Diisopropylammonium dichloroacetate

Diisopropylammonium dichloroacetate

White crystal powder 
Product Specification
Place of Origin
1 kg
Payment Term
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Diisopropylammonium dichloroacetate

CAS No.: 660-27-5   

Appearance: White crystal powder 

Purity: 99%min  

Type: Cardiovascular Agents

Usage:  Animal Pharmaceuticals
Other Names: 660-27-5; Diisopropylammonium dichloroacetate; Diisopropylamine dichloroacetate; Diisopropylamine 2,2-dichloroacetate; Vasculopatina

Grade: Medicine Grade, Tech Grade
Molecular Formula: C8H17Cl2NO2   

Molecular Weight:  230.13 g/mol

Melting point:  119-121°C



It can be used in liver disease drug for acute and chronic hepatitis, fatty liver, early cirrhosis, yellow gangrene and general liver dysfunction.


Diisopropylammonium dichloroacetate (DIPA) was found to exert a significant and prolonged hypoglycemic effect in alloxan diabetic rats, but did not alter blood sugar levels of normal rats. It did not affect blood glycerol levels in either the diabetic or nondiabetic group.
Both DIPA and sodium dichloroacetate (DCA) significantly stimulated glucose-U-14C oxidation to 14CO2 in isolated hemidiaphragms from diabetic but not from nondiabetic rats. Diisopropylammonium hydrochloride (DIA) was not effective in promoting glucose oxidation in tissues from diabetic or nondiabetic rats. Thus, the effect of the compound in vivo may be due entirely to its acid moiety.
DCA (and presumably DIPA) produced no significant changes in glycerol output or on glucose-U-14C conversion to 14C-triglyceride in hemidiaphragms or epididymal fat pads from normal or diabetic rats. In addition, DCA did not alter oleate-1-14C conversion to 14C-triglyceride in muscle or adipose tissue from diabetic animals. However, DCA markedly inhibited oleate-1-14C oxidation to 14CO2 in muscle from diabetic rats.
It is possible that the hypoglycemic activity of DIPA, and presumably DCA, may be due, at least partly, to a suppression of fatty acid oxidation in muscles of diabetic rats. The high levels of circulating free fatty acids and ketone bodies which commonly occur in diabetes increase intracellular concentrations of citrate, a known inhibitor of phosphofructokinase (PFK). By suppressing fatty acid oxidation in muscle, DIPA and DCA may thus reduce citrate levels and reactivate PFK. Such an effect may explain the selective action of both DIPA and DCA on diabetic but not on normal tissue.

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