Objective: To determine the level of B cell depletion by ublituximab in subjects with RMS Background: Patients with relapsing or primary progressive forms of multiple sclerosis have shown significant clinical improvement after B cell depletion with an anti-CD20 antibody. UTX is a novel, chimeric mAb which targets a unique epitope on the CD20 antigen and has been glycoengineered to enhance affinity for all variants of FcγRIIIa receptors, demonstrating greater antibody-dependent cellular cytotoxicity (ADCC) activity than rituximab. UTX is currently in multiple phase III trials for treatment of hematologic malignancies. Design/Methods: TG1101-RMS201 is a 52-week, phase 2, placebo-controlled, multicenter study that is designed to assess the optimal dose and infusion time as well as safety/tolerability of UTX in RMS subjects. Radiological and clinical analysis are also performed. Optimal dosing is determined by B cell depletion, defined as percentage of CD19 + B cells present following UTX administration. This is calculated by gating the entire lymphocyte/myeloid population. Within this population, CD19 + CD3 − cells were gated and % CD19 + B cells was determined. Results: To date, B cell data from 11 subjects have been analyzed up to week 4 of the 52-week study, encompassing two infusions of UTX. Further, no SAEs have been reported, including subjects receiving rapid UTX infusions. Only patients whose B cells were within a normal range (≥5% of total lymphocytes) at screening were included in the study. At week 4 (1 week post second infusion), median B cell depletion was 99% from baseline in UTX treated subjects, while placebo subjects maintained similar B cell levels as compared to baseline. [Data from ≥24 patients, will reported at the conference.] Conclusions: Ublituximab, a novel glycoengineered anti-CD20 antibody, is well tolerated and demonstrates rapid and robust B cell depletion. Unlike other anti-CD20s, ublituximab can be delivered in shorter infusions, providing a convenience benefit for patients. Study Supported by: TG Therapeutics, Inc Disclosure: Dr. Lovett-Racke has nothing to disclose. Dr. Liu has nothing to disclose. Dr. Racke has received personal compensation for activities with Abbvie, Novartis, Roche, Genentech, TG Therapeutics, and Teva Neuroscience as a consultant. Dr. Racke has received personal compensation in an editorial capacity for JAMA Neurology and The Journal of Neuroimmunology. Dr. Racke has received research support from Diogenix, Roche/Genentech, Novartis, Actelion, TG Therapeutics, and Alkermes. Dr. Shubin has nothing to disclose. Dr. Wray has received personal compensation for activities with Biogen, Genentech/Roche, Sanofi Genzyme, Novartis, and Teva. Dr. Wray has received research support from Actelion, Alkermes, Biogen Celgene, EMD Serono, Sanofi Genzyme Genentech/Roche, Novartis Receptos, TG Therapeutics. Dr. Su has received personal compensation for activities with TG Therapeutics as an employee. Dr. Eubanks has received personal compensation for activities with TG Therapeutics as an employee. Dr. Eubanks receives stock and/or stock options in TG Therapeutics. Dr. Fox has received personal compensation for activities with Acorda, Bayer, Biogen, EMD Serono, Genentech, Novartis, Roche, Sanofi Genzyme, and Teva Neuroscience. Dr. Fox has received research support from Acorda, Biogen, Chugai, EMD Serono, Novartis, Opexa, Roche, Sanofi Genzyme, and Teva Neuroscience.