By Peptide Insider Research Team · 12 min read · Last updated 11 September 2026

The tesamorelin / ipamorelin blend is a two-component research preparation that pairs a stabilised growth hormone-releasing hormone (GHRH) analog, tesamorelin (TH9507), with the selective growth hormone secretagogue-receptor (GHS-R1a) agonist ipamorelin (NNC 26-0161) [1,2]. The two peptides act on different somatotroph receptors — the Gs-coupled GHRH receptor and the Gq-coupled ghrelin receptor — and the rationale for co-formulating them rests on the synergy between the GHRH and GHRP receptor systems first described in the 1990 pituitary studies of Bowers and colleagues [6,7]. Catalogues list the preparation under many labels: tesamorelin and ipamorelin blend, tesamorelin/ipamorelin blend, ipamorelin tesamorelin blend, tesamorelin + ipamorelin, the abbreviated tesa/ipa blend, tesa/ipa peptide and tesa ipa peptide, or simply tesa/ipa. This review summarises the pharmacology of each component, explains the receptor-level basis for the pairing, sets out the separate evidence bases, and states plainly what the literature does not contain: a controlled study of the two peptides administered together. Peptide Insider's single-compound reviews of tesamorelin and ipamorelin cover each molecule in depth. All content is provided strictly for research reference.

Definition. A tesamorelin / ipamorelin blend (also catalogued as ipamorelin and tesamorelin, tesamorelin + ipamorelin or tesa/ipa) is a co-lyophilised or co-listed research preparation containing two chemically unrelated peptides: tesamorelin, a 44-residue human GHRH(1-44)-NH2 carrying an N-terminal trans-3-hexenoyl group that protects it from dipeptidyl peptidase-IV cleavage [2], and ipamorelin, a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) that activates the ghrelin receptor without the ACTH, cortisol or prolactin release seen with earlier GHRPs [1]. Neither component is a fragment or metabolite of the other; the blend is a mixture, not a conjugate.

Introduction

Growth hormone (GH) secretion from anterior-pituitary somatotrophs is governed by two hypothalamic peptides — stimulatory GHRH and inhibitory somatostatin — and by a third, later-discovered input from the ghrelin receptor [7,8]. Synthetic ligands for the first and third of these systems form the two largest families in the research-peptide catalogue: GHRH analogs (sermorelin, tesamorelin, CJC-1295, Mod GRF 1-29) and GHRPs or "ghrelin mimetics" (GHRP-6, GHRP-2, hexarelin, ipamorelin). A tesamorelin and ipamorelin blend draws one member from each family. The idea of combining the two receptor classes is not new; it dates to the observation that a GHRP given with GHRH produced GH release in normal men greater than the sum of either peptide alone [6]. What is new is the specific pairing of the longest-acting approved GHRH analog with the most receptor-selective GHRP, and the fact that this pairing has entered research catalogues ahead of any published combination study.

Biological background: two receptors, one secretory cell

The GHRH receptor is a class B G protein-coupled receptor expressed on somatotrophs. Ligand binding activates Gs, raises cyclic AMP, and stimulates both GH exocytosis and GH gene transcription. Native GHRH(1-44)-NH2 is inactivated within minutes in plasma by dipeptidyl peptidase-IV, which removes the N-terminal Tyr-Ala dipeptide to leave the inactive GHRH(3-44) fragment [12]. Every GHRH analog in the research catalogue is an attempt to slow that cleavage.

The ghrelin receptor (GHS-R1a) was cloned from pituitary and hypothalamus in 1996 as the target of the synthetic GHRPs, three years before its endogenous ligand — the octanoylated 28-residue stomach peptide ghrelin — was identified [7,8]. GHS-R1a couples to Gq/11, activates phospholipase C, and mobilises intracellular calcium. It is also expressed in the arcuate nucleus, where its activation is thought to increase GHRH neuron firing and reduce somatostatin tone, which is one proposed explanation for why GHRP-class compounds require intact hypothalamic GHRH signalling for their full effect [6,7].

Because the two receptors use different second messengers and converge on the same secretory granule pool, their simultaneous activation produces more than additive GH release in pituitary cell and human infusion studies [6]. This is the entire mechanistic premise of an ipamorelin tesamorelin blend. It is important to note that the synergy data were generated with GHRH(1-44) and the hexapeptide GHRP-6, not with tesamorelin and ipamorelin; the extrapolation is pharmacologically reasonable but has not been tested directly.

