What is the difference between sermorelin and tesamorelin?

Both are synthetic analogs of growth hormone-releasing hormone (GHRH) that agonize the same receptor, but they differ in sequence, modification, pharmacokinetics, and approval status. Sermorelin is GHRH 1-29, the 29-amino-acid N-terminal fragment with a C-terminal amide, plasma half-life roughly 12 minutes; it was FDA-approved as Geref in 1990 (diagnostic) and 1997 (pediatric therapy) and commercially discontinued in 2008. Tesamorelin is the full 44-amino-acid GHRH 1-44 sequence carrying an N-terminal trans-3-hexenoyl cap that blocks enzymatic degradation, plasma half-life roughly 26 to 38 minutes; it is FDA-approved as Egrifta (2010) for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy and remains marketed. Both are sold here for laboratory research use only and are not the approved drug products.

Which is stronger, sermorelin or tesamorelin?

The question does not have a single answer because the two molecules were studied for different purposes in different populations. Sermorelin's pivotal evidence is pediatric growth-hormone-deficiency therapy (Thorner 1996) plus small adult studies from 1997. Tesamorelin's pivotal evidence is visceral-fat reduction in HIV-associated lipodystrophy (Falutz 2007, 2010), a different endpoint in a different clinical population. The two evidence bases are not directly comparable, and the published literature does not establish either as superior for general or off-label use. This article makes no recommendation.

Is tesamorelin FDA approved? Is sermorelin?

Their regulatory histories are different. Tesamorelin is the active drug substance in Egrifta (Theratechnologies, NDA 022505), FDA-approved on November 10, 2010 for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy; a weekly formulation (Egrifta WR) was approved March 25, 2025. Tesamorelin was also reclassified as a biologic in March 2020. Sermorelin was FDA-approved twice as Geref (1990 diagnostic, 1997 pediatric therapy) and commercially discontinued in 2008; a 2013 Federal Register determination confirmed the withdrawal was not for safety or effectiveness. CJC-1295, the third analog discussed here, has never been FDA-approved. The research-grade material sold by Peerless is not any of these approved products and is for laboratory research use only.

How is ipamorelin different from sermorelin and tesamorelin?

Ipamorelin is frequently grouped with these three but belongs to a different pharmacological class. Sermorelin, tesamorelin, and CJC-1295 are GHRH analogs that agonize the GHRH receptor (GHRH-R). Ipamorelin agonizes the ghrelin receptor (GHSR1a), a separate receptor on the same pituitary cells. In the standard Bowers classification of growth-hormone secretagogues, GHRH analogs and ghrelin-receptor agonists occupy two different columns. The distinction matters because findings about one class do not automatically transfer to the other.

Can sermorelin and tesamorelin be used together?

The published literature does not characterize the combined administration of sermorelin and tesamorelin. Both agonize the same receptor (GHRH-R), so they are members of a single pharmacological class rather than complementary mechanisms. This article describes receptor pharmacology only and makes no recommendation on combining compounds, on dose, or on any protocol of use.

Peerless Research·ghrh-analog

Sermorelin vs Tesamorelin: GHRH Analog Class Review

Sermorelin, tesamorelin, and CJC-1295 are GHRH-analog peptides with three half-lives and three different FDA postures. A mechanism and evidence review.

By Peerless Research·Published May 31, 2026

Sermorelin and tesamorelin peptide structures in deep navy and warm brass, a GHRH analog class comparison on cream

Sermorelin, tesamorelin, and CJC-1295 all do the same thing at the same receptor. Each tells the pituitary to release growth hormone by agonizing the growth-hormone-releasing-hormone receptor, the way the body's own GHRH does. The differences that matter are downstream of that shared action.

What separates them, first, is time. Sermorelin clears from plasma in about twelve minutes. Tesamorelin clears in roughly half an hour. CJC-1295, tethered to a circulating blood protein, lingers for the better part of a week.

Those three half-lives map onto two design philosophies and, as it happens, three completely different positions under United States drug law. Most of the popular comparison content on these molecules sells a protocol or a stack and skips both stories. This review covers the mechanism, the evidence, and the regulatory split.

