This protein functions as a multispecific organic anion transporter, with oxidized glutathione, cysteinyl leukotrienes, and activated aflatoxin B1 as substrates.

[8] The two nucleotide binding domains have a functional asymmetry that plays a significant role in the ability of ATP to power the transporter.

[10] While ABCC1 is generally found throughout most tissues in humans, it is particularly prevalent in the lungs, spleen, testes, kidneys, placenta, thyroid, bladder, and adrenal glands.

On the other hand, an individual with a 3'-UTR G3361A polymorphism generally had a more severe case of COPD that was accompanied by a greater amount of inflammation in their airways.

As these proteins accumulate, they begin to form plaques that interfere with signaling between cells of the nervous system found within the brain.

Due to its presence in the choroid plexus and blood-brain barrier and its ability to transport multiple kinds of molecules out of cells, ABCC1 has been a point of interest in many Alzheimer's disease studies.

The transporter protein has been shown to decrease β-amyloid accumulation by nearly 80 percent when activated, leading researchers to further investigation on its use in future treatments of Alzheimer's and other neurological disorders.

[12] Similar results were found in early-stage breast cancer where the increased expression of the transporter gene correlated with shorter times until a relapse occurred and lower rates of survival.

[12] Because of its significant role in the transportation of organic anion molecules and recent association with multiple illnesses including Alzheimer's disease (AD), the ABCC1 protein has become a potential drug target.