3-Indolepropionic acid (IN-OX1; Indole-3-propionic acid; OX-1; Oxigon; SHP 22; SHP-622; VP-20629), an endogenous substance produced by bacteria in the intestine, is a deamination product of Tryptophan (T947200) that protects the hippocampus (studied in gerbils) from ischemic damage and oxidative stress. It’s ability to protect the neurons in this way is attributed to its potent antioxidative effects. 3-Indolepropionic acid is also hypothesized to have protective effects on the thyroid gland. 3-Indolepropionic acid is being studied for therapeutic use in Alzheimer's disease. 3-Indolepropionic acid (IPA) completely protected primary neurons and neuroblastoma cells against oxidative damage and death caused by exposure to Abeta, by inhibition of superoxide dismutase, or by treatment with hydrogen peroxide. In kinetic competition experiments using free radical-trapping agents, the capacity of IPA to scavenge hydroxyl radicals exceeded that of melatonin, an indoleamine considered to be the most potent naturally occurring scavenger of free radicals. In contrast with other antioxidants, IPA was not converted to reactive intermediates with pro-oxidant activity. In 2011, Intellect redirected the focus of the OX1 program from Alzheimer's disease to FA (Friedreich's Ataxia). Research suggests that the symptoms associated with FA are the result of oxidative stress caused by the abnormal accumulation of iron. OX1's ability to neutralize ROS could be an effective agent to reduce oxidative stress in FA, thereby eliminating the symptoms of FA and increasing both quality of life and longevity in affected individuals.

Protocatechuic acid (3,4-dihydroxybenzoic acid, PCA) is a simple phenolic acid. It is found in a large variety of edible plants and possesses various pharmacological activities. This bioactive compound is famous for its biological properties and pharmacological activities such as: antioxidant, antibacterial, anticancer, antiulcer, antidiabetic, antiaging, antifibrotic, antiviral, anti-inflammatory, analgesic, antiatherosclerotic, cardiac, hepatoprotective, neurological and nephroprotective. The neuroprotective effects of PCA, extracted from Alpinia oxyphylla, on H2O2 resulted in apoptosis and oxidative stress in cultured PC12 cells. Apoptotic cell death by H2O2 was dose-dependent. Enhanced effect of PCA on protecting PC12 cells against apoptosis, augmented glutathione (GSH) level and an increase in catalytic activity was investigated by flow cytometric analysis. In cytotoxic assays, PCA causes cell death in HepG2 cancerous cell line of liver showing that PCA stimulates the c-Jun N-terminal kinase (JNK) and p38 subgroups of the mitogen-activated protein kinase (MAPK) family. Treatment with PCA decreased OVA-induced airway hyper-responsiveness to inhaled methacholine. Cell inflammation and mucus hypersecretion was also decreased by PCA. Thus, PCA can be useful for treating asthma. Experimental studies strongly support the role of protocatechuic acid in the prevention of neurodegenerative processes, including Alzheimer's and Parkinson's diseases, due to its favorable influence on processes underlying cognitive and behavioral impairment, namely accumulation of the β-amyloid plaques in brain tissues, hyperphosphorylation of tau protein in neurons, excessive formation of reactive oxygen species and neuroinflammation.