Vasostatin (Chromogranin A)
The first active chromogranin-A peptides — vasoinhibitory, heart-calming and vessel-protecting. A research peptide, not a drug
Vasostatin is the name given to the two peptides cut from the front (N-terminal) end of chromogranin A — vasostatin-1 and the slightly longer vasostatin-2. They were the first fragments of chromogranin A ever shown to be biologically active, and they are named for their effect on blood vessels: they inhibit vascular tension. Together with catestatin (another chromogranin-A peptide), the vasostatins act as brakes on the cardiovascular system — they weaken the force of heart contraction, relax (dilate) blood vessels, and blunt the stimulating effect of adrenaline, working in a receptor-independent way by triggering nitric oxide release from the lining of vessels and heart. They also protect the heart from ischemia-reperfusion injury, stabilize the barrier function of the endothelium, and calm inflammation and atherosclerosis. Circulating chromogranin A rises in heart failure, hypertension and inflammatory disease, and the vasostatins are studied as the protective counterweights in that system. (This chromogranin-A vasostatin is a different molecule from the unrelated calreticulin fragment also called vasostatin.) Vasostatin is studied as a research tool; it is not an approved medicine and has not been given to people as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Chromogranin-A vasostatin is an endogenous human peptide that has never been given to people as a treatment. The work is in animals, isolated organs and cells, where vasostatin-1 and vasostatin-2 are applied or over-expressed at experimental amounts that do not carry over to people; in humans the peptides are measured, not administered.
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What is it?
Chromogranin A is a large acidic protein stored in the secretory granules of neuroendocrine cells, nerves and heart muscle, and it is cut by processing enzymes into a family of smaller active peptides. The vasostatins — vasostatin-1 (the first 76 amino acids of chromogranin A) and vasostatin-2 (the first 113) — were the earliest of these fragments shown to do something biologically, and they took their name from their ability to lower vascular tension. They are highly conserved across species, a sign of an important role.
In the cardiovascular system, the vasostatins act as brakes. On isolated hearts they produce negative inotropism (weaker contraction) and dilate the coronary vessels, and they oppose the stimulating effect of adrenaline-type signals — the same anti-beta-adrenergic, heart-calming direction as their cousin catestatin, and the opposite of serpinin. Strikingly, they do this without a classic receptor: their amphipathic structure lets them interact with the cell membrane and trigger a calcium-independent, PI3-kinase-dependent release of nitric oxide from the endothelium, which then relaxes the heart and vessels through NO-cGMP signalling.
The vasostatins are also protective. Vasostatin-1 limits the damage of ischemia and reperfusion in heart-muscle cells, including through cardiomyocyte-endothelial crosstalk, and it stabilizes the endothelial barrier — tightening the junctions between vessel-lining cells and blocking the activation those cells undergo in response to inflammatory and pro-angiogenic signals. Through these actions it has anti-inflammatory and anti-angiogenic effects relevant to vascular disease.
A growing body of work places the vasostatins against atherosclerosis. Vasostatin-1 suppresses the adhesion molecules and inflammatory signals that start a plaque, reduces foam-cell formation in macrophages, and — infused into atherosclerosis-prone mice — slows the development of aortic plaques; vasostatin-2 similarly restrains the proliferation, migration and adhesion of vascular smooth-muscle cells and is reduced in people with coronary artery disease. Because circulating chromogranin A is high in heart failure, hypertension and inflammation, the vasostatins are studied as the system's built-in protective counterweights.
Chromogranin-A vasostatin is an endogenous human peptide and a research tool, not a medicine. No published study has given it to people as a treatment — the work is in animals, isolated organs and cells — it is approved nowhere, and material sold online as 'vasostatin' is an unregulated research chemical (and may be confused with the unrelated calreticulin vasostatin). Nothing here is a dose or a therapy; this page records what the published science says about the peptide.
Mechanism of Action
The vasostatins (vasostatin-1 and vasostatin-2) are chromogranin-A N-terminal peptides that act as cardio-suppressive, vasoinhibitory regulators — anti-adrenergic negative inotropes and vasodilators — through a receptor-independent endothelial nitric-oxide pathway, and they protect vessels and heart from injury and atherosclerosis.
Cardioprotection and negative inotropism
Vasostatin-1 produces negative inotropism counteracting adrenergic stimulation (PMID 15028525) and protects heart cells from hypoxia/reoxygenation injury directly and via endothelial crosstalk (PMID 23956006).
Anti-atherogenic, endothelial-barrier protection
Vasostatin-1 suppresses endothelial/macrophage inflammation and plaque development in mice (PMID 30401690), and vasostatin-2 restrains vascular smooth-muscle proliferation, migration and adhesion (PMID 26721428).
