Peptide Medix product catalog

ET
Editorial Team
August 16, 2026 4 min read

Obesity and appetite peptide research is organised around a circuit, not a single tissue: peripheral hormones from gut and adipose report energy status to the hypothalamic arcuate nucleus, where opposing NPY/AgRP and POMC/CART neurons drive feeding behaviour through melanocortin receptors. Our obesity topic page collects the peptide standards, antisera, tracers and immunoassay kits used across that circuit. This guide maps which families sit inside the topic, what each is ordered for, and which reagent format answers which question.

What sits under the obesity topic

Families are filed here when the parent peptide regulates food intake, energy expenditure or adipose biology in published models. That spans peripheral satiety and hunger signals, hypothalamic neuropeptides, melanocortin-system components, adipokines, and the newer myokine and browning-related peptides. Overlap with other topics is heavy by design: leptin and adiponectin are shared with diabetes, while NPY, orexin and galanin also sit under neuropeptides. Every item is supplied for in-vitro and approved animal research only; nothing here is a weight-management product.

Peripheral signals: hunger, satiety and adiposity

  • Leptin — the adipose-derived adiposity signal whose discovery defined the field; ordered as recombinant standards, fragments and antagonists, plus the antisera and kits used to measure it in rodent plasma.
  • Ghrelin — the only established circulating orexigenic hormone. The octanoylated form is the receptor-active species; des-acyl ghrelin has its own, separate literature.
  • Obestatin — encoded in the same preproghrelin transcript, with a contested anorexigenic literature; a useful case where catalog inclusion reflects active investigation rather than agreement.
  • PYY — PYY(3–36) is the Y2-selective satiety fragment; the full-length PYY(1–36) has a different receptor profile, so the form must be specified.
  • Amylin and oxyntomodulin — co-secreted satiety peptides now central to combination pharmacology research.
  • CCK — the original satiety hormone; CCK-8 sulfated is the standard active form and desulfation abolishes CCK-A receptor potency.
  • GLP-1 — appetite as well as glycaemic effects; see the incretin pathway hub.

Hypothalamic and melanocortin families

  • NPY — the most potent orexigenic peptide characterised, with Y1/Y2/Y5 receptor-selective fragments for dissecting the circuit.
  • AgRP — the endogenous inverse agonist at MC3R/MC4R, co-expressed with NPY; AgRP(83–132) is the standard active fragment.
  • POMC, MSH and melanocortin — the anorexigenic arm. α-MSH acting at MC4R is the best-validated node in monogenic obesity, and the family page carries the receptor-selective analogs.
  • CART — co-expressed with POMC; the (55–102) fragment is the commonly used active form.
  • MCH — melanin-concentrating hormone, an orexigenic lateral-hypothalamic peptide.
  • Orexin — orexin-A and orexin-B link arousal state to feeding; central to the sleep–metabolism interface.
  • Galanin and spexin — opposing influences on macronutrient preference and energy balance; spexin is a comparatively recent addition with a fast-growing literature.
  • Nesfatin-1, neuromedin U and neuromedin S — anorexigenic hypothalamic peptides used in circuit-mapping and receptor work.
  • GnIH/RFRP — connects energy status to the reproductive axis, ordered where the design spans both.

Adipose, muscle and browning families

  • Adiponectin and resistin — the classical adipokines; note that adiponectin's multimeric state governs activity, which peptide fragments cannot reproduce.
  • Adipocyte-derived factors — a broad family page collecting less-studied secreted peptides from fat.
  • Irisin and FNDC5 — the exercise-induced browning candidate and its precursor; antibody specificity in this family has been publicly disputed, so validated reagents and blocking-peptide controls matter more than usual.
  • Meteorin-like (Metrnl) and musclin — myokines studied in thermogenesis and exercise adaptation.
  • Apelin and adropin — metabolic peptides bridging to cardiovascular research.
  • Visfatin and vaspin — adipose-derived peptides in insulin-sensitivity studies.

