TG 100572 is a multi-targeted kinase inhibitor which inhibitsreceptor tyrosine kinasesandSrckinases; hasIC₅₀s 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.

TG 100572 shows sub-nanomolar activity against the Src family as well as RTK such as VEGFR1 and R2, FGFR1 and R2, and PDGFRβ. TG 100572 inhibits vascular endothelial cell proliferation (ED₅₀=610±71 nM) and blocks VEGF-induced phosphorylation of extracellular signal-regulated kinase. TG 100572 induces apoptosis in rapidly proliferating, but not quiescent, endothelial cell cultures^[1]. TG 100572 is shown to inhibit hRMVEC cell proliferation, with an IC₅₀of 610±72 nM. This suggests that TG 100572 has the therapeutic potential to inhibit VEGF function in ocular endothelial cells, 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]. A concentration of 23.4 μM (C_max) of TG 100572 is reached in 30 min (T_max)=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, the compound 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].

475.97

C₂₆H₂₆ClN₅O₂

867334-05-2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

DMSO : ≥ 150 mg/mL(315.15 mM)

*"≥" means soluble, but saturation unknown.