Systemic acquired resistance (SAR) is a plant defense system against a broad range of pathogens and is induced through the salicylic acid (SA)-mediated pathway. We investigated the mode of action of SAR-inducible chemicals, N-cyanomethyl-2-chloroisonicotinamide (NCI), 3-chloro-1-methyl-1H-pyrazole-5-carboxylic acid (CMPA), and N-(3-chloro-4-methylphenyl)-4-methyl-1,2,3-thiadiazole-5-carboxamide (tiadinil, TDL), by analyzing disease resistance and the expression of SAR marker genes in tobacco and Arabidopsis. NCI, CMPA, TDL and its active metabolite 4-methyl-1,2,3-thiadiazole-5-carboxylic acid (SV-03) induced SAR by activating the site between SA accumulation and NPR1 in the SAR signaling pathway.