Catestatin

CST, chromogranin A fragment 352–372 (human), CgA(344–364) (bovine)

Sexual health, hormones & signalling

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Summary

Class: Naturally occurring 21-amino-acid peptide, cut from the chromogranin A protein stored in adrenal and nerve secretory granules
Mechanism: Blocks nicotinic acetylcholine receptors on adrenaline-releasing cells, so less catecholamine is released; also lowers blood pressure, calms the heart, improves insulin signalling and kills some microbes in animal and cell studies
Routes studied: Intraperitoneal, intravenous, intracerebroventricular injection and osmotic minipump (rodents); community: subcutaneous (rare)
Dose range reported: Mice: commonly about 2–5 µg/g (2–5 mg/kg) intraperitoneally, daily for 1–2 weeks in metabolic studies; rats: lower acute IV doses. Community: no consistent protocol. No human dosing data of any kind
Half-life: Not characterised in humans; as an unmodified 21-mer it is expected to be cleared in minutes
Storage: Lyophilised: refrigerate or freeze, protect from light. Reconstituted: refrigerate, use within days to a few weeks (community practice)
Regulatory status: Not approved anywhere; no clinical trials of administration registered to our knowledge †

Doses are as reported in studies or by the community — never recommendations.

1What it is

Catestatin is a piece of chromogranin A, a large protein packed alongside adrenaline and noradrenaline in the storage granules of the adrenal gland and sympathetic nerves. When those granules empty, chromogranin A is released and chopped by enzymes; one of the pieces is catestatin. It was identified in 1997 by Sushil Mahata and Daniel O'Connor's group in San Diego as the body's own brake on catecholamine release (Mahata 1997, J Clin Invest). It circulates in everyone at low nanomolar levels, and common genetic variants (notably Gly364Ser) change how strongly it works.

It is a natural signalling molecule, not a drug, and nearly everything known about giving it comes from mice and rats. It appears in peptide discussions as a "cardioprotective" or "anti-hypertensive" peptide; that reputation is built entirely on rodent data and on human studies that measured it rather than administered it.

2How it's thought to work

Catecholamine brake. non-competitive antagonist at nicotinic acetylcholine receptors on chromaffin cells and sympathetic neurons, reducing adrenaline and noradrenaline release.

Vasodilation. triggers histamine release from mast cells and acts on endothelium, lowering blood pressure in rodents.

Cardiac effects. negative inotropic (reduces contraction force) and anti-adrenergic actions on isolated hearts, via nitric oxide and β2/β3-adrenergic pathways (Angelone 2008, Endocrinology).

Metabolic. in obese mice it reduces liver fat and inflammation and improves insulin sensitivity, apparently through effects on macrophages and gluconeogenesis (Ying 2018, Diabetes).

Gut and microbiome. alters gut bacteria composition and mucosal inflammation in mice; chromogranin A-knockout mice have a disturbed microbiome.

Antimicrobial. kills bacteria and fungi at micromolar concentrations (Briolat 2005, Cell Mol Life Sci).

Angiogenesis and repair. promotes blood-vessel growth and improves recovery after hind-limb ischaemia and myocardial infarction in rodents (Theurl 2010, Circ Res).

Catestatin, cut out of chromogranin A — the very protein that packages catecholamine granules. It blocks the nicotinic receptor on the chromaffin cell, so the granules stay packed: a brake the adrenal medulla builds into its own secretory machinery.Schematic — not to scale

3What the research shows

Graded C (interventional); B (observational human association)

Blood pressure

Chromogranin A-knockout mice are hypertensive and catestatin replacement normalises their pressure (Mahapatra 2005, J Clin Invest). In humans, lower plasma catestatin is seen in people with hypertension and in their still-normotensive children, suggesting low catestatin precedes the disease (O'Connor 2002, J Hypertens). The Gly364Ser variant alters autonomic activity in human carriers (Rao 2007, Circulation). No human has been given catestatin in a trial. [2][3][4]

Heart protection

Reduced infarct size and improved cardiac function after experimental heart attack and ischaemia-reperfusion in rats, with anti-inflammatory and effects (Penna 2010, Cell Mol Neurobiol; Theurl 2010, Circ Res). [6]

Obesity, insulin resistance and fatty liver

Two weeks of daily injections in diet-induced obese mice reduced liver fat, hepatic inflammation and insulin resistance; effects were partly dependent on macrophage signalling (Ying 2018, Diabetes; Ying 2021, Hepatology). [7]

Graded B (observational)

Biomarker in heart failure, acute coronary syndromes and critical illness

Circulating catestatin levels associate with outcomes in heart failure, myocardial infarction, atrial fibrillation and sepsis in several cohorts, with inconsistent direction between studies (e.g. Liu 2013, Clin Chim Acta; Zhu 2015, Clin Cardiol). These tell us about the body's own catestatin, not about treatment.

