An interdisciplinary team of researchers at UC Davis, focused on finding new treatments for Alzheimer's disease (AD), have identified a novel anti-inflammatory target -- KCa3.1, a calcium-activated potassium channel which modulates microglial activation, which may help reduce the effects of beta-amyloid on the brain. Their research in transgenic AD mice has shown that KCa3.1 channel blocking drugs can reduce beta-Amyloid oligomer (AßO)-induced microglia activation. Furthermore, these potassium channel blockers also prevents the deleterious effects of AßO on the mice's memory function and a key electrophysiological process (called LTP for long-term potentiation) needed for normal hippocampal and memory function. An existing orally available KCa3.1 blocker called Senicapoc has excellent absorption in the gut and brain penetrance (passes the blood-brain barrier), and had excellent safety and tolerability in prior clinical trials for sickle cell anemia and asthma. Senicapoc (or other KCa3.1 channel blockers) have not yet been tested in persons with AD. This team at UC Davis has received a competitive grant award from the Alzheimer's Association to fund a small Phase II trial of Senicapoc in Mild or Prodromal AD.The present "IND-enabling" proposal to the ADDF is necessary for this clinical trial to start, because there is no clinical grade drug available, which is an expensive part of drug development. If funded, the below Aims can be accomplished and an IND application will be submitted to the FDA, allowing the first human clinical trial of the drug in persons with Alzheimer's disease.SPECIFIC AIMS: 1. To produce and formulate GMP grade Senicapoc. 2. To Conduct stability testing of the Senicapoc formulation. This work will be done by WuXi AppTec and its public subsidiary SynTheAll (STA) Pharmaceutical Co. in collaboration with investigators at UC Davis and its Alzheimer's Disease Center.