Structure and mechanism of each component

Tesamorelin (TH9507, Egrifta)

Tesamorelin is the full 44-residue human GHRH sequence with a trans-3-hexenoyl moiety attached to the N-terminal tyrosine. Ferdinandi and colleagues reported that this acyl group confers resistance to dipeptidyl peptidase-IV, prolongs plasma elimination relative to native GHRH, and produces sustained rises in GH and IGF-1 in rats, dogs and pigs; subchronic toxicology in the same paper attributed the adverse findings in dogs to prolonged supraphysiological GH/IGF-1 exposure rather than to the peptide itself [2]. Tesamorelin is the only GHRH analog to have completed phase 3 development, and it received United States regulatory approval in 2010 for a specific indication in HIV-associated lipodystrophy [3,4,13]. Unlike sermorelin (GHRH 1-29) and CJC-1295, it retains the full C-terminal 30-44 region of the native hormone.

Ipamorelin (NNC 26-0161)

Ipamorelin emerged from a Novo Nordisk programme that modified GHRP-1. Raun and colleagues showed in 1998 that the pentapeptide releases GH in vitro and in vivo with potency comparable to GHRP-6, acts as an agonist at the GHRP receptor, and — critically — does not raise ACTH or cortisol even at exposures more than 200-fold above its GH-releasing ED50, a selectivity profile previously seen only with GHRH itself [1]. Later rat studies reported concentration-dependent increases in longitudinal bone growth and reversal of glucocorticoid-induced suppression of periosteal bone formation [9,10]. Ipamorelin reached phase 2 as an intravenous prokinetic candidate for postoperative ileus, where it was well tolerated but did not separate from placebo on the primary endpoint [11].

Nomenclature and catalogue variants

Because the preparation is defined by its two components rather than a single chemical name, catalogue and search labels vary widely. The table below maps common variants to the underlying chemistry so that literature and lot documents can be matched unambiguously.

Catalogue or search labelWhat it denotesNotes
tesamorelin / ipamorelin blend, tesamorelin/ipamorelin blendCo-listed two-peptide preparation, GHRH analog named firstSlash with or without spaces; the most common formal listing
tesamorelin and ipamorelin blend, tesamorelin + ipamorelinSame preparation, conjunction or plus-sign formConjunction form dominates in written questions
ipamorelin and tesamorelin, ipamorelin tesamorelin blendSame preparation, GHRP named firstComponent order carries no chemical meaning
tesa/ipa blend, tesa/ipa peptide, tesa ipa peptide, tesa/ipaAbbreviated forms (tesa = tesamorelin, ipa = ipamorelin)"Ipa" alone is ambiguous in some catalogues; "tesa" is not
TH9507 + NNC 26-0161Developer code names of the two componentsUsed in the primary literature, rarely in catalogues
CJC-1295 / ipamorelinA different blend using a GHRH(1-29) analogNot interchangeable; see the CJC-1295 review

Evidence by research domain

No peer-reviewed study has evaluated tesamorelin and ipamorelin together. The evidence summarised below is therefore component-wise, and the "combination" row records an absence.

DomainTesamorelinIpamorelinCombination
Receptor pharmacologyGHRH-R agonist; DPP-IV resistant [2]Selective GHS-R1a agonist; no ACTH/cortisol release [1]Synergy inferred from GHRH + GHRP-6 data only [6]
Preclinical GH/IGF-1 axisSustained GH/IGF-1 rise in rat, dog, pig [2]GH release in rat and swine; bone growth in rat [1,9,10]None
Human clinical literaturePhase 3 in HIV lipodystrophy; 26- and 52-week data [3,4]; hepatic-fat imaging trial [5]Phase 2 postoperative ileus, negative primary endpoint [11]None
Safety signals reportedGlucose elevations early in treatment, IGF-1 monitoring [3,4,5]Well tolerated at tested exposures [11]Not characterised

Tesamorelin: the clinical evidence base

Tesamorelin carries the larger human literature. In a 26-week randomised, placebo-controlled trial in 412 HIV-infected adults with central fat accumulation, Falutz and colleagues reported a reduction in visceral adipose tissue and an increase in IGF-1 relative to placebo, with no significant between-group difference in glucose or insulin parameters [3]. A pooled analysis of two phase 3 trials with 52-week extension data described maintenance of the visceral-fat and lipid changes while treatment continued and reversal after withdrawal [4]. Stanley and colleagues later used magnetic resonance spectroscopy in 50 HIV-infected participants and reported reductions in both visceral fat and hepatic lipid content over six months, alongside a transient early rise in fasting glucose that was not significant at study end [5]. These are disease-population data generated under regulatory oversight; they describe tesamorelin alone and do not transfer to a blend.

