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  1. AU="Esbenshade, Tim"
  2. AU="Yu, S-J"
  3. AU="de Oliveira, Arao Belitardo"
  4. AU="H Charles Manning"
  5. AU=Raman Siva P
  6. AU="Gederaas, Odrun A"
  7. AU="Cho, Won-Ki"
  8. AU="Juranic Lisnic, Vanda"
  9. AU="Junzhou Wu"
  10. AU="Kevin M Haigis"
  11. AU="Brühl, Marius"
  12. AU="Hawash, Mohammed"
  13. AU="Kalra, Sarathi"
  14. AU=Schwab Frank
  15. AU="Tzung-Chi Huang"
  16. AU="Nisa, Maherun"
  17. AU="Resnick, Adam C"
  18. AU="Thomas, Brodie"
  19. AU="Yaming Wang"
  20. AU="Lee, Chun‐Tsu"
  21. AU="Albert Gargallo‐Garriga"
  22. AU="Serwin, Natalia Maria"
  23. AU="La Rosa, Stefano"
  24. AU="Yin-Yin Xie"
  25. AU=White David P
  26. AU="Maria Teresa Viadero"
  27. AU="Wingeter, Márcia A"
  28. AU="Stein, Joshua D"
  29. AU="De Vecchis, Liana"
  30. AU="Chapman, Janet"
  31. AU="Umlai, Umm-Kulthum Ismail"
  32. AU="Reddi, Jyoti M"
  33. AU=Zeissig Sebastian
  34. AU="Valentini, Mariaconsuelo"

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  1. Artikel ; Online: Superoxide produced by mitochondrial site I

    Wong, Hoi-Shan / Mezera, Vojtech / Dighe, Pratiksha / Melov, Simon / Gerencser, Akos A / Sweis, Ramzi F / Pliushchev, Marina / Wang, Zhi / Esbenshade, Tim / McKibben, Bryan / Riedmaier, Stephan / Brand, Martin D

    Free radical biology & medicine

    2021  Band 164, Seite(n) 223–232

    Abstract: Superoxide produced by mitochondria has been implicated in numerous physiologies and pathologies. Eleven different mitochondrial sites that can produce superoxide and/or hydrogen peroxide ( ... ...

    Abstract Superoxide produced by mitochondria has been implicated in numerous physiologies and pathologies. Eleven different mitochondrial sites that can produce superoxide and/or hydrogen peroxide (O
    Mesh-Begriff(e) Animals ; Hydrogen Peroxide/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Succinate Dehydrogenase ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxides/metabolism
    Chemische Substanzen Superoxides (11062-77-4) ; Hydrogen Peroxide (BBX060AN9V) ; Superoxide Dismutase (EC 1.15.1.1) ; Succinate Dehydrogenase (EC 1.3.99.1)
    Sprache Englisch
    Erscheinungsdatum 2021-01-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2020.12.447
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: NRF2 activator A-1396076 ameliorates inflammation in autoimmune disease models by inhibiting antigen dependent T cell activation.

    Goess, Christian / Terrillon, Sonia / Mayo, Martha / Bousquet, Peter / Wallace, Craig / Hart, Michelle / Mathieu, Suzanne / Twomey, Rachel / Donnelly-Roberts, Diana / Namovic, Marian / Jung, Paul / Hu, Min / Richardson, Paul / Esbenshade, Tim / Cuff, Carolyn A

    Journal of translational autoimmunity

    2020  Band 4, Seite(n) 100079

    Abstract: Nuclear factor (erythroid-derived 2) like 2 (NRF2) is a nuclear transcription factor activated in response to oxidative stress that induces a gene program that dampens inflammation and can limit cell damage that perpetuates the inflammatory response. We ... ...

