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2-PHENYL-2-(2-PHENYL-1H-INDOL-3-YL)ETHANAMINE HYDROCHLORIDE is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

102441-39-4

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102441-39-4 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 102441-39-4 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 1,0,2,4,4 and 1 respectively; the second part has 2 digits, 3 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 102441-39:
(8*1)+(7*0)+(6*2)+(5*4)+(4*4)+(3*1)+(2*3)+(1*9)=74
74 % 10 = 4
So 102441-39-4 is a valid CAS Registry Number.
InChI:InChI=1/C22H20N2/c23-15-19(16-9-3-1-4-10-16)21-18-13-7-8-14-20(18)24-22(21)17-11-5-2-6-12-17/h1-14,19,24H,15,23H2

102441-39-4SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 17, 2017

Revision Date: Aug 17, 2017

1.Identification

1.1 GHS Product identifier

Product name 2-phenyl-2-(2-phenyl-1H-indol-3-yl)ethanamine,hydrochloride

1.2 Other means of identification

Product number -
Other names 2-phenyl-2-(2-phenyl-1H-indol-3-yl)ethanamine hydrochloride

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:102441-39-4 SDS

102441-39-4Downstream Products

102441-39-4Relevant academic research and scientific papers

The Trifluoromethyl Group as a Bioisosteric Replacement of the Aliphatic Nitro Group in CB1 Receptor Positive Allosteric Modulators

Tseng, Chih-Chung,Baillie, Gemma,Donvito, Giulia,Mustafa, Mohammed A.,Juola, Sophie E.,Zanato, Chiara,Massarenti, Chiara,Dall'Angelo, Sergio,Harrison, William T. A.,Lichtman, Aron H.,Ross, Ruth A.,Zanda, Matteo,Greig, Iain R.

supporting information, p. 5049 - 5062 (2019/05/28)

The first generation of CB1 positive allosteric modulators (e.g., ZCZ011) featured a 3-nitroalkyl-2-phenyl-indole structure. Although a small number of drugs include the nitro group, it is generally not regarded as being "drug-like", and this is particularly true for aliphatic nitro groups. There are very few case studies where an appropriate bioisostere replaced a nitro group that had a direct role in binding. This may be indicative of the difficulty of replicating its binding interactions. Herein, we report the design and synthesis of ligands targeting the allosteric binding site on the CB1 cannabinoid receptor, in which a CF3 group successfully replaced the aliphatic NO2. In general, the CF3-bearing compounds were more potent than their NO2 equivalents and also showed improved in vitro metabolic stability. The CF3 analogue (1) with the best balance of properties was selected for further pharmacological evaluation. Pilot in vivo studies showed that (±)-1 has similar activity to (±)-ZCZ011, with both showing promising efficacy in a mouse model of neuropathic pain.

Identification of cb1 receptor allosteric sites using force-biased mmc simulated annealing and validation by structure-activity relationship studies

Hurst, Dow P.,Garai, Sumanta,Kulkarni, Pushkar M.,Schaffer, Peter C.,Reggio, Patricia H.,Thakur, Ganesh A.

supporting information, p. 1216 - 1221 (2019/08/27)

Positive allosteric modulation of the cannabinoid 1 receptor (CB1R) has demonstrated distinct therapeutic advantages that address several limitations associated with orthosteric agonism and has opened a promising therapeutic avenue for further drug development. To advance the development of CB1R positive allosteric modulators, it is important to understand the molecular architecture of CB1R allosteric site(s). The goal of this work was to use Force-Biased MMC Simulated Annealing to identify binding sites for GAT228 (R), a partial allosteric agonist, and GAT229 (S), a positive allosteric modulator (PAM) at the CB1R. Our studies suggest that GAT228 binds in an intracellular (IC) TMH1-2-4 exosite that would allow this compound to act as a CB1 allosteric agonist as well as a CB1 PAM. In contrast, GAT229 binds at the extracellular (EC) ends of TMH2/3, just beneath the EC1 loop. At this site, this compound can act as CB1 PAM only. Finally, these results were successfully validated through the synthesis and biochemical evaluation of a focused library of compounds.

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