Tesamorelin 10mg

Tesamorelin is an agonist at the growth hormone-releasing hormone receptor (GHRHR), a class-B1 GPCR on pituitary somatotrophs. Occupancy couples through Gs and adenylyl cyclase to raise intracellular cAMP, driving both the synthesis and the release of growth hormone, which drives hepatic IGF-1 production.

Whether pulsatile architecture survives that stimulation was measured, not assumed. Stanley et al. (J Clin Endocrinol Metab 2011;96(1):150-158) ran overnight frequent GH sampling in 13 healthy men after two weeks, measuring mean overnight GH, log₁₀ GH peak area, basal secretion rate, IGF-1 and insulin-stimulated glucose uptake. The pattern reported stayed pulsatile: existing pulses were amplified rather than replaced by a flat elevated plateau.

Because the stimulus is applied upstream at the pituitary, the effect remains subject to somatostatin tone and IGF-1 negative feedback — the brake stays connected and the response is self-limiting. Exogenous recombinant GH, by contrast, abolishes pulsatility and suppresses endogenous secretion. That is why a GHRH analogue is the right probe for physiological axis regulation rather than for GH exposure alone.

Health Canada initially refused it. The original New Drug Submission received a Notice of Non-Compliance – Withdrawal over diabetogenic effect and IGF-1-related carcinogenicity concerns. Authorisation followed only after an expert Reconsideration Panel in August 2013: a Notice of Compliance issued 29 April 2014 (NDS 131836, brand EGRIFTA, sponsor Theratechnologies Inc.), with restricted conditions of use including mandatory IGF-1 monitoring, and an indication narrower than the American one.

It was marketed in Canada from 23 June 2015, and has since been withdrawn. Verified against the Health Canada Drug Product Database:

United States. EGRIFTA was approved 27 November 2010, EGRIFTA SV in 2019, and EGRIFTA WR on 25 March 2025, available from 5 September 2025. That approval was not smooth: the FDA issued a Complete Response Letter on 24 January 2024 on chemistry, manufacturing and controls grounds — impurities, microbiological assays, and the stability of both the lyophilised and the reconstituted product — plus a request for more immunogenicity data on the concentrated formulation. Efficacy and bioequivalence were not challenged. A contract-manufacturing shutdown separately caused an EGRIFTA SV shortage from mid-January 2025.

European Union: never approved. Theratechnologies withdrew its marketing authorisation application in June 2012, citing the absence of safety data beyond 48 weeks on elevated IGF-1 and the absence of a cardiovascular endpoint.

Elsewhere: we do not know. We found no evidence either way on the United Kingdom, Australia, Japan or China, and will not call tesamorelin “US-only” on absent evidence. What we can state: approved in the US, approved and no longer marketed in Canada, never approved in the EU.

None of this makes the vial on this page an authorised drug — it is an unapproved research reagent. Tesamorelin is also named explicitly on the WADA Prohibited List under section S2, prohibited at all times.

“Which is better” is the wrong question. These compounds act on different receptors, through different second messengers, on the same cell — which is why co-administration studies of the two classes exist at all.

Three design consequences. Comparator choice: work isolating GHRH-pathway signalling cannot use a ghrelin mimetic as its comparator, or vice versa — they are two arms of a synergy model, not substitutes. Confound profile: GHS-R1a is also the orexigenic receptor and is expressed outside the pituitary, so ghrelin-receptor agonists carry food-intake and GI-motility confounds a GHRHR agonist does not. Evidence asymmetry: tesamorelin is the only compound in this class with regulatory-grade human characterisation. If a GHS-R1a probe is what the protocol needs, tesamorelin is the wrong reagent — see Ipamorelin 10mg.

Not a weight-loss agent. The FDA label carries an explicit Limitation of Use: not indicated for weight loss management. Makimura 2012, the main non-HIV randomised trial, found no significant weight change over 12 months (P = 0.52) despite a measured visceral fat effect in the same study; Clemmons 2017 found no change in weight, BMI, body fat or waist circumference over 12 weeks, and no change in glycaemic control. The effect is compartment redistribution, not mass reduction.

No cardiovascular outcome benefit demonstrated. “Long-term cardiovascular safety and benefit have not been studied” is a label Limitation of Use, and the missing cardiovascular endpoint was a stated reason for the 2012 EU withdrawal. The carotid intima-media thickness change reported in Makimura 2012 is a surrogate, not an outcome.

Cognition is not established, and the two most recent trials are negative. Baker et al. (Arch Neurol 2012) is the positive signal everyone cites: 137 completers aged 55-87, 20 weeks, measuring cognitive test performance and IGF-1 in healthy and mild-cognitive-impairment groups, with the authors themselves calling for larger trials. Those have partly happened and have not replicated it. Ellis et al. (J Infect Dis 2025) randomised 73 people with HIV and abdominal obesity over six months and missed the primary endpoint — between-group P = 0.673 — concluding no clear benefit. Stewart et al. (eNeurologicalSci 2026), a 22-participant double-blind low-dose pilot, reported that treatment “was not directly linked with significant changes in study measures”.

Liver histology is unproven. The 12-month Lancet HIV 2019 trial measured hepatic fat fraction by imaging; its authors conclude only that tesamorelin “might be beneficial” and that further studies are needed on liver histology. NASH resolution and fibrosis outcomes are not established. A general-population NASH programme was announced in September 2020; we found no published results and no discontinuation notice, and claim neither.

Population limits. Almost all human efficacy data come from people with HIV and lipodystrophy; Makimura 2012 is the main exception, and there are no paediatric data. A 2026 meta-analysis of tesamorelin RCTs exists (PMID 41545261); we have not verified its pooled estimates and quote no numbers from it.