Ipamorelin: selectivity and preclinical anabolic readouts

The defining ipamorelin finding is receptor selectivity. In pentobarbital-anaesthetised rats and conscious swine, Raun and colleagues observed GH release comparable to GHRP-6 without the ACTH and cortisol elevations produced by GHRP-6 and GHRP-2, and without changes in FSH, LH, prolactin or TSH [1]. Johansen and colleagues reported a concentration-dependent increase in tibial longitudinal growth rate and in body-weight gain in adult female rats over 15 days, without changes in total IGF-1 or bone-turnover markers [9]. Andersen and colleagues found that ipamorelin counteracted the methylprednisolone-induced fall in periosteal bone formation and in tetanic muscle tension in adult rats [10]. The single controlled human trial, in bowel-resection patients, reported good tolerability but no significant difference from placebo in time to first tolerated meal [11].

The combination: what is and is not known

Direct answer: as of this review, there is no published randomised, controlled or even open-label study in which tesamorelin and ipamorelin were co-administered and GH, IGF-1 or any downstream outcome was measured. The synergy argument rests on 1990 human infusion data with GHRH(1-44) and GHRP-6 [6] and on the receptor biology established by Howard and Kojima [7,8]. Whether tesamorelin's long duration of GHRH-receptor occupancy changes the pulsatile character of a GHRP-driven release, or alters the ACTH/cortisol neutrality that distinguishes ipamorelin, has not been examined. Researchers citing "tesa/ipa" data are, in practice, citing two separate literatures.

Limitations of the current evidence

  • No combination data. Every claim about the blend is an inference from single-agent studies or from a different GHRP (GHRP-6) paired with native GHRH.
  • Population specificity. Tesamorelin's phase 3 data come exclusively from HIV-infected adults with lipodystrophy; ipamorelin's only human trial was in surgical patients. Neither population resembles a typical research-compound context.
  • Divergent kinetics. Tesamorelin is designed for prolonged action, ipamorelin for a short GH pulse. A co-lyophilised mixture fixes the molar ratio of two peptides with very different residence times, and no pharmacokinetic study has characterised the resulting profile.
  • Analytical complexity. Two peptides of 44 and 5 residues in one vial require two identity assignments and two purity assessments; a single HPLC purity figure on a certificate of analysis does not distinguish component ratio from total peptide content.
  • Stability. The trans-3-hexenoyl group of tesamorelin and the D-amino acids of ipamorelin protect against enzymatic cleavage, not against oxidation or aggregation in solution; blend-specific stability data are unpublished.

Where to source for research

Tesamorelin and ipamorelin are available separately and as co-listed blends in lyophilised research-grade form. Laboratories comparing suppliers typically ask for a lot-specific certificate of analysis that reports HPLC purity and mass-spectrometry identity for each component, states the nominal component ratio, and labels the material for research use only. Catalogue listings for the tesamorelin / ipamorelin blend and its components can be found at Short Chain Aminos, BioPep, Catalyst Research and Apex Research Services. Peptide Insider's supplier evaluation guide and suppliers directory outline the documentation researchers generally request before purchase.

Frequently asked research questions

What is a tesamorelin / ipamorelin blend?

It is a two-peptide research preparation combining tesamorelin, a DPP-IV-resistant 44-residue GHRH analog, with ipamorelin, a selective pentapeptide ghrelin-receptor agonist. The two act on different somatotroph receptors, and the pairing is based on the GHRH–GHRP synergy described in 1990 pituitary studies, not on any study of the blend itself [1,2,6].

What does tesa/ipa stand for?

"Tesa" abbreviates tesamorelin and "ipa" abbreviates ipamorelin, so tesa/ipa, tesa/ipa blend, tesa/ipa peptide and tesa ipa peptide all refer to the same two-component preparation. The abbreviation is a catalogue convention with no chemical meaning; the component order (tesamorelin and ipamorelin, or ipamorelin and tesamorelin) is likewise arbitrary.

Is there a study of tesamorelin + ipamorelin together?

No. As of this review no peer-reviewed study has co-administered tesamorelin and ipamorelin. The synergy rationale comes from Bowers and colleagues' 1990 human infusion data with native GHRH and the hexapeptide GHRP-6 [6], and from the distinct Gs and Gq signalling of the two receptors [7,8]. Extrapolation to this specific pair remains untested.

How does tesamorelin differ from sermorelin or CJC-1295?

