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Of note, this compound failed to modulate BCR-ABL and Crkl phosphorylation at the same time, indicating that the acadesine anti-leukemic effect is independent on BCR-ABL.
The compound failed to show efficacy, and development was halted in 2008 [ 29].
However, this compound failed to extend survival time in an acute mouse model of African trypanosomiasis.
Although ZM336372 effectively inhibited purified BRAF and CRAF in vitro, the compound failed to suppress MEK phosphorylation in cells.
The doses used in the clinical program were limited by ARIA, and finally the compound failed to show efficacy.
When the ultimate DNA-damaging metabolite BPDE was directly applied to HaCaT cells, this compound failed to promote CD95L-induced apoptosis.
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In contrast, this compound fails to inhibit cell growth or induce cell apoptosis [ 137].
Unexpectedly, these compounds failed to inactivate or inhibit the enzyme, even at high concentrations.
The E.P.A. account differs from that of 3M, which said on Monday that it had voluntarily decided to stop making the chemical used in Scotchgard and many other products by the end of the year because the tests showed that the chemical compounds failed to decompose in the environment.
But these compounds failed to induce Cldn4 and NQO1 in both Nrf2−/− and AhR−/− colon explants as well as Nrf2 in AhR−/− mice colon explants (Fig. 3d, e, Supplementary Fig. 10) suggesting requirement of AhR and Nrf2 expression for UroA/UAS03 mediated activities.
Experimental animals fed purified organic compounds failed to thrive.
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