Tesamorelin

Dosing from the Literature

Published for belly fat: the label doses for HIV-related belly fat. Not published: an approved dose for people without HIV.

Each dose below names its source: an FDA label, a published trial or, once, online bodybuilding protocols. Tesamorelin is prescription-only in the United States (EGRIFTA SV label).

What It Is

Tesamorelin is a synthetic analog of human growth-hormone-releasing hormone (hGHRH) consisting of the full native 44-amino-acid GHRH (the signal that tells the pituitary to release GH) sequence with a trans-3-hexenoic acid moiety conjugated to the α-amino group of the N-terminal tyrosine residue (EGRIFTA SV label; Baker et al., 2012). The added chain was designed to resist dipeptidyl peptidase-4 (DPP-4), the serum enzyme that rapidly breaks down native GHRH (Bedimo, 2011), and tesamorelin still binds and stimulates the human GHRH receptor with potency similar to the body's own GHRH in vitro (EGRIFTA SV label). 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 visceral-fat reductions of 15.2% and 10.9% at 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 healthy adults and 38 minutes in HIV-infected patients on the original product, 8–11 minutes after single doses of the current ones; original EGRIFTA, EGRIFTA SV and EGRIFTA WR labels), so the pharmacodynamic effect is pulsatile GH release rather than a sustained plateau.

Mechanism of Action

Tesamorelin acts on the pituitary's GHRH receptor, which it binds and stimulates in vitro with potency similar to the body's own GHRH (EGRIFTA SV label); its added chain protects it from breakdown (Bedimo, 2011). In the trials it caused no clinically significant change in other pituitary hormones such as TSH, LH, ACTH or prolactin (EGRIFTA SV label).

• GHRH receptor (pituitary somatotropes) — Tesamorelin carries the full 44-amino-acid sequence of human GHRH and, in vitro, binds and stimulates the human GHRH receptor with potency similar to the body's own GHRH. GHRH acts on the pituitary's somatotroph cells to stimulate the synthesis and pulsatile release of growth hormone (EGRIFTA SV label).
• DPP-4 resistance via N-terminal acylation — Native GHRH is rapidly broken down in the blood by the enzyme DPP-4; tesamorelin's added hydrophobic chain was designed to resist it (Bedimo, 2011). The chain is a trans-3-hexenoyl group on the N-terminal tyrosine (Baker et al., 2012), and receptor potency stays similar to native GHRH in vitro (EGRIFTA SV label). Its elimination half-life after injection under the skin was 26 minutes in healthy adults and 38 minutes in people with HIV on the original 2 mg product (original EGRIFTA label), and 8–11 minutes after single doses of Egrifta SV or WR in healthy adults (EGRIFTA SV and EGRIFTA WR labels).
• Endogenous pulsatile GH release — The cognition-trial authors describe GHRH treatment as producing a natural pulsatile GH release, rather than the prolonged rise that follows GH injections, and as keeping the normal negative feedback of IGF-1 on GH (Baker et al., 2012). Tesamorelin raises GH and, after it, IGF-1 and IGFBP-3 (EGRIFTA SV label).
• IGF-1 elevation (pharmacodynamic marker) — IGF-1 rose 81% over 26 weeks on 2 mg daily in the first Phase 3 trial (Falutz et al., 2007) and 117% over 20 weeks on 1 mg daily in older adults (Baker et al., 2012). The labels call for monitoring IGF-1 during treatment and for considering stopping if it stays high (for example above 3 SDS), particularly if the response is not robust (EGRIFTA SV label).
• Visceral fat reduction (downstream of GH lipolysis) — The effect behind its FDA approval; growth hormone is lipolytic, breaking down fat (EGRIFTA SV label). In the pooled Phase 3 trials, visceral fat fell 15.4% more than on placebo over 26 weeks, while abdominal fat under the skin did not change significantly (Falutz et al., 2010, JCEM). The two trials' own results were −15.2% and −10.9% at 26 weeks (Falutz et al., 2007; Falutz et al., 2010, JAIDS), and about −18% at 52 weeks in those kept on it (Falutz et al., 2008).
• Liver fat (MASH/NAFLD context) — In the Stanley et al. 2019 Lancet HIV trial, tesamorelin reduced hepatic fat fraction by 4.1% absolute (37% relative) compared with placebo in HIV-infected adults with NAFLD, and fewer showed fibrosis progression on biopsy (10.5% vs 37.5%). The mechanism is unknown (Stanley et al., 2014); in that 6-month trial the fall in liver fat tracked the fall in visceral fat. Fourman and colleagues propose two routes: visceral fat drains to the liver through the portal vein, and growth hormone lowers the liver's de novo lipogenesis in HIV (Fourman et al., 2017).
• Cognition (Baker 2012) — In healthy older adults and adults with amnestic mild cognitive impairment, 20 weeks of 1 mg/day tesamorelin improved executive function, with a non-significant trend for verbal memory. The authors note that GHRH, growth hormone and IGF-1 act on the brain and decline with age (Baker et al., 2012).
• Lipid profile — In the pooled Phase 3 trials, triglycerides fell 12.3% more than on placebo over 26 weeks, and the total-to-HDL cholesterol ratio 7.2% more; non-HDL cholesterol was 7 mg/dL below baseline at 52 weeks in those kept on it (Falutz et al., 2010, JCEM). In the first trial, total and HDL cholesterol also improved (Falutz et al., 2007).

