High impact information on SU 10603

• Likewise, the FeSO4-induced formation of D was not blocked by the P450c17 inhibitor, SU-10603 [1].
• This increase in both activity and amount was enhanced by inhibiting testosterone production with aminoglutethimide, an inhibitor of cholesterol side-chain cleavage or SU 10603, an inhibitor of 17 alpha-hydroxylase [2].
• SU 10603 failed to inhibit D formation by astrocytes [3].
• The sum of the different steroids produced by Leydig cells from immature rats incubated in the presence of a 5 alpha-reductase inhibitor was only 80% of pregnenolone production in the presence of SU-10603 and epostane [4].
• The efficiency and specificity of inhibition of pregnenolone metabolism in mature, immature rat Leydig cells, mouse and tumour Leydig cells by SU-10603, a 17 alpha-hydroxylase inhibitor and epostane (WIN-32729), a 3 beta-hydroxysteroid dehydrogenase inhibitor, were studied [4].

Anatomical context of SU 10603

• Metabolism of [14C]pregnenolone by mature rat Leydig cells was inhibited for more than 95% in the presence of 20 microM SU-10603 and 5 microM epostane [4].
• Treatment of oligodendrocytes with the P450c17 inhibitor SU 10603 in the presence or absence of P failed to inhibit D production [3].
• However, the lutropin-stimulated steroid production in the tumour cells was quantitatively comparable with the normal rat Leydig cell when the metabolism of pregnenolone in intact cells and mitochondria was inhibited by addition of SU-10603 and/or cyanoketone [5].

Gene context of SU 10603

• The reactions convering delta5-3beta-hydroxysteroids to delta4-3-ketosteroids were studied in testes infused with SU-10603 (7-chloro-3,4-dihydro-2-[3-pyridyl]-1(2H)-naphthalenone. Ciba-Geigy), an inhibitor of 17alpha-hydroxylation and C-17, C-20 cleavage reactions [6].

References