Early studies with the non-selective Chk1 inhibitor UCN-01 established plasma concentrations that exceeded 20 μM (far higher than the 100 nM needed to inhibit Chk1) with a half-life of >200 h, but it was discovered that the drug was bound avidly to the plasma protein alpha-1-acid glycoprotein and hence was not bioavailable to the tumor [22, 23]. Here, CHEK1 is linked to neoplasm.