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    Tolbutamide (HLS-831)
    Tolbutamide (HLS-831)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0192
    CAS #: 64-77-7 Purity ≥98%

    Description: Tolbutamide (also known as HLS 831; trade names: Artosin, Diabetol, Orinase), a sulfonylurea analog, is a potent and selective inhibitor of potassium channel used as an oral blood-glucose-lowering/hypoglycemic medication. It may be used for the treatment of type II diabetes.  

    References: Biochem Biophys Res Commun. 1973 Jul 2;53(1):291-4; Glia. 2006 Aug 1;54(2):125-34.

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    Molecular Weight (MW)270.35 
    CAS No.64-77-7 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 54 mg/mL (199.7 mM) 
    Water: <1 mg/mL
    Ethanol: 54 mg/mL (199.7 mM) 
    Other info

    Chemical Name: 1-butyl-3-(4-methylphenyl)sulfonylurea


    InChi Code: InChI=1S/C12H18N2O3S/c1-3-4-9-13-12(15)14-18(16,17)11-7-5-10(2)6-8-11/h5-8H,3-4,9H2,1-2H3,(H2,13,14,15)

    SMILES Code: O=C(NS(=O)(C1=CC=C(C)C=C1)=O)NCCCC

    SynonymsTolbutamide, trade names: Artosin, Diabetol, Orinase, HLS 831, HLS831, HLS-831

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    In Vitro

    In vitro activity: Tolbutamide belongs to a class of medications called sulfonylureas. Tolbutamide lowers blood sugar by causing the pancreas to produce insulin (a natural substance that is needed to break down sugar in the body) and helping the body use insulin efficiently. This medication will only help lower blood sugar in people whose bodies produce insulin naturally. Tolbutamide is not used to treat type 1 diabetes (condition in which the body does not produce insulin and, therefore, cannot control the amount of sugar in the blood) or diabetic ketoacidosis (a serious condition that may occur if high blood sugar is not treated). Tolbutamide inhibits both the basal and the cyclic AMP-stimulated protein kinase activities and the IC50 of Tolbutamide is 4 mM. Similar Tolbutamide concentrations are required for half maximal inhibition of in vitro lipolysis induced by hormones (norepinephrine and ACTH) or by dibutyryl cyclic AMP plus theophylline. Tolbutamide also inhibits both soluble and membrane-bound protein kinase from canine heart. The Tolbutamide inhibition of adipose tissue cyclic AMP-dependent protein kinase is one possible explanation for the antilipolytic effects of this drug. Tolbutamide inhibits C6-glioma cell proliferation by increasing Cx43, which correlates with a reduction in pRb phosphorylation due to the up-regulation of the Cdk inhibitors p21 and p27. Cytosolic nucelotides enhance the Tolbutamide sensitivity of the ATP-dependent K+ channel in mouse pancreatic B cells by their combined actions at inhibitory and stimulatory receptors.

    Kinase Assay: Diced epididymal fat pads from fed Wistar rats (175-225 gm) are obtained after decapitation and incubated at 37 °C for two hours in Krebs-bicarbonate buffer containing 1.27 mM CaCl2. When added, Tolbutamide is present only during the incubation. After incubation fat pads are rinsed and sonicated in cold Krebs-bicarbonate buffer. The aqueous supematants from centrifugation at 50,000 × g for 30 minutes at 4 °C contained 0.75 to 1.25 mg protein per mL and are assayed for cyclic AMP-stimulated protein kinase activity. The assay is performed in 0.2 mL with these additions, 10 μmoles sodium glycerofiosphate pH 7.0, 2 μmoles sodium fluoride, 0.4 μmoles theophylline, 0.1 μmoles ethylene glyool bis (β-aminoethyl ether)-N, N'-tetraaoetic acid, 3 μmoles magnesium chloride, 0.3 mg mixed histone, 2 nmoles (γ- 32P) ATP, 1 nmoles cyclic AMP when indicated, and 0.05 ml of supernatant. 

    Cell Assay: C6 glioma cells are incubated in serum-free DMEM at 37 °C for at least 24 hours before each experiment. Tolbutamide (400 μM) is incubated for 24 hours in serum-free medium. Incubations are performed at 37 °C in an atmosphere of 95% air/5% CO2 with 90–95% humidity. 

    In Vivo450 mg Tolbutamide/kg/day given for 7 days significantly increases the binding of insulin to isolated adipocytes. The binding curves reflect an increase in the number of receptor sites rather than in the affinity. The effect is associated with an enhanced response to insulin of the adipose tissue, since the fat cells obtained from animals treated with Tolbutamide convert significantly more glucose to lipids in the presence of insulin than those obtained from the control group. However, the augmentation of insulin binding sites is observed only at a large tolbutamide dosage, which reduces the pancreatic insulin content, the secretory response of the isolated pancreas, and the serum insulin levels. Smaller doses, sufficient to produce metabolic effects via a stimulation of insulin secretion, do not provide additional insulin binding sites 
    Animal modelMale albino Wistar rats
    Formulation & DosageTolbutamide is given as powder and mixed with food; 450 mg/kg; oral gavage 

    Biochem Biophys Res Commun. 1973 Jul 2;53(1):291-4; Glia. 2006 Aug 1;54(2):125-34; Biochem Pharmacol. 1982 Apr 1;31(7):1227-31. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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