Krüppel-like factor 5 (KLF5), part of the SP/KLF group of zinc finger transcription factors, is overexpressed in human colorectal cancer examples, which overabundance is connected with aggressive cancer development and progression. We shown that rodents haploinsufficient for Klf5 had reduced intestinal tumor burden without anyone’s knowledge of germline mutation in Apc, a gatekeeper of intestinal tumorigenesis. With different high-throughput screening strategy, we developed ML264, a little-molecule compound that inhibits KLF5, and demonstrated it inhibits development of colorectal cancer in vitro as well as in vivo Through optimization efforts in line with the structure of ML264, we now have identified a brand new lead compound, SR18662. We discover that treatment with SR18662 considerably reduces growth and proliferation of colorectal cancer cells compared to treatment with vehicle control, ML264, or SR15006 (a less enhanced analogue from SAR efforts resulting in SR18662). SR18662 demonstrated improved effectiveness in lessening the viability of multiple colorectal cancer cell lines. Flow cytometry analysis following SR18662 treatment demonstrated a rise in cells taken either in S or G2-M phases from the cell cycle along with a significant rise in the amount of apoptotic cells, the second a distinctive property in contrast to ML264 or SR15006. SR18662 treatment also cuts down on the expression of cyclins and aspects of the MAPK and WNT signaling pathways. Importantly, we observed a substantial dose-dependent inhibition of xenograft development in rodents following SR18662 treatment that exceeded the result of ML264 at equivalent doses. These bits of information support further growth and development of SR18662 and it is analogues for colorectal cancer therapy.