Which formats the obesity topic contains

Synthetic peptide standards dominate: central administration studies in rodents, receptor pharmacology and assay calibration all start here, and receptor-selective fragments are the main tool for separating Y-receptor and melanocortin-receptor contributions. ELISA and EIA kits quantify leptin, ghrelin, PYY and adipokines in plasma. Polyclonal antisera support hypothalamic immunohistochemistry, where co-localisation of NPY/AgRP and POMC/CART markers is standard. Labeled peptides supply binding tracers and fluorescent ligands for receptor-trafficking imaging. Magnetic beads underpin multiplex metabolic panels.

How laboratories choose within a family

Fragment identity is the first decision and the one most often got wrong: PYY(3–36) and PYY(1–36), AgRP(83–132) and full-length AgRP, CART(55–102) and CART(62–102) behave differently, and substituting one for another changes the pharmacology rather than the potency. Modification state is the second: sulfated CCK-8, acylated ghrelin and amidated C-termini are functional requirements, not cosmetic details — see C-terminal amidation. Species is the third; rodent and human sequences diverge in several of these families, and antibody cross-reactivity cannot be assumed, so check species reactivity. Finally, if the question is a concentration in a sample, a validated kit beats assembling components; if it is localisation or mechanism, order peptide and antiserum separately.

Handling notes for this topic

Three cautions. Acyl-ghrelin is labile — samples need acidification and protease inhibition or you measure des-acyl ghrelin by default. Amylin aggregates; it is amyloidogenic by nature, so freshly prepared solutions and appropriate solvents are essential, and old stock may give irreproducible results (see peptide solubility). Central-administration peptides need vehicle compatibility checked before the experiment, not during it. Otherwise the standard workflow holds: sealed vials at −20 °C, single-use aliquots, minimal freeze–thaw — the storage guide, aliquoting guide and COA guide cover the details.

Where to go next

Browse the full obesity topic, the adipose tissue hub or the melanocortin pathway hub. Adjacent guides cover the diabetes and metabolism section and the neuropeptide section, which shares most of the hypothalamic families.

Frequently Asked Questions

PYY(3–36) or PYY(1–36) — which should I order?
They are different tools. PYY(3–36), produced by DPP-4 cleavage, is Y2-selective and is the form used in satiety studies. Full-length PYY(1–36) retains Y1 activity and behaves differently in feeding assays. Specify the fragment explicitly; catalog entries list both because both appear in the literature.
Why does CCK need to be sulfated?
The sulfated tyrosine at position 7 from the C-terminus is required for high-affinity CCK-A receptor binding. Desulfated CCK-8 loses that potency almost entirely while remaining active at CCK-B. Since sulfation is labile under acidic conditions, confirm the modification on the certificate of analysis rather than assuming it.
Are peptide standards suitable for central administration studies?
They are the standard tools for it in approved animal protocols, but check vehicle compatibility, endotoxin status and solubility at the required concentration before the study. Research-grade peptides are not sterile or endotoxin-controlled unless a specific item states so, which matters for intracerebroventricular work.
Why is irisin controversial in the catalog?
Early irisin measurements relied on antibodies later shown to cross-react with unrelated proteins, and the human FNDC5 start codon is atypical. The molecule is real and the field continues, but reagent validation matters unusually much here — use blocking-peptide controls and mass-spectrometry-validated antibodies where the conclusion depends on absolute quantitation.
Do I need melanocortin receptor-selective analogs, or is α-MSH enough?
α-MSH activates MC1R, MC3R, MC4R and MC5R, so it cannot attribute a feeding effect to a specific receptor. Selective agonists and antagonists on the melanocortin family page exist precisely for that dissection. Use α-MSH as the physiological ligand and the selective tools to assign the receptor.
Are these peptides for weight-loss use?
No. Everything in the research catalog is supplied for in-vitro assays and approved animal research. Several molecules in this topic have approved therapeutic counterparts, but catalog material is not manufactured to pharmaceutical standards and is not for human or veterinary administration.

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