<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ashraf-Uz-Zaman M</submitter><funding>National Institute of Neurological Disorders and Stroke</funding><funding>South Plains Foundation</funding><funding>NIMH NIH HHS</funding><funding>National Cancer Institute</funding><funding>NINDS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Institute of Mental Health</funding><funding>Cancer Prevention and Research Institute of Texas</funding><pagination>217-228</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9365315</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(2)</volume><pubmed_abstract>The dopaminergic system is involved in the regulation of immune responses in various homeostatic and disease conditions. For conditions such as Parkinson's disease and multiple sclerosis (MS), pharmacological modulation of dopamine (DA) system activity is thought to have therapeutic relevance, providing the basis for using dopaminergic agents as a treatment of relevant states. In particular, it was proposed that restoration of DA levels may inhibit neuroinflammation. We have recently reported a new class of dopamine transporter (DAT) inhibitors with high selectivity to the DAT over other G-protein coupled receptors tested. Here, we continue their evaluation as monoamine transporter inhibitors. Furthermore, we show that the urea-like DAT inhibitor (compound &lt;b>5&lt;/b>) has statistically signi</pubmed_abstract><journal>ACS chemical neuroscience</journal><pubmed_title>Evaluation of Urea-Based Inhibitors of the Dopamine Transporter Using the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.</pubmed_title><pmcid>PMC9365315</pmcid><funding_grant_id>NS109255</funding_grant_id><funding_grant_id>RP210154</funding_grant_id><funding_grant_id>NS106902</funding_grant_id><funding_grant_id>1R15CA231339-0</funding_grant_id><funding_grant_id>R01 NS106902</funding_grant_id><funding_grant_id>R01 NS109255</funding_grant_id><funding_grant_id>HHSN-271-2013-00017-C</funding_grant_id><funding_grant_id>R15 CA231339</funding_grant_id><funding_grant_id>RP170003</funding_grant_id><funding_grant_id>R01 NS038261</funding_grant_id><funding_grant_id>HHSN271201300017C</funding_grant_id><funding_grant_id>NS038261</funding_grant_id><pubmed_authors>Shahi S</pubmed_authors><pubmed_authors>Ji G</pubmed_authors><pubmed_authors>Sajib MS</pubmed_authors><pubmed_authors>Mikelis CM</pubmed_authors><pubmed_authors>Neugebauer V</pubmed_authors><pubmed_authors>Ashraf-Uz-Zaman M</pubmed_authors><pubmed_authors>German NA</pubmed_authors><pubmed_authors>Thakolwiboon S</pubmed_authors><pubmed_authors>Tidwell D</pubmed_authors><pubmed_authors>Griffin Z</pubmed_authors><pubmed_authors>Pan J</pubmed_authors><pubmed_authors>Das H</pubmed_authors><pubmed_authors>Junell R</pubmed_authors><pubmed_authors>Trippier PC</pubmed_authors><pubmed_authors>Barthels D</pubmed_authors><pubmed_authors>Yin L</pubmed_authors><pubmed_authors>Avila M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Evaluation of Urea-Based Inhibitors of the Dopamine Transporter Using the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.</name><description>The dopaminergic system is involved in the regulation of immune responses in various homeostatic and disease conditions. For conditions such as Parkinson's disease and multiple sclerosis (MS), pharmacological modulation of dopamine (DA) system activity is thought to have therapeutic relevance, providing the basis for using dopaminergic agents as a treatment of relevant states. In particular, it was proposed that restoration of DA levels may inhibit neuroinflammation. We have recently reported a new class of dopamine transporter (DAT) inhibitors with high selectivity to the DAT over other G-protein coupled receptors tested. Here, we continue their evaluation as monoamine transporter inhibitors. Furthermore, we show that the urea-like DAT inhibitor (compound &lt;b>5&lt;/b>) has statistically signi</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2025-04-19T22:58:13.206Z</modification><creation>2024-11-14T18:20:05.736Z</creation></dates><accession>S-EPMC9365315</accession><cross_references><pubmed>34978174</pubmed><doi>10.1021/acschemneuro.1c00647</doi></cross_references></HashMap>