PDGF1-3) is a glycoprotein that is produced by a large number of normal as well as transformed cell types, and it acts not only on connective tissue cells but also on other types of cells. It is also well known that PDGF participates in the onset of illness, e.g., arteriosclerosis and restenosis, [4][5][6][7][8] fibrosis, 9,10) nephritis, 11) along with its role in physiological phenomena such as generating processes in living organisms and aiding the wound healing process. An attractive target to treat proliferative disorders is to block abnormal PDGF-induced cell proliferation. PDGF-induced cell proliferation is caused by the ligand binding to its cell surface receptor, followed by dimerization of the receptor and auto-phosphorylation of tyrosine kinase domain. [12][13][14][15][16] Various recent approaches to blocking the pathways mediated by PDGFR tyrosine kinase have led to the discovery of a wide range of small-molecule inhibitors, e.g., the indole-2-ones, [17][18][19][20] the quinoxalines, 21-23) the tyrophostines, 24,25) the pyridylpyrimidines, 26,27) the quinolines and quinazolines, [28][29][30][31][32][33][34] the indoles, 35,36) the imidazoles, 37,38) the pyrazoles. 39) We also found previously that the in-house compound 7-[3-(cyclohexylmethyl)ureido]-3-{1-methyl-1H-pyrrolo [2,3-b]pyridin-3-yl}quinoxalin-2(1H)-one (7d-6) showed potent inhibitory activity toward PDGF-induced CPA and APA. Table 1 shows the inhibitory activity of 7d-6 (IC 50 ϭ0.05 mmol/l in CPA, 0.03 mmol/l in APA) against PDGF compared to the inhibitory activity of 26,27) CT52923 28) and SU6668, 17) which have been evaluated in a clinical trial. As the data show, 7d-6 had a more potent inhibitory activity in CPA and APA against PDGF than did the other compounds. Encouraged by these promising results, we carried out a more extensive Structure-Activity Relationships (SAR) study of 3-