Research content. The article below reviews published clinical and preclinical literature on three growth-hormone-releasing-hormone analogs. The compounds discussed are sold by Peerless Peptides for laboratory research use only and are not for human or veterinary administration. Two of the three (sermorelin and tesamorelin) have separate FDA-approval histories as prescription drugs; the research-grade material sold here is not those approved drug products.

Last reviewed: May 31, 2026 by Peerless Research.

Summary

Sermorelin, tesamorelin, and CJC-1295 are synthetic analogs of growth hormone-releasing hormone (GHRH), the hypothalamic peptide that signals the pituitary to release growth hormone. All three agonize the GHRH receptor. They differ in sequence length, in the chemical modification that protects them from enzymatic breakdown, and in how long they stay in circulation^[1].

A fourth molecule, ipamorelin, is frequently compared alongside them but belongs to a separate class: it agonizes the ghrelin receptor, not the GHRH receptor. Conflating the two classes is the most common mechanism error in the popular comparison literature.

The human evidence base is uneven. Sermorelin's strongest data is in pediatric growth-hormone deficiency; its adult data is small and decades old.

Tesamorelin's strongest data comes from HIV-associated lipodystrophy trials and does not automatically generalize to healthy populations. CJC-1295's human pharmacology rests on two sponsor-internal papers from 2006 with no independent replication. The three also occupy three different regulatory postures, which the final section sets out.

Note: Much of the human evidence below was generated in specific clinical-trial populations (children with growth-hormone deficiency, adults with HIV-associated lipodystrophy) using FDA-approved drug products. It does not establish safety or efficacy for off-label or general use. This article is a literature review, not a recommendation of use.

The Three Molecules at a Glance

All three derive from the same parent sequence, native human GHRH, isolated in 1982 from a pancreatic tumor by the Salk Institute group of Roger Guillemin^[1]. Brazeau and colleagues then showed that the first 29 amino acids retained the full activity of the 44-residue parent, which became the chemical basis for sermorelin^[2].

Property	Sermorelin	Tesamorelin	CJC-1295 (with DAC)
Backbone	GHRH 1-29, C-terminal amide	GHRH 1-44, trans-3-hexenoyl on Tyr1	GHRH 1-29, four substitutions + DAC
Residues	29	44	30
Molecular weight (g/mol)	3357.93	5135.86	3647.25
CAS registry	86168-78-7	218949-48-5	863288-34-0
PubChem CID	16132413	16137828	91971820
Plasma half-life	~12 min	~26 to 38 min	~6 to 8 days
US FDA status	Approved 1990 and 1997; discontinued 2008	Approved 2010; marketed	Never approved

The table holds the whole comparison in miniature. One receptor, one parent sequence, and three engineering answers to a single problem: native GHRH is destroyed in the bloodstream within minutes.

One Receptor: GHRH-R Agonism and the Secretagogue Distinction

The shared target is the growth-hormone-releasing-hormone receptor (GHRH-R), a class B G-protein-coupled receptor on the somatotroph cells of the anterior pituitary. Agonism there raises intracellular cyclic AMP through the Gαs pathway, which drives growth-hormone gene transcription and the pulsatile release of growth hormone into circulation^[1]. Sermorelin, tesamorelin, and CJC-1295 differ in sequence and pharmacokinetics, but they converge on this one receptor.

That shared target is why the three are grouped as the GHRH-analog class. It is also why one common point of confusion is worth correcting directly. Ipamorelin, frequently grouped with these three, does not act at this receptor. It agonizes the ghrelin receptor (GHSR1a), a different receptor expressed on the same pituitary cells.

The published pharmacology places GHRH analogs and ghrelin-receptor secretagogues in two distinct classes, the two columns of the Bowers classification of growth-hormone secretagogues. Findings about one class do not transfer to the other by default. A study of ipamorelin is not evidence about sermorelin, and the reverse is equally true.

