In therapeutic models, NIBR-0213 demonstrates significant biological effects. When administered orally at 30 mg/kg to rats, it dramatically reduces peripheral blood lymphocyte (PBL) counts by 75%-85% within 14 hours, maintaining this suppression up to 24 hours post-treatment. This effect suggests a strong immunomodulatory capability, which is critical for diseases where lymphocyte migration and activation play pivotal roles^[1].

Moreover, the efficacy of NIBR-0213 extends to disease models, as doses of 30 mg/kg and 60 mg/kg have been effective in a mouse model of experimental autoimmune encephalomyelitis (EAE), a standard model for studying multiple sclerosis. This outcome suggests its potential for therapeutic application in autoimmune diseases, particularly for conditions that mimic the pathophysiology of multiple sclerosis^[1].

NIBR-0213 showcases targeted inhibitory activity on the hS1P1 receptor with a notably low IC50 of 2.5 nM, indicating its high potency. Its effectiveness is highly specific, as it does not significantly inhibit S1P2, S1P3, and S1P4 receptors in calcium mobilization assays, where the IC50 values exceed 10 μM, underscoring its selective action^[1].

NIBR-0213's potency is consistent across species, displaying IC50 values of 2.0 nM for human S1P1 and 2.3 nM for rat S1P1 in GTPγ35S assays. This potency slightly decreases in mouse S1P1 with an IC50 of 8.5 nM, but it remains highly effective. Additionally, NIBR-0213 exhibits approximately 3,000-fold selectivity against the human S1P5 receptor in the same assay, reinforcing its selectivity towards S1P1^[1].

As a competitive antagonist of S1P1, NIBR-0213's affinity for the receptor is further quantified by a calculated Kd of 0.37 ± 0.031 nM, which is indicative of its strong binding efficiency and potential for high efficacy in vivo^[1].