Idiopathic basal ganglia calcification (IBGC) is an intractable disease characterized by bilateral calcification in basal ganglia and other regions. The most frequent causative gene of familial IBGC is SLC20A2 which codes inorganic phosphate (Pi) transporter, PiT2. Then Pi homeostasis was thought to be disturbed in the brain of patients with SLC20A2 mutations. This suggested that repairing Pi homeostasis in the brain led to the improvement of symptoms in patients with IBGC. Here, we aimed to screen drugs which stimulate PiT2 activity. The past study showed that some transcriptional factor bound promoter region of SLC20A2. Among them, Tamibarotene was proposed as a potential candidate by analyses of transcriptional factors-binding site in the SLC20A2 promoter. We examined the effects of the candidate drugs using bEnd.3 cells. As a results, Tamibarotene significantly increased the levels of both SLC20A2 mRNA and PiT2 protein. The amount of Pi uptake into cells was measured using radioisotope ³²P. The increases of Pi uptake was observed in the Tamibarotene-treated group. In conclusion, Tamibarotene increases PiT2 expression, suggesting a possibility improving Pi homeostasis.