Because sermorelin, tesamorelin, and CJC-1295 all occupy the same receptor, combining two of them is a different matter from combining two pharmacological classes. That is a question of receptor pharmacology, not a protocol. The published literature does not characterize the combined administration of these analogs, and nothing here should be read as a recommendation on use, dose, or combination.

Pulsatile Versus Sustained: The Half-Life Axis

The reason native GHRH needs engineering at all is a single enzyme. Dipeptidyl peptidase IV (DPP-IV) cleaves the N-terminal Tyr-Ala dipeptide off GHRH within minutes, producing an inactive fragment^[3]. Each of the three analogs solves this problem differently, and each solution sets the molecule's half-life.

Sermorelin keeps the native sequence and accepts the short half-life, roughly twelve minutes. The bet is that a clean, brief growth-hormone pulse that decays before the next dose more closely mimics the body's own episodic GHRH signaling than a sustained signal would. Tesamorelin takes a similar pulsatile path by a different route: it keeps the full 44-residue sequence and caps the N-terminus with a trans-3-hexenoyl group that blocks DPP-IV, extending the half-life modestly to roughly twenty-six to thirty-eight minutes without converting the signal to a continuous one.

CJC-1295 takes the opposite path. The four protease-resistance substitutions in its backbone already extend its life relative to sermorelin, and the Drug Affinity Complex (DAC) modification then tethers the peptide covalently to circulating serum albumin through a maleimide linker^[11]. The albumin tether stretches the half-life to roughly six to eight days, converting pulsatile receptor occupancy into sustained, multi-day occupancy.

This is the structural spine of the whole comparison. Sermorelin and tesamorelin preserve pulsatile signaling by design; CJC-1295 with DAC deliberately abolishes it in favor of sustained exposure. Whether sustained GHRH-receptor signaling reproduces the biology of pulsatile signaling over months is an open question in the published record, not a settled one.

Sermorelin: An Approved-Drug Pedigree and a Thin Adult Base

Sermorelin is the only molecule of the three with a finished FDA-approval history, and that history is specific. Serono developed sermorelin acetate as Geref and received two approvals: Geref Diagnostic in December 1990 for growth-hormone-deficiency provocation testing, and Geref in September 1997 for chronic therapy of idiopathic growth-hormone deficiency in children with growth failure.

The registration trial behind the 1997 approval was the Geref International Study Group study reported by Thorner and colleagues in 1996, which enrolled 110 previously untreated prepubertal growth-hormone-deficient children and reported an increase in height velocity over the first year of once-daily therapy^[4]. Prakash and Goa later reviewed the pediatric program and positioned sermorelin as a secondary option to recombinant growth hormone, whose height-velocity readouts were larger. That relative efficacy gap contributed to the 2008 commercial discontinuation.

The adult evidence is much thinner, and this is the gap most commercial copy elides. The contemporary off-label market is adult age-related supplementation, but the supporting human literature is two small academic studies from 1997. Vittone and colleagues enrolled 19 older men and women in a 16-week nightly dosing protocol and reported increases in nocturnal growth hormone and IGF-1^[5]. Khorram and colleagues enrolled 14 age-advanced subjects using a closely related analog over the same 16 weeks^[6].

Two studies, fourteen and nineteen subjects, sixteen weeks each, nearly three decades old. No Phase 3 randomized trial of sermorelin in adult age-related indications has been published. The adult case rests largely on surrogate endpoints, principally IGF-1 and lean-mass measures, rather than on hard clinical outcomes, and that distinction is rarely drawn in the comparisons that dominate the topic.

Tesamorelin: Phase 3 Evidence in a Specific Population

Tesamorelin has the strongest and most modern evidence base of the three, and it comes attached to a specific population that is easy to lose. The molecule is the active substance in Egrifta (Theratechnologies), FDA-approved in November 2010 for the reduction of excess abdominal fat in HIV-infected adults with lipodystrophy. That HIV-lipodystrophy population is the entire basis of the approval.