Tesamorelin retains the full GHRH(1-44) sequence with an N-terminal trans-3-hexenoyl group, whereas sermorelin is the unmodified 1-29 fragment and CJC-1295 is a 1-29 analog with four substitutions and, in the DAC form, an albumin-binding linker. Tesamorelin is the only one with completed phase 3 trials and regulatory approval [2,3,4,13].

Why is ipamorelin called a selective secretagogue?

Raun and colleagues reported that ipamorelin released GH with potency similar to GHRP-6 but, unlike GHRP-6 and GHRP-2, did not raise ACTH or cortisol even at exposures far above its GH-releasing ED50, and left FSH, LH, prolactin and TSH unchanged. That endocrine profile had previously been seen only with GHRH itself [1].

What human data exist for each component?

Tesamorelin has 26-week and 52-week phase 3 data in HIV-infected adults with abdominal fat accumulation and a six-month imaging trial of visceral and hepatic fat [3,4,5]. Ipamorelin has one phase 2 trial in postoperative ileus that was well tolerated but negative on its primary endpoint [11]. Neither dataset involves the blend.

What should a certificate of analysis for the blend show?

Because two peptides are present, a useful certificate reports identity by mass spectrometry and purity by HPLC for each component separately, states the nominal component ratio, and specifies research-use-only status. A single aggregate purity figure cannot confirm that both peptides are present in the stated proportion.

Works Cited

  1. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. DOI: 10.1530/eje.0.1390552. PMID: 9849822.
  2. Ferdinandi ES, Brazeau P, High K, et al. Non-clinical pharmacology and safety evaluation of TH9507, a human growth hormone-releasing factor analogue. Basic Clin Pharmacol Toxicol. 2007;100(1):49-58. DOI: 10.1111/j.1742-7843.2007.00008.x. PMID: 17214611.
  3. Falutz J, Allas S, Blot K, et al. Metabolic effects of a growth hormone-releasing factor in patients with HIV. N Engl J Med. 2007;357(23):2359-2370. DOI: 10.1056/NEJMoa072375. PMID: 18057338.
  4. Falutz J, Mamputu JC, Potvin D, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in HIV-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010;95(9):4291-4304. DOI: 10.1210/jc.2010-0490. PMID: 20554713.
  5. Stanley TL, Feldpausch MN, Oh J, et al. Effect of tesamorelin on visceral fat and liver fat in HIV-infected patients with abdominal fat accumulation: a randomized clinical trial. JAMA. 2014;312(4):380-389. DOI: 10.1001/jama.2014.8334. PMID: 25038357.
  6. Bowers CY, Reynolds GA, Durham D, et al. Growth hormone (GH)-releasing peptide stimulates GH release in normal men and acts synergistically with GH-releasing hormone. J Clin Endocrinol Metab. 1990;70(4):975-982. DOI: 10.1210/jcem-70-4-975. PMID: 2108187.
  7. Howard AD, Feighner SD, Cully DF, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 1996;273(5277):974-977. DOI: 10.1126/science.273.5277.974. PMID: 8688086.
  8. Kojima M, Hosoda H, Date Y, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402(6762):656-660. DOI: 10.1038/45230. PMID: 10604470.
  9. Johansen PB, Nowak J, Skjaerbaek C, et al. Ipamorelin, a new growth-hormone-releasing peptide, induces longitudinal bone growth in rats. Growth Horm IGF Res. 1999;9(2):106-113. PMID: 10373343.
  10. Andersen NB, Malmlöf K, Johansen PB, et al. The growth hormone secretagogue ipamorelin counteracts glucocorticoid-induced decrease in bone formation of adult rats. Growth Horm IGF Res. 2001;11(5):266-272. PMID: 11735244.
  11. Beck DE, Sweeney WB, McCarter MD; Ipamorelin 201 Study Group. Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients. Int J Colorectal Dis. 2014;29(12):1527-1534. DOI: 10.1007/s00384-014-2030-8. PMID: 25331030.
  12. Frohman LA, Downs TR, Williams TC, et al. Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive product cleaved at the NH2 terminus. J Clin Invest. 1986;78(4):906-913. DOI: 10.1172/JCI112679. PMID: 3093533.
  13. U.S. Food and Drug Administration. EGRIFTA (tesamorelin for injection) prescribing information; approval 2010. accessdata.fda.gov.

All content strictly for research reference. The tesamorelin / ipamorelin blend and its components are research chemicals; nothing in this review constitutes guidance for human or veterinary use, and the preparation is not for human or veterinary use. Peptide Insider does not sell peptides.

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