Graded D/C

Antimicrobial and wound-healing

activity against skin bacteria and fungi; some rodent wound and inflammatory-bowel data.

4Reported side effects and interactions

Literature-reported

No human administration data exist, so there is no human safety profile. In rodents, high acute doses lower blood pressure and heart contractility; mast-cell histamine release is part of the mechanism.

Community-reported

too few reports to characterise; occasional mentions of lightheadedness after injection, which would be consistent with its vasodilatory and histamine-releasing actions.

Theoretical. hypotension and reflex changes in heart rate; histamine-type reactions (flushing, itching, wheeze) in susceptible people; action carries the standard caution for anyone with a cancer history; reduced catecholamine release could blunt the response to exercise or to low blood sugar.

Interactions. additive hypotension with blood-pressure medicines, β-blockers or nitrates is plausible; antihistamines could mask part of its action in rodents. None studied in humans.

Markers researchers commonly monitor

No human monitoring data exist. Based on its physiology:

Marker	Why it's watched
Blood pressure and heart rate, seated and standing	the compound's primary action in animals is on both; a home cuff before and after is the most relevant measure available.
Fasting glucose, insulin, HbA1c	metabolic effects in mice; also catecholamine suppression could affect glucose counter-regulation.
Liver enzymes (ALT/AST)	fatty-liver effects in mice are the headline metabolic claim.
Plasma or urine catecholamines/metanephrines	direct read-out of the proposed mechanism, though normal-range changes are hard to interpret.
CBC and CMP	general baseline for an injected compound with zero human safety data.
Plasma catestatin	measurable by research ELISA only; not a routine clinical test.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Rarely supplied; where it is, as a powder in low-milligram vials. with , swirl gently, protect from light. Given mg/kg rodent dosing, a human-equivalent amount would be tens of milligrams, far beyond anything the community uses, which means community doses are not modelled on the animal data at all.

Open in calculator, pre-loaded →

6Commonly studied alongside

Nothing established. Mechanistically it sits with other naturally occurring regulatory peptides discussed on this site — vasoactive intestinal peptide (VIP), humanin and MOTS-c (see set 2) — rather than with repair peptides. Community pairing with GH secretagogues or recovery peptides has no study basis.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; no IND-stage trials known. Not on the Category 2 compounding list to our knowledge †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Not named by WADA; as a non-approved substance it falls under S0 †

8Open questions

Does exogenous catestatin do anything at all in humans at any dose? No one has looked.
Which variant (wild-type, Gly364Ser, Pro370Leu) is in any given vial, and does it matter for activity?
Whether histamine release at effective doses would be tolerable in people.

9References

1Mahata SK et al. (1997). Novel autocrine feedback control of catecholamine release: a discrete chromogranin A fragment is a noncompetitive nicotinic cholinergic antagonist. J Clin Invest. PubMed · DOI
2O'Connor DT et al. (2002). Early decline in the catecholamine release-inhibitory peptide catestatin in humans at genetic risk of hypertension. J Hypertens. PubMed · DOI
3Mahapatra NR et al. (2005). Hypertension from targeted ablation of chromogranin A can be rescued by the human ortholog. J Clin Invest. PubMed · DOI
4Rao F et al. (2007). Catecholamine release-inhibitory peptide catestatin (chromogranin A352–372): naturally occurring amino acid variant Gly364Ser causes profound changes in human autonomic activity and alters risk for hypertension. Circulation. PubMed · DOI
5Angelone T et al. (2008). The antihypertensive chromogranin A peptide catestatin acts as a novel endocrine/paracrine modulator of cardiac inotropism and lusitropism. Endocrinology. PubMed · DOI
6Theurl M et al. (2010). The neuropeptide catestatin acts as a novel angiogenic cytokine via a basic fibroblast growth factor-dependent mechanism. Circ Res. PubMed · DOI
7Ying W et al. (2018). Catestatin inhibits obesity-induced macrophage infiltration and inflammation in the liver and suppresses hepatic glucose production, leading to improved insulin sensitivity. Diabetes. PubMed · DOI
8Briolat J et al. (2005). New antimicrobial activity for the catecholamine release-inhibitory peptide from chromogranin A. Cell Mol Life Sci. PubMed · DOI
9Mahata SK, Corti A (2019). Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation. Ann N Y Acad Sci. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

26 Oct 2026Profile published — awaiting medical review

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