Author ORCID Identifier

https://orcid.org/0009-0000-6783-2010

Date Available

8-14-2027

Year of Publication

2025

Document Type

Doctoral Dissertation

Degree Name

Doctor of Philosophy (PhD)

College

Pharmacy

Department/School/Program

Pharmaceutical Sciences

Faculty

Dr. Chang-Guo Zhan

Faculty

Dr. David Feola

Abstract

Butyrylcholinesterase (BChE), a close cousin of acetylcholinesterase (AChE), is a serine hydrolase possessing activity primarily for ester hydrolysis for a diverse set of substrates. It is found in a variety of species and in humans is expressed in approximately 10-fold greater quantities than AChE (itself crucial for terminating signaling at cholinergic synapses), indicating one or more important physiological roles, of which the leading theories are (1) protection from exogenous compounds by binding and/or metabolism of said compounds into inactive metabolites, (2) providing reserve cholinesterase activity under instances of exposure to AChE inhibitors, and (3) regulating signaling of the peptide hormone ghrelin. Previous work in our group has led to the discovery of BChE mutants with dramatically improved catalytic efficiency for ester hydrolysis of cocaine (yielding inactive metabolites). This improved catalytic activity, in combination with design of fusion proteins of BChE mutants fused with the IgG1 Fc domain (resulting in markedly improved enzyme pharmacokinetics), yielded enzyme constructs with highly promising safety and efficacy results for treatment of cocaine use disorder in in vivo models of cocaine addiction and cocaine overdose.

In this work, we explored BChE mutants for accelerated biotransformation of other clinically-relevant compounds to inactive metabolites. The first of these is ghrelin, a peptide hormone—requiring acylation at Ser-3 for signaling activity—that has been found to play a central role in reinforcement and motivation of rewarding behaviors, including addiction-seeking behavior for heavily-abused substances such as alcohol, nicotine, stimulants (cocaine, amphetamines, etc.), and opioids. Additionally, we explored the use of BChE mutants for the treatment of carbamate and organophosphate (OP) poisoning, which arises from cholinergic excess from carbamate/OP reaction with the catalytic serine residue of AChE. Each year, hundreds of thousands of individuals die from carbamate/OP poisoning, with an estimate of millions of annual serious exposure events, representing a major threat to human health and a burden on healthcare infrastructure. We selected aldicarb and paraoxon as representative carbamate and OP inhibitors (respectively), given their potent toxicity (LD50 < 1 mg/kg) and commercial availability as pesticides.

From these efforts, we discovered a BChE mutant—E23-7Fc(M6)—with 44-fold (4300%) greater activity for ghrelin deacylation compared to mutant CocH5-Fc(M6), which itself was previously found to exhibit greater activity than wild-type BChE. Additionally, from screening of previously-explored mutants from our efforts in cocaine addiction treatments, we identified mutant construct CocH3-Fc(M3) from in silico screening as a promising enzyme for treatment of aldicarb as well as paraoxon poisoning. In vitro kinetic characterization confirmed that CocH3-Fc(M3) exhibited improved activity for accelerating conversion of aldicarb and paraoxon into inactive metabolites, and in vivo studies confirmed its safety and efficacy for rescue of mice from carbamate/OP poisoning after administration of a lethal dose of aldicarb or paraoxon. Building upon prior successful efforts for treatment of cocaine use disorder, these findings confirm that the iterative design/screening approach applied herein allows for the discovery of BChE mutants for targeted and accelerated metabolism of clinically-relevant compounds.

Digital Object Identifier (DOI)

https://doi.org/10.13023/etd.2025.440

Available for download on Saturday, August 14, 2027

Share

COinS