SBI-553

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Chemical Structure| 1849603-72-0 同义名 : -
CAS号 : 1849603-72-0
货号 : A1216662
分子式 : C26H31FN4O2
纯度 : 99%+
分子量 : 450.548
MDL号 : MFCD08141843
存储条件：

Pure form Sealed in dry,2-8°C

In solvent -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 16 mg/mL(35.51 mM)，配合低频超声，并水浴加热至45℃助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 Neurotensin receptor 1 (NTSR1) is a G-protein-coupled receptor (GPCR) that engages multiple subtypes of G protein, and is involved in the regulation of blood pressure, body temperature, weight and the response to pain[1].SBI-553 not only acts as a β-arrestin-biased agonist but also extends profound β-arrestin bias to the endogenous ligand by selectively antagonizing G protein signaling. SBI-553 shows efficacy in animal models of psychostimulant abuse, including cocaine self-administration, without the side effects characteristic of balanced NTSR1 agonism. SBI-553 administration (12 mg/kg, i.p.) to attenuate cocaine-induced hyperlocomotion relative to the vehicle control (saline, 5 ml/kg, i.p.) (Fig 5A,B). By contrast, responses to the vehicle and SBI-553 were comparable in non-stimulant exposed animals. This SBI-553 dose also reduced methamphetamine (2 mg/kg) -induced hyperlocomotion and blocked the expression of methamphetamine conditioned place preference.[2]. SBI-553 increases NTS binding affinity and Bmax,, and its binding affinity is reciprocally increased by NTS. These behaviors are characteristic of positive allosteric modulation and are concordant with the Monod-Wyman-Changeux model of allosteric transitions[3].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.22mL

0.44mL

0.22mL

11.10mL

2.22mL

1.11mL

22.20mL

4.44mL

2.22mL
参考文献

[1] Hideaki E Kato, Yan Zhangi,et al. Conformational transitions of a neurotensin receptor 1-G i1 complex. Nature. 2019 Aug;572(7767):80-85.

[2] Lauren M Slosky, Yushi Bai,et al. β-Arrestin-Biased Allosteric Modulator of NTSR1 Selectively Attenuates Addictive Behaviors. Cell. 2020 Jun 11;181(6):1364-1379.e14.

[3] Canals M, Lane JR, Wen A, Scammells PJ, Sexton PM, and Christopoulos A (2012). A MonodWyman-Changeux Mechanism Can Explain G Protein-coupled Receptor (GPCR) AllostericModulation. J Biol Chem 287, 650–659.