OPTIMIZATION OF THE BROMINATION OF THE BIS-FURAN INTERMEDIATE IN THE SYNTHESIS OF PHIDIANIDINE ANALOGUES
Presentation Type
Event
Full Name of Faculty Mentor
Bryan Wakefield
Major
Biochemistry
Second Major
Biology
Presentation Abstract
Alzheimer's Disease onset is characterized by memory loss due to extracellular deposits of amyloid B and plaque formation, often causing diminishing neurological synaptic functioning and neurodegeneration. Oxidative stressors, caused by radical oxidative species such as H2O2, have shown to enhance and/or initiate Alzheimer's disease through lipid peroxidation, DNA damage, and apoptosis. Phidianidine A analogues derived from Phidiana militaris have exhibited neuroprotective effects in neuroblastoma cell lines. Guo's group, through substituting the linker region of phidianidine A with a biaryl linker, showed the greatest of antioxidant activity against H2O2. The addition of aromatic compounds, 4-ethoxy benzene bound to furan, has shown potential in reducing H2O2-induced damage along with prevention towards oxygenglucose deprived neurotoxicity. Development of further phidianidine analogues, such as replacing the 1,2,4-oxadiazole ri g with a furan ring or substitution on the indole ring with additional aromatic substituents, may help to produce more potent ROS inhibitors. New phidianidine analogues will be synthesized through a cross-coupling approach that will enable the late-stage installation of different aromatic groups and substituted indoles. A necessary step in this approach is the selective introduction of bromine to the 5-position of a substituted furan. A variety of conditions have been studied to identify the most effective procedure.
External Presentation
1
Location
Lib Jackson Student Union, Atrium
Start Date
17-4-2019 4:30 PM
End Date
17-4-2019 6:30 PM
Disciplines
Biochemistry
Recommended Citation
Hatton, James, "OPTIMIZATION OF THE BROMINATION OF THE BIS-FURAN INTERMEDIATE IN THE SYNTHESIS OF PHIDIANIDINE ANALOGUES" (2019). Undergraduate Research Competition. 22.
https://digitalcommons.coastal.edu/ugrc/2019/poster/22
OPTIMIZATION OF THE BROMINATION OF THE BIS-FURAN INTERMEDIATE IN THE SYNTHESIS OF PHIDIANIDINE ANALOGUES
Lib Jackson Student Union, Atrium
Alzheimer's Disease onset is characterized by memory loss due to extracellular deposits of amyloid B and plaque formation, often causing diminishing neurological synaptic functioning and neurodegeneration. Oxidative stressors, caused by radical oxidative species such as H2O2, have shown to enhance and/or initiate Alzheimer's disease through lipid peroxidation, DNA damage, and apoptosis. Phidianidine A analogues derived from Phidiana militaris have exhibited neuroprotective effects in neuroblastoma cell lines. Guo's group, through substituting the linker region of phidianidine A with a biaryl linker, showed the greatest of antioxidant activity against H2O2. The addition of aromatic compounds, 4-ethoxy benzene bound to furan, has shown potential in reducing H2O2-induced damage along with prevention towards oxygenglucose deprived neurotoxicity. Development of further phidianidine analogues, such as replacing the 1,2,4-oxadiazole ri g with a furan ring or substitution on the indole ring with additional aromatic substituents, may help to produce more potent ROS inhibitors. New phidianidine analogues will be synthesized through a cross-coupling approach that will enable the late-stage installation of different aromatic groups and substituted indoles. A necessary step in this approach is the selective introduction of bromine to the 5-position of a substituted furan. A variety of conditions have been studied to identify the most effective procedure.