CART peptide
A neuropeptide named after a drug response, what it does to appetite in animals, and what human studies have found
CART peptide takes its name from the cocaine- and amphetamine-regulated transcript, a gene found switched on in rat brains after those stimulants. Its peptide turned out to be one of the brain's appetite brakes: in rats it reduces eating and opposes neuropeptide Y. In people it has only been measured: low in a family with an obesity mutation, high in many neuroendocrine tumours, low in the spinal fluid of depressed patients. No one agrees yet on its receptor, and it has never been given to humans.
No established human dose Details ↓
Recommended Dosing
No established human dose
CART peptide has not been given to people in any study on this page. The human studies measure it in serum, plasma, spinal fluid or post-mortem tissue, or study its gene; every study that gave the peptide was done in rats or mice, by injection into the brain.
What is it?
CART stands for cocaine- and amphetamine-regulated transcript, a gene found in the rat striatum in 1995 and named for its response to those drugs. The gene, CARTPT, makes a precursor that is cut into several peptides; the main active one in people is a 48-residue peptide held in shape by three disulfide bonds, numbered CART(42-89) in humans; rat work uses its counterpart, CART(55-102). 'CART peptide' usually means this one.
Its first clear effect was on eating. Injected into the brain ventricles of rats, CART fragments cut food intake, an antibody that soaked up the rat's own CART made them eat more, and CART blunted the strong feeding drive that neuropeptide Y produces. Since then it has been tied in animal work to reward and addiction, stress, pain, bone and insulin release. Mice without it, for example, drink less alcohol.
Human evidence is mostly measurement. In a family with obesity, a single change in the precursor, Leu34Phe, sends it down the wrong route inside cells, and carriers have very little bioactive CART in their blood. Screening Danish people with early-onset obesity, by contrast, found no harmful variants, so CART mutations are a rare cause at most. Blood CART was higher in severe obesity and normal a year after gastric bypass, but it did not follow body fat in lean adults.
Outside appetite, plasma CART is high in more than half of people with neuroendocrine tumours and adds a little to chromogranin A as a blood test, and spinal-fluid CART was lower in a small group with depression. In the human brain it is made mainly in the hypothalamus and thalamus, and along the gut it sits in nerves and some endocrine cells.
What CART binds is still open. In 2021 a group reported that the orphan receptor GPR160 was needed for CART's effects on eating and drinking in rats; in 2023 another group found CART does not bind GPR160 at all. Without a confirmed receptor or a drug that blocks it, CART has not reached human trials, and it has never been given to people.
Mechanism of Action
CART peptide is a brain and gut signal that reduces eating in animals; how it acts is uncertain because its receptor has not been confirmed.
Appetite brake
Given into the brain of rats it lowers food intake, and blocking the rat's own CART increases eating.
Opposes neuropeptide Y
CART given before neuropeptide Y blunts the extra feeding NPY causes, and NPY nerve endings sit on CART cells in the hypothalamus.
Unconfirmed receptor
GPR160 was reported to be needed for its effects in rats, but binding studies found CART does not attach to GPR160.
Neuroendocrine release
Endocrine cells and tumours release it into blood, where it can be measured.
Published Research
These are studies of CART peptide and its gene, read from their PubMed abstracts: the first feeding study in rats, human genetic, brain, gut, blood and spinal-fluid studies, two animal studies and one cell study on its receptor and behaviour, and three reviews. CART is measured in every human study here; none gave it to people.
CART peptide stops rats eating
Fragments of CART peptide injected into the brain ventricles of rats reduced feeding, the first behavioural effect shown for the peptide. An antibody against CART increased feeding, suggesting the body's own CART holds appetite down, and CART given before neuropeptide Y blunted the extra eating that neuropeptide Y causes. Neuropeptide Y nerve endings were seen around CART cells in the hypothalamus.
No obesity variants in Danish early-onset obesity
Mapping placed the human CART gene at chromosome 5q13-14, near a reported obesity locus. Screening the coding region in 84 people with early-onset obesity found only two silent variants outside the protein-coding part, and neither was linked to obesity or later weight gain in 757 obese and 890 control subjects.
Where CART is made in the human brain
In post-mortem human brains, CART messenger RNA was most abundant in the hypothalamus and the thalamus, with high levels in parts of the prefrontal and piriform cortex, the amygdala, the nucleus accumbens and the hippocampus. The thalamus was the clearest difference from the rat, which has almost none there.
An obesity mutation that starves the body of CART
People carrying the Leu34Phe mutation in the CART precursor, first found in a family with obesity, had greatly reduced bioactive CART in their serum and more partly processed precursor. In cultured cells the mutant precursor was sent down the wrong secretory route, poorly processed and released unregulated, which would explain the shortfall.
A blood marker for neuroendocrine tumours
In 401 people, the upper normal limit for plasma CART immunoreactivity was set at 150 pmol/l. Patients with neuroendocrine malignancy averaged 440 pmol/l and 56% were above the limit; adding CART to chromogranin A raised detection from 85% to 91%, and 95% of patients with progressive pancreatic neuroendocrine tumours were above the limit.
