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Advances in Targeting GIRK Channels in Disease
Open accessAbstract
G protein-gated inwardly rectifying potassium (GIRK) channels are essential regulators of cell excitability in the brain. While they are implicated in a variety of neurological diseases in both human and animal model studies, their therapeutic potential has been largely untapped. Here, we review recent advances in the development of small molecule compounds that specifically modulate GIRK channels and compare them with first-generation compounds that exhibit off-target activity. We describe the method of discovery of these small molecule modulators, their chemical features, and their effects in vivo. These studies provide a promising outlook on the future development of subunit-specific GIRK modulators to regulate neuronal excitability in a brain region-specific manner.
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GIRK modulators can quiet hyperactive cortical-limbic ensembles while preserving information throughput, an effect profile that differs from global CNS suppressants.
“By converting inhibitory GPCR signals into stabilizing potassium currents, GIRK modulators can quiet hyperactive cortical–limbic ensembles while preserving information throughput, an effect profile that differs from global central nervous system (CNS) suppressants [305,323].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [323]
The ML297-related GIRK Modulators section reports that GAT1508 increased currents in basolateral amygdala neurons and facilitated fear extinction without affecting cognitive or motor functions; the GiGA1 section reports reduced excitability in hippocampal neurons. These findings support parts of the proposed effect profile, but the paper does not establish preserved information throughput across cortical–limbic ensembles or compare GIRK modulators with global CNS suppressants. It also reports sedation at high doses of GiGA1. (LLM, conf=0.86)
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Lüscher, C., & Slesinger, P. A. (2010) · Nature Reviews Neuroscience · doi:10.1038/nrn2834 · Cited by 617
Self-citationWydeven, N., Marron Fernandez de Velasco, E., Du, Y., Benneyworth, M. A., Hearing, M. C., Fischer, R. A., Thomas, M. J., Weaver, C. D., & Wickman, K. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1405190111 · Cited by 109
Xu, Y., Cantwell, L., Molosh, A. I., Plant, L. D., Gazgalis, D., Fitz, S. D., Dustrude, E. T., Yang, Y., Kawano, T., Garai, S., et al. (2020) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.011527 · Cited by 32
Kozek, K. A., Du, Y., Sharma, S., Prael, F. J., Spitznagel, B. D., Kharade, S. V., Denton, J. S., Hopkins, C. R., & Weaver, C. D. (2019) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.8b00287 · Cited by 26
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Research works printed but not linked: 91
- Kubo, 1993, Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel, Nature, 364, 802, 10.1038/364802a0 · DOI
- Lesage, 1995, Molecular properties of neuronal G-protein-activated inwardly rectifying K+ channels, J. Biol. Chem., 270, 28660, 10.1074/jbc.270.48.28660 · DOI
- Lujan, 2015, Localization and targeting of GIRK channels in mammalian central neurons, Int. Rev. Neurobiol., 123, 161, 10.1016/bs.irn.2015.05.009 · DOI
