• Archives of Pharmacal Research
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• v.8 no.4
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• pp.221-227
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• 1985

Acetyl-11-ketopomolic acid methyl ester (VI), mp 276-$278^{\circ}$ was synthesized from pomolic acid (III). The mild alkaline treatment of VI induced the opening of ring E on carbone skeleton to yield VII, and then VII was deacetylated to give VIII, mp 82-$84^{\circ}$ Compound VIII was established as 11, 19-diketo-18, 19-secoursolic acid methylester. The E-ring opening was believed to be due to regrograde aidol condensation.

• Korean Journal of Pharmacognosy
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• v.17 no.2
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• pp.178-183
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• 1986

It was our working hypothesis that introduction of 11-keto groups to 12-oleanene/ursene series of triterpenoids should endow them with corticoid-like activities, since pharmacological actions of glycyrrhetinic acid (GA) are known to be caused by inhibition on $corticoid-{\delta}^4-reductase$. 11-Keto-triterpenoids derived artificially in these studies, such as 11, 19-diketo-18, 19-secoursolic acid methyl ester(I), $11-keto-{\beta}-boswellic$ acid derivatives (IIa-IIc), 11-Keto-presenegenin dimethyl ester (III), II-keto-oleanolic acid derivatives (IVa-IVd) and 11-keto-hederagenin (V) possess the fundamental functions of ${\alpha},\;{\beta}-unsaturated$ ketone on C-11 and hydroxyl group on C-3, as like GA (VI). Additionally, they involve the carboxyl groups on rings A (II, III), D (I, III, IV, V) and E (VI), and the hydroxyl groups on rings A (III, V) and C (III). All the compounds competitively inhibited $corticoid-5{\beta}-reductase$, and the highest inhibitory potency appeared in I. All of them except $3,\;11-diketo-{\beta}-boswellic$ acid methyl ester (IIc) were more effective about five times to twice than GA. On carrageenin-induced edema test, compounds I and IVa-IVd showed anti-inflammatory activities, but III enhanced rather edema. Structure-activity relations were found in the aspects of hydrophilicity of ring A and hydrophobicity of rings C/D. The more they were hydrophilic in ring A and hydrophobic in rings C/D, the more they inhibited the enzyme. And the more they were hydrophobic in rings C/D, the more they exhibited antiiflammatory activities. However, the increased hydrophilicity in ring A resulted in increasing edema, probably due to a nonspecific inhibition on $aldosterone-5{\beta}-reductase$.