    Abstract Nuclear factor (erythroid-derived 2) like 2 (NRF2) is a nuclear transcription factor activated in response to oxidative stress that induces a gene program that dampens inflammation and can limit cell damage that perpetuates the inflammatory response. We have identified A-1396076, a potent and selective NRF2 activator with demonstrated KEAP1 binding and modulation of cellular NRF2 mediated effects.
    Sprache Englisch
    Erscheinungsdatum 2020-12-23
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ISSN 2589-9090
    ISSN (online) 2589-9090
    DOI 10.1016/j.jtauto.2020.100079
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Discovery of histamine H3 antagonists for the treatment of cognitive disorders and Alzheimer's disease.

    Brioni, Jorge D / Esbenshade, Tim A / Garrison, Tiffany Runyan / Bitner, Scott R / Cowart, Marlon D

    The Journal of pharmacology and experimental therapeutics

    2011  Band 336, Heft 1, Seite(n) 38–46

    Abstract: H(3) antagonists increase the release of brain histamine, acetylcholine, noradrenaline, and dopamine, neurotransmitters that are known to modulate cognitive processes. The ability to release brain histamine supports the effect on attention and vigilance, ...

    Abstract H(3) antagonists increase the release of brain histamine, acetylcholine, noradrenaline, and dopamine, neurotransmitters that are known to modulate cognitive processes. The ability to release brain histamine supports the effect on attention and vigilance, but histamine also modulates other cognitive domains such as short-term and long-term memory. A number of H(3) antagonists, including 1-{3-[3-(4-chlorophenyl)propoxy]propyl}piperidine hydrochloride (BF2.649), (1R,3R)-N-ethyl-3-fluoro-3-[3-fluoro-4-(pyrrolidin-1-ylmethyl)phenyl]cyclobutane-1-carboxamide (PF-03654746), 6-[(3-cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254), MK-0249 (structure not yet disclosed), JNJ-17216498 (structure not yet disclosed), and ABT-288 (structure not yet disclosed), have advanced to the clinical area for the potential treatment of human cognitive disorders. H(3) antagonists exhibited wake-promoting effects in humans and efficacy in narcoleptic patients, indicating target engagement, but some of them were not efficacious in patients suffering from attention-deficit hyperactivity disorder and schizophrenic patients. Preclinical studies have also shown that H(3) antagonists activate intracellular signaling pathways that may improve cognitive efficacy and disease-modifying effects in Alzheimer's disease. Ongoing clinical studies will be able to determine the utility of H(3) antagonists for the treatment of cognitive disorders in humans.
    Mesh-Begriff(e) Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/psychology ; Animals ; Cognition Disorders/drug therapy ; Cognition Disorders/metabolism ; Cognition Disorders/psychology ; Drug Discovery/trends ; Histamine H3 Antagonists/metabolism ; Histamine H3 Antagonists/therapeutic use ; Humans ; Receptors, Histamine H3/metabolism ; Treatment Outcome
    Chemische Substanzen Histamine H3 Antagonists ; Receptors, Histamine H3
    Sprache Englisch
    Erscheinungsdatum 2011-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.110.166876
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Lack of cataleptogenic potentiation with non-imidazole H3 receptor antagonists reveals potential drug-drug interactions between imidazole-based H3 receptor antagonists and antipsychotic drugs.

    Zhang, Min / Ballard, Michael E / Pan, Liping / Roberts, Stanley / Faghih, Ramin / Cowart, Marlon / Esbenshade, Tim A / Fox, Gerard B / Decker, Michael W / Hancock, Art A / Rueter, Lynne E

    Brain research

    2005  Band 1045, Heft 1-2, Seite(n) 142–149

    Abstract: Since H3 receptor (H3R) antagonists/inverse agonists can improve cognitive function in animal models, they may have the potential to be used as add-on therapy in the treatment of schizophrenia, a disease with significant cognitive deficits. However, a ... ...

