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Weight Loss & Metabolic

Peptides used for weight management, insulin sensitivity, and metabolic dysfunction.

Clinical Overview

Weight Loss & Metabolic

Peptides used for weight management, insulin sensitivity, and metabolic dysfunction.

7 peptides1 FDA-approvedSubcutaneous injection (Ozempic · Wegovy) · oral (Rybelsus) · Subcutaneous injection (once weekly) · SC once weekly · Subcutaneous injection (oral formulation was also investigated)Last reviewed · April 22, 2026

Weight-loss and metabolic peptides span several mechanism classes that prescribers commonly combine, stack, or sequence — from FDA-approved GLP-1 receptor agonists to emerging triple agonists, growth-hormone-derived fragments, and mitochondrial peptides.

Mechanism Classes

  • GLP-1 receptor agonists

    Drive appetite suppression, delayed gastric emptying, and improved glycemic control. Semaglutide is the FDA-approved workhorse in this class.

  • Dual GLP-1 / GIP agonists

    Tirzepatide adds GIP receptor activity for greater weight loss than single-target GLP-1s in head-to-head trials.

  • Triple agonists (emerging)

    Retatrutide adds glucagon-receptor activity (GLP-1 + GIP + glucagon) for even greater weight loss in early Phase 2 data.

  • GHRH analogs & GH fragments

    Tesamorelin (GHRH analog, FDA-approved for HIV lipodystrophy) and AOD-9604 (GH fragment) target visceral adiposity and lipolysis.

  • Mitochondrial & metabolic peptides

    MOTS-c, 5-Amino-1MQ (NNMT inhibitor), and cagrilintide (amylin analog, stacks with semaglutide) target insulin sensitivity and adipocyte metabolism through distinct pathways.

Regulatory Status

FDA-Approved

  • Semaglutide
  • Tirzepatide
  • Tesamorelin (HIV lipodystrophy)

Investigational / Off-Label

  • AOD-9604
  • MOTS-c
  • Retatrutide
  • Cagrilintide
  • 5-Amino-1MQ

Compounding eligibility for semaglutide and tirzepatide is tied to FDA drug-shortage status. Verify current status before writing compounded prescriptions.

Evidence Base

Heterogeneous — Phase 3 RCT data for FDA-approved agents; early-phase trials for emerging triple agonists (retatrutide, cagrilintide); preclinical-to-pilot data for compounded peptides (AOD-9604, MOTS-c, 5-Amino-1MQ).

Primary-Literature References

90

Across 7 linked monographs

Prescribing Considerations

  1. 1Verify FDA drug-shortage status for semaglutide and tirzepatide before writing compounded prescriptions.
  2. 2Screen for personal or family history of medullary thyroid carcinoma before starting GLP-1 or dual agonists (contraindication).
  3. 3Titrate GLP-1-based agents gradually to manage GI tolerability during dose escalation.
  4. 4Baseline and periodic monitoring: CMP, HbA1c, lipid panel, thyroid function, body composition.
  5. 5Monitor for gallbladder disease and rare pancreatitis reports on chronic therapy.
  6. 6Set patient expectations on time-to-effect, adherence, and long-term weight maintenance.
Peer-reviewed clinical references · last reviewed April 22, 2026PeptidePrescriber · Clinical Reference

Peptides in this category(7)

Clinical monographs for each agent — dosing ranges, safety profile, evidence, and prescribing considerations.

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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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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1 additional monograph in this category is in clinical review and will be published soon.

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