Through slowing the degradation of EETs (via SEH inhibition), it has been hypothesized to induce neuroprotective, cardioprotective, and anti-inflammatory effects. In vitro studies with murine models found that SEH inhibition significantly lowered blood pressure, bolstering its hypothesized role in blood pressure regulation. Here, we apply docking, MD, and (NCMC+MD) BLUES simulations on a small set of 12 fragments which bind to SEH and evaluate their effectiveness in identifying their binding modes.