the randomized, double-blind, placebo controlled Single Ascending Dose (SAD) study of VU319. This presentation includes both data from the initial SAD study, and the Food Effect substudy. The main pharmacodynamic objectives of the SAD were to identify early markers of functional engagement. Following the ascending dose cohorts, a Food Effect substudy was conducted to assess whether there was any change in the cognitive performance if VU319 was dosed with food compared to in a fasted state. Methods: VU319 was given orally to 52 healthy volunteers aged 18-55?years. The SAD study tested 40 participants in five dose escalating cohorts of eight participants, in which six received VU319 and two received placebo. The Food Effect substudy consisted of 12 participants, in which ten received oral VU319 and two received placebo. The five doses for the SAD study were 60, 120, 240, 400 and 600mg. Participants in the Food Effect substudy received VU319 at a single dose of 120mg. For the 5 cohorts of the SAD study, all participants were dosed in a fasted stated. In contrast, all 12 participants in the Food Effect substudy completed were dosed twice; once fasted, and once following breakfast. Cognitive and electrophysiological tasks were examined pre-dosing and at 5?hours post-dose. The tasks were selected for their sensitivity to cholinergic tone. Cognitive tasks tested spatial and sustained attention, episodic and working memory, perceptual vigilance and psychomotor speed. Recorded ERP examined auditory and visual discrimination using oddball tasks, and an incidental memory task in which participants passively observed novel and repeated complex images. Results: The analysis showed a trend for improvements in cognitive and ERP performance on the higher doses of VU319 compared to placebo. Participants on the highest dose of VU319 responded significantly faster to targets on the continuous performance test compared to participants on placebo (p = 0.03, effect size d = 1.2). Additionally, on the incidental memory task, participants who received the higher two doses of VU319 exhibited larger P300 amplitudes compared to placebo, when present with repeated compared to novel images (d > 0.8). Examination of the relationship between plasma levels of VU319 and cognitive performance showed that the response time on the continuous performance task decreased in relation to increasing concentration of VU319 in the bloodstream. Conclusions: We conclude that these results demonstrate potential enhancement of the cholinergic system functioning in healthy adults following a single dose of VU319. These results provide an indication of the potential measures that are sensitive to cognitive activity by VU319 and therefore provide a potential framework to examine the cognitive impact of multiple doses of VU319 in AD patients. This research was funded by: This work was supported by the following grants: VKC Hobbs Discovery Grant 4-04-218-9745, Alzheimer’s Association PCTR-16-383171; NICHD U54 HD083211, NCATS UL1 TR000445, 2RO1MH082867, R01MH073676, R01MH86601, MH087965, MH093366. Poster Number: EI-56 HALOPERIDOL DECANOATE INDUCED PANCYTOPENIA: A CASE REPORT Amit Jagtiani; Sandra Veigne; Elisabeth Lescouflair; Sabish Balan Harlem Hospital Center, New York Introduction: Blood dyscrasias can occur secondary to antipsychotic drug use which may be due to direct drug toxicity or immunologic mechanisms causing bone marrow suppression. Antipsychotic use mostly causes neutropenia and less frequently thrombocytopenia. Drug-induced pancytopenia is a very rare side-effect of psychotropic medications and is even rarer with butyrophenones like haloperidol Methods: We reviewed the case of a geriatric patient who developed pancytopenia while on haloperidol decanoate monthly injection Results: We present the case of an 85-year-old African-American woman with a long history of schizophrenia, who was stabilized on Haloperidol Decanoate 50?mg monthly IM for a few years at another hospital. She was then maintained on the Haloperidol decanoate for a few months after she moved outpatient care to our hospital. She was noted to have pancytopenia at initial presentation in the clinic and her RBC, Platelets, and WBC (including neutrophil) counts gradually declined to the point where her Haloperidol Decanoate was placed on hold in order to further monitor the blood counts. Baseline leukocyte count was 3000/mm 3 when she started outpatient treatment at our clinic, which gradually dropped to 1860/mm 3 within 6 months of Haloperidol decanoate treatment. During this time, hemoglobin dropped 0.8 points (10.9?g/?dL to 10.1 g/dL), and platelet count decreased from 154,000/mm3 to 140,000/mm3. Within one month of discontinuation of haloperidol decanoate, patient decompensated and was admitted to the psychiatry inpatient unit. Hematology was consulted; lab work to exclude other causes of pancytopenia was completed and haloperidol induced pancytopenia was suspected. She didn’t receive any more haloperidol decanoate during her hospital stay. She consistently refused oral medications and became catatonic. Court order for medication- over-objection was obtained but she continued refusing oral medications. As a result, she received Olanzapine 5?mg IM consistently for few days which ultimately resulted in clinical improvement. She was discharged after 2 months of inpatient stay. Her cell counts gradually trended upwards during the inpatient stay. At the time of discharge from the inpatient unit, her WBC Poster Abstracts Am J Geriatr Psychiatry 28:4S, April 2020 S115