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Record W2969583663 · doi:10.1002/jbm4.10230

Development of Macrocycle Kinase Inhibitors for ALK2 Using Fibrodysplasia Ossificans Progressiva‐Derived Endothelial Cells

2019· article· en· W2969583663 on OpenAlexfundno aff
Gonzalo Sánchez‐Duffhues, Eleanor Williams, Pascal Benderitter, Valeria V. Orlova, Michiel van Wijhe, Amaya García de Vinuesa, Georgina Kerr, Josselin Caradec, Kirsten Lodder, Hetty C. de Boer, Marie‐José Goumans, Elisabeth M. W. Eekhoff, Antonio Morales‐Piga, Javier Bachiller‐Corral, Pieter Koolwijk, Alex N. Bullock, Jan Hoflack, Peter ten Dijke

Bibliographic record

VenueJBMR Plus · 2019
Typearticle
Languageen
FieldMedicine
TopicHeterotopic Ossification and Related Conditions
Canadian institutionsnot available
FundersEshelman Institute for Innovation, University of North Carolina at Chapel HillNederlandse Federatie van Universitair Medische CentraMinistero dello Sviluppo EconomicoMerck Sharp and DohmeAFM-TéléthonNovartis PharmaCanada Foundation for InnovationAO FoundationWellcome TrustFundação de Amparo à Pesquisa do Estado de São PauloGenome CanadaOntario Ministry of Economic Development and InnovationInnovative Medicines InitiativeCancer Genomics CentreDiamond Light SourceInstituto de Salud Carlos IIIBoehringer IngelheimTakeda Pharmaceutical CompanyAbbVieEuropean Federation of Pharmaceutical Industries and AssociationsJanssen PharmaceuticalsMerck KGaAPfizer
KeywordsFibrodysplasia ossificans progressivaActivin receptorOssificationMesenchymal stem cellHeterotopic ossificationCancer researchCell biologyBone morphogenetic proteinSignal transductionBone morphogenetic protein 2BMPR2Myositis ossificansMedicineBioinformaticsChemistryBiologyPathologyBiochemistryAnatomyGeneIn vitro

Abstract

fetched live from OpenAlex

ABSTRACT Fibrodysplasia ossificans progressiva (FOP) is an extremely rare congenital form of heterotopic ossification (HO), caused by heterozygous mutations in the activin A type I receptor (ACVR1), that encodes the bone morphogenetic protein (BMP) type I receptor ALK2. These mutations enable ALK2 to induce downstream signaling in response to activins, thereby turning them into bone‐inducing agents. To date, there is no cure for FOP. The further development of FOP patient‐derived models may contribute to the discovery of novel biomarkers and therapeutic approaches. Nevertheless, this has traditionally been a challenge, as biopsy sampling often triggers HO. We have characterized peripheral blood‐derived endothelial colony‐forming cells (ECFCs) from three independent FOP donors as a new model for FOP. FOP ECFCs are prone to undergo endothelial‐to‐mesenchymal transition and exhibit increased ALK2 downstream signaling and subsequent osteogenic differentiation upon stimulation with activin A. Moreover, we have identified a new class of small molecule macrocycles with potential activity against ALK2 kinase. Finally, using FOP ECFCs, we have selected OD36 and OD52 as potent inhibitors with excellent kinase selectivity profiles that potently antagonize mutant ALK2 signaling and osteogenic differentiation. We expect that these results will contribute to the development of novel ALK2 clinical candidates for the treatment of FOP. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.003

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.028
GPT teacher head0.301
Teacher spread0.274 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations45
Published2019
Admission routes1
Has abstractyes

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