What the Research Shows

The HIV-lipodystrophy Phase 3 program enrolled 806 patients in two trials (Falutz et al., 2010, JCEM). Later trials tested tesamorelin on liver fat in people with HIV (Stanley et al., 2014; Stanley et al., 2019) and on cognition in older adults (Baker et al., 2012).

• 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 fell 50 mg/dL, against a 9 mg/dL rise on 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 (second trial) — 404 patients randomized 2:1 to tesamorelin 2 mg SC daily or placebo for 6 months, then a 6-month extension. VAT fell 10.9% on tesamorelin vs 0.6% on placebo in the efficacy phase (P < 0.0001) (J Acquir Immune Defic Syndr 53:311-322).
• Phase 3 — Falutz 2010 JCEM (pooled) — Pooled analysis of the two pivotal trials (806 patients). Treatment effect on VAT −15.4% at week 26, and VAT −17.5% at week 52 in patients kept on tesamorelin; triglycerides −12.3% vs placebo; better patient- and physician-rated belly profile. No clinically meaningful differences in glucose parameters; generally well tolerated (J Clin Endocrinol Metab 95:4291-4304).
• 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. The 8% cut-off was set in advance in the trials' analysis plan (Clin Infect Dis 54:1642-1651); the labels advise weighing the risks and benefits of continuing in people whose visceral fat has not gone down (EGRIFTA SV label).
• 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, a net −2.9% in lipid-to-water percentage over 6 months. The fall in liver fat tracked the fall in visceral fat, independent of weight change; the authors call the mechanism unknown.
• 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 change in HFF): −4.7% on tesamorelin vs 0.0% on placebo, a treatment effect of −4.1 percentage points (p = 0.018), or −37% relative. On repeat biopsy, fibrosis progressed in 10.5% on tesamorelin vs 37.5% on placebo (p = 0.04); the NAFLD Activity Score did not change significantly. 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. An exploratory analysis after a 10-week washout suggested a lingering benefit for executive function (P = .08) but not for verbal memory (Arch Neurol 69:1420-1429).
• Inflammatory markers — Stanley 2011 — Tesamorelin lowered tPA antigen more than placebo, while CRP and PAI-1 did not change significantly; among treated patients, changes in PAI-1, tPA and adiponectin tracked the change in visceral fat.
• Liver enzymes — Fourman 2017 — Among trial patients with raised baseline ALT or AST, VAT responders on tesamorelin had larger falls in ALT and AST over 26 weeks than non-responders. Liver fat was not measured; the authors suggest the change may reflect less fat in the liver.
• 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 — Two placebo-controlled trials in HIV-infected adults with abdominal fat accumulation: NCT00123253 (412 patients; Falutz 2007 NEJM) and a second trial of 404 patients (Falutz 2010 JAIDS), each a 26-week efficacy phase followed by a 26-week extension. Their pooled analysis covers 806 patients (Falutz 2010 JCEM). Consistent VAT and triglyceride effects.
• Liver-fat / NAFLD trials — NCT01263717 (Stanley 2014 JAMA), NCT02196831 (Stanley 2019 Lancet HIV NAFLD histology).
• Cognition trial — NCT00257712 (Baker 2012 Arch Neurol, N = 137).
• Pharmacokinetics — Tmax ~0.15 h SC; half-life 26 min in healthy adults and 38 min in HIV-infected patients after 14 days of 2 mg on the original product (original EGRIFTA label), and 8–11 min after a single dose of Egrifta SV or WR in healthy adults (EGRIFTA SV and EGRIFTA WR labels); 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.

