| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| Other Sizes |
| Targets |
The specific molecular target of phenyl sulfate is not definitively identified in this study. However, it is shown to be a substrate for the human organic anion transporting polypeptide SLCO4C1 (OATP4C1). In an uptake study using SLCO4C1-overexpressing MDCKII cells, the uptake of phenyl sulfate was significantly increased, confirming it as a substrate for this transporter. Additionally, the SLCO4C1 inhibitor ritonavir inhibited the uptake of phenyl sulfate by human proximal tubular HK-2 cells. [1]
|
|---|---|
| ln Vitro |
Phenyl sulfate was shown to be toxic to differentiated human podocytes. Cell survival analysis revealed that phenyl sulfate induced significant cell toxicity at concentrations from 100 µM. [1]
Phenyl sulfate decreased glutathione levels in differentiated podocytes. Exposure to 30 µM phenyl sulfate caused a reduction in glutathione levels, which became significant at the 100 µM concentration. [1] Phenyl sulfate impaired mitochondrial bioenergetics in cultured podocytes. Exposure to phenyl sulfate at concentrations ranging from 100 µM to 1 mM significantly decreased mitochondrial basal respiration, ATP production, proton leak, and maximum respiratory capacity. Phenyl sulfate also increased non-mitochondrial respiration, suggesting a compensatory respiration mechanism, while glycolysis (measured by extracellular acidification rate) remained unchanged. [1] |
| ln Vivo |
In db/db mice (a model of type 2 diabetes), oral administration of phenyl sulfate (50 mg/kg) for 6 weeks significantly increased plasma phenyl sulfate levels by approximately 5-fold (to 27.3 ± 9.17 µM) and significantly increased albuminuria compared to control db/db mice. Electron microscopy revealed increased foot process effacement and glomerular basement membrane thickening in phenyl sulfate-treated db/db mice. [1]
In KKAy mice fed a high-fat diet (another DKD model), oral administration of phenyl sulfate (50 mg/kg) for 6 weeks significantly increased plasma phenyl sulfate levels (to 6.09 ± 3.18 µM) and increased albuminuria. Electron micrographs showed podocyte effacement, glomerular basement membrane thickening, and perivascular fibrosis in the treated group. [1] In eNOS-knockout mice with the Akita mutation (a severe diabetes model), plasma phenyl sulfate levels were significantly higher in diabetic mice (15.4 ± 2.73 µM) compared to non-diabetic controls (5.97 ± 0.47 µM). Histological examination revealed significant glomerulosclerosis changes in the diabetic mice. [1] |
| Cell Assay |
Podocyte cell viability assay: Differentiated human urinary podocyte-like epithelial cells were cultured in 96-well collagen-coated plates. Phenyl sulfate was applied at final concentrations indicated (0, 3, 10, 30, 100, 300, 1000 µM), and cells were cultured for 72 hours. Cell viability was then measured. Results showed significant cell toxicity at concentrations from 100 µM. [1]
Glutathione measurement: Differentiated podocytes were exposed to phenyl sulfate (30 µM and 100 µM) for 72 hours. Glutathione levels were measured using a luminescent cell viability assay kit. Exposure to 30 µM phenyl sulfate decreased glutathione levels, with a significant reduction observed at the 100 µM concentration. [1] Mitochondrial function measurement (Seahorse assay): Bioenergetic analysis of human cultured podocytes was carried out. Cells were cultured in a specialized assay medium without CO₂ for 60 minutes. After equilibration, oxygen consumption rate and extracellular acidification rate were measured using a Seahorse XF24 analyzer by sequentially injecting inhibitors of oxidative phosphorylation. Phenyl sulfate exposure (100 µM to 1 mM) significantly decreased mitochondrial basal respiration, ATP production, proton leak, and maximum respiration capacity. [1] |
| Animal Protocol |
Oral administration in db/db mice: Phenyl sulfate was administered orally to db/db mice at a dose of 50 mg/kg/day for 6 weeks. Water intake was measured to estimate drug intake. Plasma phenyl sulfate levels were measured 1 hour after administration in a separate cohort (n=3) to confirm rapid absorption, showing a rise to 64.53 ± 5.87 µM. [1]
