–1.0 lbs range
Fat Loss
4.1 lbs
3.1–5.1 lbs range
Fat Loss by Week
Risks & mistakes
Common (most users)#
- Injection-site reactions (erythema, itching, induration): the most frequent complaint, affecting ~25% of users in trials. Rotate between abdominal quadrants daily, warm the reconstituted peptide to room temp before injecting, and use a fresh 29–31g insulin syringe. Usually fades after the first 2–3 weeks.
- Peripheral edema / puffiness (hands, ankles, face): classic GH-axis water retention. Typically settles by week 4–6 as the axis acclimates. If it doesn't, drop to 1–1.4 mg/day.
- Arthralgia and myalgia (joints, fingers, wrists): dose-dependent, usually mild. Hydration and magnesium help; persistent pain is a signal to reduce dose.
- Transient paresthesias / numbness or tingling in hands: early-cycle, tied to fluid shifts. Resolves on its own or with a dose reduction. Persistent symptoms pointing to carpal-tunnel–type compression warrant backing off.
- Vivid dreams / altered sleep architecture with pre-bed dosing: common with any GH-axis stimulator. Move the injection to AM fasted if it bothers you — efficacy is similar.
- Mild IGF-1 elevation into upper-normal range: expected and desired. Only a problem if it blows past the reference range — check at week 12.
Uncommon (dose-dependent or individual)#
- Elevated fasting glucose (+3 to +10 mg/dL) and HbA1c creep: GH is diabetogenic. Most users stay within reference range; pre-diabetics and users on heavy carb intakes drift higher.
"Improvements in visceral adipose tissue and triglyceride concentrations were observed, although glucose homeostasis was modestly impaired, with a mean increase in fasting glucose of 0.30 mmol/L at week 26." — Falutz et al., JAIDS 2010
Check fasting glucose and HbA1c at baseline and week 12. Hold or reduce if HbA1c rises >0.4 points. Running metformin 500–1000 mg/day is the common community answer for users who want to stay on through a borderline result.
- IGF-1 above 2× ULN: back the dose down to 1 mg/day or pause for 2–4 weeks and retest. Sustained supra-physiological IGF-1 is the mechanistic basis for most of tesamorelin's long-term theoretical risks.
- Carpal tunnel symptoms: night-time numbness, grip weakness. Reduce dose; if it doesn't resolve within 1–2 weeks, come off.
- Worsened lipid picture in non-responders: VAT responders improve lipids; non-responders sometimes don't. Check a fasted lipid panel at week 12 and decide whether to continue based on VAT and triglyceride response, not time on cycle.
- Fatigue or lethargy in the first 1–2 weeks: usually a water-shift effect. Persistent fatigue plus no VAT response by week 12–16 means you're a non-responder — don't push the dose higher, stop.
Rare but serious#
- Symptomatic hyperglycemia / new-onset type 2 diabetes: rare but documented in users with pre-existing insulin resistance. Warning signs: polyuria, polydipsia, fasting glucose >126 mg/dL on two readings. Stop immediately and work up the metabolic panel.
- Severe hypersensitivity reactions to the peptide or mannitol excipient: rash, urticaria, angioedema. Stop and do not re-challenge.
- Acute pancreatitis (case reports on the GH axis generally, not tesamorelin-specific): severe epigastric pain radiating to the back, nausea, vomiting. Emergency evaluation.
- Pituitary / malignancy signal: any new visual disturbance, persistent headache, or unexplained mass warrants stopping and imaging. GH/IGF-1 stimulation is theoretically pro-tumorigenic — don't ignore red flags.
- Fluid retention severe enough to worsen heart failure or uncontrolled hypertension: not a general-population issue but relevant for lifters already running heavy orals with BP in the 140s+. Get BP controlled before starting.
Hard contraindications#
- Active malignancy or history of cancer under surveillance — GH/IGF-1 axis stimulation is off the table.
- Pituitary tumor, prior pituitary surgery, head irradiation, or hypopituitarism — the axis is broken or dysregulated; tesamorelin is either useless or unsafe.
- Pregnancy (Category X) and active attempts at conception in women — do not run it. No adequate human data; fetal risk cannot be excluded.
- Uncontrolled type 2 diabetes or HbA1c >7.5% — get glycemic control first, then revisit.
- Known hypersensitivity to mannitol (the excipient in clinical formulations and most research-grade lyo powders).
- Stacking tesamorelin on top of full-dose exogenous HGH (4+ IU/day) — mechanistically redundant and worsens IGF-1 and insulin resistance without proportional VAT benefit. Pick one.
Gender-specific and PCT considerations#
Tesamorelin is non-hormonal with respect to sex steroids — no aromatization, no HPG-axis suppression, no androgen receptor activity. Women can run the same 1–2 mg/day dose as men with the same side-effect profile, and it's one of the few peptides without sex-specific dosing concerns. Pregnancy and attempted conception are absolute contraindications (Category X); women of reproductive age should be on reliable contraception through the cycle and for at least 2 weeks after discontinuation (the peptide clears in hours but IGF-1 elevation lingers for weeks).
No PCT required. You can stop cold — there's nothing to restart. The trade-off is that the VAT benefit is not permanent: discontinuation without dietary and training follow-through leads to VAT rebound toward baseline within ~6 months. Plan the next phase before you pin the last dose.
Stack & combine
Multipliers applied when these compounds run together. Values > 1 indicate a bonus on that axis. Tap a partner to expand the mechanism.
| Partner | Type | Lean | Fat loss | Recovery |
|---|---|---|---|---|
| synergistic | ×1.15 | ×1.22 | ×1.25 | |
| synergistic | ×1.12 | ×1.23 | ×1.10 | |
| synergistic | ×1.10 | ×1.08 | ×1.22 | |
| synergistic | ×1.15 | ×1.22 | ×1.07 | |
| synergistic | ×1.15 | ×1.22 | ×1.05 | |
| synergistic | ×1.15 | ×1.20 | ×1.10 | |
| synergistic | ×1.08 | ×1.20 | ×1.12 | |
| synergistic | ×1.05 | ×1.18 | ×1.10 | |
| synergistic | ×1.13 | ×1.18 | ×1.14 | |
| synergistic | ×1.10 | ×1.18 | ×1.10 | |
| additive | ×1.00 | ×1.08 | ×1.00 |
Featured in stacks1 curated protocol include Tesamorelin
FAQ — Tesamorelin
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Research & citations
5 studies cited on this page.
Conclusion
Tesamorelin is the go-to GHRH analog for targeted visceral fat reduction and NAFLD — especially when you want the VAT loss and IGF-1 elevation of growth hormone, but prefer a pulsatile, endogenous axis approach over exogenous HGH.
Key takeaways:
- Standard dose: 1.4–2 mg/day SubQ, once daily, AM fasted or pre-bed for best GH response
- Cycle length: 12–26 weeks — VAT loss is slow and requires commitment; short cycles rarely deliver visible results
- Stacks well with ipamorelin (GHRH + GHRP synergy) for stronger GH pulses and enhanced recomp
- Routine bloodwork: monitor IGF-1, glucose, and HbA1c before and during the cycle
- Headline benefit: 15–18% reduction in visceral fat, significant liver-fat loss, modest lean-mass preservation (Falutz 2007; Stanley 2019)
- Side effects are mostly injection site reactions and mild water retention; mitigate by rotating sites and managing dose
For a clinically-backed method to reduce visceral fat, tighten the waistline, or reverse early fatty liver, tesamorelin is among the most targeted and well-characterized tools in the peptide arsenal.