Clinical Monographs

Peptide Guides

Comprehensive clinical monographs for prescribing professionals. Each guide covers mechanisms, dosing, safety, and practical considerations.

New guideMetabolicLimited EvidenceRemoved from Category 2 notice; PCAC review pendingSubcutaneous injection in common compounding workflows; no clinically validated prescribing standard

MOTs-C

Flagship clinician reference on MOTs-C, covering mechanism, evidence limits, metabolic signaling, and the April 2026 FDA update.

Primary indication: Investigational metabolic-resilience and insulin-sensitivity support; no FDA-approved indication

A clinician-first MOTs-C guide covering what the peptide is, how the mitochondrial stress-response biology actually works, where the evidence is strongest, where it remains weak, and how the April 2026 FDA update changes the regulatory conversation.

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MetabolicStrong EvidenceapprovedSubcutaneous injection

Tesamorelin

GHRH Analog - FDA-Approved Growth Hormone Secretagogue

Primary indication: Reduction of excess abdominal fat in HIV-infected patients with lipodystrophy (FDA-approved)

Tesamorelin (Egrifta/Egrifta SV) is an FDA-approved synthetic growth hormone-releasing hormone (GHRH) analog indicated for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy, with emerging evidence for cognitive enhancement and hepatic steatosis.

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Weight LossModerate EvidenceavailableSubcutaneous injection (oral formulation was also investigated)

AOD-9604

Growth Hormone Fragment - Fat Metabolism Guide

Primary indication: Fat reduction and body composition improvement (investigational; no regulatory approval for therapeutic use)

AOD-9604 is a modified fragment of human growth hormone (hGH fragment 177-191) studied for its fat-reducing properties without the diabetogenic or growth-promoting effects of full GH.

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Tissue RepairPreclinicalcategory2Multiple (SC, IM, IV, oral, intra-articular, topical)

BPC-157

Body Protection Compound - Complete Clinical Guide

Primary indication: Gastrointestinal cytoprotection and mucosal healing (investigational)

BPC-157 is a 15-amino acid peptide derived from human gastric juice that has demonstrated tissue-protective and healing properties across multiple organ systems.

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Growth HormoneLimited EvidenceavailableSubcutaneous injection (SC)

CJC-1295/Ipamorelin

Growth Hormone Secretagogue Combination - Prescriber Guide

Primary indication: Growth hormone deficiency and age-related GH decline (investigational combination)

CJC-1295/Ipamorelin is a synergistic combination of a growth hormone-releasing hormone (GHRH) analog and a growth hormone secretagogue used to stimulate natural growth hormone production.

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LongevityPreclinicalavailableSubcutaneous injection (SC), intramuscular injection (IM), intranasal (investigational)

Epithalon

Telomerase Activator Peptide - Anti-Aging Guide

Primary indication: Telomerase activation and telomere maintenance (investigational anti-aging peptide)

Epithalon (Epitalon) is a synthetic tetrapeptide based on the natural epithalamin produced by the pineal gland, studied for its effects on telomerase activation and potential anti-aging properties.

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Skin/HealingModerate EvidenceavailableTopical (most common), subcutaneous injection (SC), mesotherapy/microneedling delivery

GHK-Cu

Copper Peptide Complex - Regenerative Medicine Guide

Primary indication: Wound healing and tissue repair (topical and injectable formulations)

GHK-Cu (Glycyl-L-Histidyl-L-Lysine Copper) is a naturally occurring copper-binding peptide with demonstrated wound healing, anti-aging, and tissue remodeling properties.

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Sexual HealthStrong EvidenceapprovedSubcutaneous injection (SC); auto-injector available (Vyleesi)

PT-141 (Bremelanotide)

Melanocortin Receptor Agonist - Sexual Dysfunction Guide

Primary indication: Hypoactive sexual desire disorder (HSDD) in premenopausal women (FDA-approved as Vyleesi)

PT-141 (bremelanotide) is a melanocortin receptor agonist FDA-approved for hypoactive sexual desire disorder in premenopausal women, also used off-label for male sexual dysfunction.

