New findings are detailed in a research paper that appeared on-line in the Journal of Neurotrauma recently. The paper, which will appear in the next print edition of the journal, was authored by doctoral college students Lingxing Zheng, Jonghyuck Park, Michael Walls and Melissa Tully; Amber Jannasch, laboratory manager of the Metabolite Profiling Service; and Cooper and Shi. The method will not detect acrolein directly but determines the presence of a byproduct, or metabolite, of acrolein in the urine. The metabolite is certainly a chemical compound called N-acetyl-S-3-Hydroxypropylcysteine, or 3-HPMA. Acrolein is very volatile, so it doesn't remain stable long plenty of to monitor, but 1 molecule of acrolein will make one molecule of 3-HPMA, which is very stable in urine, Shi said.This efficacy was comparable to CYC with respect to suppression of experimental SLE. However, vidofludimus didn’t cause myelosuppression like the unselective cell proliferation inhibitor CYC which might relate with the more specific setting of actions of vidofludimus. Vidofludimus acquired an excellent activity profile than MMF in this mouse style of SLE. Thus, vidofludimus may represent a novel medication that could control active SLE like CYC but prevent CYC toxicity and may, therefore, be considered for induction and maintenance therapy of SLE. Dr Bernd Hentsch, Chief Development Officer of 4SC, commented: ‘In addition to vidofludimus’ primary focus on indications rheumatoid arthritis and inflammatory bowel disease, vidofludimus demonstrated the potential to effectively control active SLE within an experimental preclinical model without the sort of side effects often seen with standard therapies.