Salusin-alpha
The vessel-wall peptide that slows foam-cell formation in the laboratory and runs low in the blood of many people with heart and vessel disease
Salusin-alpha was found in 2003 by a computer search of human gene transcripts. It is cut from the same precursor as salusin-beta, and in cells and animals the two pull in opposite directions: salusin-alpha reduced cholesterol storage in macrophages and shrank plaques in mice and rabbits, while salusin-beta did the reverse. In people it has only been measured, and its blood level is lower in many, though not all, studies of coronary disease, hypertension and diabetes. It is not a medicine and has no human dose.
No established human dose Details ↓
Recommended Dosing
No established human dose
Salusin-alpha has never been given to people in any study read. The human evidence is entirely blood and urine measurement: assays that detect it in healthy serum and urine, and observational comparisons of its level in coronary disease, hypertension, diabetes, thyroid disease, dialysis and other conditions.
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What is it?
Salusin-alpha is a 28-amino-acid peptide that the body makes from the same precursor as its sister, salusin-beta. Both were found in 2003, not by isolating them from tissue but by a computer search of human gene transcripts for sequences that looked like hidden hormone precursors. The precursor, prosalusin, comes from an alternatively spliced message of the TOR2A gene, a member of the torsion dystonia family. Salusin-alpha sits at the very end of that protein and finishes in an amidated lysine, a common mark of active peptide hormones.
Injected into rats, salusin-alpha lowered blood pressure and slowed the heart, though later papers describe that effect as mild next to salusin-beta's. The more lasting finding was in the artery wall. In human macrophages, the cells that swell with cholesterol to become the foam cells of a plaque, salusin-alpha reduced cholesterol storage by turning down the enzyme ACAT-1, while salusin-beta pushed it up. Infusions then shrank plaques in mice and in cholesterol-fed rabbits. In the research the two peptides keep turning up as a pair with opposite effects: salusin-alpha protecting the vessel wall and salusin-beta promoting damage.
In people, salusin-alpha has only ever been measured, never given. The first assay, in 2006, found it in healthy serum and urine and confirmed the peptide is cut where the gene predicted. Since then many groups have compared its blood level between patients and controls. Many report it lower in coronary artery disease, hypertension, type 2 diabetes and underactive thyroid, often falling further as disease worsens, and one study found it rose in older adults after eight weeks of aerobic training as their arteries became less stiff.
The picture is not tidy. Other studies found salusin-alpha higher in rheumatoid arthritis, in people on haemodialysis and in children with obesity, or no different in pre-eclampsia and in one coronary angiography series. A head-to-head analysis judged salusin-beta the better marker of coronary narrowing. Part of the spread is technical: the radioimmunoassay used in the early work reported healthy serum in the tens of picomoles per litre, while commercial ELISA and electrochemiluminescence kits report hundreds to thousands of picograms per millilitre, so figures from different papers cannot be set side by side.
Salusin-alpha is not a medicine anywhere and has no human dose. Everything known about what it does comes from cells and animals, and everything known about it in people comes from blood tests in observational studies, most of them small and single-centre. A low level goes with vascular disease in much of that work, but a link of this kind cannot show that the peptide protects anyone, or that raising it would help. Its sister peptide, salusin-beta, is a separate molecule with its own literature and its own entry here, which covers the plaque-promoting half of the pair.
Mechanism of Action
Salusin-alpha is cut from prosalusin, made in many tissues, and acts on vessel-wall cells and macrophages in laboratory work; its receptor has not been identified in the studies read.
One precursor, two peptides
Prosalusin comes from an alternatively spliced TOR2A message and is cut into salusin-alpha and salusin-beta, which often act in opposite directions in the same cell types.
Less cholesterol storage in macrophages
In human monocyte-derived macrophages, salusin-alpha turned down ACAT-1, the enzyme that stores cholesterol as droplets, so fewer cells became foam cells; G-protein, c-Src, protein kinase C and MEK blockers abolished the effect.
Quieter vessel-wall cells
In cultured cells it slowed smooth muscle growth and migration through lower Akt and mTOR activity and damped inflammatory cytokines in endothelial cells; in mouse kidneys it kept the filter sealed by holding back YAP.