- Liao, 1996, Heteromultimerization of G-protein-gated inwardly rectifying K+ channel proteins GIRK1 and GIRK2 and their altered expression in weaver brain, J. Neurosci., 16, 7137, 10.1523/JNEUROSCI.16-22-07137.1996 · DOI
- Cruz, 2004, Bi-directional effects of GABAB receptor agonists on the mesolimbic dopamine system, Nat. Neurosci., 7, 153, 10.1038/nn1181 · DOI
- Wickman, 1998, Abnormal heart rate regulation in GIRK4 knockout mice, Neuron, 20, 103, 10.1016/S0896-6273(00)80438-9 · DOI
- Logothetis, 1987, The beta gamma subunits of GTP-binding proteins activate the muscarinic K+ channel in heart, Nature, 325, 321, 10.1038/325321a0 · DOI
- Reuveny, 1994, Activation of the cloned muscarinic potassium channel by G protein beta gamma subunits, Nature, 370, 143, 10.1038/370143a0 · DOI
- Aryal, 2009, A discrete alcohol pocket involved in GIRK channel activation, Nat. Neurosci., 12, 988, 10.1038/nn.2358 · DOI
- Kobayashi, 1999, Ethanol opens G-protein-activated inwardly rectifying K+ channels, Nat. Neurosci., 2, 1091, 10.1038/16019 · DOI
- Lewohl, 1999, G-protein-coupled inwardly rectifying potassium channels are targets of alcohol action, Nat. Neurosci., 2, 1084, 10.1038/16012 · DOI
- Glaaser, 2017, Dual activation of neuronal G protein-gated inwardly rectifying potassium (GIRK) channels by cholesterol and alcohol, Sci. Rep., 7, 4592, 10.1038/s41598-017-04681-x · DOI
- Bukiya, 2017, Cholesterol up-regulates neuronal G protein-gated inwardly rectifying potassium (GIRK) channel activity in the hippocampus, J. Biol. Chem., 292, 6135, 10.1074/jbc.M116.753350 · DOI
- Signorini, 1997, Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2, Proc. Natl. Acad. Sci. U. S. A., 94, 923, 10.1073/pnas.94.3.923 · DOI
- Horvath, 2018, Gain-of-function KCNJ6 mutation in a severe hyperkinetic movement disorder phenotype, Neuroscience, 384, 152, 10.1016/j.neuroscience.2018.05.031 · DOI
- Yang, 2010, Identification of a Kir3.4 mutation in congenital long QT syndrome, Am. J. Hum. Genet., 86, 872, 10.1016/j.ajhg.2010.04.017 · DOI
- Rifkin, 2018, GIRK currents in VTA dopamine neurons control the sensitivity of mice to cocaine-induced locomotor sensitization, Proc. Natl. Acad. Sci. U. S. A., 115, E9479, 10.1073/pnas.1807788115 · DOI
- Herman, 2015, GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol, Proc. Natl. Acad. Sci. U. S. A., 112, 7091, 10.1073/pnas.1416146112 · DOI
- Whorton, 2011, Crystal structure of the mammalian GIRK2 K+ channel and gating regulation by G proteins, PIP2, and sodium, Cell, 147, 199, 10.1016/j.cell.2011.07.046 · DOI
- Whorton, 2013, X-ray structure of the mammalian GIRK2-βγ G-protein complex, Nature, 498, 190, 10.1038/nature12241 · DOI
- Pegan, 2005, Cytoplasmic domain structures of Kir2.1 and Kir3.1 show sites for modulating gating and rectification, Nat. Neurosci., 8, 279, 10.1038/nn1411 · DOI
- Pegan, 2006, Andersen’s syndrome mutation effects on the structure and assembly of the cytoplasmic domains of Kir2.1, Biochemistry, 45, 8599, 10.1021/bi060653d · DOI
- Niswender, 2008, A novel assay of Gi/o-linked G protein-coupled receptor coupling to potassium channels provides new insights into the pharmacology of the group III metabotropic glutamate receptors, Mol. Pharmacol., 73, 1213, 10.1124/mol.107.041053 · DOI
