Tesamorelin (5mg & 10mg)

Tesamorelin Peptide

Tesamorelin is a synthetic analogue of growth hormone-releasing hormone (GHRH) containing 44 amino-acid residues. It carries an N-terminal trans-3-hexenoyl group and a C-terminal amide; the sequence is listed below.
Tesamorelin is studied for its activity at GHRH receptors and its effects on growth hormone secretion. Related compounds, such as sermorelin, have distinct structures and research evidence; findings should not be assumed to transfer between them.
This product is supplied for laboratory and analytical research only. Published clinical findings concern specific study formulations and populations and do not establish the safety or suitability of this product for human use.

Specifications

Molecular Formula: C₂₂₁H₃₆₆N₇₂O₆₇S

Molecular Weight: 5136 g/mol

Sequence: (3E)-hex-3-enoyl-Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-Arg-Gly-Ala-Arg-Ala-Arg-Leu-NH₂. This notation describes the 44 amino-acid residues, N-terminal modification and C-terminal amide shown in the WHO Recommended INN List 58, page 260.

Tesamorelin Research

Tesamorelin and the Pituitary Gland
Tesamorelin might potentially interact with the pituitary gland by possibly binding to GHRH receptors, which might initiate a sequence of molecular events. Researchers propose that it may cause structural alterations in the receptor, thereby activating intracellular signaling pathways.^{[1, 2]} They have noted that this binding process is likely followed by a significant conformational change, involving the transmembrane helix 6 (TM6), which may open the intracellular face for G protein coupling. One potential pathway might involve the stimulation of cyclic adenosine monophosphate (cAMP) production within pituitary cells. This might be achieved through the activation of the enzyme adenylate cyclase, which may convert ATP (adenosine triphosphate) to cAMP. It is suggested that increased cAMP levels might activate protein kinase A (PKA), leading to protein phosphorylation and GHRH receptor activation by Tesamorelin. This cascade might stimulate the synthesis and secretion of growth hormone (hGH) from somatotrophs in the pituitary gland. A 2011 open-label physiology study followed 13 healthy men through two weeks of tesamorelin exposure and two weeks of withdrawal. Mean 12-hour GH area under the curve rose from 531 to 897 (reported as μg/litre per 12 hours).^[3]
Mean non-log-transformed GH pulse area increased from 2.2 to 3.4 μg/litre, and mean IGF-1 increased from 148 to 329 μg/litre. These are short-term changes from baseline in a small study without a placebo group. GH and IGF-1 measurements largely returned to baseline after withdrawal. The findings do not establish long-term safety, general clinical benefits, or suitability of this research product for human use. Read the published GH physiology study.

Tesamorelin, HIV and Growth Hormone Research
A 2017 review discusses altered growth hormone (GH) secretion in human patients living with HIV, especially those with lipodystrophy. The authors report biochemical GH deficiency in about one-third of patients in the literature they review.^[4] This is not a prevalence estimate for experimental models or proof that antiretroviral therapy alone causes GH deficiency. HIV, treatment, comorbidities and changes in body fat can contribute, and the mechanisms remain incompletely understood. The review discusses tesamorelin research on visceral fat in HIV-associated lipodystrophy; it does not establish this research product as a general treatment for GH deficiency or as suitable for human use. Read the published GH and HIV review.

Tesamorelin and Lipodystrophy
Clinical research has evaluated tesamorelin in adults with HIV and excess abdominal visceral fat. These studies do not establish the suitability of this laboratory research product for human use.
Lipodystrophy is characterized by an irregular distribution and storage of fat cells, which can often result in visceral obesity. Visceral obesity refers to the abnormal accumulation of fat around and within internal organs, and it has been tentatively linked to a range of metabolic disturbances.
These disturbances may include insulin resistance, which impairs the organism’s ability to regulate blood sugar levels; elevated levels of low-density lipoprotein (LDL) cholesterol, often referred to as “bad” cholesterol due to its association with increased risk of cardiovascular disease; and hyperuricemia, which is an excessive concentration of uric acid in the blood.
A 2015 exploratory analysis of two phase 3 trials found that the adjusted odds of reaching a visceral adipose tissue (VAT) area below 140 cm² after six months were 3.9 times higher with tesamorelin than placebo (95% confidence interval 2.03–7.44). This is an odds ratio for a specified threshold, not a percentage of participants losing fat.^[5] Read the exploratory analysis.
A 2010 pooled analysis combined two phase 3 trials that initially randomised 806 adults with HIV receiving antiretroviral therapy. Among participants who continued tesamorelin through week 52, mean VAT decreased by 17.5% from their original baseline. Mean changes in triglycerides, total cholesterol and non-HDL cholesterol in this continuation group were −48, −8 and −7 mg/dl, respectively; these were changes from baseline, not placebo-adjusted treatment effects at week 52.^[6] Read the pooled trial analysis.
A 2011 systematic review of 10 trials involving 1,511 patients examined several growth hormone axis treatments, not tesamorelin alone. Its pooled VAT difference versus placebo was −25.20 cm² (95% confidence interval −32.18 to −18.22 cm²), an area measurement rather than a 25% reduction. The review reported increased arthralgia and oedema and limited evidence for individual drug classes.^[7] Read the systematic review.

