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NIBR0213
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
NIBR0213图片
CAS NO:1233332-14-3
包装与价格:
包装价格(元)
1mg电议
5mg电议
10mg电议
25mg电议

产品介绍
NIBR-0213 是一种有效的选择性 S1P1 拮抗剂,对实验性自身免疫性脑脊髓炎有效。
Cas No.1233332-14-3
化学名N-[[3'-[[(1R)-1-(4-chloro-3-methylphenyl)ethyl]amino]-3,5-dimethyl[1,1'-biphenyl]-4-yl]carbonyl]-L-alanine
Canonical SMILESCC1=C(Cl)C=CC([C@@H](C)NC2=CC(C3=CC(C)=C(C(N[C@@H](C)C(O)=O)=O)C(C)=C3)=CC=C2)=C1
分子式C27H29ClN2O3
分子量465
溶解度25mg/mL in DMSO, 25mg/mL in DMF, 25mg/mL in Ethanol
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

NIBR0213 is an orally bioavailable, potent, and selective antagonist of sphingosine-1-phosphate receptor-1 (S1P1) with IC50 values of 2.5 and 2.0 nM for the hS1P1 in a Ca2+ mobilization assay and GTPγS assay, respectively. [1] It is inactive at S1P2, S1P3, and S1P4 receptors (IC50s = >20, >10, and >10 uM, respectively in a Ca2+ mobilization assay). S1P1 plays a key role in the immune system, regulating lymphocyte egress from lymphoid tissues into the circulation.[2] In rats, NIBR0213 (30 mg/kg) reduces peripheral blood lymphocytes by 75-85% for up to 24 hours. [1] In a mouse model of experimental autoimmune encephalitis (EAE), it significantly reduces disease severity up to 26 days, when administered at 30 mg/kg twice per day for three days, then 60 mg/kg twice per day. However, in a rat model of adjuvant-induced arthritis, chronic administration of 30 mg/kg induces pulmonary damage and chronic lung inflammation.[3]

Reference:
[1]. Quancard, J., Bollbuck, B., Janser, P., et al. A potent and selective S1P1 antagonist with efficacy in experimental autoimmune encephalomyelitis. Chem. Biol. 19(9), 1142-1151 (2012).
[2]. Huwiler, A., Kolter, T., Pfeilschifter, J., et al. Physiology and pathophysiology of sphingolipid metabolism and signaling. Biochim. Biophys. Acta. 1485(2-3), 63-99 (2000).
[3]. Bigaud, M., Dincer, Z., Bollbuck, B., et al. Pathophysiological consequences of a break in S1P1-dependent homeostasis of vascular permeability revealed by S1P1 competitive antagonism. PLoS One 11(12), e0168252 (2016).