24587-98-2

Basic information

• Product Name: 2',6'-dihydroxy-4'-methoxyacetophenone 2'-O-(2,3,4,6-O-tetraacetyl)-β-D-glucopyranoside
• Synonyms: 2',6'-dihydroxy-4'-methoxyacetophenone 2'-O-(2,3,4,6-O-tetraacetyl)-β-D-glucopyranoside
• CAS NO: 24587-98-2
• Molecular Weight: 512.468
• Mol File: 24587-98-2.mol
• Article Data: 1

Chemical Properties

• CAS DataBase Reference: 2',6'-dihydroxy-4'-methoxyacetophenone 2'-O-(2,3,4,6-O-tetraacetyl)-β-D-glucopyranoside(CAS DataBase Reference)
• NIST Chemistry Reference: 2',6'-dihydroxy-4'-methoxyacetophenone 2'-O-(2,3,4,6-O-tetraacetyl)-β-D-glucopyranoside(24587-98-2)
• EPA Substance Registry System: 2',6'-dihydroxy-4'-methoxyacetophenone 2'-O-(2,3,4,6-O-tetraacetyl)-β-D-glucopyranoside(24587-98-2)

Safety Data

• Hazardous Substances Data: 24587-98-2(Hazardous Substances Data)

Upstream product

• 480-66-0 2,4,6-trihydroxyacetophenone 
• 7507-89-3 2,6-dihydroxy-4-methoxy-acetophenone 
• 572-09-8 2,3,4,6-tetra-O-acetyl-α-D-glucopyranosyl bromide 

Relevant articles and documents

Na+-glucose cotransporter (SGLT) inhibitors as antidiabetic agents. 4. Synthesis and pharmacological properties of 4'- dehydroxyphlorizin derivatives substituted on the B ring

In our studies of Na+-glucose cotransporter (SGLT) inhibitors as antidiabetic agents, a series of novel 4'- dehydroxyphlorizin derivatives substituted on the B ring was prepared and their effects on urinary glucose excretion were evaluated in rats. Introduction of only a small alkyl group at the 4'-position increased the activity, and 3-(benzo[b]furan-5- yl)-2',6'-dihydroxy-4'-methylpropiophenone 2'-O-β-D- glucopyranoside (4) showed the most potent effect. To overcome hydrolysis of compound 4 by β-glucosidase in the digestive tract, the OH groups on the glucose moiety of compound 4 were modified. Three prodrugs (5, 42, and 55) were more potent than the parent compound 4 by oral administration, and finally 3- (benzo[b]furan-5-yl)-2',6'-dihydroxy-4'-methylpropiophenone 2'-O- (6-O-methoxycarbonyl-β-D-glucopyranoside) (5) was selected as a new promising candidate. Compound 5 was metabolized mainly by liver esterase to the active form (4), which was about 10 times more potent than 5 in inhibiting SGLT. In oral glucose tolerance test in db/db mice, compound 5 dose-dependently suppressed the elevation of glucose levels. Single administration of 5 reduced hyperglycemia concurrently with increase of glucose excretion into urine in diabetic KK-A(y) mice. Furthermore, compound 5 suppressed the elevation of blood glucose levels but did not lower it below the normal level even in fasted conditions in KK- A(y) mice. Additionally, long-term treatment with 5 dose- dependently reduced hyperglycemia and HbA1c in KK-A(y) mice. These pharmacological data strongly suggest that compound 5 has a therapeutic potential in the treatment of NIDDM.