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Submission Date

Fall 2021


Cystic fibrosis is an autosomal disease that is caused by a defect in the CFTR, or cystic fibrosis transmembrane conductance regulator. It affects more than 70,000 people world-wide and is life-threatening to those affected. To treat this disease there are two drug classes: correctors and potentiators. Correctors aim to correct the misfolded CFTR proteins, while potentiators aid in increasing ion concentration outside of the cells by keeping the channels open for longer periods of time. The aim of this project was to identify the key differences between two similar potentiator drugs, Ivacaftor (Kalydeco®) and GLPG 1837. The research question posed was: How does a model show the difference in efficacy of GLPG1837 compared to Ivacaftor? The comparison was done through the research and rendering of protein models through the Jmol software. The Jmol files that were used were 6O2P (Ivacaftor) and 6O1V (GLPG 1837) from the Protein Data Bank (PDB), which displayed the drugs in their binding site within the CFTR protein. It was shown that GLPG 1837 contained a sulfur molecule, while Ivacaftor did not. It is believed that this difference is what causes GLPG 1837 to appear more effective than Ivacaftor (in clinical trials) because the hinge region of the CFTR protein also contains a sulfur molecule. These models can be used by providers to explain treatments to patients who are using these medications much more effectively. By providing tools to break down the science behind these medications to all age groups it can further rapport between patient and provider. As well as reduce stress of patients due to a better understanding of their treatment.

Cystic Fibrosis Poster.pptx (1280 kB)
Cystic Fibrosis Poster

CF Presentation - Updated (1).pptx (14098 kB)
Cystic Fibrosis Presentation

Comparing the Effectiveness between Ivacaftor and GLPG 1837