"It worked better than Nexavar because Nexavar is another crap MULTI-TARGETED Kinase inhibitor. "
You are embarrassing yourself. Having a specific kinase inhibitor can work well in very defined one hit cancers, as in the case of Gleevec inhibition of the abl kinase activation via the famous Philadelphia chromosome translocation. However, having a single kinase more specifically targeted means it is easier to generate resistance by activation of other growth pathways. That is why multi-kinase inhibitors can have broader usage and be more effective in the longer run. I would guess that the PLX drug would work better in increasing survival by combining it with other inhibitors.
I will have to look into PLX4032 and the nature of its action but I find it extremely unlikely it is truly specific for only one kinase. The only example I know if is called a shokat mutated kinase (as allele) used in research both in vivo and in vitro. A specific kinase is mutated by site directed mutagenesis so that the size of the ATP binding pocket is altered to allow an ATP analog to be able to fit in and inhibit that kinase alone. It is specific because the analog is too large to fit into the binding pocket of a normal kinase.
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