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Nootropic & AnxiolyticLimited Evidenceavailableintranasal

Selank

Synthetic tuftsin-analog heptapeptide with anxiolytic, nootropic, and immunomodulatory properties

Primary indication: Generalized anxiety disorder and neurasthenia (approved in Russia as intranasal spray)

Selank (TP-7) is a synthetic heptapeptide analog of the endogenous immunomodulatory peptide tuftsin, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. Approved in Russia since 2009 as an intranasal anxiolytic and nootropic, Selank provides clinically meaningful anxiety reduction through GABAergic modulation without the sedation, tolerance, or dependence associated with benzodiazepines. Its tuftsin core also confers immunomodulatory properties, creating a unique dual anxiolytic-immunomodulatory pharmacological profile.

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MetabolicStrong EvidenceshortageSubcutaneous injection (Ozempic, Wegovy) or oral (Rybelsus)

Semaglutide

GLP-1 Receptor Agonist - Prescriber Reference

Primary indication: Type 2 diabetes mellitus (FDA-approved: Ozempic, Rybelsus) and chronic weight management (FDA-approved: Wegovy)

Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist with FDA approval for type 2 diabetes and chronic weight management.

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Hormone OptimizationModerate Evidenceavailablesubcutaneous

Sermorelin

Synthetic GHRH(1-29) fragment for physiologic growth hormone optimization

Primary indication: Growth hormone optimization and anti-aging (off-label via compounding pharmacies)

Sermorelin acetate is a synthetic 29-amino-acid peptide corresponding to the biologically active N-terminal segment of endogenous growth hormone-releasing hormone (GHRH). Originally FDA-approved as Geref/Geref Diagnostic for diagnosing and treating GH deficiency, the commercial product was discontinued around 2008 due to manufacturing and business reasons — not safety concerns. Today, sermorelin is one of the most widely prescribed peptides in functional and regenerative medicine, stimulating the pituitary to release GH in a physiologic, pulsatile pattern that preserves natural feedback mechanisms.

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RegenerativePreclinicalavailableMultiple (SC, IM, IV, topical, ophthalmic)

TB-500

Thymosin Beta-4 Fragment - Tissue Repair Guide

Primary indication: Wound healing and tissue repair (investigational; pharmaceutical Tbeta4 in Phase II trials for epidermolysis bullosa and dry eye)

TB-500 is a synthetic peptide representing the active region of Thymosin Beta-4, studied for its roles in tissue repair, wound healing, and anti-inflammatory effects.

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Immune SupportModerate EvidenceavailableSubcutaneous injection

Thymosin Alpha-1

Immune-Modulating Peptide - Clinical Monograph

Primary indication: Chronic hepatitis B (approved in 35+ countries as Zadaxin); immune modulation (compounded use in US)

Thymosin Alpha-1 is a naturally occurring thymic peptide that modulates immune function and has been studied for various infectious and oncologic applications.

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Weight LossStrong EvidenceshortageSubcutaneous injection (once weekly)

Tirzepatide

Dual GIP/GLP-1 Receptor Agonist - Clinical Guide

Primary indication: Type 2 diabetes mellitus (FDA-approved: Mounjaro, 2022) and chronic weight management (FDA-approved: Zepbound, 2023; expanded in 2024 for moderate-to-severe obstructive sleep apnea in adults with obesity)

Tirzepatide is a first-in-class dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist with FDA approval for type 2 diabetes and chronic weight management.

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MetabolicPreclinicalOral (compounded clinical use)

5-Amino-1MQ

Investigational metabolic and adipose-targeting agent for obesity, adipose-tissue dysfunction, and related metabolic conditions (no FDA-approved indication; no registered human clinical trials as of April 2026)

Primary indication: Investigational metabolic and adipose-targeting agent for obesity, adipose-tissue dysfunction, and related metabolic conditions (no FDA-approved indication; no registered human clinical trials as of April 2026)

