Autism spectrum disorder (ASD) is a brain disorder of early childhood onset which is characterized by core social impairments. Although ASD is one of the most devastating childhood disorders in terms of prevalence (1 in 68 U.S. children) and societal cost ($236 billion expended annually in the U.S.), its basic disease mechanisms remain poorly understood. Few biomarkers of ASD have been identified, hindering the understanding of its basic biology; nor are there any laboratory-based diagnostic tests to detect, or any medications to treat, ASD’s core social deficits. Creating animal models with reliable behavioral and biological correlates to the human disease, and in humans, elucidating the underlying neurobiology of social deficits, testing promising medications that improve social functioning, and identifying biomarkers of treatment response are important challenges that require urgent attention. Addressing these barriers to progress is the principal goal of the Parker Lab Social Neurosciences Research Program at Stanford University, which spans primate models to patients with ASD. A particular interest of our group is testing whether “social” neuropeptide (e.g., oxytocin and arginine vasopressin) signaling pathways are robust biomarkers of, and treatment targets for, social impairments in ASD. Accordingly, this presentation will review behavioral and biomarker findings from our monkey model of naturally occurring social impairments and from pediatric ASD patients. Implications of these research findings for targeted therapies will be discussed, as will preliminary findings from our ongoing neuropeptide treatment trials in children with ASD.