Sorafenib and Sunitinib have been approved by the FDA respectively in December 2005 for RCC, and in January 2006 for RCC and GIST.
The aim of this drawing is not to show differences in chemical structure,
efficacy or safety, but to pinpoint differences in biological mechanisms of action.
Although there are many similar targets (VEGFR2, VEGFR3, PDGFR, c Kit), Sunitinib is also active on VEGFR1, and on the RET receptor (which is becoming an exciting target for other cancers, such as thyroid, where trials are ongoing with a few molecules).
Sorafenib is active on intra-cellular kinases, such as those active on CRAF and BRAF, hence blocking the MEK/ERK pathway, which is a strategic target for many cancers.