TG 100572 is a inhibitor of multi-targeted kinase which inhibits receptor tyrosine kinases and Src kinases(IC50s of 2, 7, 2, 16, 13, 5, 0.5, 6, 0.1, 0.4, 1, 0.2 nM for VEGFR1, VEGFR2, FGFR1, FGFR2, PDGFRβ, Fgr, Fyn, Hck, Lck, Lyn, Src, Yes, respectively).

PDGFRβ:13 nM, FGFR1:2 nM, FGFR2:16 nM, VEGFR1:2 nM, VEGFR2:7 nM

TG 100572 induces apoptosis in rapidly proliferating, but not quiescent, endothelial cell cultures[1]. TG 100572 is shown to inhibit hRMVEC cell proliferation with IC50 of 610±72 nM. in ocular endothelial cells,TG 100572 has the therapeutic potential to inhibit VEGF function, a contributing factor to pathological angiogenesis in diseases such as AMD and PDR[2].

Systemic delivery of TG 100572 in a murine model of laser-induced choroidal neovascularization (CNV) causes significant suppression of CNV, but with an associated weight loss suggestive of systemic toxicity[1]. TG 100572(23.4 μM) is reached in 30 min (Tmax)=0.5 h) in the choroid and the sclera. However, the levels of TG 100572 in the retina are relatively low. The half-life of TG 100572 in ocular tissues is very short; hence, TG 100572 is administered topically minimum t.i.d. to maintain appropriate drug levels in the eye. The maximum concentration one can achieve in formulations using TG 100572 is 0.7% w/v[2].