N-Methyl-D-aspartic acid is an amino acid derivative acting as a specific agonist at the NMDA receptor, and therefore mimics the action of the neurotransmitter glutamate on that receptor. Unlike glutamate, NMDA only binds to and regulates the NMDA receptor and has no effect on other glutamate receptors (such as those for AMPA and kainate). NMDA receptors are particularly important when they become overactive during withdrawal from alcohol as this causes symptoms such as agitation and, sometimes, epileptiform seizures. NMDA is a water-soluble synthetic substance that is not normally found in biological tissue.

Buthionine sulfoximine (BSO) is a selective inhibitor of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting enzyme in glutathione (GSH) synthesis. In cancer cells, glutathione depletion significantly increased cytotoxicity via oxidative stress. In addition, in neuroblastoma cells susceptible to Buthionine sulfoximine treatment, DNA damage and cell apoptosis occurred via ROS production. Buthionine sulfoximine plus melphalan was effective in treatment for patients with recurrent/refractory neuroblastoma. Buthionine sulfoximine may also be used to increase the sensitivity of parasites to oxidative antiparasitic drugs. Buthionine sulfoximine has been shown to increase the efficacy of nifurtimox against T. cruzi and has also been shown to be an effective modulator of GSH-mediated chemoresistance by increasing the in vitro cytotoxicity of alkylating agents and radiation. Buthionine sulfoximine has been tested in animal studies and in human phase I trials for adults with solid tumors, with documented clinical responses in patients with melanoma, ovarian carcinoma and small cell carcinoma of the lung treated with the combination of Buthionine sulfoximine and melphalan.