Thomas Dix

Thomas Dix

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Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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20 June 2019 in Pharmaceuticals
Verified
Journal Article
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TBTyler Beck
Tyler Beck
MHMatthew A. Hapstack
Matthew A. Hapstack
KBKyle Beck
Kyle Beck
TDThomas Dix
Thomas Dix
Many original research articles have been published that describe findings and outline areas for the development of kappa-opioid agonists (KOAs) as novel drugs; however, a single review article that summarizes the broad potential for KOAs in drug development does not exist. It is well-established that KOAs demonstrate efficacy in pain attenuation; however, KOAs also have proven to be beneficial in treating a variety of novel but often overlapping conditions including cardiovascular disease, pruritus, nausea, inflammatory diseases, spinal anesthesia, stroke, hypoxic pulmonary hypertension, multiple sclerosis, addiction, and post-traumatic cartilage degeneration. This article summarizes key findings of KOAs and discusses the untapped therapeutic potential of KOAs in the treatment of many human diseases.

15 October 1998 in Biochemical Journal
Verified
Journal Article
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TSTiberiu Simandan
Tiberiu Simandan
JSJing Sun
Jing Sun
TDThomas Dix
Thomas Dix
DNA base oxidation is considered to be a key event associated with disease initiation and progression in humans. Peroxyl radicals (ROO•) are important oxidants found in cells whose ability to react with the DNA bases has not been characterized extensively. In this paper, the products resulting from ROO• oxidation of the DNA bases are determined by gas chromatography/MS in comparison with authentic standards. ROO• radicals oxidize adenine and guanine to their 8-hydroxy derivatives, which are considered biomarkers of hydroxyl radical (HO•) oxidations in cells. ROO• radicals also oxidize adenine to its hydroxylamine, a previously unidentified product. ROO• radicals oxidize cytosine and thymine to the monohydroxy and dihydroxy derivatives that are formed by oxidative damage in cells. Identical ROO• oxidation profiles are observed for each base when exposed as deoxyribonucleosides, monohomopolymers and base-paired dihomopolymers. These results have significance for the development, utilization and interpretation of DNA base-derived biomarkers of oxidative damage associated with disease initiation and propagation, and support the idea that the mutagenic potential of N-oxidized bases, when generated in cellular DNA, will require careful evaluation. Adenine hydroxylamine is proposed as a specific molecular probe for the activity of ROO• in cellular systems.

31 December 2005 in Neuropharmacology
Verified
Journal Article
Closed access
MHM. Kyle Hadden
M. Kyle Hadden
KOKevin S. Orwig
Kevin S. Orwig
KKKyle P. Kokko
Kyle P. Kokko
JMJean Mazella
Jean Mazella
TDThomas Dix
Thomas Dix

1 August 2019 in European Journal of Pharmacology
Verified
Journal Article
Closed access
TBTyler Beck
Tyler Beck
CRCarmela M. Reichel
Carmela M. Reichel
KHKristi L. Helke
Kristi L. Helke
SBSanat S. Bhadsavle
Sanat S. Bhadsavle
TDThomas Dix
Thomas Dix

19 May 2010 in Journal of Medicinal Chemistry
Verified
Journal Article
Open access
FHFrancis Monroe Hughes
Francis Monroe Hughes
BSBrooke E. Shaner
Brooke E. Shaner
LMLisa A. May
Lisa A. May
LZLyndsay Zotian
Lyndsay Zotian
JBJustin O. Brower
Justin O. Brower
TDThomas Dix
Thomas Dix
The neurotensin hexapapetide fragment NT(8−13) is a potent analgesic when administered directly to the central nervous system but does not cross the blood−brain barrier. A total of 43 novel derivatives of NT(8−13) were evaluated, with one, ABS212 (1), being most active in four rat models of pain when administered peripherally. Compound 1 binds to human neurotensin receptors 1 and 2 with IC50 of 10.6 and 54.2 nM, respectively, and tolerance to the compound in a rat pain model did not develop after 12 days of daily administration. When it was administered peripherally, serum levels and neurotensin receptor binding potency of 1 peaked within 5 min and returned to baseline within 90−120 min; however, analgesic activity remained near maximum for >240 min. This could be due to its metabolism into an active fragment; however, all 4- and 5-mer hydrolysis products were inactive. This pharmacokinetic/pharmacodynamic dichotomy is discussed. Compound 1 is a candidate for development as a first-in-class analgesic.