Chlorpropamide 94-20-2

99%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

氯磺bing脲

白色結(jié)晶性粉末

DMSO : 51 mg/mL (184.3 mM)

Ethanol : 51 mg/mL (184.3 mM)

Na(addition)_K(addition) ATPase

Chlorpropamide acts through a cyclic AMP-independent mechanism. The addition of 0.2 mM Chlorpropamide 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 Chlorpropamide (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 pyruvate converted to glucose/g of cells). Chlorpropamide enhances the inhibitory action evoked by insulin on glucagon-stimulated gluconeogenesis. Chlorpropamide treatment has no effect on insulin binding, altering neither receptor number nor affinity in rat adipocytes. Chlorpropamide (175 μg/mL) enhances 2-deoxyglucose transport in both the absence (17%) and presence (20%) of insulin. Chlorpropamide significantly increases glucose metabolism and total lipids in both the absence (30%) and presence (31%) of insulin. Chlorpropamide 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. Chlorpropamide (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 Chlorpropamide 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).