uremic

Iptacopan hydrochloride (LNP023 hydrochloride) is an orally bioavailable, highly potent and highly selective factor B inhibitor with an IC50 of 10 nM. Iptacopan hydrochloride shows direct, reversible, and high-affinity binding to human factor B with a KD of 7.9 nM.

Indican (Indoxyl-β-D-glucoside) is a natural protective compound that is used to protect the liver.

Phytic acid dipotassium salt is an endogenous metabolite that inhibits β-secretase 1 (BACE1).

Penicillamine (Artamine), possessing antineoplastic properties, induces apoptosis by a p53-mediated mechanism and inhibits angiogenesis by chelating with copper, a cofactor for angiogenesis. Artamine is a beta dimethyl analog of the amino acid cysteine. As a degradation product of penicillin antibiotics, Artamine chelates with heavy metals and increases their urinary excretion.

N-Acetyl-L-arginine (Ac-Arg-OH), an N-acyl-L-alpha-amino acid with a strong basic nature (based on its pKa), has elevated serum levels in hyperargininemic patients and is associated with several diseases, including uremia and colorectal cancer. In untreated hyperargininemic patients, it reaches its highest levels in cerebrospinal fluid. It has also been detected in apples and loquats, suggesting it could be a potential biomarker for consumption of these foods. Additionally, a low-arginine diet combined with sodium benzoate therapy leads to a marked decrease in plasma N-acetyl-L-arginine concentrations.

4-Ethylphenyl Sulfate is an intestinal microbial metabolite that reduces mature oligodendrocytes and myelin formation in the brain, affects PVT gene expression, and promotes anxiety-like behaviour in mice.

p-Cresyl sulfate potassium (p-Tolyl sulfate potassium salt) is a prototype protein-bound uremic toxin derived from the metabolites of tyrosine and phenylalanine through liver.

p-Cresyl Sulfate is the major uremic toxin present in the blood of patients with chronic kidney disease and is derived from the metabolites of tyrosine and phenylalanine in the liver.

Potassium 1H-indol-3-yl sulfate (Potassium 3-indoxyl sulfate) is an agonist for the human Aryl Hydrocarbon Receptor (AhR), a key regulator of immune-inflammatory conditions. A metabolite of tryptophan derived from dietary protein, it is produced by intestinal bacteria and metabolized in the liver. In chronic kidney disease patients with impaired renal function, it accumulates in serum as a uremic toxin, inducing oxidative stress and accelerating disease progression. At 250 μM, it activates NF-Κb, promoting TGF-β1 and Smad3 expression in rat proximal tubular cells, which is associated with profibrotic activity.

N-Acetyl-L-arginine dihydrate (N-Ac-L-arg-OH) is one of the guanidino compounds found elevated in the serum of a hemodialyzed renal insufficient (uremic) pediatric population.

Indoxyl sulfate-d5 is intended for use as an internal standard for the quantification of indoxyl sulfate by GC- or LC-MS. Indoxyl sulfate is a uremic toxin and a metabolite of tryptophan. It is formed via sulfation of indole, an intermediate generated from tryptophan by intestinal bacteria, by the sulfotransferase (SULT) isoform 1A1 variant 2 (SULT1A1*2) in the liver. Indoxyl sulfate activates the aryl hydrocarbon receptor (AhR) in HepG2 40/6 hepatoma cells (EC50 = 12.1 nM in a reporter assay). It also inhibits the organic anion transporter (OAT) isoforms OAT1 and OAT3 (Kis = 34.2 and 74.4 µM, respectively for the rat transporters) in S2 proximal tubule cells. Indoxyl sulfate (0.2 and 1 mM) increases superoxide anion and nitric oxide levels in isolated human mononuclear blood cells. It increases serum creatinine and blood urea nitrogen (BUN) levels in the 5/6 nephrectomized rat model of chronic renal failure when administered at a dose of 50 mg/kg.

Guanidinosuccinic acid (GSA) has been identified as a uremic toxin, is a nitrogenous metabolite isolated in excess from serum and urine.

pTH (1-37) (human), a fragment of parathyroid hormone (PTH), promotes cAMP formation and enhances alkaline phosphatase activity. Additionally, it fosters growth, elevates bone calcium content, and augments bone mineral density (BMD) in uremic animals. This compound shows promise for osteoporosis research [1] [2] [3].

Ravulizumab (ALXN1210) is a humanized monoclonal antibody that specifically binds to human complement protein C5 with high affinity, targeting complement factor 5 to block complement activation. It can be used for the prevention and treatment of paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and myasthenia gravis.

