Language

English

Publication Date

11-19-2024

Journal

Proceedings of the National Academy of Sciences of the United States of America

DOI

10.1073/pnas.2413108121

PMID

39541346

PMCID

PMC11588046

PubMedCentral® Posted Date

11-14-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Activin receptor type 1 (ACVR1; ALK2) and activin receptor like type 1 (ACVRL1; ALK1) are transforming growth factor beta family receptors that integrate extracellular signals of bone morphogenic proteins (BMPs) and activins into Mothers Against Decapentaplegic homolog 1/5 (SMAD1/SMAD5) signaling complexes. Several activating mutations in ALK2 are implicated in fibrodysplasia ossificans progressiva (FOP), diffuse intrinsic pontine gliomas, and ependymomas. The ALK2 R206H mutation is also present in a subset of endometrial tumors, melanomas, non-small lung cancers, and colorectal cancers, and ALK2 expression is elevated in pancreatic cancer. Using DNA-encoded chemistry technology, we screened 3.94 billion unique compounds from our diverse DNA-encoded chemical libraries (DECLs) against the kinase domain of ALK2. Off-DNA synthesis of DECL hits and biochemical validation revealed nanomolar potent ALK2 inhibitors. Further structure-activity relationship studies yielded center for drug discovery (CDD)-2789, a potent [NanoBRET (NB) cell IC

Keywords

Humans, Activin Receptors, Type I, Protein Kinase Inhibitors, Activin Receptors, Type II, DNA, Drug Discovery, Small Molecule Libraries, Signal Transduction, DEL, kinase inhibitors, X-ray Crystallography

Published Open-Access

yes

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