    Abstract Since H3 receptor (H3R) antagonists/inverse agonists can improve cognitive function in animal models, they may have the potential to be used as add-on therapy in the treatment of schizophrenia, a disease with significant cognitive deficits. However, a recent study showed potentiation of haloperidol-induced catalepsy by ciproxifan, an imidazole-containing H3R antagonist/inverse agonist, suggesting there is a potential risk of exacerbating extrapyramidal symptoms (EPS) if H3R antagonists were used as adjunctive treatment [Pillot, C., Ortiz, J., Heron, A., Ridray, S., Schwartz, J.C. and Arrang, J.M., Ciproxifan, a histamine H3-receptor antagonist/inverse agonist, potentiates neurochemical and behavioral effects of haloperidol in the rat, J Neurosci, 22 (2002) 7272-80]. In order to clarify the basis of this finding, we replicated this result and extended the work with another imidazole and two non-imidazole H3R antagonists. The results indicate that ciproxifan significantly augmented the effects of haloperidol and risperidone on catalepsy. Another imidazole H3R antagonist, thioperamide, also potentiated the effect of risperidone on catalepsy. In contrast, no catalepsy-enhancing effects were observed when selective non-imidazole H3R antagonists, ABT-239 and A-431404, were coadministered with haloperidol and/or risperidone. As ciproxifan and thioperamide are inhibitors of cytochrome P450 enzymes, responsible for metabolizing risperidone and haloperidol, the possibility that the augmentation of antipsychotics by imidazoles resulted from drug-drug interactions was tested. A drug metabolism study revealed that an imidazole, but not a non-imidazole, potently inhibited the metabolism of haloperidol and risperidone. Furthermore, ketoconazole, an imidazole-based CYP 3A4 inhibitor, significantly augmented risperidone-induced catalepsy. Together, these data suggest the potentiation of antipsychotic-induced catalepsy may result from pharmacokinetic drug-drug interactions and support the potential utility of non-imidazole H3R antagonists in treatment of cognitive impairment in schizophrenia without increased risk of increased EPS in patients.
    Mesh-Begriff(e) Animals ; Antipsychotic Agents/adverse effects ; Antipsychotic Agents/pharmacokinetics ; Benzofurans/chemistry ; Benzofurans/pharmacokinetics ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Cataplexy/chemically induced ; Cataplexy/physiopathology ; Cataplexy/prevention & control ; Cytochrome P-450 Enzyme System/drug effects ; Cytochrome P-450 Enzyme System/metabolism ; Drug Combinations ; Drug Synergism ; Haloperidol/pharmacokinetics ; Histamine/metabolism ; Histamine Antagonists/chemistry ; Histamine Antagonists/pharmacokinetics ; Imidazoles/chemistry ; Imidazoles/pharmacokinetics ; Ketoconazole/pharmacokinetics ; Male ; Metabolic Clearance Rate/drug effects ; Metabolic Clearance Rate/physiology ; Piperidines/chemistry ; Piperidines/pharmacokinetics ; Pyrrolidines/chemistry ; Pyrrolidines/pharmacokinetics ; Rats ; Rats, Sprague-Dawley ; Receptors, Histamine H3/drug effects ; Receptors, Histamine H3/metabolism ; Risperidone/pharmacokinetics ; Schizophrenia/drug therapy
    Chemische Substanzen Antipsychotic Agents ; Benzofurans ; Drug Combinations ; Histamine Antagonists ; Imidazoles ; Piperidines ; Pyrrolidines ; Receptors, Histamine H3 ; ciproxifan (5EVQ7IRG99) ; Histamine (820484N8I3) ; benzonitrile, 4-(2-(2-((2r)-2-methyl-1-pyrrolidinyl)ethyl)-5-benzofuranyl)- (86H6B395PI) ; Cytochrome P-450 Enzyme System (9035-51-2) ; thioperamide (II4319BWUI) ; Haloperidol (J6292F8L3D) ; Risperidone (L6UH7ZF8HC) ; Ketoconazole (R9400W927I)
    Sprache Englisch
    Erscheinungsdatum 2005-05-31
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2005.03.018
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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