Published Research
These are studies of salusin-alpha itself, read from their PubMed abstracts: the discovery paper, the first human assays, observational studies comparing its blood level between patients and controls, and cell and animal work in which the peptide was given. No study read gave salusin-alpha to a person.
Found by searching the human genome's transcripts
Researchers screened libraries of full-length human gene transcripts by computer and picked out two related peptides, 28 and 20 residues long, which they named salusin-alpha and salusin-beta. Both are cut from a protein encoded by an alternatively spliced message of the TOR2A gene. Injected into a vein in rats, either peptide made blood pressure and heart rate fall quickly and steeply, and both raised calcium inside cells and made cells divide. The precursor was found in every tissue looked at, and both peptides were detected in human tissues, plasma and urine.
First measurement in human blood and urine
A radioimmunoassay built for human salusin-alpha, with negligible cross-reaction with salusin-beta, found it in the serum of 31 healthy people at 11.0 to 40.4 pmol/L (mean 23.3) and in urine at a mean of 156.8 pmol/L. On chromatography the main measured peak ran at the same position as synthetic salusin-alpha, which confirmed that the precursor is cut where the gene sequence predicted.
Human cells make and release it
Every human cell line tested carried the precursor's message and protein, but how much of it was cut down to salusin-alpha differed from one cell type to another. HeLa cells held the most and released it into their culture fluid, where a single measured peak matched the synthetic peptide. This was the first direct evidence that human cells produce and secrete salusin-alpha.
Low in coronary disease, and it slows foam-cell formation
Serum salusin-alpha averaged 4.9 pmol/L in 173 people with coronary artery disease shown on angiography, against 15.4 pmol/L in 40 people with mild hypertension and 20.7 pmol/L in 55 healthy volunteers. Both salusins were found in coronary plaques. In macrophages grown from human blood monocytes, salusin-alpha cut the build-up of stored cholesterol and lowered the cholesterol-storing enzyme ACAT-1, while salusin-beta did the reverse.
Lower in hypertension, and lower still with carotid plaque
Among 70 people with essential hypertension and 20 with normal blood pressure, serum salusin-alpha was lower in the hypertensive group. Across everyone it fell as carotid plaque scores rose, and in a stepwise regression it stayed independently and inversely linked to the thickest carotid wall measurement after other risk factors were considered.
Eight weeks of infusion shrank plaques in mice
Apolipoprotein E-deficient mice, which develop atherosclerosis, were given a continuous infusion of salusin-alpha, salusin-beta or saline from implanted pumps. Salusin-alpha lowered total cholesterol by 15% and foam-cell formation in macrophages by 68%, and after eight weeks the aortic lesions were 54% smaller than in controls. Salusin-beta had the opposite effect, with lesions 2.6 times larger after four weeks.
Where it sits in the rat body
An antibody specific for rat salusin-alpha stained nerve cells and fibres widely and the epithelial linings of organs throughout the body, a pattern unlike salusin-beta, which sat mainly in hormone-producing and blood-forming tissue. Fragments matching rat salusin-alpha were seen in spleen extracts, supporting cleavage of the rat precursor even though it lacks the paired basic residues that usually mark a cutting site.
Higher, not lower, in rheumatoid arthritis
In 56 people with rheumatoid arthritis, 37 with Behcet's disease and 29 healthy controls, serum salusin-alpha was higher in both disease groups, which also had thicker carotid walls. Its level did not track carotid wall thickness in any group, so the authors concluded it does not drive the faster atherosclerosis seen in these inflammatory diseases.
No difference in pre-eclampsia
Serum salusin-alpha and salusin-beta did not differ between 48 women with pre-eclampsia and 21 women with healthy pregnancies, and were similar in the mild and severe forms. Apelin, measured in the same samples, was higher in pre-eclampsia.
Lower with more coronary disease
In 172 people with coronary artery disease and 91 controls, measured by ELISA, serum salusin-alpha was lower in the patients and fell as the angiographic severity score rose. The inverse link held as an independent factor in the analysis, and the authors proposed it as a candidate marker for coronary disease.
Lower in underactive thyroid
Serum salusin-alpha was lower than in 25 healthy controls both in 32 people with overt hypothyroidism taking levothyroxine and in 18 with untreated subclinical hypothyroidism. Treated and untreated patients did not differ from each other in salusin-alpha.
