Unbound reagents were removed by washing, and the bound antibodies on the chips were visualized utilizing the GenePix 4000B microarray scanner. The signal intensities were analyzed and relative phosphorylation levels determined with the GenePix Pro application. Research was done using multiple t check with the STATA program. Topoisomerase Data was analyzed by class, g _ 0. 05 was considered significant. MP470, a novel receptor tyrosine kinase inhibitor shows growth inhibitory activity against many different cancer cell lines. MP470 is in Phase I clinical trial testing. In this review, the cytotoxicity of MP470 was considered on prostate cancer cell lines. The drug was successful on LNCaP and PC 3 cells with an IC50 of 8 M and 4 M, respectively. However, MP470 had only a small influence on the viability of DU145 cells. Since it Cabozantinib structure could be the most favored in vitro type of prostate cancer here we focused on LNCaP cells. Since the HER family is implicated by growing evidence in prostate cancer development, we evaluated the cytotoxic effect of Erlotinib on LNCaP cells and exhibited a cytotoxic effect having an IC50 of 10 M. But, when Erlotinib was coupled with different amounts of MP470, the IC50 of MP470 decreased to 2 M. This suggests that Erlotinib has an additive impact on the cytotoxicity of MP470. We next examined whether apoptosis is involved in the inhibition of cell proliferation by MP470. LNCaP cells were treated with DMSO and increasing amounts of MP470 alone or in mixture with Erlotinib for 48 hr. Apoptosis quantified by morphologic changes was caused in a dose dependent manner and this effect was synergistic with Erlotinib. Treatment of LNCaP cells with either Erlotinib or MP470 Ribonucleic acid (RNA) induced 9% or 21% apoptosis respectively, while apoptosis with the combination, risen up to 36%. These morphologic changes were established by Annexin V staining and PARP cleavage assays respectively. Since MP470 inhibits c Kit and PDGFR RTKs, we examined Imatinib Mesylate, a well established c Kit and PDGFR TKI. IM had an of ~12 M in LNCaP cells just like that observed for Erlotinib alone. Interestingly, IM did not induce apoptosis in LNCaP cells either alone or in combination with Erlotinib. This implies that c Kit and PDGFR do not play a role in defending apoptosis and that MP470 inhibits LNCaP cells by a mechanism independent of c Kit and PDGFR. In order to learn whether MP470 inhibits cell cycle progression, we treated the lung cancer cell line A549 and two prostate cell lines, pan Caspase inhibitor LNCaP and PC 3 with DMSO, 10 M of Erlotinib, MP470, IM or combinations for 32 hr. The cells were then left unsynchronized or synchronized at the mitotic stage by nocodazole for 16 hr. Cell cycle progression analyzed by flow cytometry showed that MP470 induced G1 arrest in A549 and LNCaP cells while they can not be synchronized in G2/M by nocodazole compared to DMSO control. Nevertheless, MP470 didn’t induce G1 arrest in PC three cells, implicating that this arrest is cell line specific.