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CertaPeptides

Research reference

Peptides studied in adipose-tissue laboratory literature

Not everything on this page is a peptide — 5-Amino-1MQ is a small molecule, and the page is titled accordingly. It indexes the published research on compounds studied against adipose-tissue and metabolic endpoints — what was measured, in what model, and where to read the record. The literature here is preclinical (cell-culture, rodent and primate work), and one summary also notes an observational finding in people. Those are different kinds of evidence and the page keeps them distinct. None of these compounds is approved for general human use.

How to read this page. Compounds are ordered by how much published preclinical literature exists for the research area — not by how well anything is claimed to work. An "Extensive literature" label means many peer-reviewed studies exist to read, including negative and inconclusive ones. It is not a statement that the compound produces any effect, in a laboratory model or in a person. Every summary below describes what a specific study reported, with the PubMed record linked so you can read the source yourself.

01

5-Amino-1MQ

Moderate literature

A small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme whose knockdown in fat and liver tissue was shown to affect diet-induced obesity in mice. The compound is studied as a way to inhibit that target pharmacologically rather than genetically.

Literature depth: A young literature built on solid target-validation work, including a Nature paper on the underlying enzyme target.

NNMT inhibitionAdipocyte lipogenesisNAD+ metabolismRodent obesity models

What the research reports

[1] NNMT inhibition in adipocytes. In cultured adipocytes, membrane-permeable methylquinolinium NNMT inhibitors were reported to lower intracellular 1-methylnicotinamide, raise NAD+ and SAM, and suppress lipogenesis. In diet-induced obese mice, a potent inhibitor of this series reduced body weight and white adipose mass with no change in food intake.

Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology (2018). PMID 29155147

[2] NNMT target validation. Antisense knockdown of nicotinamide N-methyltransferase in white adipose tissue and liver of diet-induced obese mice was reported to protect against diet-induced obesity. This target-validation work in mice underpins the later small-molecule NNMT inhibitor literature.

Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature (2014). PMID 24717514
View 5-Amino-1MQ specifications and COA
02

MOTS-c

Moderate literature

A mitochondrial-derived peptide studied in metabolic regulation research. It is one of the few compounds in this area whose primary literature appears in top-tier journals, covering metabolic homeostasis, insulin resistance, and exercise-response signalling in rodent models.

Literature depth: A young but high-quality literature, including papers in Cell Metabolism and Nature Communications.

Metabolic homeostasisInsulin-resistance modelsExercise-response signallingAMPK pathway

What the research reports

[1] Metabolism and insulin resistance. This research characterised the mitochondrial-derived peptide MOTS-c as a regulator of metabolic homeostasis, reporting effects on insulin sensitivity in laboratory models.

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism (2015). PMID 25738459

[2] Exercise and muscle homeostasis. This paper reports two distinct things that should not be merged: endogenous MOTS-c rose with exercise in human subjects, while ADMINISTERED MOTS-c affected physical capacity in mice. The mouse arm is the interventional result; the human arm is observational.

MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications (2021). PMID 33473109
View MOTS-c specifications and COA
03

Adipotide

Emerging literature

A ligand-directed peptidomimetic designed to target the blood vessels supplying white adipose tissue rather than fat cells themselves. Its mechanism is deliberately destructive — it triggers apoptosis in that vasculature — which is why the published work sits in cancer-adjacent targeting literature and why it has not progressed to human study.

Literature depth: A short, high-profile preclinical trail — mouse and non-human primate work from one research group — with no human data at all.

Adipose vasculature targetingProhibitin as a vascular markerNon-human primate research

What the research reports

[1] Adipose vasculature targeting in mice. In mouse research, a peptide motif (CKGGRAKDC) was reported to home to white fat vasculature and to associate with prohibitin, identifying prohibitin as a vascular marker of adipose tissue. Coupling a proapoptotic peptide to that motif produced targeted ablation of adipose tissue in the animals studied.

Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine (2004). PMID 15133506

[2] Non-human primate research. In obese Old World monkeys, the ligand-directed peptidomimetic termed adipotide was reported to induce apoptosis within blood vessels of white adipose tissue, with associated weight loss and changes in insulin resistance. The same study also reported reversible renal proximal-tubule changes in the treated animals — a finding that belongs alongside the efficacy result. These are preclinical primate data and were not followed by human trials.

A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science Translational Medicine (2011). PMID 22072637

Choosing between them for a study

The compounds here answer different questions. Some are studied for direct effects on adipose tissue, others for broader metabolic regulation where adiposity is one measured outcome among several. A crucial distinction when reading this literature: a finding in a rodent model and a finding from a controlled trial in a specific patient population are not interchangeable, and neither transfers to a healthy person. Check which kind of study each citation is before drawing any conclusion from it.

Frequently asked questions

Will any of these cause fat loss?

We make no such claim, and the literature indexed here does not support one for general use. These records report what was measured in defined laboratory models, or in specific clinical trial populations where noted. None of these compounds is an approved weight-loss treatment, and all are supplied for research purposes only.

Why are Semaglutide and Tirzepatide not listed?

We no longer supply them, so they are outside this index. This page covers only compounds whose per-batch certificate of analysis we publish and that can be independently verified on a public certificate page hosted by the testing lab or its certificate provider.

What does the evidence level mean?

It describes how much published peer-reviewed literature exists for that compound in this research area — nothing more. It is not a ranking of effect, and a higher level does not imply a compound does anything.

Related: Peptides studied in skeletal-muscle literature · COA Vault · Reconstitution calculator

This page summarises published laboratory research for reference. It is not medical guidance and makes no human safety, dosing, or efficacy claim. All referenced compounds are for research purposes only. Inclusion in this reference does not establish current catalogue availability.

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