TUSP should not be thought of as just a Flt3 inhibitor.
Each molecule needs to be assessed in the context of all of its kinase inhibitory targets at the mechanistic level for the target disease and indication.
As you just posted, Lux is being looked at as a SYK inhibitor in context of auto-immune disease.
Lux inhibits PDGFa and CSF1R. Why is that important in AML? There is a rational. When and where does AURA/B inhibition potentially play a role. There is a rational.
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