Sodium nitrophenate (CSN) enhanced cold tolerance of cucumber. However, at the omics-level, the molecular mechanism of CSN to cold stress remains unclear. Here, we found that CSN was comparable to abscisic acid and much stronger than 2, 4-epibrassinolide (EBR) in enhancing cold tolerance. RNA-seq indicated that CSN regulated the brassinolides (BR) and cytokinin (CK) synthesis in the late stage of cold stress (LS-CS). CSN reduced the source of BR synthesis, accelerated the conversion of intermediate substances to BR and the deactivation of BR. While, CSN accelerated CK synthesis and CK deactivation by cytokinin dehydrogenase. Hormone content determination showed that CSN increased BR and decreased CK contents during most time-points of cold stress. Kinds of hormone signaling genes at LS-CS were activated by CSN, which may be due to changes in BR and CK contents. CSN also enhanced the expression of 90 % phenylalanine ammonia-lyase genes, participated in phenylpropanoid biosynthesis, at LS-CS. Genes of phenylpropanoid biosynthesis pathway and hormones signal were co-expression during cold stress. The metabolome also showed that CSN participated phenylpropanoid biosynthesis at LS-CS too. However, as for lipid metabolome, CSN up-regulated anthocyanin, flavones and flavonols metabolism at the early stage of cold stress. The autumn and winter field yield test showed that CSN increase cucumber yield by approximately 17.67 % and economic income by 207.67 dollars/667 m