Mitochondria have a central role in bioenergetics and are most well known for their role in cellular respiration and the production of ATP. Thus, it is not surprising that mitochondrial dysfunction is a large contributor to many human diseases. Previously, the lipophilic mitochondrial-targeted cation, Triphenylphosphonium (TPP+) has been used to target bioactive molecules to mitochondria in vivo. This is accomplished by chemically coupling a TPP+ moiety to the bioactive molecule, typically through a linking group. It has been found that the TPP+ moiety coupled to a linking group only, with no bioactive molecule attached, can alter mitochondrial oxygen consumption and uncouple ATP production. Recently, the Kerns group discovered that structural changes to the TPP+ moiety can alter the effect of TPP+ on mitochondrial function. Decyl TPP derivatives were studied and electron-donating as well as electron-withdrawing substituents on the TPP+ phenyl rings were shown to have an effect on the degree of mitochondrial oxygen consumption and uncoupling. In the study presented here, structural analogs of the TPP+ moiety were coupled with butyl and benzyl groups to synthesize novel TPP+ conjugates. Each conjugate was structurally characterized, and the electrostatic potential for each was determined. Ongoing studies will determine if the new TPP+ conjugates target mitochondria, and the effect of electron-donating and withdrawing substituents on mitochondrial function and cellular respiration.