Oral administration in KKAy mice: Phenyl sulfate was administered orally to high-fat diet-fed KKAy mice at a dose of 50 mg/kg/day for 6 weeks. [1] Streptozotocin-induced diabetic rat model: Diabetes was induced in 8-week-old SLCO4C1-Tg and wild-type rats by intraperitoneal injection of streptozotocin (50 mg/kg) dissolved in citrate-phosphate buffer (pH 4.2). Blood was collected on day 7, and rats with blood glucose levels greater than 300 mg/dl were selected for further analysis. [1] |
| ADME/Pharmacokinetics |
After oral administration of phenyl sulfate (50 mg/kg) to db/db mice, the plasma concentration rose rapidly, reaching 64.53 ± 5.87 µM within 1 hour, and then decreased quickly. Following 6 weeks of oral administration in db/db mice, the plasma level was significantly increased by approximately 5-fold (to 27.3 ± 9.17 µM). [1]
In the human U-CARE diabetic cohort study, plasma phenyl sulfate levels in patients ranged from 0 to 68.1 µM. [1] |
| Toxicity/Toxicokinetics |
Phenyl sulfate administration induced podocyte damage. Electron microscopy revealed increased foot process effacement and glomerular basement membrane thickening in phenyl sulfate-treated db/db and KKAy mice. [1]
Phenyl sulfate was directly toxic to differentiated human podocytes in vitro, with significant cell toxicity observed at concentrations of 100 µM and above. [1] Phenyl sulfate decreased glutathione levels in differentiated podocytes, rendering cells vulnerable to oxidative stress, with a significant reduction at 100 µM. [1] Phenyl sulfate impaired mitochondrial function in podocytes, significantly decreasing basal respiration, ATP production, and maximum respiratory capacity at concentrations of 100 µM to 1 mM. [1] |
| References |
[1]. Gut microbiome-derived phenyl sulfate contributes to albuminuria in diabetic kidney disease. Nat Commun. 2019 Apr 23;10(1):1835.
|
| Additional Infomation |
Phenylacetyl hydrogen sulfate is an aryl sulfate ester, a phenolic compound with an O-sulfonyl substituent. It is a human heterologous metabolite, functionally related to phenolic compounds, and is the conjugate acid of phenyl sulfate esters. Aryl sulfate esters are found in or produced by Escherichia coli (K12 strain, MG1655 strain). Phenylacetyl hydrogen sulfate has also been reported in Trypanosoma brevicornu, and relevant data are available for reference.
Role in disease: Phenyl sulfate is identified as a gut microbiota-derived metabolite that contributes to albuminuria and podocyte damage in diabetic kidney disease (DKD). In a diabetic patient cohort (U-CARE study, n=362), plasma phenyl sulfate levels significantly correlated with baseline albuminuria (urinary albumin-to-creatinine ratio) and predicted 2-year progression of albuminuria, particularly in patients with microalbuminuria. Among known risk factors, phenyl sulfate was the only factor that served as a predictor of 2-year albuminuria progression in microalbuminuric patients. [1] Source and metabolism: Phenyl sulfate is produced from dietary tyrosine. Gut bacterial tyrosine phenol-lyase converts tyrosine to phenol, which is then absorbed and metabolized to phenyl sulfate in the liver. [1] Therapeutic targeting: Inhibition of the bacterial enzyme tyrosine phenol-lyase (using inhibitors such as 2-aza-tyrosine or L-meta-tyrosine) reduced plasma phenyl sulfate levels and ameliorated albuminuria and renal damage in diabetic mice, suggesting a potential therapeutic strategy. [1] |
| Molecular Formula |
C6H6O4S
|
|---|---|
| Molecular Weight |
174.17
|
| Exact Mass |
173.999
|
| CAS # |
937-34-8
|
| Related CAS # |
1733-88-6 (potassium salt)
|
| PubChem CID |
74426
|
| Appearance |
White to off-white solid at room temperature
|
| LogP |
1.949
|
| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
2
|
| Heavy Atom Count |
11
|
| Complexity |
197
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
O=S(OC1C=CC=CC=1)(O)=O
|
| InChi Key |
CTYRPMDGLDAWRQ-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C6H6O4S/c7-11(8,9)10-6-4-2-1-3-5-6/h1-5H,(H,7,8,9)
|
| Chemical Name |
phenyl hydrogen sulfate
|
| Synonyms |
phenyl hydrogen sulfate; Phenylsulfate; Phenol sulfate; 937-34-8; Sulfuric acid, monophenyl ester;
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
H2O: ~250 mg/mL (1435.4 mM)
|
|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.7415 mL | 28.7076 mL | 57.4152 mL | |
| 5 mM | 1.1483 mL | 5.7415 mL | 11.4830 mL | |
| 10 mM | 0.5742 mL | 2.8708 mL | 5.7415 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