5-Amino-1MQ is a selective, membrane-permeable small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine (SAH). NNMT is highly expressed in white adipose tissue, liver, and skeletal muscle, and its expression is upregulated in obesity, insulin resistance, and several cancers. By methylating and thereby trapping nicotinamide, NNMT reduces the salvageable pool of nicotinamide available for NAD+ biosynthesis — NNMT inhibition thus indirectly raises intracellular NAD+ levels and restores sirtuin activity. In adipocytes, NNMT inhibition with 5-Amino-1MQ has been shown to reduce lipogenesis, reduce intracellular 1-MNA, increase cellular NAD+, promote adipocyte lipolysis, and decrease adipocyte size and white adipose mass in preclinical models. Additional proposed effects include improved mitochondrial function, restored sirtuin-mediated transcriptional programs, and altered methylation-pathway flux. Critically, the human therapeutic implications of these preclinical findings remain unvalidated — no human clinical trials have been registered or completed.

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NeuromodulationModerate EvidenceIV infusion (standard) · IM · slow IV push

Cerebrolysin

Neurorehabilitation after ischemic stroke and traumatic brain injury (approved in 35+ countries including Austria, Germany, Russia, China; NOT FDA-approved in the United States)

Primary indication: Neurorehabilitation after ischemic stroke and traumatic brain injury (approved in 35+ countries including Austria, Germany, Russia, China; NOT FDA-approved in the United States)

Cerebrolysin is a standardized preparation of low-molecular-weight peptides and free amino acids derived from purified porcine brain tissue by enzymatic hydrolysis. Its proposed mechanisms are pleiotropic and mimic the actions of endogenous neurotrophic factors. Preclinical work demonstrates effects consistent with brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and glial-derived neurotrophic factor (GDNF) signaling — including upregulation of neuronal survival pathways (PI3K/Akt), inhibition of calcium-dependent proteases (calpains) and caspase-3-mediated apoptosis, attenuation of glutamate excitotoxicity, and enhancement of neurogenesis in subventricular and hippocampal niches. Additional reported actions include anti-inflammatory modulation of microglia, reduction of oxidative stress, and improvement of energy metabolism in neurons. In acute stroke, the presumed benefit is neuroprotection of the ischemic penumbra and enhancement of endogenous recovery mechanisms; in chronic cognitive indications, the hypothesis is sustained neurotrophic support.

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Sexual HealthModerate EvidenceIV bolus · IV infusion · SC (research)

Kisspeptin-10

Investigational stimulation of the hypothalamic-pituitary-gonadal (HPG) axis: diagnostic evaluation of hypogonadotropic hypogonadism, research in fertility induction, and adjunct investigation alongside testosterone replacement therapy (not FDA-approved for any indication)

Primary indication: Investigational stimulation of the hypothalamic-pituitary-gonadal (HPG) axis: diagnostic evaluation of hypogonadotropic hypogonadism, research in fertility induction, and adjunct investigation alongside testosterone replacement therapy (not FDA-approved for any indication)

Kisspeptin-10 is the shortest active fragment of the kisspeptin neuropeptide family encoded by the KISS1 gene. It binds the G-protein-coupled receptor GPR54 (KISS1R) expressed on hypothalamic GnRH neurons. Activation triggers pulsatile release of gonadotropin-releasing hormone (GnRH) into the hypophyseal portal system, which drives pituitary secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Downstream, LH stimulates testosterone production in Leydig cells in men and progesterone/estradiol production in the ovary, while FSH drives spermatogenesis in men and follicular development in women. The KISS1/KISS1R pathway sits upstream of GnRH and is the principal gatekeeper of puberty onset and normal reproductive function — loss-of-function mutations in KISS1 or KISS1R cause congenital hypogonadotropic hypogonadism. Exogenous kisspeptin-10 therefore serves as a probe of this axis: a brisk LH response confirms intact GnRH and pituitary function (central hypogonadism with preserved hypothalamic response), while a blunted response localizes the defect further upstream. Kisspeptin administration also has potential therapeutic applications in fertility (triggering physiologic-pattern LH surges) and in hypogonadism phenotypes responsive to pulsatile stimulation.