Published Research
These are studies of chromogranin-A vasostatin read from their PubMed abstracts on November 6, 2026. They include two reviews of vasostatin-1 and catestatin as cardiovascular regulatory peptides, an isolated-heart study of vasostatin-1 as a cardiostatin, an animal study of vasostatin-1 against atherosclerosis, a cardiomyocyte-endothelial study of its protection in hypoxia/reoxygenation, and a vascular-smooth-muscle study of vasostatin-2. Vasostatin has not been given to people as a treatment in any published study; the human evidence is tissue expression and circulating levels.
Vasostatin-I and catestatin as cardiovascular regulators
A review linking high circulating chromogranin A in inflammatory conditions to cardiovascular dysfunction, and positioning the CgA peptides vasostatin-I and catestatin as protective regulators. Both carry membrane-penetrating properties and act through pertussis-toxin-sensitive, receptor-independent signalling via Gi/o proteins to produce inhibitory effects on vascular and cardiac responses — supporting vasostatin-I as a regulatory peptide that alleviates cardiovascular dysfunction.
Endothelium-dependent cardiovascular effects of vasostatin-1
A review of the signalling of vasostatin-1 and catestatin behind their negative inotropic and vasodilator, cardioprotective actions. Both act as vasoactive peptides indirectly on cardiomyocytes through a calcium-independent, PI3-kinase-dependent nitric-oxide release from endothelial cells, triggered by interaction with the plasma membrane and notably without a specific membrane receptor — a receptor-independent eNOS activation.
Vasostatin-1 is a cardiostatin on the frog heart
On the isolated working frog heart, human recombinant vasostatin-1 (CgA1-76) and a synthetic CgA7-57 peptide produced a significant negative inotropism (weaker contraction). The effect was independent of nitric oxide, adrenergic or muscarinic receptors and G proteins, but depended on extracellular calcium and potassium channels — and it counteracted adrenergic positive inotropism, supporting a cardio-regulatory 'cardiostatin' role (a preclinical result).
Vasostatin-1 against atherosclerosis
Vasostatin-1 suppressed inflammatory activation of human endothelial cells and macrophages, reduced macrophage foam-cell formation, and modulated vascular smooth-muscle migration and matrix production. Infused for four weeks into atherosclerosis-prone ApoE-deficient mice it reduced aortic plaque development, plaque inflammation and macrophage infiltration — the first evidence that vasostatin-1 is anti-atherogenic and a possible therapeutic target (a preclinical result).
Vasostatin-1 protects heart cells in hypoxia/reoxygenation
In a cardiomyocyte-endothelial co-culture, over-expressing vasostatin-1 reduced cardiomyocyte apoptosis and the damage markers AST and CK-MB after hypoxia/reoxygenation, and endothelial vasostatin-1 protected neighbouring cardiomyocytes. A nitric-oxide scavenger partly reversed the protection, showing vasostatin-1 guards heart cells directly and indirectly through cardiomyocyte-endothelial interaction (a cell result).
Vasostatin-2 restrains vascular smooth-muscle cells
Vasostatin-2 was down-regulated in atherosclerotic vascular smooth-muscle cells and tissue. Over-expressing it inhibited the proliferation and migration of these cells, reduced inflammatory cytokine release, and lowered soluble adhesion molecules (sICAM-1, sVCAM-1) — identifying vasostatin-2 as an atherosclerosis-related factor and a potential biomarker and therapeutic target (a cell result).
No Established Human Dose
Chromogranin-A vasostatin is an endogenous human peptide that has never been given to people as a treatment. The work is in animals, isolated organs and cells, where vasostatin-1 and vasostatin-2 are applied or over-expressed at experimental amounts that do not carry over to people; in humans the peptides are measured, not administered. No regulator has approved any dose, and no published human dose exists, so no amount is printed here.
What this rests on: PMID 15028525, PMID 30401690, PMID 19640932.
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 Vasostatin (Chromogranin A) 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 Vasostatin (Chromogranin A) 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 Vasostatin (Chromogranin A), 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 Vasostatin (Chromogranin A) stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Vasostatin (Chromogranin A). What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
How long it stays in the body: a half-life of not established for humans as a drug; an endogenous signalling peptide. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Vasostatin (Chromogranin A). Results reported in the studies are under Published Research.
Source: half-life: PMID 19640932.
