Ferroptosis is a form programmed of cell death that can happen following injury and is receiving increased attention. It is being studied to possibly develop therapeutics for neurological diseases such as stroke and Alzheimer’s disease. Programmed cell death means the cell actively participates in its own demise via the synthesis of “death” proteins. It can be triggered by inhibiting the XC- transporter, a cell surface antiporter. This antiporter can import and export amino acids; in this case, it imports cysteine and exports glutamate. If this antiporter is inhibited, there will be an accumulation of glutamate in a cell causing it to die. In this experiment, ferroptosis was examined in mouse hippocampal cells, also known as HT22 cells. These cells are popular in glutamate-toxicity studies because they are sensitive to glutamate-induced ferroptosis. UK5099 is a drug that is known to inhibit the mitochondrial pyruvate carrier (MPC). By inhibiting the MPC, the intracellular glutamate will be utilized by other processes in a cell like the TCA cycle and less glutamate is released into the synapse. I hypothesized that using UK5099 would protect cells from ferroptosis. Previous positive results were obtained in primary cultured neurons from embryonic mouse brains. The UK5099 has not been tested on the HT22 cells. To examine the effects of UK5099, I first determined the LD50 for erastin in these cells. Erastin is a drug that induces ferroptosis and the LD50 is where the erastin will kill 50% of cells at a certain density. The LD50 for erastin was found to be 180,000 cells/mL. After the LD50 was established, a 96-well plate was used with all wells at 180,000 cells/mL. Half of the wells had cells with erastin in them, and half without. The cells were subjected to distinct treatments. UK5099 was then added into these cells to see if this drug would protect HT22 cells from ferroptosis. I found that UK5099 did not protect against ferroptosis. The lack of protection was confirmed using MTT measures of cell viability and a live/dead assay. Limitations of our experimental design could explain the negative results, which will be taken into account in the future.