Reconstitution & Storage

The branded products are supplied as lyophilized powder with their own diluent: Egrifta SV in a 2 mg single-dose vial with sterile water for injection, Egrifta WR in an 11.6 mg vial with bacteriostatic water (EGRIFTA SV and EGRIFTA WR labels). The last two rows are arithmetic only, at example vial sizes and volumes: no label or document read for this page gives a vial size or mixing volume for compounded tesamorelin.

• Reconstitution — The Egrifta SV instructions describe pushing the water slowly down the inside wall of the vial, with the needle at a slight angle, then rolling the vial gently in the hands for 30 seconds without shaking; Egrifta WR is swirled, not shaken. Both labels describe the mixed solution as clear and colorless (EGRIFTA SV and EGRIFTA WR labels).
• Storage — Egrifta SV 2 mg vials, before reconstitution: room temperature, 20–25°C (68–77°F), with excursions to 15–30°C permitted, kept in the original box to protect from light (EGRIFTA SV label, section 16). The Egrifta SV label calls for using reconstituted solution immediately and discarding the rest; it says not to refrigerate or freeze it. Egrifta WR vials are also kept at 20–25°C before mixing; once mixed, a vial stays at room temperature, is neither refrigerated nor frozen, and is discarded 7 days later (EGRIFTA WR label). The original 1 mg Egrifta vials were refrigerated at 2–8°C (original EGRIFTA label). No document read for this page gives storage for compounded vials.
• Injection site — The labels describe injecting into the abdomen, at least 2 inches (5 cm) from the navel and not into scar tissue or bruises, and changing the site with each dose to lower the risk of injection-site reactions (EGRIFTA SV and EGRIFTA WR labels).
• Needle — Egrifta SV comes with 1-inch 20-gauge needles for mixing and ½-inch 30-gauge needles for injecting; Egrifta WR comes with syringes that have the needle attached (EGRIFTA SV and EGRIFTA WR labels).
• Inspection — The labels say to use the solution only if it is clear and colorless, without particles (EGRIFTA SV and EGRIFTA WR labels).

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Side Effects & Risks

Tesamorelin's FDA labels list the adverse reactions seen in the Phase 3 program: 740 people with HIV were treated in the trials, 543 of them in the 26-week placebo-controlled phase, for up to 52 weeks in all (EGRIFTA SV label).

