Experimental study demonstrates immune-enzyme-triggered degradation of conjugated polymer transistors, indicating a pathway for transient bioelectronics.
Degradable imine linkers within the polymer backbone enabled acid-triggered organic mixed ionic–electronic conductors (OMIECs). Yet, for many bioelectronic applications, OMIECs must work in direct contact with physiological fluids, making it challenging to achieve both excellent mixed ionic-electronic transport and degradation. A degradation mechanism that is triggered by specific reagents not continuously present in physiological environments (pH 7.4 and 37 °C) is therefore needed. Here, we show that myeloperoxidase (MPO), an enzyme expressed by immune cells, enables the degradation of conjugated polymer films. Specifically, hypochlorite generated by MPO drives the degradation of f-BTI2g-TVTCN, an n-type donor–acceptor polymer with excellent organic electrochemical transistor (OECT) performance (µC* 41.3 F cm−1 V−1 s−1). The process is concentration-dependent, with 50 μM hypochlorite leading to a complete loss of OECT performance within 42 days, whereas devices stored in phosphate buffer retained 42 ± 4% of their initial drain current. Mechanistic studies reveal that degradation proceeds via cleavage of the vinylene bonds accompanied by side-chain oxidation, yielding low-molecular-weight fragments. High-resolution mass spectrometry combined with machine-learning models shows that degradation products have low predicted toxic concern. This work opens a new generation of high-performance OMIECs whose degradation is enabled by immune-specific enzymatic activity under physiological conditions.
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Batista et al. (2026) studied this question.
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