Author

Mohamad Saoud

Heidelberg UniversityORCID 0000-0003-0749-8692Unclaimed ORCID profile · follow to get notified of new preprints

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Mohamad Saoud1 paper · Metabolomics Core Technology Platform (MCTP), Heidelberg University, 69120, Heidelberg, Germany;

Biology Disciplines

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Cancer Biology· 1 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:benchmarking· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Research Focus:perturbation response prediction· 1 Assay:proteomics· 1 Approach:wet-lab / biochemical assay· 1

Frequent Co-Authors

Alexander SonntagiD· 1 shared Aubry K. MilleriD· 1 shared Bozhidar S. IvanoviD· 1 shared Frank H. DeisiD· 1 shared Franziska SchanbacheriD· 1 shared Gernot PoschetiD· 1 shared Giorgia Del FaveroiD· 1 shared Hana NůskováiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperPharmacology & Toxicology

Alexander SonntagORCID

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2 papers

Recent·Most cited

Cancer BiologybioRxivPreprintApr 24, 2026

Disrupting linearity of PROTAC scaffolds prevents off-target complex I inhibition

Nick Richert, Hana Nůsková, Jana Samarin…·Aubry K. Miller

The paper identifies that linear PROTAC scaffolds inhibit mitochondrial complex I, leading to ATP depletion, and proposes structural modifications to mitigate this off-target effect.

DOI 10.64898/2026.02.13.702718

humanproteomics

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Pharmacology & ToxicologyChemical Research in ToxicologyPeer-reviewedJul 25, 2025

Aetokthonotoxin, the causative agent of vacuolar myelinopathy, uncouples oxidative phosphorylation due to protonophore activity

Valerie I. C. Rebhahn, Mohamad Saoud, Mathias Winterhalter…·Timo H. J. Niedermeyer

This study identifies Aetokthonotoxin as a protonophore that uncouples oxidative phosphorylation, leading to ATP depletion and neurotoxic effects in wildlife.

5 citations

experimental assayhost-pathogen & immune response

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