• Injection site reactions (most common) — In the first 26 weeks of the trials, 25% on tesamorelin vs 14% on placebo had injection-site reactions, such as redness, itching, pain, irritation or bruising; the labels advise rotating sites across the abdomen to lower the risk (EGRIFTA SV label). In the 2019 fatty-liver trial, none of the injection-site complaints was judged serious (Stanley et al., 2019).
• Arthralgia and myalgia — In the first 26 weeks, joint pain was reported by 13% on tesamorelin vs 11% on placebo, muscle pain by 6% vs 2%, and pain in the arms or legs by 6% vs 5%. The label ties joint pain to fluid retention caused by the growth hormone the drug releases (EGRIFTA SV label).
• Peripheral edema — Reported by 6% on tesamorelin vs 2% on placebo in the first 26 weeks, and carpal tunnel syndrome by 1% vs none. The label describes these fluid-retention effects as either passing or resolving when treatment stops (EGRIFTA SV label).
• Paresthesias / hypoesthesias — Tingling was reported by 5% on tesamorelin vs 2% on placebo in the first 26 weeks, and numbness by 4% vs 2% (EGRIFTA SV label).
• Hyperglycemia / glucose intolerance — The labels warn that tesamorelin can cause glucose intolerance: by week 26, HbA1c reached 6.5% or more in 5% on tesamorelin vs 1% on placebo, a higher risk of diabetes (hazard ratio 3.3). They call for checking glucose status before starting and periodically during treatment (EGRIFTA SV label). In the Phase 3 trials, fasting glucose and HbA1c rose more in people whose visceral fat fell less than 8% than in those whose fell more (Stanley et al., 2012); in a smaller trial, fasting glucose rose at 2 weeks but not significantly over 6 months (Stanley et al., 2014).
• IGF-1 elevation — In the first Phase 3 trial, IGF-1 rose 81% over 26 weeks (Falutz et al., 2007). The labels say the effects of prolonged IGF-1 elevation are unknown, and call for monitoring IGF-1 and for considering stopping if it stays high (for example above 3 SDS), particularly if the response is not robust (EGRIFTA SV label).
• Hypersensitivity — Hypersensitivity reactions occurred in 4% of trial patients: itching, redness, flushing, hives and rash. The labels say to stop treatment and seek prompt medical attention if one is suspected (EGRIFTA SV label).
• Fluid retention / weight — The labels call tesamorelin weight neutral: over 26 weeks, body weight changed by −0.4 kg and +0.5 kg in the two trials, against 0.0 and +0.3 kg on placebo, while lean body mass rose 1.3 and 1.2 kg (EGRIFTA SV label).
• Contraindications — Pregnancy (it could harm the fetus), active cancer, disruption of the hypothalamic-pituitary axis (pituitary removal, tumor or surgery, hypopituitarism, head radiation or head trauma), and known hypersensitivity to tesamorelin or the product's other ingredients, such as mannitol. Because the drug releases growth hormone, a known growth factor, the labels call for careful weighing before starting given the higher background risk of cancer in people with HIV, and for stopping if a cancer comes back. They advise considering stopping in critically ill patients, since pharmacologic doses of growth hormone have been linked to increased deaths in acute critical illness (EGRIFTA SV label).
• Discontinuation effect reversal — In people switched to placebo after 26 weeks, visceral fat came back over the next 26 weeks; the effect lasted only as long as treatment (Falutz et al., 2008).
• Pediatric use — Not indicated, and not recommended, in children with open or closed growth plates; in children whose growth plates are still open, it may cause accelerated and excessive growth (EGRIFTA SV label).

What to Expect — Timeline

Tesamorelin is the most comprehensively characterized GHRH analogue in regulatory and clinical-trial terms (Dominikowski et al., 2026). The timeline below gives what those trials measured, in people with HIV.

• Week 26 (6 months) — The Phase 3 trials' primary end point: visceral fat fell 15.2% and 10.9% in the two trials (Falutz et al., 2007; Falutz et al., 2010, JAIDS). Responders (≥8% VAT reduction, defined in advance) had larger falls in triglycerides, better adiponectin and steadier glucose than non-responders, whose fasting glucose and HbA1c rose more (Stanley et al., 2012).
• Week 26–52 (extension phase) — In people kept on tesamorelin, the fall in visceral fat held at about 18% at 52 weeks (Falutz et al., 2008). In people with HIV and fatty liver, liver fat fell over 12 months, a 37% relative reduction compared with placebo (Stanley et al., 2019).
• Post-discontinuation (months 1–6 off) — In people switched to placebo at 26 weeks, visceral fat rose again by 22% and 16% over the next 26 weeks in the two trials (EGRIFTA SV label); the effect lasts only as long as treatment (Falutz et al., 2008).
• Non-responders — In the combined Phase 3 trials, 69% of people on tesamorelin reached the 8% reduction, against 33% on placebo, so 31% did not (Fourman et al., 2017).

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.
• 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.
• 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: its half-life is minutes (EGRIFTA SV and EGRIFTA WR labels). Relevant for pregnancy planning, pre-operative considerations, and anti-doping wash-out.

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

Bloodwork & Monitoring

What the FDA labels list, and what the trials measured:

