Mia 

Noonan Syndrome (NS) is a RASopathy, a genetic disease caused by mutations in the RAS/MAPK cell signaling pathway, most commonly in the PTPN11 and RAF1 genes, resulting in atypical development. In order to study NS-associated gene mutations, we use Drosophila (fruit flies), as they are easy to genetically manipulate, have a short life cycle, and share 75% of human disease-related genes. NS has very few therapeutic options. Therefore, the purpose of our research is to determine whether certain drugs increase the survival of Drosophila flies expressing PTPN11 variants, and whether these drugs may serve as possible therapeutics for NS. Various drug candidates were administered through food media in vials housing Drosophila flies expressing specific NS-associated PTPN11 variants, introduced into the fly genome using a temperature-sensitive Gal80ts system to control the timing of gene expression. Offspring were then scored by phenotype to determine whether the drugs produced changes in expected trait ratios, indicating therapeutic potential. After testing various drugs, Statins (particularly Locastatin and Atrovastatin) and Rigosertib demonstrated the highest increase in survival rates across several PTPN11 variants, suggesting their potential as therapeutics for Noonan Syndrome. However, drug effectiveness varied across variants, indicating that NS treatment may need to be tailored to specific mutations. These findings lay the groundwork for developing therapeutics for Noonan Syndrome. Future studies will aim to test more drug candidates, retest current drug candidates, and apply findings for clinical applications for NS.