The registration data is two identically designed Phase 3 trials. Falutz and colleagues reported the first in 2007 in the New England Journal of Medicine (NCT00123253, 412 HIV-infected adults), with a reduction in visceral adipose tissue measured by CT against placebo^[7]. The 2010 pooled analysis of that trial plus its confirmatory companion (NCT00435136, combined 816 adults) reported sustained visceral-fat reduction over 52 weeks^[8].

A separate academic program at Massachusetts General Hospital extended tesamorelin into HIV-associated fatty liver disease. Stanley and colleagues reported in 2019 in Lancet HIV (NCT02196831, 61 adults) a reduction in liver fat fraction over twelve months in that HIV population^[9]. The work is rigorous, and it remains within HIV-associated disease.

Here is the load-bearing critique. Every one of these readouts was generated in people living with HIV and lipodystrophy or HIV-associated fatty liver. Generalization to healthy adults seeking body-composition or anti-aging effects is not Phase 3 evidence-supported, and a non-HIV NAFLD program announced in 2020 has not reported a confirmatory readout.

There is also a frequent citation error worth flagging: the Baker 2012 cognition trial in Archives of Neurology used tesamorelin, not sermorelin, yet is routinely cited in commercial sermorelin copy^[10]. The two molecules are not interchangeable, and neither is their evidence.

CJC-1295: A Corporate-Orphan Evidence Base Frozen at 2006

CJC-1295 has the thinnest human record of the three, and the reason is corporate rather than scientific. The entire peer-reviewed human pharmacology consists of two papers published in 2006 by the developer, ConjuChem. Teichman and colleagues reported two randomized controlled trials in healthy adults, observing a plasma half-life of roughly six to eight days and multi-day growth-hormone and IGF-1 elevation per dose^[11]. Ionescu and Frohman reported that pulsatile growth-hormone secretion persisted over seven days of continuous receptor activation in eight healthy men^[12].

Both papers were authored by the sponsor, the molecule and the funding were internal, and neither has been independently replicated. The corpus has not grown because the program ended. ConjuChem terminated its one registered Phase 2 trial in HIV-associated visceral adiposity (NCT00267527) in 2006 following a participant death at the Argentina site, attributed by the attending physician to pre-existing coronary disease; the company filed for bankruptcy in 2010, and the successor pivoted away from the GHRH program entirely.

The result is an evidence base structurally frozen at two papers from one sponsor, nearly twenty years old. A further complication routinely lost in vendor catalogs is that two chemically distinct molecules are sold under the name CJC-1295. The with-DAC form carries the albumin-binding modification and the multi-day half-life; the without-DAC form (Mod GRF 1-29) lacks it and clears in roughly thirty minutes. The two differ by about 280 daltons in mass, and confirming which one a Certificate of Analysis describes is the only reliable way to tell them apart.

Research Limitations: Population, Sample Size, and an Open Receptor Question

Read together, the three evidence bases share a set of gaps that the popular comparison content rarely names. Naming them is the point of this section.

The first is population transfer. Tesamorelin's best data is in HIV-associated disease, and sermorelin's best data is in pediatric deficiency. Neither is a study of healthy adults, and importing those results into a general-use or anti-aging frame is an extrapolation, not a finding.

The second is sample size and endpoint. Sermorelin's adult literature is two studies under twenty subjects each, built on surrogate endpoints, and CJC-1295's human literature is two sponsor-internal papers with no replication.

The third is a mechanism question that applies across the class. GHRH-receptor splice variants, notably SV1, are documented on multiple human cancer cell lines, and cells expressing them gain mitogenic responsiveness to GHRH agonists^[13]. The Schally laboratory has spent decades developing GHRH antagonists as anti-tumor agents precisely because GHRH-receptor-positive tumors can expand under agonist exposure. Whether chronic agonism by any of these analogs carries a meaningful signal in people with occult GHRH-receptor-positive tumors is unresolved in the peer-reviewed record, and none of the existing trials was powered to detect it.

None of these limitations is a verdict against the molecules. Each describes the current grade and reach of the evidence. A careful reading weights the population mismatch, the small adult samples, the unreplicated CJC-1295 data, and the open receptor question accordingly.

