TargetMol

Potassium 1H-indol-3-yl sulfate

Product Code:
 
TAR-T4938
Product Group:
 
Inhibitors and Activators
Supplier:
 
TargetMol
Regulatory Status:
 
RUO
Shipping:
 
cool pack
Storage:
 
-20℃
1 / 1
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CodeSizePrice
TAR-T4938-10mg10mg£115.00
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TAR-T4938-25mg25mg£145.00
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TAR-T4938-50mg50mg£184.00
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TAR-T4938-100mg100mg£257.00
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TAR-T4938-200mg200mg£350.00
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TAR-T4938-500mg500mg£550.00
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Further Information

Bioactivity:
Indoxyl sulfate (potassium salt) is an agonist for the human aryl hydrocarbon receptor (AHR). The aryl hydrocarbon receptor (AhR) has recently emerged as a pathophysiological regulator of immune-inflammatory conditions and Indoxyl sulfate has been shown to be a ligand for AhR. Indoxyl sulfate is also a metabolite of tryptophan derived from dietary protein. Tryptophan is metabolized by intestinal bacteria into indole, which is absorbed into the blood and then further metabolized to indoxyl sulfate in the liver, which is normally excreted in urine. In chronic kidney disease patients where renal function is compromised, indoxyl sulfate can accumulate in serum as a uremic toxin, inducing oxidative stress and accelerating progression of the disease. Indoxyl sulfate at 250 μM can induce the activation of NF-κB, promoting the expression of both TGF-β1 and Smad3 expression in proximal tubular cells of rats, which is associated with profibrotic activity.
CAS:
2642-37-7
Formula:
C8H6KNO4S
Molecular Weight:
251.3
Pathway:
Immunology/Inflammation; Metabolism
Purity:
0.9987
SMILES:
[K+].[O-]S(=O)(=O)Oc1c[nH]c2ccccc12
Target:
AhR; Endogenous Metabolite

References

Zgoda-Pols J R , Chowdhury S , Wirth M , et al. Metabolomics analysis reveals elevation of 3-indoxyl sulfate in plasma and brain during chemically-induced acute kidney injury in mice: Investigation of nicotinic acid receptor agonists[J]. Toxicology & Applied Pharmacology, 2011, 255(1):48-56. Ito S , Osaka M , Edamatsu T , et al. Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation.[J]. Journal of Atherosclerosis & Thrombosis, 2016, 23(8):iii510-iii511.