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Table 28: Growth inhibition values for compounds I-IV against TK-10, UACC-62<br />

<strong>and</strong> MCF-7 cell lines<br />

Compound<br />

I<br />

II<br />

III<br />

IV<br />

Doseresponse<br />

parameters<br />

Line 1<br />

(TK-10)<br />

renal<br />

Line 2<br />

(UACC-62)<br />

melanoma<br />

Line 3<br />

(MCF-7)<br />

breast<br />

GI50 21.02 13.42 20.57<br />

TGI 49.10 44.71 51.20<br />

LC50 77.18 76.00 81.84<br />

LC100 N/A N/A N/A<br />

GI50 24.06 12.05 23.63<br />

TGI 55.84 42.18 52.72<br />

LC50 87.63 72.32 81.82<br />

LC100 N/A N/A N/A<br />

GI50 26.50 13.53 39.08<br />

TGI 53.99 44.64 81.22<br />

LC50 81.48 75.74 N/A<br />

LC100 N/A N/A N/A<br />

GI50 N/A 48.67 92.57<br />

TGI N/A N/A N/A<br />

LC50 N/A N/A N/A<br />

LC100 N/A N/A N/A<br />

Etoposide TGI 27.00 36.20 >100<br />

NB. N/A denotes inactivity<br />

The GI50 values for compounds I <strong>and</strong> II are compared to that <strong>of</strong> their isomers (Gaspar-<br />

Marques et al., 2002) in Table 29. In our results, the GI50 values <strong>of</strong> both I <strong>and</strong> II are<br />

similar. However, this is not the case with the GI50 values for the isomers, compounds 33<br />

<strong>and</strong> 36 reported in the literature. Compound 36 displayed significantly better activity<br />

than any <strong>of</strong> the other three compounds against the three cell lines used. Our two<br />

compounds I <strong>and</strong> II however showed better activity than the dihydroxy isomer (33).<br />

Table 29: GI50 values (µM) <strong>of</strong> compounds I <strong>and</strong> II <strong>and</strong> their 7α-isomers<br />

Compound<br />

MCF-7<br />

Cell line<br />

TK-10 UACC-62<br />

I 34.41 53.90 52.74<br />

36 6.4 7.4 4.5<br />

II 34.63 69.14 67.90<br />

33 48.3 107.6 77.9<br />

Doxorubicin 0.055 0.570 0.094<br />

152

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