- Kaufmann, 2013, ML297 (VU0456810), the first potent and selective activator of the GIRK potassium channel, displays antiepileptic properties in mice, ACS Chem. Neurosci., 4, 1278, 10.1021/cn400062a · DOI
- Huang, 2018, GIRK1-mediated inwardly rectifying potassium current suppresses the epileptiform burst activities and the potential antiepileptic effect of ML297, Biomed. Pharmacother., 101, 362, 10.1016/j.biopha.2018.02.114 · DOI
- Zou, 2019, Direct activation of G-protein-gated inward rectifying K+ channels promotes nonrapid eye movement sleep, Sleep, 42, 10.1093/sleep/zsy244 · DOI
- Wen, 2013, Discovery of ‘molecular switches’ within a GIRK activator scaffold that afford selective GIRK inhibitors, Bioorg. Med. Chem. Lett., 23, 4562, 10.1016/j.bmcl.2013.06.023 · DOI
- Wen, 2014, Discovery of potent and selective GIRK1/2 modulators via ‘molecular switches’ within a series of 1-(3-cyclopropyl-1-phenyl-1H-pyrazol-5-yl)ureas, Bioorg. Med. Chem. Lett., 24, 5102, 10.1016/j.bmcl.2014.08.061 · DOI
- Abney, 2019, Analgesic effects of the GIRK activator, VU0466551, alone and in combination with morphine in acute and persistent pain models, ACS Chem. Neurosci., 10, 1294, 10.1021/acschemneuro.8b00370 · DOI
- Marker, 2004, Spinal G-protein-gated K+ channels formed by GIRK1 and GIRK2 subunits modulate thermal nociception and contribute to morphine analgesia, J. Neurosci., 24, 2806, 10.1523/JNEUROSCI.5251-03.2004 · DOI
- Ramos-Hunter, 2013, Discovery and SAR of a novel series of GIRK1/2 and GIRK1/4 activators, Bioorg. Med. Chem. Lett., 23, 5195, 10.1016/j.bmcl.2013.07.002 · DOI
- Barber, 2016, Optical control of neuronal activity using a light-operated GIRK channel opener (LOGO), Chem. Sci., 7, 2347, 10.1039/C5SC04084A · DOI
- Trads, 2016, Optical control of GIRK channels using visible light, Org. Biomol. Chem., 15, 76, 10.1039/C6OB02153K · DOI
- Trads, 2019, Sign inversion in photopharmacology: incorporation of cyclic azobenzenes in photoswitchable potassium channel blockers and openers, Angew. Chem. Int. Ed. Engl., 58, 15421, 10.1002/anie.201905790 · DOI
- Wieting, 2017, Discovery and characterization of 1H-pyrazol-5-yl-2-phenylacetamides as novel, non-urea-containing GIRK1/2 potassium channel activators, ACS Chem. Neurosci., 8, 1873, 10.1021/acschemneuro.7b00217 · DOI
- Vo, 2019, VU0810464, a non-urea G protein-gated inwardly rectifying K+ (Kir 3/GIRK) channel activator, exhibits enhanced selectivity for neuronal Kir 3 channels and reduces stress-induced hyperthermia in mice, Br. J. Pharmacol., 176, 2238, 10.1111/bph.14671 · DOI
- Sharma, 2019, Discovery, synthesis and characterization of a series of (1-alkyl-3-methyl-1H-pyrazol-5-yl)-2-(5-aryl-2H-tetrazol-2-yl)acetamides as novel GIRK1/2 potassium channel activators, Bioorg. Med. Chem. Lett., 29, 791, 10.1016/j.bmcl.2019.01.027 · DOI
- Mahan, 2012, Fear conditioning, synaptic plasticity and the amygdala: implications for posttraumatic stress disorder, Trends Neurosci., 35, 24, 10.1016/j.tins.2011.06.007 · DOI
- Rifkin, 2017, G protein-gated potassium channels: a link to drug addiction, Trends Pharmacol. Sci., 38, 378, 10.1016/j.tips.2017.01.007 · DOI
- Kotecki, 2015, GIRK channels modulate opioid-induced motor activity in a cell type- and subunit-dependent manner, J. Neurosci., 35, 7131, 10.1523/JNEUROSCI.5051-14.2015 · DOI
- McCall, 2019, GIRK channel activity in dopamine neurons of the ventral tegmental area bidirectionally regulates behavioral sensitivity to cocaine, J. Neurosci., 39, 3600, 10.1523/JNEUROSCI.3101-18.2019 · DOI
