Optimization and Characterization of SHIP1 Ligands for Cellular Target Engagement and Activity in Alzheimer’s Disease Models

Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1), encoded by the gene INPP5D, is a lipid phosphatase that negatively regulates immune receptor signaling in hematopoietic cells and microglia. Here, we describe a pyridyl-pyrazole-piperidine scaffold and the lead compound 3-((2-chlorobenzyl)oxy)-5-(1-(piperidin-4-yl)-1H-pyrazol-4-yl)pyridine (<b>32</b>), which demonstrates SHIP1 target engagement, brain exposure, and evidence of a central pharmacodynamic response <i>in vivo</i>. Structure-activity relationship studies, guided by biochemical and cellular assays using multiple human and murine protein constructs and cells, identified SHIP1-active ligands. A thermal shift assay using full-length SHIP1 was used to assess compounds for cellular target engagement, while studies in IL-4 conditioned THP-1 cells was used to demonstrate changes in downstream AKT signaling. Targeted lipidomics revealed changes in the overall phosphoinositide pool consistent with SHIP1 target engagement and reduction of phospho-AKT levels. In a protein-lipid overlay assay, compound <b>32</b> induced changes in the relative association of SHIP1 with multiple phosphatidylinositols on a membrane surface. In high-content cellular imaging assays, compound <b>32</b> enhanced the uptake of myelin/membrane debris and fibrillar amyloid by primary murine microglia, phenocopying a genetic model with reduced SHIP1 expression. Finally, oral administration of compound <b>32</b> resulted in brain exposure sufficient to alter gene expression and reduce IL-1β levels as pharmacodynamic markers of microglial activation and neuroinflammation in an amyloidosis mouse model of Alzheimer's disease. Collectively, these results define a scaffold with SHIP1 target engagement, CNS exposure, and <i>in vivo</i> activity, providing a foundation for the optimization of brain-penetrant SHIP1 ligands suitable for further mechanistic studies and therapeutic development for the treatment of Alzheimer's disease.

Authors

Institutions

Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-01-02
DOI
https://doi.org/10.64898/2025.12.31.697127
Primary Topic
PI3K/AKT/mTOR signaling in cancer
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Optimization and Characterization of SHIP1 Ligands for Cellular Target Engagement and Activity in Alzheimer’s Disease Models

Alan D. Palkowitz, Andrew D. Mesecar, Peter J. Meikle, Philip A. Hipskind et al.
bioRxiv (Cold Spring Harbor Laboratory)
PI3K/AKT/mTOR signaling in cancer
article

Optimization and Characterization of SHIP1 Ligands for Cellular Target Engagement and Activity in Alzheimer’s Disease Models

Alan D. Palkowitz, Andrew D. Mesecar, Peter J. Meikle, Philip A. Hipskind, Daniel E. Beck, Kratika Singhal, Ashton Faulkner, Suzanne Doolen, Disha Soni, Jeffrey L. Dage, Hasi Huhe, Sara K. Quinney, Travis S. Johnson, Lais Da Silva, Steven P. Angus, Mustapha Moussaif, Brent Clayton, Cynthia D. Jesudason, Ryan D. Imhoff, Emily R. Mason, Kevin Huynh, Shaoyou Chu, Matilda van Buuren-Milne, Adrian L Oblak, Isaac Caballero-Floran, Stacey J Sukoff Rizzo, Sean-Paul Williams, Juliane C David, Colin J Beach, Timothy I Richardson, June Javens-Wolfe, Rima Fathi Kadurah-Dauok, Bruce T Lamb, Adam K Hamdani, Claudia Rangel-Barajas
article en

Abstract

Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP1), encoded by the gene INPP5D, is a lipid phosphatase that negatively regulates immune receptor signaling in hematopoietic cells and microglia. Here, we describe a pyridyl-pyrazole-piperidine scaffold and the lead compound 3-((2-chlorobenzyl)oxy)-5-(1-(piperidin-4-yl)-1H-pyrazol-4-yl)pyridine (<b>32</b>), which demonstrates SHIP1 target engagement, brain exposure, and evidence of a central pharmacodynamic response <i>in vivo</i>. Structure-activity relationship studies, guided by biochemical and cellular assays using multiple human and murine protein constructs and cells, identified SHIP1-active ligands. A thermal shift assay using full-length SHIP1 was used to assess compounds for cellular target engagement, while studies in IL-4 conditioned THP-1 cells was used to demonstrate changes in downstream AKT signaling. Targeted lipidomics revealed changes in the overall phosphoinositide pool consistent with SHIP1 target engagement and reduction of phospho-AKT levels. In a protein-lipid overlay assay, compound <b>32</b> induced changes in the relative association of SHIP1 with multiple phosphatidylinositols on a membrane surface. In high-content cellular imaging assays, compound <b>32</b> enhanced the uptake of myelin/membrane debris and fibrillar amyloid by primary murine microglia, phenocopying a genetic model with reduced SHIP1 expression. Finally, oral administration of compound <b>32</b> resulted in brain exposure sufficient to alter gene expression and reduce IL-1β levels as pharmacodynamic markers of microglial activation and neuroinflammation in an amyloidosis mouse model of Alzheimer's disease. Collectively, these results define a scaffold with SHIP1 target engagement, CNS exposure, and <i>in vivo</i> activity, providing a foundation for the optimization of brain-penetrant SHIP1 ligands suitable for further mechanistic studies and therapeutic development for the treatment of Alzheimer's disease.

bioRxiv (Cold Spring Harbor Laboratory)
Indiana Institute of Technology (US), Baker Heart and Diabetes Institute (AU), University of Pittsburgh (US), Duke University (US), La Trobe University (AU), Purdue University West Lafayette (US), Indiana Biosciences Research Institute (US), Duke Institute for Health Innovation (US), Duke University Hospital (US), Indiana University School of Medicine, Indiana University – Purdue University Indianapolis (US)
Purdue University, University of Pittsburgh, Partenariat Canadien Contre Le Cancer, National Institutes of Health, School of Medicine, Indiana University, Melvin and Bren Simon Cancer Center, Indiana University, Medical Research Council, National Health and Medical Research Council, National Institute on Aging
Openalex Percentile: Top 98%
PI3K/AKT/mTOR signaling in cancer
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.