Calms inflammatory signals in vessel-lining cells
In human umbilical vein endothelial cells, salusin-alpha reduced the message and protein of the inflammatory cytokines IL-6 and IL-8, among others, raised the anti-inflammatory IL-1 receptor antagonist, and damped the response to TNF-alpha. Blocking NF-kappaB did not change these effects, so they seem to run through some other route.
Protection in kidney ischaemia in rats
Rats had one kidney removed and the other starved of blood for an hour, then received salusin-alpha or salusin-beta under the skin. The injury lowered salusin-alpha in serum but raised it in kidney tissue. Both peptides improved antioxidant enzyme activity and lowered inflammatory markers, and the lower salusin-alpha amount also brought down urea and creatinine.
Smaller aortic lesions in cholesterol-fed rabbits
In rabbits on a cholesterol diet, an infusion of salusin-alpha reduced the lesion area by 39% in the aortic arch and by 71% in both the thoracic and abdominal aorta, without changing blood lipids. Plaques held fewer macrophages and smooth muscle cells. In cultured vascular smooth muscle cells, salusin-alpha slowed growth and migration and reduced activation of the Akt and mTOR signalling proteins.
Linked to diastolic pressure in children with obesity
Levels of both salusins were similar in 75 children with obesity and 101 healthy children, and neither tracked body mass index. The authors report a negative correlation between salusin-alpha and diastolic blood pressure and suggest it may be an early sign of heart and vessel involvement, while calling for more work.
Higher on haemodialysis, yet lower with stiffer arteries
In 180 people on haemodialysis and 90 healthy controls, mean salusin-alpha was higher in the dialysis group (726 versus 326 pg/mL). Within both groups, people with lower salusin-alpha had thicker carotid walls and faster pulse waves, a sign of stiffer arteries. Among dialysis patients, a higher salusin-beta to salusin-alpha ratio went with worse values, and diabetic patients had lower salusin-alpha.
Falls with age and rises with aerobic training
Serum salusin-alpha was lower in 60 adults aged 40 to 80 than in 45 adults aged 20 to 39, and it fell as age, blood pressure and arterial stiffness rose. In the exercise part of the study, eight weeks of aerobic training raised salusin-alpha in the middle-aged and older group, and the people whose levels rose most showed the largest falls in arterial stiffness and blood pressure.
Salusin-beta reads coronary narrowing better
In 256 people having coronary angiography for chest pain, the two salusins together explained much of the variation in the SYNTAX narrowing score. Salusin-beta carried the larger weight (standardised coefficient 0.797) and salusin-alpha a smaller, inverse one (-0.367), so the authors judged salusin-beta the more useful marker.
Lower when blood pressure does not dip at night
Among 88 people with newly diagnosed hypertension, the 47 whose blood pressure failed to fall at night had lower salusin-alpha than the 41 whose pressure dipped normally (about 1,819 versus 1,963 pg/mL by an electrochemiluminescence test), and salusin-alpha remained an independent predictor of the non-dipping pattern.
No link to coronary narrowing in this group
In 168 people having coronary angiography, 55 with normal arteries and 113 with disease of varying extent, serum salusin-alpha did not differ between any of the groups. Salusin-beta and C-reactive protein were higher in the disease groups.
Lower in type 2 diabetes, lowest with poor control
Serum salusin-alpha was lower in 55 people with type 2 diabetes than in 35 healthy volunteers, and lower still in those with HbA1c above 9%. Within the patient group it fell as fasting glucose and HbA1c rose, while salusin-beta moved the other way. Body weight made no difference to either peptide.
Kidney protection in diabetic rats
Diabetic rats had less salusin-alpha in plasma and kidney. Giving the peptide reduced kidney scarring and the change of tubular cells toward a scar-forming type, lowered oxidative stress by restraining NADPH oxidase subunits, and switched off the overactive Akt-mTOR growth signalling chain.
Higher in children with obesity
In 125 children with obesity and 33 healthy-weight peers, both salusins were higher in the children with obesity, and only salusin-alpha rose further with more severe obesity. It went with body mass index and C-reactive protein, which led the authors to suggest it as an early inflammation marker, the opposite direction to most adult findings.