- Zhao, 2020, Identification of a G-protein-independent activator of GIRK channels, Cell Rep., 31, 107770, 10.1016/j.celrep.2020.107770 · DOI · Paper page
- Harris, 2008, Ethanol’s molecular targets, Sci. Signal., 1, 10.1126/scisignal.128re7 · DOI
- Abrahao, 2017, Alcohol and the brain: neuronal molecular targets, synapses, and circuits, Neuron, 96, 1223, 10.1016/j.neuron.2017.10.032 · DOI
- Blednov, 2001, Potassium channels as targets for ethanol: studies of G-protein-coupled inwardly rectifying potassium channel 2 (GIRK2) null mutant mice, J. Pharmacol. Exp. Ther., 298, 521, 10.1016/S0022-3565(24)29410-6 · DOI
- Blednov, 2003, A pervasive mechanism for analgesia: activation of GIRK2 channels, Proc. Natl. Acad. Sci. U. S. A., 100, 277, 10.1073/pnas.012682399 · DOI
- Ikeda, 2002, Molecular mechanisms of analgesia induced by opioids and ethanol: is the GIRK channel one of the keys?, Neurosci. Res., 44, 121, 10.1016/S0168-0102(02)00094-9 · DOI
- Hill, 2003, Reduced ethanol-induced conditioned taste aversion and conditioned place preference in GIRK2 null mutant mice, Psychopharmacology, 169, 108, 10.1007/s00213-003-1472-4 · DOI
- Tipps, 2016, G protein-gated inwardly rectifying potassium channel subunit 3 knock-out mice show enhanced ethanol reward, Alcohol. Clin. Exp. Res., 40, 857, 10.1111/acer.13012 · DOI
- Bodhinathan, 2013, Molecular mechanism underlying ethanol activation of G-protein-gated inwardly rectifying potassium channels, Proc. Natl. Acad. Sci. U. S. A., 110, 18309, 10.1073/pnas.1311406110 · DOI
- Luscher, 2011, Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling, Neuron, 69, 650, 10.1016/j.neuron.2011.01.017 · DOI · Paper page
- Iwanir, 2008, Adrenaline-induced hyperpolarization of mouse pancreatic islet cells is mediated by G protein-gated inwardly rectifying potassium (GIRK) channels, Pflugers Arch., 456, 1097, 10.1007/s00424-008-0479-4 · DOI · Paper page
- Shankar, 2004, Role of G protein-gated inwardly rectifying potassium channels in P2Y12 receptor-mediated platelet functional responses, Blood, 104, 1335, 10.1182/blood-2004-01-0069 · DOI
- Magyar, 1996, Effects of volatile anesthetics on the G protein-regulated muscarinic potassium channel, Mol. Pharmacol., 50, 1520, 10.1016/S0026-895X(25)09610-5 · DOI
- Milovic, 2004, The sensitivity of G protein-activated K+ channels toward halothane is essentially determined by the C terminus, J. Biol. Chem., 279, 34240, 10.1074/jbc.M403448200 · DOI
- Yamakura, 2001, Differential effects of general anesthetics on G protein-coupled inwardly rectifying and other potassium channels, Anesthesiology, 95, 144, 10.1097/00000542-200107000-00025 · DOI
- Weigl, 2001, G protein-gated inwardly rectifying potassium channels are targets for volatile anesthetics, Mol. Pharmacol., 60, 282, 10.1124/mol.60.2.282 · DOI
- Nimitvilai, 2016, Differential effects of toluene and ethanol on dopaminergic neurons of the ventral tegmental area, Front. Neurosci., 10, 434, 10.3389/fnins.2016.00434 · DOI
- Kollert, 2020, Chloroform is a potent activator of cardiac and neuronal Kir3 channels, Naunyn Schmiedeberg's Arch. Pharmacol., 393, 573, 10.1007/s00210-019-01751-x · DOI
- Patel, 2020, Structural determinants mediating tertiapin block of neuronal Kir3.2 channels, Biochemistry, 59, 836, 10.1021/acs.biochem.9b01098 · DOI
