Our goal was to develop a smart polymer, controlled release delivery system and evaluate its capabilities for use with salmon calcitonin and rivastigmine. Thermosensitive and phase sensitive smart polymers were evaluated for their potential as controlled release delivery systems. Thermosensitive triblock copolymers were synthesized with increasing lactide to glycolide ratios of 3.5:1, 4.5:1, and 5:1. Characterization was via analytical techniques including proton nuclear magnetic resonance, gel permeation chromatography, critical micellar concentration, sol-gel transition test tube inversion, and cellular biocompatibility assay. Only the 5:1 lactide to glycolide copolymer transitioned into gel at body temperature. Release duration in vitro was 70 days when salmon calcitonin was incorporated at 40% (w/v) in 5:1 thermosensitive copolymer while retaining the native conformation of salmon calcitonin as analyzed via micro bicinchoninic acid assay, circular dichroism and differential scanning calorimetry. Optimization of thermosensitive and phase sensitive copolymers for delivery of rivastigmine was extensively studied thereafter by comparing key variables of: rivastigmine hydrophobicity, polymer concentration, rivastigmine concentration, and depot volume. The optimal thermosensitive formulation was composed of 35% (w/v) copolymer at an injection volume of 0.5 ml containing 40 mg/ml of rivastigmine base. The release of rivastigmine base was observed for ~16 days in a zero-order fashion. For phase sensitive polymer, we found the best formulation after optimization was that of 5% (w/v) 50:50 poly(lactic-co-glycolic acid) in 95:5 benzyl benzoate to benzyl alcohol with rivastigmine base incorporated at 216 mg/ml. Release was observed over the course of ~42 days. In vivo testing was performed using the optimized phase sensitive smart polymer composed of 50:50 PLGA at 5% (w/v) in 95:5 benzyl benzoate with rivastigmine tartrate incorporated as a suspension. Using this formulation, we achieved controlled release for 7 days. Acetylcholinesterase activity was evaluated in the brains of the rats at different time points for all conditions. Acetylcholinesterase was inhibited during controlled release of rivastigmine by 42% in 7 days, compared to healthy controls. The results demonstrate that controlled release of rivastigmine was accomplished and shows promise as a method to increase dosing interval and improve quality of life for those suffering from Alzheimer’s Disease.