Protects the kidney filter in hypertensive mice
Mice made hypertensive with angiotensin II and a high-salt diet had about 43% less salusin-alpha in serum and 55% less in the kidney. Treatment restored a tight-junction protein that seals the filter and roughly halved protein loss in urine. In human glomerular endothelial cells the peptide kept the cell layer sealed by stopping the regulator YAP from entering the nucleus, and forcing YAP up removed the protection.
No Established Human Dose
Salusin-alpha has never been given to people in any study read. The human evidence is entirely blood and urine measurement: assays that detect it in healthy serum and urine, and observational comparisons of its level in coronary disease, hypertension, diabetes, thyroid disease, dialysis and other conditions. The amounts injected or infused in rats, mice and rabbits are animal research conditions and do not translate to a human amount, so there is no dose to state.
What this rests on: PMID 16889872, PMID 18212280, PMID 31918410.
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 Salusin-alpha 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 Salusin-alpha 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 Salusin-alpha, 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 Salusin-alpha stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Salusin-alpha. 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 Salusin-alpha 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: In the discovery study, an intravenous injection in rats caused a fast, steep fall in blood pressure and heart rate (PMID 12910263); No human safety data exist: every human study read only measured it (PMID 16889872). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Salusin-alpha. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Salusin-alpha has not been given to people, so no human side effects are known”).
Interactions
Unknown: a PubMed search for human interaction studies of Salusin-alpha (reviewed 2026-11-03) 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 Salusin-alpha 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 Salusin-alpha's expected mass, 2,603.0 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 anywhere in the sources read: Drugs@FDA (openFDA) returns no record for salusin (November 3, 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
Salusin-alpha has not been given to people, so no human side effects are known.
Contraindications & Cautions
No product label exists. These cautions follow from the evidence.
Legal Status
Salusin-alpha is an endogenous research peptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is salusin-alpha?
A 28-amino-acid peptide cut from prosalusin, the same precursor that yields salusin-beta. It was identified in 2003 by a computer search of human gene transcripts and has since been measured in human blood, urine and coronary plaques.
?Is salusin-alpha a drug or a supplement?
Neither. No medicine contains it, no regulator has approved it, and no study read has given it to a person. In people it has only been measured in blood and urine.
?How is it different from salusin-beta?
They come from the same precursor but are different peptides, 28 and 20 residues long. In laboratory and animal work salusin-alpha reduced cholesterol storage in macrophages and plaque growth, while salusin-beta increased both.
?Does a low salusin-alpha level mean heart disease?
Many studies found lower levels in coronary disease, hypertension and diabetes, but others found higher or unchanged levels, the assays disagree with one another, and no clinical test uses it. It is a research marker, not a diagnosis.
?Can exercise raise it?
One study found serum salusin-alpha rose after eight weeks of aerobic training in middle-aged and older adults, and the rise went with less arterial stiffness. That is a single trial of exercise, not of the peptide.
?Is there a safe dose?
No dose exists. The only amounts ever given were to animals in laboratory studies, and those cannot be turned into a human amount.
References
- [pubmed] Shichiri M, et al. "Salusins: newly identified bioactive peptides with hemodynamic and mitogenic activities." Nat Med, 2003;9(9):1166-72. PMID: 12910263.
- [pubmed] Sato K, et al. "Presence of immunoreactive salusin-alpha in human serum and urine." Peptides, 2006;27(11):2561-6. PMID: 16889872.
- [pubmed] Sato K, et al. "Biosynthesis and secretion of salusin-alpha from human cells." Peptides, 2008;29(12):2203-7. PMID: 18804130.
- [pubmed] Watanabe T, et al. "Impact of salusin-alpha and -beta on human macrophage foam cell formation and coronary atherosclerosis." Circulation, 2008;117(5):638-48. PMID: 18212280.
- [pubmed] Watanabe T, et al. "Serum salusin-alpha levels are decreased and correlated negatively with carotid atherosclerosis in essential hypertensive patients." Hypertens Res, 2008;31(3):463-8. PMID: 18497465.
- [pubmed] Nagashima M, et al. "Chronic infusion of salusin-alpha and -beta exerts opposite effects on atherosclerotic lesion development in apolipoprotein E-deficient mice." Atherosclerosis, 2010;212(1):70-7. PMID: 20684826.