- Yow, 2011, Naringin directly activates inwardly rectifying potassium channels at an overlapping binding site to tertiapin-Q, Br. J. Pharmacol., 163, 1017, 10.1111/j.1476-5381.2011.01315.x · DOI
- Campbell, 1983, Ivermectin: a potent new antiparasitic agent, Science, 221, 823, 10.1126/science.6308762 · DOI
- Su, 2016, Novel cell-free high-throughput screening method for pharmacological tools targeting K+ channels, Proc. Natl. Acad. Sci. U. S. A., 113, 5748-553, 10.1073/pnas.1602815113 · DOI
- Chen, 2018, Ivermectin and its target molecules: shared and unique modulation mechanisms of ion channels and receptors by ivermectin, J. Physiol., 596, 1833, 10.1113/JP275236 · DOI
- Osborne, 1998, Flupirtine, a nonopioid centrally acting analgesic, acts as an NMDA antagonist, Gen. Pharmacol., 30, 255, 10.1016/S0306-3623(97)00355-8 · DOI
- Klinger, 2012, Concomitant facilitation of GABAA receptors and KV7 channels by the non-opioid analgesic flupirtine, Br. J. Pharmacol., 166, 1631, 10.1111/j.1476-5381.2011.01821.x · DOI
- Friedel, 1993, Flupirtine. A review of its pharmacological properties, and therapeutic efficacy in pain states, Drugs, 45, 548, 10.2165/00003495-199345040-00007 · DOI
- Kornhuber, 1999, Flupirtine shows functional NMDA receptor antagonism by enhancing Mg2+ block via activation of voltage independent potassium channels. Rapid communication, J. Neural Transm. (Vienna), 106, 857, 10.1007/s007020050206 · DOI
- Kobayashi, 2000, Inhibition by various antipsychotic drugs of the G-protein-activated inwardly rectifying K+ (GIRK) channels expressed in xenopus oocytes, Br. J. Pharmacol., 129, 1716, 10.1038/sj.bjp.0703224 · DOI
- Kobayashi, 2004, Modulators of G protein-activated inwardly rectifying K+ channels: potentially therapeutic agents for addictive drug users, Ann. N. Y. Acad. Sci., 1025, 590, 10.1196/annals.1316.073 · DOI
- Khan, 2017, Clozapine: improvement of negative symptoms of schizophrenia, Cureus, 9
- Kobayashi, 2003, Inhibition of G protein-activated inwardly rectifying K+ channels by fluoxetine (Prozac), Br. J. Pharmacol., 138, 1119, 10.1038/sj.bjp.0705172 · DOI
- Kobayashi, 2006, Inhibition of G protein-activated inwardly rectifying K+ channels by the antidepressant paroxetine, J. Pharmacol. Sci., 102, 278, 10.1254/jphs.FP0060708 · DOI
- Wong, 1995, Prozac (fluoxetine, Lilly 110140), the first selective serotonin uptake inhibitor and an antidepressant drug: twenty years since its first publication, Life Sci., 57, 411, 10.1016/0024-3205(95)00209-O · DOI
- Perchenet, 2001, Effects of anorexinogen agents on cloned voltage-gated K+ channel hKv1.5, J. Pharmacol. Exp. Ther., 298, 1108, 10.1016/S0022-3565(24)29480-5 · DOI
- Thomas, 2002, The antidepressant drug fluoxetine is an inhibitor of human ether-a-go-go-related gene (HERG) potassium channels, J. Pharmacol. Exp. Ther., 300, 543, 10.1124/jpet.300.2.543 · DOI
- Takahama, 2012, Multiple pharmacological actions of centrally acting antitussives – do they target G protein-coupled inwardly rectifying K+ (GIRK) channels?, J. Pharmacol. Sci., 120, 146, 10.1254/jphs.12R07CP · DOI
- Sasaki, 2014, Tipepidine in children with attention deficit/hyperactivity disorder: a 4-week, open-label, preliminary study, Neuropsychiatr. Dis. Treat., 10, 147, 10.2147/NDT.S58480 · DOI