Tesamorelin and Lipid Research
A 2007 randomised trial enrolled 412 human participants with HIV and excess abdominal fat. Over 26 weeks, triglycerides decreased by 50 mg/dl in the tesamorelin group and increased by 9 mg/dl in the placebo group. The total-cholesterol-to-HDL ratio also improved relative to placebo.^[8] These findings apply to the studied population and do not establish general cardiovascular benefits. Read the published lipid study.
A 2012 post hoc analysis of two phase 3 trials compared human participants receiving tesamorelin who achieved at least an 8% reduction in visceral adipose tissue with those who did not. Responders had greater improvements in triglycerides and adiponectin and smaller changes in glucose measures through 52 weeks.^[9] This comparison by response status shows associations; it does not prove that fat reduction causes an anti-inflammatory effect or that tesamorelin cannot impair glucose regulation. Read the published responder analysis. These studies do not establish the safety or suitability of this research product for human use.

Tesamorelin and Peripheral Nerve Damage
Peripheral nerve damage may potentially trigger debilitating motor and sensory challenges. Research in intervention of such damage is limited, as nerve cells present a challenge to regenerate.
A 2016 review discusses growth hormone (GH)-based approaches to peripheral nerve regeneration, including mechanistic and translational research.^[10] It is not a tesamorelin clinical trial and does not establish that tesamorelin improves nerve repair in humans. Read the published GH and nerve-injury review.
Johns Hopkins separately lists a tesamorelin clinical study, NCT03150511, designed to test functional recovery after peripheral nerve injury. Its description sets out a research hypothesis, not evidence of a demonstrated benefit. Read the university study description. Neither the review nor the study description establishes the safety or suitability of this research product for human use.

Tesamorelin, Mild Cognitive Impairment and Healthy Ageing
Tesamorelin has been studied in human participants with mild cognitive impairment (MCI) and in older adults with normal cognitive function. The cited 2013 randomised, double-blind, placebo-controlled brain imaging substudy included 30 adults aged 55–87 years, 17 of whom had MCI, and followed participants for 20 weeks. The investigators reported increased GABA ratios in three measured brain regions and decreased myo-inositol ratios in the posterior cingulate. Neurochemical changes were not significantly associated with changes in cognitive outcomes.^[11] This small substudy does not establish prevention or treatment of dementia. Its clinical findings do not establish the safety or suitability of this research product for human use. Read the published study abstract.

Tesamorelin and Muscle Imaging Research
A 2019 exploratory secondary analysis of two clinical trials compared 193 selected tesamorelin responders with 148 placebo participants, all living with HIV and abdominal obesity.^[12] Responders had achieved at least an 8% decrease in visceral adipose tissue. CT scans assessed the density and cross-sectional area of four trunk muscle groups over 26 weeks.
Adjusted comparisons found greater increases in total muscle density across all four groups, total muscle area in the rectus and psoas, and lean muscle area across all four groups.
These imaging findings come from a selected responder subgroup and do not establish improved muscle strength or everyday physical function. Longer studies in people with and without HIV are needed. They do not establish the safety or suitability of this research product for human use. Read the published muscle-imaging study.

Tesamorelin and Liver Adiposity
A 2019 randomised, double-blind trial enrolled 61 human participants with HIV and non-alcoholic fatty liver disease and assessed hepatic fat fraction (HFF) over 12 months.^[13]
These findings concern a specific clinical population; they do not establish the safety or suitability of this research product for human use. Longer studies are needed to assess effects on liver histology. Read the published trial abstract. The adjusted absolute treatment effect versus placebo was a decrease of 4.1 percentage points in HFF,
corresponding to a relative treatment effect of 37%, which might suggest a potential benefit in reducing liver fat accumulation. Furthermore, 35% of the Tesamorelin group achieved a hepatic fat fraction below 5%, in contrast to 4% in the placebo group.
In terms of liver tissue fibrosis, Tesamorelin appeared to slow its progression, with only 10.5% of the Tesamorelin group showing fibrosis progression, compared to 37.5% in the placebo. Nevertheless, Tesamorelin did not seem to significantly improve pre-existing fibrosis.
Secondary associations do not establish a causal mechanism or a general anti-inflammatory effect.
In this trial, Tesamorelin did not significantly impact liver enzymes, such as alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT), overall. An exploratory subgroup analysis reported an ALT decrease in participants with elevated baseline ALT; this does not establish a general liver-enzyme benefit.
Changes in fasting glucose and glycated haemoglobin (HbA1c) did not differ significantly between groups at 12 months. This finding does not establish an absence of glucose-related risk. Local injection-site complaints were more frequent in the tesamorelin group.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing. This product must not be administered to humans or animals. All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

References