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. 2021 Apr;62(4):536–544. doi: 10.2967/jnumed.120.243600

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© 2021 by the Society of Nuclear Medicine and Molecular Imaging.

Immediate Open Access: Creative Commons Attribution 4.0 International License (CC BY) allows users to share and adapt with attribution, excluding materials credited to previous publications. License: https://creativecommons.org/licenses/by/4.0/. Details: http://jnm.snmjournals.org/site/misc/permission.xhtml.

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FIGURE 2. — LW223 binding to TSPO is not affected by human rs6971 genetic polymorphism. (A) Chemical structures of established (PK11195, PBR28) and novel (AB5186, LW223) TSPO ligands investigated. (B) Competition binding assays using these TSPO ligands in human brain homogenates genotyped and grouped as HAB, MAB, and LAB (PK11195: HAB = 6, MAB = 8, LAB = 4; PBR28: HAB = 4, MAB [2-site fitting] = 5, LAB = 4; AB5186: HAB = 6, MAB [2-site fitting] = 6, LAB = 5; LW223: HAB = 5, MAB = 5, LAB = 4). Only PK11195 and LW223 were not affected by polymorphism, as is also demonstrated in human heart homogenates (C) (PK11195: HAB = 4, MAB = 5, LAB = 4; PBR28: HAB = 4, MAB = 5, LAB = 4; AB5186: HAB = 4, MAB = 5 [2-site fitting], LAB = 4; LW223: HAB = 5, MAB = 5, LAB = 4).