Phenyl sulfate is a gut microbiota-derived metabolite of tyrosine and a recognized uremic toxin. At a concentration of 30 µM, phenyl sulfate reduces the survival of differentiated human urinary podocyte-like epithelial cells (HUPECs), decreases intracellular glutathione (GSH) levels, and induces mitochondrial dysfunction. In a db/db mouse model of diabetes, phenyl sulfate administered at a dose of 50 mg/kg induces podocyte damage and albuminuria. Elevated plasma levels of phenyl sulfate are correlated with the progression of albuminuria in patients suffering from diabetic kidney disease, highlighting its role as a biomarker and potential therapeutic target.

Danicopan (ACH-4471) (ACH-4471) is a selective, orally active small molecule factor D inhibitor with high binding affinity to human factor D, with a Kd value of 0.54 nM. Danicopan (ACH-4471) inhibits the activity of the complement replacement pathway (APC) and may block the complement replacement pathway in paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS).

p-Cresol-d3 (methyl-d3) is a deuterated compound of p-Cresol, suitable for isotope tracing. p-Cresol (4-methylphenol) is the terminal product of protein degradation, capable of inhibiting mitochondrial respiration and mitochondrial autophagy.

p-Cresol sulfate-d7 (potassium) is the deuterated form of p-Cresyl sulfate potassium. This compound, also known as p-Methylphenyl potassium sulfate, is a uremic toxin that binds to prototype proteins.

p-Cresyl sulfate (Standard) is a reference standard for research and analysis in studies involving p-Cresyl sulfate. p-Cresyl Sulfate is the major uremic toxin present in the blood of patients with chronic kidney disease and is derived from the metabolites of tyrosine and phenylalanine in the liver.

Potassium 1H-indol-3-yl sulfate (Standard) is a reference standard for research and analysis in studies involving Potassium 1H-indol-3-yl sulfate. Potassium 1H-indol-3-yl sulfate (Potassium 3-indoxyl sulfate) 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 potassium 1H-indol-3-yl sulfate has been shown to be a ligand for AhR. Potassium 1H-indol-3-yl 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, potassium 1H-indol-3-yl sulfate can accumulate in serum as a uremic toxin, inducing oxidative stress and accelerating progression of the disease. Potassium 1H-indol-3-yl 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.

N-Acetyl-L-arginine (Standard) is a reference standard for research and analysis in studies involving N-Acetyl-L-arginine. N-Acetyl-L-arginine (Ac-Arg-OH) belongs to the class of organic compounds known as n-acyl-l-alpha-amino acids. These are n-acylated alpha amino acids which have the L-configuration of the alpha-carbon atom. N-a-Acetyl-L-arginine serum levels (and other guanidino compounds) were elevated of all the hyperargininemic patients are higher than the normal range. N-a-Acetyl-L-arginine is a very strong basic compound (based on its pKa). Untreated hyperargininemic patients have the highest guanidino compound levels in cerebrospinal fluid. N-a-Acetyl-L-arginine is one of the guanidino compounds found elevated in the serum of an hemodialyzed renal insufficient (uremic) pediatric population. Outside of the human body, N-a-Acetyl-L-arginine has been detected, but not quantified in, apples and loquats. This could make N-a-acetyl-L-arginine a potential biomarker for the consumption of these foods. N-a-Acetyl-L-arginine, with regard to humans, has been found to be associated with several diseases such as uremia and colorectal cancer; N-a-acetyl-L-arginine has also been linked to the inborn metabolic disorder hyperargininemia. During a low-arginine diet, together with sodium benzoate therapy, there was a marked decrease in plasma N-alpha-acetylarginine. N-a-Acetyl-L-arginine increases in urine hyperargininemic patients.

4-Ethylphenyl sulfate sodium is a metabolite produced by gut microbes. It is also a protein-bound uremic toxin and a xenobiotic substrate that contributes to endothelial dysfunction.

NAB815 is a specific inhibitor of Stx2a (Kd= 0.01 μM)/TLR4 interactions. It inhibits the interaction between neutrophils and Stx2a with an IC50 of 0.057 μg/mL. NAB815 also prevents the formation of extracellular vesicles (EV) containing Stx2 from leukocytes and platelets, reducing its toxicity in cells (Vero cells) and in animal models (CD-1 mice). Additionally, NAB815 decreases the bacterial load in the kidneys, urine, and bladder of mice infected with Escherichia coli. It is applicable for research in hemolytic uremic syndrome (HUS).