Side effects, and when to stop or get help
From the Side Effects section: No human adverse-event data exist: no published study has administered vasostatin to people; Vasostatin-1 is a negative inotrope and vasodilator in animal hearts (PMIDs 15028525, 22834796), so cardiovascular effects would be expected if administered; The vasostatins are reduced in atherosclerosis and act protectively (PMIDs 30401690, 26721428) — an association and a research target, not an effect of taking them; Material sold online as 'vasostatin' is an unregulated research chemical, and may be the unrelated calreticulin vasostatin rather than the chromogranin-A peptide. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Vasostatin (Chromogranin A). Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Chromogranin-A vasostatin is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Vasostatin (Chromogranin A) (reviewed 2026-11-06) 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 Vasostatin (Chromogranin A) 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. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a drug: Drugs@FDA and the openFDA label endpoint hold no record, and FDA GSRS and ChEMBL hold no substance record for chromogranin-A vasostatin (searched November 6, 2026)). 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
Chromogranin-A vasostatin is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status.
Contraindications & Cautions
Chromogranin-A vasostatin has no approved use and no label. These points reflect its endogenous, research status.
Legal Status
Chromogranin-A vasostatin is an endogenous human peptide studied as a research compound; it is not a drug and is not approved in any country.
Frequently Asked Questions
?What is vasostatin?
In this entry, the chromogranin-A vasostatins — vasostatin-1 (the first 76 amino acids of chromogranin A) and vasostatin-2 (the first 113). They were the first active chromogranin-A fragments found, named for lowering vascular tension, and are cousins of catestatin, pancreastatin and serpinin. (A different peptide from calreticulin is also called vasostatin.)
?What does it do?
It calms the cardiovascular system — weakening heart contraction, dilating vessels and opposing adrenaline through receptor-independent nitric-oxide release (PMIDs 22834796, 15028525) — protects the heart and endothelium from injury (PMID 23956006), and is anti-atherogenic (PMIDs 30401690, 26721428).
?Is it a treatment for anything?
No. Vasostatin is a research peptide used to study how chromogranin A protects the cardiovascular system. No human trial has administered it, and it is approved nowhere.
?Is it approved or available to buy?
No. Chromogranin-A vasostatin is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as vasostatin is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [review] Helle KB. "The chromogranin A-derived peptides vasostatin-I and catestatin as regulatory peptides for cardiovascular functions." Cardiovasc Res, 2010;85(1):9-16. PMID: 19640932.
- [review] Fornero S, et al. "Endothelium dependent cardiovascular effects of the Chromogranin A-derived peptides Vasostatin-1 and Catestatin." Curr Med Chem, 2012;19(24):4059-67. PMID: 22834796.
- [animal] Corti A, et al. "Chromogranin A N-terminal fragments vasostatin-1 and the synthetic CGA 7-57 peptide act as cardiostatins on the isolated working frog heart." Gen Comp Endocrinol, 2004;136(2):217-24. PMID: 15028525.
- [animal] Sato Y, et al. "Inhibitory effects of vasostatin-1 against atherogenesis." Clin Sci (Lond), 2018;132(23):2493-2507. PMID: 30401690.
- [mechanism] Liu J, et al. "Overexpression of vasostatin-1 protects hypoxia/reoxygenation injuries in cardiomyocytes-endothelial cells transwell co-culture system." Cell Biol Int, 2014;38(1):26-31. PMID: 23956006.
- [mechanism] Hou J, et al. "Vasostatin-2 inhibits cell proliferation and adhesion in vascular smooth muscle cells, which are associated with the progression of atherosclerosis." Biochem Biophys Res Commun, 2016;469(4):948-53. PMID: 26721428.
- [other] UniProt P10645 (CMGA_HUMAN), read November 6, 2026: the vasostatin peptides are the N-terminal fragments of chromogranin A (vasostatin-1 = CgA1-76, vasostatin-2 = CgA1-113), the product of the CHGA gene and a member of the granin family. https://www.uniprot.org/uniprotkb/P10645/entry
- [other] Vasostatin-1 and vasostatin-2 were the first chromogranin A fragments shown to be biologically active, named for their inhibitory effect on vascular tension; their cardiovascular biology is set out in the regulatory-peptide reviews carded on this page (read November 6, 2026). They are distinct from the unrelated calreticulin-derived peptide also called vasostatin.
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 6, 2026: no application and no label record for chromogranin-A vasostatin. It is an endogenous human peptide, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it.
Sources & Citations
The six studies carded above were read from their PubMed records on November 6, 2026. Identity comes from UniProt (P10645, gene CHGA); vasostatin-1 (CgA1-76) and vasostatin-2 (CgA1-113) as the first active chromogranin-A fragments, their receptor-independent endothelial-NO cardio-suppressive mechanism, their cardioprotective and anti-atherogenic actions, and their distinction from the calreticulin-derived vasostatin are from the reviews and studies carded here; the absence of US approval and of a drug substance record from Drugs@FDA, openFDA, FDA GSRS and ChEMBL was checked 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.