The visceral fat comes back, and this is measured rather than inferred. Falutz et al. (AIDS 2008;22(14):1719-1728) re-randomised 410 participants at week 26. Those continuing on tesamorelin sustained the visceral adipose tissue change over 52 weeks; those switched to placebo reaccumulated VAT across weeks 26 to 52. The authors conclude that the effects do not last beyond the duration of treatment.

No published evidence shows a durable post-treatment benefit, and the mechanism makes that unsurprising: a secretagogue acting on an intact, feedback-regulated axis leaves little trace once the stimulus is removed. Labelled fluid-retention effects conversely tend to resolve after stopping. Any protocol asking about persistence therefore needs an off-treatment arm.

In the clinical record documented in the FDA label, 49.5% of treated patients developed anti-tesamorelin IgG antibodies by 26 weeks and 47.4% by 52 weeks, with cross-reactivity to endogenous GHRH in roughly 60% of antibody-positive patients. Antibody presence did not reduce the visceral fat or IGF-1 response. Of patients with hypersensitivity reactions, 85.2% were antibody-positive; labelled hypersensitivity reactions occurred in 3.6% overall.

Why that is interesting rather than merely a safety line: tesamorelin is a self-sequence peptide with one small non-native acyl modification, and it still elicits antibodies in about half of exposed subjects, much of it cross-reactive with the endogenous hormone — a well-quantified natural experiment in tolerance and epitope formation.

That makes it a substantive model antigen for anti-drug-antibody assay development, analogue-versus-parent cross-reactivity, and epitope-mapping method work. It is also why the FDA requested more immunogenicity data when reviewing the concentrated formulation in 2024.

Lot CS-te10-0616 was submitted to Janoshik Analytical, an independent third-party laboratory, and reported under report #198440, analysis conducted 1 July 2026: purity 99.174%, measured peptide content 11.56 mg against a 10 mg nominal fill. This is the Janoshik Analytical assay; Testides (Toronto) confirmation is still pending. Every current lot is indexed on our lab results page.

Those two figures do different jobs, and conflating them is the commonest error in reading a COA. Purity is the proportion of peptide-containing material that is the target peptide, as resolved by HPLC; it says nothing about how much is in the vial. Content is the quantitative mass determination; it says nothing about what the remainder is. A vial can be 99% pure and underfilled, or correctly filled and 90% pure — you need both, from the same lot, with the lot number matching the vial label. Full walkthrough: how to read a peptide COA.

One caveat almost no supplier mentions: the pharmaceutical drug substance is the acetate salt, the label formula being the free base plus roughly seven acetic acid equivalents — around 8% heavier. We do not print an acetate CAS number or acetate molecular weight as established, because the figures circulating online rest on a single secondary source and on arithmetic estimation rather than a primary measurement. Either way, a vial characterised by peptide content and one characterised by total salt mass are not the same quantity.

The two label generations disagree, so we show both rather than pick one. The EGRIFTA prescribing information, section 12.3, reports a terminal half-life after 14 days of subcutaneous administration of 26 minutes in healthy subjects and 38 minutes in HIV-infected patients. The later EGRIFTA SV / EGRIFTA WR label states 8 minutes in healthy subjects. Both are label-sourced, and volume of distribution likewise differs across label versions (9.4–10.5 L/kg versus 4.8 L/kg). The widely copied “26 to 38 minutes” is one of these figures reproduced without the label version, formulation or route it belongs to.

Worth pairing with it: subcutaneous bioavailability is documented at under 4%. That is genuinely unusual, and it is why exposure and effect decouple so sharply here — a short plasma residence with very low systemic availability still produces sustained IGF-1 elevation, because the readout is a downstream secretory cascade rather than the peptide itself.

No. The synonym list attached to CAS 218949-48-5 in at least one widely scraped chemical database carries contaminated entries, including “Adipotide/FTTP”. Adipotide is an unrelated prohibitin-targeting peptidomimetic with a different structure, target and mechanism, so any listing reproducing a scraped synonym block publishes a false synonym. Two neighbouring corrections while we are here: tesamorelin is not sermorelin, which is the shorter GHRH(1-29)NH₂ fragment rather than tesamorelin’s parent; and EGRIFTA is not a different molecule, but the brand name of the product formulated from tesamorelin acetate.

Falutz J, et al. N Engl J Med. 2007;357(23):2359-2370 — pivotal 26-week phase III, placebo-controlled; measured visceral adipose tissue and IGF-1.

Falutz J, et al. AIDS. 2008;22(14):1719-1728 — 410 patients re-randomised at week 26: continued treatment sustained the VAT change; on discontinuation VAT reaccumulated.

Falutz J, et al. J Clin Endocrinol Metab. 2010;95(9):4291-4304 — pooled phase 3 dataset behind the label safety table; VAT measured at 26 and 52 weeks.

Stanley TL, et al. J Clin Endocrinol Metab. 2011;96(1):150-158 — the pulsatility paper: GH pulse amplitude and mean overnight GH increased with the pulsatile pattern preserved.

Makimura H, et al. J Clin Endocrinol Metab. 2012;97(12):4769-4779 — main non-HIV RCT, 12 months: measured VAT, with no significant weight change (P=0.52).

Baker LD, et al. Arch Neurol. 2012;69(11):1420-1429 — the positive cognition signal: 137 completers, 20 weeks, favourable effect in healthy and MCI groups; authors called for larger trials.

Stanley TL, et al. Lancet HIV. 2019;6(12):e821-e830 — 12-month NAFLD trial: measured hepatic fat fraction by imaging; histology left undetermined.

Ellis RJ, et al. J Infect Dis. 2025;231(5):1230-1238 — negative: open-label phase 2, n=73, six months, between-group P=0.673 on the primary endpoint.