L-Glutamate, a major neurotransmitter in the central nervous system, has been known to be extensively released during brain ischemia and induces subsequent neuronal cell death.1,2) Recent studies indicate that oxygen radicals are produced through a variety of intracellular cascades in such events.2) It was also reported that blockage of glutamate toxicity by free radical scavengers was effective to ameliorate brain ischemia injury.3,4) Recently, some glutamate toxicity inhibitors of microbial origin such as carquinostatin A,5) lavanduquinocin,6) and aestivophoenins A and B7) have been reported. In the course of our screening for free radical scavengers or inhibitors of glutamate toxicity using the neuronal hybridoma N18-RE-105 cells to prevent the brain ischemia injury, we previously isolated benzastatins A~G8~10) and phenazostatins A (2) and B11,12) Further investigation on metabolites of Streptomyces sp. 833 which is the producer of phenazostatins A and B has resulted in isolation of a unique diphenazine compound, phenazostatin C (1) (Fig. 1). We report here the isolation, physico-chemical properties, structure determination, and biological activities of 1.