DX3-234 is an oxidative phosphorylation (OXPHOS) inhibitor. DX3-234 shows significant tumor suppression in the Pan02 syngeneic model of pancreatic cancer.

Menadiol (Dihydrovitamin K3), a menaquinol analogue, is an electron donor for reversed oxidative phosphorylation in submitochondrial particles.

Mito-TEMPO is a mitochondria-targeted antioxidant that possesses superoxide and alkyl radical scavenging properties. Mito-TEMPO helps protect against oxidative damage to the mitochondria.

Mitochondrial fusion promoter M1 is a mitochondrial dynamic modulator. Mitochondrial fusion promoter M1 preserves the mitochondrial function and promotes cellular respiration. Mitochondrial fusion promoter M1 alleviates cardiac and brain damage in rats with cardiac ischemia/reperfusion injury.

Senecionine acetate (O-Acetylsenecionine) is a pyrrolizidine alkaloid. Senecionine acetate inhibits the sequestration of Ca2+ in extramitochondrial and mitochondrial compartments possibly by inactivating free sulfhydryl groups.

HQNO, secreted by P. aeruginosa, is a potent electron transport chain inhibitor with a Kd of 64 nM for complex III. HQNO is a potent inhibitor of mitochondrial NDH-2 in many species.

Antimycin A1 is a specific electron transfer inhibitor of ubiquinol-cytochrome c oxidoreductase. Antimycin A1 inhibits angiogenesis through decrease in VEGF production caused by inhibition of HIF-1α activation.

MPP+ iodide, a toxic metabolite of the neurotoxin MPTP, causes symptom of Parkinson's disease in animal models by selectively destroying dopaminergic neurons in substantia nigra. MPP+ iodide is taken up by the dopamine transporter into dopaminergic neurons where it exerts its neurotoxic action on mitochondria by affecting complex I of the respiratory chain. MPP+ iodide is also a high affinity substrate for the serotonin transporter (SERT).

Mitochondrial respiration-IN-1 hydrobromide (compound 49) is a potent mitochondrial (IC50=8.8 mg/ml) extracted from patent US20110301180A1, compound 49. Mitochondrial respiration-IN-1 hydrobromide significantly reduces mitochondrial respiration in platelets.