CART along the human gut
Immunostaining of human gut tissue found CART nerve fibres in every segment from the oesophagus to the colon, most dense in the muscle layers and the myenteric plexus. CART-containing endocrine cells sat mainly in the pylorus, duodenum and stomach fundus and were absent from the large-bowel lining.
Higher CART on clozapine
Fasting serum CART was higher in 24 people with schizophrenia on clozapine than in 24 matched controls, and higher in those with metabolic syndrome, but it did not correlate with weight, body mass index, clozapine dose or insulin resistance. The authors could not tell whether the rise was a response to drug-related weight gain or part of the illness.
Knockout mice drink less alcohol
Mice lacking CART drank and preferred alcohol less than normal mice in a two-bottle test, in both sexes, with no difference in taste for bitter or sweet solutions or in how fast they cleared alcohol.
Low CART in spinal fluid in depression
Cerebrospinal fluid CART was lower in 24 patients with major depression than in 25 matched controls. Within the patients, lower CART went with higher antidepressant doses and with more psychomotor slowing, somatic anxiety and physical symptoms.
Raised in severe obesity, normal a year after bypass
Serum CART was higher in 27 people with morbid obesity than in 30 healthy-weight controls and returned to control levels a year after Roux-en-Y gastric bypass, moving with insulin and leptin. The hormone and neuropeptide profile explained most of the variation in weight loss.
No link with body fat in lean adults
In 30 healthy, non-obese adults, fasting serum CART correlated with neuropeptide Y but not with body fat or other body measures; leptin was the only appetite peptide in the panel that tracked body composition.
GPR160 proposed as the receptor
Blocking the orphan receptor GPR160 with an antibody in the fourth ventricle of rats stopped CART peptide from reducing food and water intake and, on its own, increased overnight eating and drinking. A GLP-1 receptor blocker interrupted CART's effect on food but not on water.
GPR160 does not bind CART
Radiolabelled CART peptides showed no specific binding to cells with high natural GPR160 or to cell lines engineered to make GPR160, and cells that do bind CART did not express GPR160. The authors concluded GPR160 cannot be CART's receptor and that the true receptor remains unknown.
What knockout mice show
This short review summarises studies of mice lacking CART peptide, the main tool for studying its functions because no antagonist that blocks CART specifically has been found.
A peptide with many jobs and no receptor
This review traces CART from its discovery in the rat striatum in 1995 and lists the functions proposed for it, from feeding, addiction and stress to pain, bone, insulin secretion and sleep. It names three obstacles: no cloned receptor, no specific agonist or antagonist, and several processed fragments.
Twenty-five years of CART and energy balance
This review covers where CART is made in the brain, vagal nerves and gut, how its expression changes with feeding state, and its effects as an appetite-reducing signal and on energy expenditure in pharmacological and genetic animal studies. It makes the case for CART as a possible obesity target.
No Established Human Dose
CART peptide has not been given to people in any study on this page. The human studies measure it in serum, plasma, spinal fluid or post-mortem tissue, or study its gene; every study that gave the peptide was done in rats or mice, by injection into the brain. There is no human dose to state.
What this rests on: PMID 16210370, PMID 18211969, PMID 29486339.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes CART peptide is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of CART peptide has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store CART peptide, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long CART peptide stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking CART peptide. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
Unknown: no cited half-life and no label or trial duration on this page says how long CART peptide lasts or how long it was given. Results reported in the studies are under Published Research.
Side effects, and when to stop or get help
From the Side Effects section: No study here administered CART to humans; its effects in people are unknown; In animals it is given straight into the brain, a route that says little about injecting it under the skin; Raised plasma CART can come from a neuroendocrine tumour, so a high value is a reason for medical follow-up, not a sign of good appetite control (PMID 18211969). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping CART peptide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“CART peptide has never been given to people, so no human side effects are known”).
Interactions
Unknown: a PubMed search for human interaction studies of CART peptide (reviewed 2026-10-30) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of CART peptide products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against CART peptide's expected mass, 5,245.2 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine: CART peptide is a research neuropeptide measured in human blood and spinal fluid and given only to animals in the studies read). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
CART peptide has never been given to people, so no human side effects are known.
Contraindications & Cautions
There is no CART medicine. These cautions follow from the evidence.
Legal Status
CART peptide is a research neuropeptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is CART peptide?
A 48-amino-acid neuropeptide from the cocaine- and amphetamine-regulated transcript gene. It is made in the brain, especially the hypothalamus, and in some gut and endocrine cells.
?Why is it named after cocaine and amphetamine?
Because its messenger RNA was first noticed rising in the rat brain after those stimulants. The name describes how the gene was found, not what the peptide mainly does.
?Does CART peptide reduce appetite?
In rats, yes: injected into the brain it cuts food intake and blunts the feeding effect of neuropeptide Y. No study has tested it in people.
?Is CART linked to human obesity?