Regulatory Context: One Class, Three Postures

The most underreported fact about these three molecules is that they sit in three different places under United States drug law, despite sharing a receptor and a parent sequence.

Sermorelin has an approved-drug pedigree. Geref was withdrawn commercially in 2008, and a Federal Register determination on March 4, 2013 confirmed the withdrawal was not for reasons of safety or effectiveness. That determination is what allows sermorelin to be compounded under the "component of an approved drug product" pathway in section 503A of the Federal Food, Drug, and Cosmetic Act, a pathway distinct from the bulk-substance route that governs most research peptides.

Tesamorelin sits differently again. It is an actively marketed FDA-approved drug, and it was reclassified as a biologic in March 2020. That reclassification closes the 503A bulk-substance compounding pathway to it, because biologics are categorically ineligible for that list.

CJC-1295 sits at the far end: it has never been approved, the FDA Pharmacy Compounding Advisory Committee voted against bulk-list inclusion for all of its variants in December 2024, and it was named in a 2026 federal indictment of a prescriber. The broader compounding framework that produced these decisions is covered in our 503A vs 503B compounding primer.

All three are prohibited in sport. The World Anti-Doping Agency lists growth-hormone-releasing factors, including this class, under category S2.2.4, banned at all times. For current chemistry, certificate-of-analysis detail, and the full reference set on each molecule, see the sermorelin, tesamorelin, and CJC-1295 product pages.

References

Guillemin R, Brazeau P, Böhlen P, Esch F, Ling N, Wehrenberg WB. Growth hormone-releasing factor from a human pancreatic tumor that caused acromegaly. Science. 1982;218(4572):585-587. PMID: 6812220.
Brazeau P, Ling N, Esch F, Böhlen P, Mougin C, Guillemin R. Growth hormone releasing factor, somatocrinin, releases pituitary growth hormone in vitro. Proc Natl Acad Sci USA. 1982;79(24):7909-7913. PMID: 6817210.
Frohman LA, Downs TR, Williams TC, Heimer EP, Pan YC, Felix AM. 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. PMID: 3093534.
Thorner M, Rochiccioli P, Colle M, et al. Once daily subcutaneous growth hormone-releasing hormone therapy accelerates growth in growth hormone-deficient children during the first year of therapy. J Clin Endocrinol Metab. 1996;81(3):1189-1196. PMID: 8772599.
Vittone J, Blackman MR, Busby-Whitehead J, et al. Effects of single nightly injections of growth hormone-releasing hormone (GHRH 1-29) in healthy elderly men. Metabolism. 1997;46(1):89-96. PMID: 8995816.
Khorram O, Laughlin GA, Yen SS. Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women. J Clin Endocrinol Metab. 1997;82(5):1472-1479. PMID: 9141536.
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. PMID: 18057338. Trial NCT00123253.
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. PMID: 20554713. Trial NCT00435136.
Stanley TL, Fourman LT, Feldpausch MN, et al. Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial. Lancet HIV. 2019;6(12):e821-e830. PMID: 31611038. Trial NCT02196831.
Baker LD, Barsness SM, Borson S, et al. Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial. Arch Neurol. 2012;69(11):1420-1429. PMID: 22869065. (Used tesamorelin, not sermorelin; frequently miscited.)
Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799-805. PMID: 16352683.
Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-4797. PMID: 17018654.
Rekasi Z, Czompoly T, Schally AV, Halmos G. Isolation and sequencing of cDNAs for splice variants of growth hormone-releasing hormone receptors from human cancers. Proc Natl Acad Sci USA. 2000;97(19):10561-10566. PMID: 10984544.
U.S. Food and Drug Administration. Determination That GEREF (Sermorelin Acetate) Injection Was Not Withdrawn From Sale for Reasons of Safety or Effectiveness. Federal Register Notice 2013-04827, 78 FR 14104, March 4, 2013.
FDA Pharmacy Compounding Advisory Committee. Meeting record, December 4, 2024. Vote against 503A bulks-list inclusion for CJC-1295 (all variants).
World Anti-Doping Agency. The 2026 Prohibited List. International Standard, Section S2.2.4 Growth Hormone Releasing Factors. Effective January 1, 2026.

