Decoding non-faradaic signal transduction in organic electrochemical transistor based biosensors

Abstract

Organic electrochemical transistors (OECTs) combine amplification and transduction, making them attractive for biochemical sensing. Yet, the fundamental mechanisms by which OECTs convert biochemical binding events into electrical signals remain poorly understood, limiting their optimization and broader use in biomarker detection. Here, we demonstrate how binding-induced changes in surface potential and capacitance at OECT interfaces can either translate into amplified output signals or result in destructive interaction and signal cancellation. By integrating electrochemical principles with solid-sate device physics, we establish a rational sensing model and provide design and operation rules to maximize biosensor performance. These include guidelines for operating voltage selection, optimal output signal choice, gate electrode geometry, and channel material properties (n-type versus p-type, doped versus undoped). This framework can enable the rational design of OECT-based sensors with enhanced response, lower detection limits, and improved resistance to interference, paving the way for reliable and versatile use of these devices as the enabler of next generation, high-performance biosensors. The mechanism underlying non-faradaic signal transduction in organic electrochemical transistor (OECT) sensors remains poorly defined. Here, the authors establish a rational model for non-faradaic OECT biosensor operation and provide actionable design rules to optimize sensitivity, detection limits, and robustness, ultimately establishing a quantitative link between molecular binding and transistor output.