In one family, a precursor mutation that leaves carriers with very little bioactive CART was found alongside obesity. A larger Danish screen found no harmful variants, so it is at most a rare cause.
?What is its receptor?
Unknown. GPR160 was proposed in 2021 from rat studies, but a 2023 binding study found that CART does not attach to GPR160.
?Is CART peptide used as a medical test?
It has been studied as a blood marker for neuroendocrine tumours, where adding it to chromogranin A raised detection a little. It is not a routine test.
?Can you take CART peptide?
It has never been given to people in the studies read. Any product sold as CART peptide is unregulated.
References
- [other] UniProt Q16568 (CART_HUMAN), CART(42-89) = residues 69-116 with three disulfide bonds (82-100, 88-108, 102-115); read October 30, 2026. Formula and mass computed from the sequence with three disulfides. https://www.uniprot.org/uniprotkb/Q16568/entry
- [pubmed] Lambert PD, et al. "CART peptides in the central control of feeding and interactions with neuropeptide Y." Synapse, 1998;29(4):293-8. PMID: 9661247.
- [pubmed] Echwald SM, et al. "Sequence variants in the human cocaine and amphetamine-regulated transcript (CART) gene in subjects with early onset obesity." Obes Res, 1999;7(6):532-6. PMID: 10574510.
- [pubmed] Hurd YL, et al. "Human cocaine- and amphetamine-regulated transcript (CART) mRNA is highly expressed in limbic- and sensory-related brain regions." J Comp Neurol, 2000;425(4):583-98. PMID: 10975881.
- [pubmed] Yanik T, et al. "The Leu34Phe ProCART mutation leads to cocaine- and amphetamine-regulated transcript (CART) deficiency: a possible cause for obesity in humans." Endocrinology, 2006;147(1):39-43. PMID: 16210370.
- [pubmed] Bech P, et al. "Elevated cocaine- and amphetamine-regulated transcript immunoreactivity in the circulation of patients with neuroendocrine malignancy." J Clin Endocrinol Metab, 2008;93(4):1246-53. PMID: 18211969.
- [pubmed] Kasacka I, et al. "Cocaine- and amphetamine-regulated transcript : identification and distribution in human gastrointestinal tract." J Biol Regul Homeost Agents, 2012;26(3):419-28. PMID: 23034261.
- [pubmed] Wysokiński A, et al. "Blood serum levels of CART peptide in patients with schizophrenia on clozapine monotherapy." Psychiatry Res, 2014;220(1-2):170-4. PMID: 25219614.
- [pubmed] Salinas AG, et al. "Reduced ethanol consumption and preference in cocaine- and amphetamine-regulated transcript (CART) knockout mice." Addict Biol, 2014;19(2):175-84. PMID: 22823101.
- [pubmed] Yoon HS, et al. "Low cocaine- and amphetamine-regulated transcript (CART) peptide levels in human cerebrospinal fluid of major depressive disorder (MDD) patients." J Affect Disord, 2018;232:134-138. PMID: 29486339.
- [pubmed] Muñoz-Rodríguez JR, et al. "Cocaine and amphetamine regulated transcript and brain-derived neurotrophic factor in morbid obesity. One-year follow-up after gastric bypass." Surg Obes Relat Dis, 2018;14(11):1732-1739. PMID: 30274741.
- [pubmed] Lucka A, et al. "Association between adiposity and fasting serum levels of appetite-regulating peptides: Leptin, neuropeptide Y, desacyl ghrelin, peptide YY(1-36), obestatin, cocaine and amphetamine-regulated transcript, and agouti-related protein in nonobese participants." Chin J Physiol, 2019;62(5):217-225. PMID: 31670286.
- [pubmed] Haddock CJ, et al. "Signaling in rat brainstem via Gpr160 is required for the anorexigenic and antidipsogenic actions of cocaine- and amphetamine-regulated transcript peptide." Am J Physiol Regul Integr Comp Physiol, 2021;320(3):R236-R249. PMID: 33206556.
- [pubmed] Freitas-Lima LC, et al. "GPR160 is not a receptor of anorexigenic cocaine- and amphetamine-regulated transcript peptide." Eur J Pharmacol, 2023;949:175713. PMID: 37054941.
- [review] Moffett M, et al. "Studies of cocaine- and amphetamine-regulated transcript (CART) knockout mice." Peptides, 2006;27(8):2037-45. PMID: 16762458.
- [review] Ahmadian-Moghadam H, et al. "Cocaine- and amphetamine-regulated transcript (CART): A multifaceted neuropeptide." Peptides, 2018;110:56-77. PMID: 30391426.
- [review] Singh A, et al. "Demystifying functional role of cocaine- and amphetamine-related transcript (CART) peptide in control of energy homeostasis: A twenty-five year expedition." Peptides, 2021;140:170534. PMID: 33757831.
Sources & Citations
Every study on this page was read from its PubMed record on October 30, 2026. Status comes from Drugs@FDA (openFDA), read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.