research use only
Cat.No.S4166
| Related Targets | CFTR CRM1 CD markers AChR Calcium Channel Sodium Channel Potassium Channel GABA Receptor TRP Channel GluR |
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| Other ATPase Inhibitors | (-)-Blebbistatin Thapsigargin Brefeldin A (BFA chemical) CB-5083 Sodium orthovanadate Golgicide A BTB06584 Ginsenoside Rb1 CDN1163 Periplocin |
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In vitro |
DMSO
: 55 mg/mL
(198.74 mM)
Ethanol : 55 mg/mL Water : Insoluble |
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In vivo |
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
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| Molecular Weight | 276.74 | Formula | C10H13ClN2O3S |
Storage (From the date of receipt) | |
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| CAS No. | 94-20-2 | Download SDF | Storage of Stock Solutions |
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| Synonyms | N/A | Smiles | CCCNC(=O)NS(=O)(=O)C1=CC=C(C=C1)Cl | ||
| Targets/IC50/Ki |
Na(+),K(+)-ATPase
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| In vitro |
Chlorpropamide acts through a cyclic AMP-independent mechanism. The addition of 0.2 mM this compound to hepatocytes isolated from fed rats, raises the cellular concentration of fructose-2,6-bisphosphate (F-2, 6-P2). The accumulation of F-2, 6-P2 caused by this chemical (1 mM) is parallel to the stimulation of L-lactate production (36.6 versus 26.1 μmol of lactate/g of cells) and to the inhibition of gluconeogenesis (0.57 versus 0.94 μmol of [U-14C]pyruvate converted to glucose/g of cells). This compound enhances the inhibitory action evoked by insulin on glucagon-stimulated gluconeogenesis. This chemical treatment has no effect on insulin binding, altering neither receptor number nor affinity in rat adipocytes. It (175 μg/mL) enhances 2-deoxyglucose transport in both the absence (17%) and presence (20%) of insulin. This compound significantly increases glucose metabolism and total lipids in both the absence (30%) and presence (31%) of insulin. It competitively inhibits antidiuretic hormone (ADH) binding and adenylyl cyclase (AC) stimulation with Ki of 2.8 mM and 250 μM, respectively, in the LLC-PK1 cell line. This chemical (333 μM) increases the apparent Ka of ADH for AC activation (0.31 vs. 0.08 nM) without affecting a maximal response. Twenty-four-hour this compound exposure (100 μM) upregulates the ADH receptors without affecting affinity, which lowers Ka and increases basal AC activity and maximal response (1.86 vs. 1.35 and 14.9 vs. 10.6 fmol cAMP/min/1000 cells). |
References |
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