Therapeutic Editing Toward a Proof of Principle

At a cellular level, the purported sorafenib editors should be assayed using the renal cancer cell line RCC-786-O and NRVMs (neonatal rat ventricular monocytes). In RCCs, the sorafenib/WBZ 4 combination yields agonistic synergy, marked by an increased inhibition of cell proliferation when compared to sorafenib-alone levels at equivalent bulk concentrations (Fig. 12.5a) The dose-dependent inhibition is greater than the Loewe-additive values [20, 21] (Fig. 12.5b). By contrast, the sorafenib-induced recruitment of the pro-apoptotic pathway in cardiomyocytes should be impaired by the downstream interference of WBZ 4 through JNK inhibition (Fig. 12.3a). Consequently, cytosolic release of 

12 Wrapper Drugs as Therapeutic Editors of Side Effects 

The editors impact a set of therapeutic targets that are more limited than that of the parent compounds [13], probably precluding the editors from serving as therapeutic agents by themselves. This is evident in RCC786-0-proliferation assays. Thus, in contrast with sorafenib effects (Fig. 12.5a), cell growth decreases by a 

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