• IGF-1 (age-adjusted, expressed as SDS) — The labels call for monitoring IGF-1 during treatment and for considering stopping if it stays high (for example above 3 SDS), particularly if the response is not robust; they set no schedule. At 26 weeks in the trials, 47% had IGF-1 above 2 SDS and 36% above 3 SDS (EGRIFTA SV label).
• Fasting glucose + HbA1c — The labels call for checking glucose status before starting and periodically during treatment, for considering stopping in people who develop glucose intolerance or diabetes without a clear response, and for monitoring people with diabetes for new or worse retinopathy (EGRIFTA SV label). In the Phase 3 trials, fasting glucose and HbA1c rose more in non-responders than in responders (Stanley et al., 2012).
• Lipid panel — The Phase 3 trials tracked triglycerides and the total-to-HDL cholesterol ratio as secondary end points (EGRIFTA SV label); triglycerides fell more in responders than in non-responders (Stanley et al., 2012).
• Waist circumference + imaging (VAT indication) — The trials measured visceral fat by CT at the L4–L5 level, and waist circumference (EGRIFTA SV label); a fall in visceral fat of 8% or more at 26 weeks was defined in advance as a response (Stanley et al., 2012). The labels advise weighing the risks and benefits of continuing in people whose visceral fat has not gone down (EGRIFTA SV label).
• Liver fat (NAFLD trials) — The liver-fat trials measured liver fat by proton MR spectroscopy, and the 2019 trial also took liver biopsies (Stanley et al., 2014; Stanley et al., 2019).
• Other medicines — The labels call for monitoring people taking drugs cleared by CYP450 liver enzymes (such as corticosteroids, sex steroids, anticonvulsants and cyclosporine), since growth hormone may change their clearance, and note that people on glucocorticoid replacement for adrenal insufficiency may need higher doses (EGRIFTA SV label).

Practical User Notes

• The 26-week response — In the Phase 3 trials, a fall in visceral fat of 8% or more at 26 weeks was defined in advance as a response; responders had larger falls in triglycerides, better adiponectin and steadier glucose over 52 weeks than non-responders (Stanley et al., 2012). The labels advise weighing the risks and benefits of continuing in people whose visceral fat has not gone down (EGRIFTA SV label).
• Timing of injection — The FDA labels do not specify a time of day. The cognition trial gave it 30 minutes before bedtime (Baker et al., 2012).
• Fasting considerations — The labels say nothing about food or fasting.
• Abdominal injection — The labels direct injection into the abdomen, changing the site with each dose, at least 2 inches (5 cm) from the navel and not into scar tissue or bruises (EGRIFTA SV and EGRIFTA WR labels).
• Glucose before starting — The labels call for checking glucose status before starting. Diabetes is not a contraindication, but the Phase 3 trials required fasting glucose below 150 mg/dL and listed type 1 or type 2 diabetes and past use of insulin or diabetes pills among their exclusions (EGRIFTA SV label).
• Cost — A 2012 review lists high cost among tesamorelin's limitations (Spooner & Olin, 2012). Clinic sites offer compounded tesamorelin for off-label use.
• Discontinuation — In the trials, visceral fat came back within 26 weeks of switching to placebo; the effect lasted only as long as treatment (Falutz et al., 2008).
• What tesamorelin does NOT do — The labels say it is not for weight loss: its effect on weight is neutral (EGRIFTA SV label). In the trials, abdominal fat under the skin did not change significantly (Falutz et al., 2010, JCEM), and glucose rose more in non-responders than in responders (Stanley et al., 2012).
• When the labels call for stopping — Pregnancy, a cancer that comes back, or a suspected allergic reaction, with prompt medical attention; the labels advise considering stopping when IGF-1 stays high or glucose intolerance develops without a clear response, and in critical illness (EGRIFTA SV label).

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References

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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.
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24. World Anti-Doping Agency. The 2026 Prohibited List. Section S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics. wada-ama.org.
25. Theratechnologies Inc. EGRIFTA SV (tesamorelin) for injection, 2 mg vial — Prescribing Information, section 16: How Supplied/Storage and Handling. BLA 022505; revised July 2026. DailyMed set ID 3d783378-b02d-4f19-99dd-0fc91a042224.
26. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
27. Makimura H, Feldpausch MN, Rope AM, Hemphill LC, Torriani M, Lee H, Grinspoon SK. Metabolic effects of a growth hormone-releasing factor in obese subjects with reduced growth hormone secretion: a randomized controlled trial. J Clin Endocrinol Metab. 2012;97(12):4769-4779. PMID: 23015655.
28. Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, Ruchała M. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475. PMID: 42395176.

Related Research

• CJC-1295Growth Hormone Releasing Hormone (GHRH) Analog
• SermorelinGHRH Analog, Growth Hormone Secretagogue
• Follistatin-344Myostatin / Activin-Binding Glycoprotein
• GHRP-2Growth Hormone Secretagogue (Ghrelin Receptor Agonist)
• FDA TrackerPCAC voted on 7 of the 12 peptides on July 23–24, 2026; FDA plans a PCAC review of the other 5 before the end of February 2027.