- Hamasaki, 2013, Tipepidine activates VTA dopamine neuron via inhibiting dopamine D2 receptor-mediated inward rectifying K+ current, Neuroscience, 252, 24, 10.1016/j.neuroscience.2013.07.044 · DOI
- Soeda, 2016, Centrally acting non-narcotic antitussives prevent hyperactivity in mice: involvement of GIRK channels, Pharmacol. Biochem. Behav., 144, 26, 10.1016/j.pbb.2016.02.006 · DOI
- Hamao, 2015, Tipepidine increases dopamine level in the nucleus accumbens without methamphetamine-like behavioral sensitization, Behav. Brain Res., 284, 118, 10.1016/j.bbr.2015.02.012 · DOI
- Jin, 1998, A novel high-affinity inhibitor for inward-rectifier K+ channels, Biochemistry, 37, 13291, 10.1021/bi981178p · DOI
- Hashimoto, 2006, Tertiapin, a selective IKACh blocker, terminates atrial fibrillation with selective atrial effective refractory period prolongation, Pharmacol. Res., 54, 136, 10.1016/j.phrs.2006.03.021 · DOI
- Walsh, 2011, Targeting GIRK channels for the development of new therapeutic agents, Front. Pharmacol., 2, 64, 10.3389/fphar.2011.00064 · DOI
- Kuzhikandathil, 2002, Classic D1 dopamine receptor antagonist R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH23390) directly inhibits G protein-coupled inwardly rectifying potassium channels, Mol. Pharmacol., 62, 119, 10.1124/mol.62.1.119 · DOI
- Matsuda, 2006, Blockade by NIP-142, an antiarrhythmic agent, of carbachol-induced atrial action potential shortening and GIRK1/4 channel, J. Pharmacol. Sci., 101, 303, 10.1254/jphs.FP0060324 · DOI
- Machida, 2011, Effects of a highly selective acetylcholine-activated K+ channel blocker on experimental atrial fibrillation, Circ. Arrhythm. Electrophysiol., 4, 94, 10.1161/CIRCEP.110.951608 · DOI
- Yamamoto, 2014, Effects of the selective KACh channel blocker NTC-801 on atrial fibrillation in a canine model of atrial tachypacing: comparison with class Ic and III drugs, J. Cardiovasc. Pharmacol., 63, 421, 10.1097/FJC.0000000000000065 · DOI
- Chen, 2019, Non-sedating antihistamines block G-protein-gated inwardly rectifying K+ channels, Br. J. Pharmacol., 176, 3161, 10.1111/bph.14717 · DOI
- Woodward, 1982, Terfenadine, the first non-sedating antihistamine, Arzneimittelforschung, 32, 1154
- Taglialatela, 1999, Cardiac ion channels and antihistamines: possible mechanisms of cardiotoxicity, Clin. Exp. Allergy, 29, 182, 10.1046/j.1365-2222.1999.0290s3182.x · DOI
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Metadata
- Authors
- Zhao, Y., Gameiro-Ros, I., Glaaser, I. W., & Slesinger, P. A.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Slesinger, Paul A.
- Venue
- Trends in Pharmacological Sciences
- Publisher
- Elsevier BV
- Published
- 2021-03
- Volume
- 42
- Issue
- 3
- Pages
- 203-215
- ISSN
- 0165-6147 (ISSN-L)
- PMC
- PMC7990506
- OpenAlex
- W3123022377
- Cited by
- 44
- References
- 4
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 4 · 2023: 14 · 2022: 7 · 2021: 3
- FWCI
- 0.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Pharmacological Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- GIRK channels, G protein-coupled inwardly rectifying potassium channels, small molecule modulators, neuronal excitability, off-target effects, drug discovery, neurological disorders
- MeSH terms
- Animals, Brain, Humans, Neurons, GTP-Binding Proteins, G Protein-Coupled Inwardly-Rectifying Potassium Channels
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