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Immune ModulationPreclinicalOral (PepT1-mediated) · SC · topical · intranasal

KPV

Investigational anti-inflammatory therapy for inflammatory bowel disease and other chronic inflammatory conditions (no FDA-approved indication)

Primary indication: Investigational anti-inflammatory therapy for inflammatory bowel disease and other chronic inflammatory conditions (no FDA-approved indication)

KPV is the C-terminal tripeptide (Lys-Pro-Val) of alpha-melanocyte-stimulating hormone (alpha-MSH). Despite its origin, KPV does not act through classical melanocortin receptors (MC1R-MC5R) — its anti-inflammatory effects are mediated by a melanocortin-receptor-independent mechanism. The key molecular pathway is cellular uptake via the proton-coupled oligopeptide transporter PepT1 (SLC15A1), which is normally expressed on the apical surface of small-intestinal enterocytes but is markedly upregulated on inflamed colonic epithelium and on activated immune cells during inflammation. This upregulation of PepT1 on inflamed tissue provides tissue selectivity for KPV delivery. Once internalized, KPV suppresses the nuclear factor-kappa B (NF-kB) signaling cascade — a master regulator of inflammatory gene expression — by inhibiting IkB degradation, reducing nuclear translocation of p65, and attenuating downstream transcription of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-8). Additional reported actions include reduction of neutrophil chemotaxis, attenuation of mast-cell degranulation, and dampening of pro-inflammatory signaling in dendritic cells and macrophages. In preclinical models, KPV demonstrated equal or greater anti-inflammatory potency than full-length alpha-MSH.

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LongevityLimited EvidenceIV · SC · IM · intranasal (oral NAD+ poorly absorbed; use NR/NMN precursors)

NAD+

Cellular energetics and mitochondrial support in age-related decline, metabolic dysfunction, and post-exertional recovery (all investigational; no FDA-approved indication for injectable NAD+)

Primary indication: Cellular energetics and mitochondrial support in age-related decline, metabolic dysfunction, and post-exertional recovery (all investigational; no FDA-approved indication for injectable NAD+)

NAD+ is a central redox coenzyme required for oxidative phosphorylation, glycolysis, the TCA cycle, and beta-oxidation. Beyond its redox role, NAD+ is a substrate consumed by three major enzyme families: sirtuins (SIRT1-7, NAD+-dependent deacylases regulating stress response, mitochondrial biogenesis, and metabolic homeostasis); poly-ADP-ribose polymerases (PARPs, which consume NAD+ during DNA damage repair); and CD38 (a cell-surface ectoenzyme that degrades NAD+ and increases with age). Age-related decline in tissue NAD+ is driven by increased CD38 activity and chronic PARP activation, contributing to mitochondrial dysfunction and cellular senescence. Exogenous NAD+ replenishment — via IV administration, or indirectly through oral NAD+ precursors nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) — is hypothesized to restore sirtuin activity, improve mitochondrial function, and attenuate age-related metabolic decline.

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MetabolicStrong EvidenceSC once weekly

Retatrutide

Chronic weight management and type 2 diabetes (investigational; Phase 3 TRIUMPH program ongoing. NOT FDA-approved as of April 2026)

Primary indication: Chronic weight management and type 2 diabetes (investigational; Phase 3 TRIUMPH program ongoing. NOT FDA-approved as of April 2026)

Retatrutide is a single-molecule triple-hormone-receptor agonist that activates three incretin and counter-regulatory hormone receptors: the glucagon-like peptide-1 receptor (GLP-1R), the glucose-dependent insulinotropic polypeptide receptor (GIPR), and the glucagon receptor (GCGR). GLP-1R agonism suppresses appetite via central and peripheral pathways, delays gastric emptying, and stimulates glucose-dependent insulin secretion. GIPR agonism adds complementary insulinotropic and adipose-tissue effects, paralleling the dual mechanism of tirzepatide. Glucagon receptor agonism — absent from semaglutide and tirzepatide — increases hepatic energy expenditure and lipid oxidation, contributing to additional weight loss beyond what GLP-1/GIP alone achieves. The net result in clinical trials is the largest magnitude of weight loss reported to date for an incretin-based therapy. The molecule is a synthetic 39-residue peptide conjugated to a C18 fatty-diacid linker that enables albumin binding and supports once-weekly subcutaneous dosing.

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