- [pubmed] Suzuki N, et al. "Distinct systemic distribution of salusin-α and salusin-β in the rat." Peptides, 2011;32(4):805-10. PMID: 21193001.
- [pubmed] Ozgen M, et al. "Serum salusin-alpha level in rheumatoid arthritis." Regul Pept, 2011;167(1):125-8. PMID: 21185876.
- [pubmed] Simsek Y, et al. "Serum levels of apelin, salusin-alpha and salusin-beta in normal pregnancy and preeclampsia." J Matern Fetal Neonatal Med, 2012;25(9):1705-8. PMID: 22533552.
- [pubmed] Du SL, et al. "Serum salusin-α levels are inversely correlated with the presence and severity of coronary artery disease." Scand J Clin Lab Invest, 2013;73(4):339-43. PMID: 23611255.
- [pubmed] Usta Atmaca H, et al. "IS SALUSIN-ALPHA A NEW MARKER OF CARDIOVASCULAR DISEASE RISK IN HYPOTHYROIDISM?." Acta Endocrinol (Buchar), 2017;13(1):53-59. PMID: 31149148.
- [pubmed] Esfahani M, et al. "Salusin-α Attenuates Inflammatory Responses in Vascular Endothelial Cells." Biochemistry (Mosc), 2017;82(11):1314-1323. PMID: 29223158.
- [pubmed] Cakir M, et al. "Protective effects of salusin-α and salusin-β on renal ischemia/reperfusion damage and their levels in ischemic acute renal failure." Biotech Histochem, 2017;92(2):122-133. PMID: 28296550.
- [pubmed] Gao S, et al. "Salusin-α Inhibits Proliferation and Migration of Vascular Smooth Muscle Cell via Akt/mTOR Signaling." Cell Physiol Biochem, 2018;50(5):1740-1753. PMID: 30384378.
- [pubmed] Dervişoğlu P, et al. "Salusin-α levels are negatively correlated with diastolic blood pressure in children with obesity." Cardiol Young, 2019;29(10):1225-1229. PMID: 31486354.
- [pubmed] Sipahi S, et al. "Relationship of salusin-alpha and salusin-beta levels with atherosclerosis in patients undergoing haemodialysis." Singapore Med J, 2019;60(4):210-215. PMID: 30311629.
- [pubmed] Fujie S, et al. "Increased serum salusin-α by aerobic exercise training correlates with improvements in arterial stiffness in middle-aged and older adults." Aging (Albany NY), 2020;12(2):1201-1212. PMID: 31918410.
- [pubmed] Wang Y, et al. "Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis." J Int Med Res, 2020;48(2):300060520903868. PMID: 32054363.
- [pubmed] Alpsoy S, et al. "Assessment of salusin alpha and salusin beta levels in patients with newly diagnosed dipper and non-dipper hypertension." Clin Exp Hypertens, 2021;43(1):42-48. PMID: 32723189.
- [pubmed] Arkan A, et al. "The importance of circulating levels of salusin-α, salusin-β, and heregulin-β1 in atherosclerotic coronary arterial disease." Clin Biochem, 2021;87:19-25. PMID: 33031820.
- [pubmed] Argun D, et al. "Evaluation of salusin-α and salusin-β levels in patients with type 2 diabetes mellitus and determination of the impact of severity of hyperglycemia on salusin levels." Ir J Med Sci, 2021;190(4):1403-1411. PMID: 34109528.
- [pubmed] Wang WJ, et al. "Salusin-α mitigates diabetic nephropathy via inhibition of the Akt/mTORC1/p70S6K signaling pathway in diabetic rats." Drug Chem Toxicol, 2022;45(1):283-290. PMID: 31665937.
- [pubmed] Medyńska A, et al. "Can Serum Salusin-α and Salusin-β Serve as Biomarkers for Early Atherosclerotic Lesions in Obese Children?." Int J Mol Sci, 2025;26(8). PMID: 40332043.
- [pubmed] Li L, et al. "Salusin-α preserves glomerular endothelial barrier function in hypertension via YAP/ZO-1 signaling pathway." Peptides, 2025;193:171441. PMID: 40972875.
Sources & Citations
Every study on this page was read from its PubMed record on November 3, 2026. The sequence and precursor positions come from UniProt Q8N2E6; regulatory 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.