3064 Background: In cells undergoing DNA synthesis,antimetabolite-induced replication arrest results in the induction of CHK1, halting the progression of cells through G1/S to allow for DNA damage repair. Inhibition of CHK1 by SCH 900776 is hypothesized to synergize with Gem to promote replication fork collapse and apoptosis, even in the setting of anti-metabolite resistance. Methods: A dose escalation study of SCH 900776 alone and in combination with fixed doses of Gem was conducted in subjects with advanced solid tumors. Subjects were assessed for safety, tolerability, dose-limiting toxicity (DLT), and maximal administered dose (MAD). A recommended phase II dose (RP2D) was determined based on the safety profile at pharmacologically active exposures. Results: Twenty-six subjects have been enrolled and treated with 10 (n=3), 20 (n=3), 40 (n=7), 80 (n=6), and 112 mg/m2 (n=7) of SCH 900776 administered alone and following Gem (800 mg/m2) on days 1 and 8 every 21 days. No SAEs or DLTs have been observed duri...