113 Background: The soluble form of the VEGFR2 receptor (sVEGFR2) neutralizes circulating VEGF, and functions as a negative feedback mechanism to enable partial inhibition of VEGF-stimulated endothelial cell migration and proliferation. In response to inhibition of VEGFR2 tyrosine kinase activity, up-regulation of VEGF expression and down-regulation of sVEGFR2 expression levels have been observed (Murukesh et al., 2010). Telatinib (tel) is a novel orally available kinase inhibitor that is highly selective for the VEGFR, PDGFR, and KIT tyrosine kinases at nanomolar concentrations with potent antiangiogenic activity. Correlation between telatinib exposure and reduction in plasma sVEGFR2 levels from baseline has previously been demonstrated in patient serum samples in phase I studies. Methods: TEL0805, a phase II study administered tel with capecitabine (X) and cisplatin (P) in previously untreated metastatic or unresectable gastric or GEJ adenocarcinoma pts. Patient serum samples were obtained on day -7, [6 plasma samples (pre-dose, and at 30 min, 1, 2, 3 and 4 hours)] and on day 1, [4 plasma samples (pre-dose and at 1, 2 and 3 hours)] and evaluated for the levels of telatinib and its M2 metabolite (M2). Additional serum samples were collected every 42 days and evaluated for VEGF and sVEGFR2 levels. Results: Measurement of tel and M2 levels confirmed previous pharmacokinetic findings and demonstrated no drug accumulation following continuous daily dosing. Baseline plasma sVEGFR2 levels have previously not been reported for advanced gastric cancer patients and displayed a wide range at disease presentation. Reduction in sVEGFR2 levels were noted for nearly all treated patients and correlated with the duration of stay on tel therapy. Conclusions: Telatinib continuous dosing is possible in combination with XP with little effect on tel exposure or accumulation. Reduction in sVEGFR2 levels may be useful in identifying patients who may benefit from tel treatment in this combination setting. [Table: see text]