ObjectiveTo evaluate the clinical efficacy of modified Zhibai Dihuangwan on children （female） with idiopathic precocious puberty （ICPP） and to explore the mechanism. MethodA total of 78 children with ICPP who were treated in Henan Children's Hospital from July 2019 to July 2020 were randomized into the observation group and control group by sealed envelope randomization with 39 in either group. The observation group was given modified Zhibai Dihuangwan （1 dose/day， oral， divided into two times） and the control group Zhibai Dihuangtang （1 dose/day， oral， divided into two times orally）. The treatment lasted 3 months for both groups. The changes of mammary nucleus length， maximum follicular diameter， uterus， and ovarian volume before and after treatment in the two groups were observed， and serum luteinizing hormone （LH） level， follicle-stimulating hormone （FSH） level， prolactin （PRL） level， and estrogen （E₂） level were detected in the two groups. At the cellular level， the secretion of gonadotropin releasing hormone （GnRH） and mRNA expression of precocious puberty-related genes Kiss-1 and G protein-coupled receptor 54 （GPR54） were measured. ResultLevels of serum sex hormones of the two groups were significantly decreased after treatment as compared with those before treatment （P<0.01）. After treatment， the length of the mammary nucleus and the maximum follicular diameter in the observation group were smaller than those in the control group （P<0.01）. The total clinical effective rate in the observation group was higher than that in the control group （P<0.01）. At the cellular level， the expression levels of GnRH， Kiss-1 and GPR54 mRNA in GT1-7 cells treated with modified Zhibai Dihuangwan were lower than those treated with traditional Zhibai Dihuangtang. ConclusionModified Zhibai Dihuangwan can effectively inhibit levels of serum sex hormones in children with ICPP and delay the development of mammary nucleus and ovary in children with precocious puberty. It is more effective than traditional Zhibai Dihuangtang， which is worthy of clinical promotion. The mechanism is the likelihood that it inhibits the expression of Kiss-1 and GPR54 mRNA.