NIBR-0213 是S1P1选择性拮抗剂，有抗实验性自身免疫性脑脊髓炎的作用。在 GTPγ35S 试验中，它作用于人和大鼠S1P1的IC50分别为 2.0 nM 和 2.3 nM。

NIBR-0213, a potent and selective S1P(1) antagonist, has efficacy in experimental autoimmune encephalomyelitis.

In Ca2+?mobilization assays, NIBR-0213 displayed an inhibitory activity on hS1P1?with an IC50?of 2.5?nM whereas it was inactive (IC50?>10?μM) on S1P2, S1P3, and S1P4. In GTPγ35S assays, NIBR-0213 displayed potent and comparable potency on human and rat S1P1?(IC50?of 2.0?nM and 2.3?nM, respectively), whereas on mouse S1P1?a slightly reduced IC50?of 8.5?nM was?measured. NIBR-0213 showed an ～3,000-fold selectivity against human S1P5?in the GTPγ35S assay (Figure?3A). On S1P4, a weak agonistic activity was detected with an EC50?of 245?nM. Schild plot analysis indicated that NIBR-0213 is a competitive S1P1?antagonist with a calculated Kd?of 0.37?± 0.031?nM[2].

NIBR-0213 increased in a dose-dependent manner the leakage of?plasma proteins?into lung parenchyma, as measured by the increase in EBD in lung tissues at 6?hr posttreatment (time of Emax on PBL). A maximum of 4–5-fold EBD increase versus vehicle controls was observed with 0.3?mg/kg. An ED50?of ～0.1?mg/kg could be estimated, i.e., in the range of the ED50?for the effects on PBL counts[2]. NIBR-0213 given orally at 30 mg/kg to rats reduced the PBL counts by 75%–85% within 14 hr and maintained this effect up to 24 hr posttreatment[2].

1233332-14-3

C27H29ClN2O3

464.98

NIBR 0213

DMSO:55 mg/ml (118.28 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years