CAMBRIDGE, Mass., Nov. 16, 2016 /PRNewswire/ -- EIP Pharma, LLC ( www.eippharma.com) today announced that the results of each of two recently completed Phase 2a clinical trials of neflamapimod have been accepted as separate oral presentations at the Clinical Trials in Alzheimer's Disease (CTAD) scientific conference in San Diego, CA ( Dec 8-10, 2016; www.ctad-alzheimer.com). Each trial was conducted in patients with Mild Cognitive Impairment due to Alzheimer's disease ("MCI due to AD") or mild Alzheimer's disease. Thursday, December 8th2:15 PMAbstract OC10 - Quantitative PET study of the effects of the p38a kinase inhibitor VX-745 on brain amyloid plaque load in patients with Early Alzheimer's disease (AD). Scheltens et al. This presentation will be given by Professor Philip Scheltens, Director of the Alzheimer Centre, VU Medical Center in Amsterdam, Netherlands; and will provide clinical and PET results from a 12-week treatment study of neflamapimod (NCT02423122; clinicaltrials.gov). Friday, December 9th7:45 AMAbstract OC19 - Clinical pharmacology study of p38 alpha MAP Kinase Inhibitor, neflamapimod (VX-745), in Mild Cognitive Impairment (MCI) Due to Alzheimer's Disease (AD) or Mild AD. Alam et al. This presentation will be given by Dr John Alam, scientific founder of EIP Pharma, and will provide clinical and CSF biomarker results from a 6-week treatment study of neflamapimod (NCT02423200; clinicaltrials.gov). About neflamapimod (VX-745) and p38 MAPKaNeflamapimod is the nonproprietary name recently adopted by the USAN council for the investigational drug that had previously been code designated VX-745. Neflamapimod is a brain-penetrant oral small molecule that inhibits the intra-cellular enzyme p38 mitogen activated protein kinase alpha (MAPKa ). In the healthy brain, p38 MAPKa regulates inflammation through effects on immune cells. In conditions of stress and disease, p38 MAPKa is also expressed in neurons; where it plays a major role in inflammation and/or amyloid beta induced synaptic toxicity, including the impairment of synaptic plasticity that is a major driver of the development of deficits in learning and memory formation which are defining characteristics of Alzheimer's disease.