Not intended to diagnose, treat, cure, mitigate, or prevent any disease. Sold for research, laboratory, or analytical purposes only.

Research Compounds Referenced

The compounds discussed in this article are sold by Peerless Peptides for laboratory research use only. They are not FDA-approved for human or veterinary administration. Per-batch Certificates of Analysis are available.

Sermorelin: 29-amino-acid synthetic GHRH 1-29 analog with C-terminal amide.PDP entry →
Tesamorelin: Synthetic 44-amino-acid GHRH 1-44 analog with N-terminal trans-3-hexenoyl modification.PDP entry →
CJC-1295: 30-amino-acid GHRH analog with Drug Affinity Complex (DAC) albumin-binding modification.PDP entry →

Frequently Asked Questions

What is the difference between sermorelin and tesamorelin?: Both are synthetic analogs of growth hormone-releasing hormone (GHRH) that agonize the same receptor, but they differ in sequence, modification, pharmacokinetics, and approval status. Sermorelin is GHRH 1-29, the 29-amino-acid N-terminal fragment with a C-terminal amide, plasma half-life roughly 12 minutes; it was FDA-approved as Geref in 1990 (diagnostic) and 1997 (pediatric therapy) and commercially discontinued in 2008. Tesamorelin is the full 44-amino-acid GHRH 1-44 sequence carrying an N-terminal trans-3-hexenoyl cap that blocks enzymatic degradation, plasma half-life roughly 26 to 38 minutes; it is FDA-approved as Egrifta (2010) for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy and remains marketed. Both are sold here for laboratory research use only and are not the approved drug products.
Which is stronger, sermorelin or tesamorelin?: The question does not have a single answer because the two molecules were studied for different purposes in different populations. Sermorelin's pivotal evidence is pediatric growth-hormone-deficiency therapy (Thorner 1996) plus small adult studies from 1997. Tesamorelin's pivotal evidence is visceral-fat reduction in HIV-associated lipodystrophy (Falutz 2007, 2010), a different endpoint in a different clinical population. The two evidence bases are not directly comparable, and the published literature does not establish either as superior for general or off-label use. This article makes no recommendation.
Is tesamorelin FDA approved? Is sermorelin?: Their regulatory histories are different. Tesamorelin is the active drug substance in Egrifta (Theratechnologies, NDA 022505), FDA-approved on November 10, 2010 for reduction of excess abdominal fat in HIV-infected adults with lipodystrophy; a weekly formulation (Egrifta WR) was approved March 25, 2025. Tesamorelin was also reclassified as a biologic in March 2020. Sermorelin was FDA-approved twice as Geref (1990 diagnostic, 1997 pediatric therapy) and commercially discontinued in 2008; a 2013 Federal Register determination confirmed the withdrawal was not for safety or effectiveness. CJC-1295, the third analog discussed here, has never been FDA-approved. The research-grade material sold by Peerless is not any of these approved products and is for laboratory research use only.
How is ipamorelin different from sermorelin and tesamorelin?: Ipamorelin is frequently grouped with these three but belongs to a different pharmacological class. Sermorelin, tesamorelin, and CJC-1295 are GHRH analogs that agonize the GHRH receptor (GHRH-R). Ipamorelin agonizes the ghrelin receptor (GHSR1a), a separate receptor on the same pituitary cells. In the standard Bowers classification of growth-hormone secretagogues, GHRH analogs and ghrelin-receptor agonists occupy two different columns. The distinction matters because findings about one class do not automatically transfer to the other.
Can sermorelin and tesamorelin be used together?: The published literature does not characterize the combined administration of sermorelin and tesamorelin. Both agonize the same receptor (GHRH-R), so they are members of a single pharmacological class rather than complementary mechanisms. This article describes receptor pharmacology only and makes no recommendation on combining compounds, on dose, or on any protocol of use.