Discovery of a selective alpha-kinase 1 inhibitor for the rare genetic disease ROSAH syndrome

J Jieqing Fan D Danyang Liu Z Zhu Ming C Chunyu Yan H Huaixin Dang Y Yanfang Pan X Xiong Wei Z Zhengle Zhao W Wenzhi Wang S Shuai Zhang L Linlin Chen S Shuo Cai (Centre of Biomedical Systems and Informatics, Zhejiang University—University of Edinburgh Institute, Zhejiang University School of Medicine) J Jiangbin Ke Y Yaru Luo L Linjie Rao J Jingjing Chen (School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences) Z Zhenjie Chen J Junlin Zhou F Feixiang Chen (College of Smart Materials and Future Energy, State Key Laboratory of Molecular Engineering of Polymers) X Xiaodi Duan B Boyue Ren T Tong-Ruei R. Li L Lawrence Melvin J Jeysen Yogaratnam V Vinit B. Mahajan H Hongmei Song H Henri Lichenstein T Tian Xu (Department of Chemical and Biomolecular Engineering and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 North Charles Street, Baltimore, Maryland 21218, United States) C Cong Xu (Department of Statistics and Data Science, College of Science)

Abstract

Abstract ROSAH (retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome is a rare genetic disease caused by variants in alpha-kinase 1 (ALPK1) resulting in downstream pro-inflammatory signaling mediated by the TIFA/TRAF6/NF-κB pathway. Here, we report the design of an ALPK1 inhibitor, DF-003, with pharmacokinetic properties suitable for daily oral dosing. In biochemical assays, DF-003 potently inhibits human ALPK1 (IC50 = 1.5 nM) and the ROSAH disease-causing mutant ALPK1[T237M] (IC50 = 16 nM). When tested against a panel of 394 human kinases, DF-003 exhibits ≥860-fold selectivity over the closest kinase. In cell-based assays, DF-003 suppresses inflammatory cytokine signaling mediated both by wild-type ALPK1 and the disease-causing ALPK1[T237M] mutant. Using mice heterozygous for wild-type human ALPK1 and ALPK1 T237M established to model ROSAH syndrome that exhibit retinal microglial infiltration, astrocyte activation, and inflammatory cytokine upregulation in the retina, optic nerve, and cortex, we show that orally administered DF-003 is sufficient to inhibit these inflammatory phenotypes.

Article Details

Volume / Issue Vol. 16, Issue 1
Published September 09, 2025
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (29)

J

Jieqing Fan

D

Danyang Liu

Z

Zhu Ming

C

Chunyu Yan

H

Huaixin Dang

Y

Yanfang Pan

X

Xiong Wei

Z

Zhengle Zhao

W

Wenzhi Wang

S

Shuai Zhang

L

Linlin Chen

S

Shuo Cai

Centre of Biomedical Systems and Informatics, Zhejiang University—University of Edinburgh Institute, Zhejiang University School of Medicine

J

Jiangbin Ke

Y

Yaru Luo

L

Linjie Rao

J

Jingjing Chen

School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences

Z

Zhenjie Chen

J

Junlin Zhou

F

Feixiang Chen

College of Smart Materials and Future Energy, State Key Laboratory of Molecular Engineering of Polymers

X

Xiaodi Duan

B

Boyue Ren

T

Tong-Ruei R. Li

L

Lawrence Melvin

J

Jeysen Yogaratnam

V

Vinit B. Mahajan

H

Hongmei Song

H

Henri Lichenstein

T

Tian Xu

Department of Chemical and Biomolecular Engineering and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 North Charles Street, Baltimore, Maryland 21218, United States

C

Cong Xu

Department of Statistics and Data Science, College of Science