FtsZ polymerizes to form a cytokinetic Z-ring at the mid-cell and coordinates the partitioning of a bacterial cell. Its crucial role in bacterial cell division and widely conserved nature makes it a promising target for antibacterial drugs. Streptococcus pneumoniae, a prevalent respiratory pathogen, is acquiring antimicrobial resistance at an alarming rate, highlighting the need for developing potent anti-pneumococcal agents. In this work, we identified the FtsZ-inhibitory property of an N- heterocyclic imine derivative, 3-methyl-2-(3-(p-tolyl)-1,3-thiazetidin-2-ylidene)amino-6-trifluoromethoxy-benzo[d]thiazolium trifluoromethanesulfonate (TTMB). TTMB inhibited the growth of S. pneumoniae, Staphylococcus aureus, Bacillus subtilis, Vibrio cholerae, Staphylococcus saprophyticus, and Mycobacterium smegmatis, indicating its broad-spectrum antibacterial activity. Further, TTMB inhibited biofilm formation by the pathogenic strain of S. pneumoniae. TTMB destroyed the Z-ring in S. pneumoniae and B. subtilis. The compound binds to purified FtsZ, increases the GTPase activity of FtsZ, and inhibits FtsZ assembly. FtsZ forms short and thin polymers and aggregates in the presence of TTMB. Importantly, TTMB exhibited low cytotoxicity to mammalian cells and did not inhibit tubulin polymerization or the activity of metabolic enzymes like alkaline phosphatase and alcohol dehydrogenase, suggesting its safety for mammalian systems. The dual-acting property of TTMB, targeting both planktonic and biofilm-forming S. pneumoniae, makes it a promising antibacterial agent.