Quercetin is a plant flavonoid that is being investigated as a potential therapy for cystic fibrosis (CF). Flavonoids are a group of naturally occurring compounds in plants that are known to confer health benefits by altering enzyme function within the cell.

Foods rich in quercetin include onions, green tea, apple, cherries, broccoli, and citrus fruits. Quercetin is not approved by the U.S. Food and Drug Administration (FDA) or the European Food Safety Authority (EFSA) for therapeutic purposes. However, in 2011 the FDA granted “generally recognized as safe” (GRAS) status to QU995, a highly pure form of quercetin made by Quercegen Pharmaceuticals.

Quercetin and Cystic Fibrosis

CF is an inherited disease characterized by the production of thick, sticky mucus in various organs such as the lungs, intestines, and pancreas. It is caused by mutations in the CFTR gene, which encodes for a transmembrane protein channel responsible for carrying chloride ions in and out of cells. The most common mutation seen in the CFTR gene is the so-called F508del mutation, in which the amino acid phenylalanine is deleted or missing at position 508 in the CFTR protein. (Amino acids are building blocks of proteins). This results in the improper folding of the CFTR protein and prevents it from moving to the cell membrane, where it normally exerts its function. This particular mutation is categorized as a class 2 mutation.

There also are other CFTR mutations (called class 3 and class 4 mutations) in which the CFTR protein is created and transported to the cell membrane, but the channel does not function properly. For those mutations, CFTR potentiators, a type of CFTR modulators, help by opening the CFTR channel and increase chloride ion transport.

Quercetin is being investigated in CF therapy as a CFTR potentiator that can improve the function of the CFTR protein after it has been transported to the cell membrane.

The exact mechanism of action of quercetin is still not clear. However, recent clinical studies have shown that compounds with anti-oxidant and anti-inflammatory activity, such as quercetin, may improve lung function in CF patients.

The lungs are a site of very high oxidative stress that potentially can have a negative effect on the proper functioning of the CFTR protein. Antioxidants such as quercetin can help lower oxidative stress in the lungs and minimize the effects of mutations on the CFTR protein function.

Quercetin in clinical trials

A Phase 2 clinical trial (NCT01348204) to measure the change in nasal potential difference (NPD) upon administration of quercetin was completed in 2011. NPD is a well-established parameter to assess the functioning of the CFTR protein in the nasal epithelium. The results of the study are yet to be published.

However, investigators noted that preliminary results from in vivo studies in humans suggest quercetin activates the defective F580del CFTR protein and increases its availability at the cell membrane.


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