Evidence map›Paper›PMID 42094496›Full record

ArticlebioRxiv : the preprint server for biology2026

DrugPTM-Bench: A Large-Scale Dataset for Predictive Modeling of Drug-Induced Cell Type-Specific Protein Post-Translational Modifications.

Amitesh Badkul, Mohammadsadeq Mottaqi, Li Xie, Lei Xie

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Amitesh BadkulComputer Science, The Graduate Center, CUNY, 365 Fifth Avenue, New York City, New York, USA.ORCID 0009-0000-9207-1954
Mohammadsadeq MottaqiBiochemistry, The Graduate Center, CUNY, 365 Fifth Avenue, New York City, New York, USA.ORCID 0000-0002-1398-7540
Li XieComputer Science, Hunter College, 695 Park Avenue, New York City, New York, USA.
Lei XieComputer Science, Hunter College, 695 Park Avenue, New York City, New York, USA.ORCID 0000-0001-9051-2111

Funding

Drug repurposing for Alzheimer's disease using structural systems pharmacology.R01AG057555 · NIA · NORTHEASTERN UNIVERSITY · PI Lei Xie · 2018 to 2026
$6.7M
Omics data integration and analysis for structure-based multi-target drug designR01GM122845 · NIGMS · NORTHEASTERN UNIVERSITY · PI Lei Xie · 2017 to 2026
$3.0M
AI-powered cross-level cross-species omics data integration to elucidate mechanisms of ELR21AG083302 · NIA · HUNTER COLLEGE · PI MELENDEZ, ALICIA, XIE, LEI · 2023 to 2023
$459k
NIA NIH HHS R01 AG057555NIA NIH HHS R21 AG083302NIGMS NIH HHS R01 GM122845
6 · The paper itself

Abstract

Protein post-translational modifications (PTMs), particularly phosphorylation, serve as the primary "molecular switches" that orchestrate cellular signaling and drug response. While PTM dysregulation is a hallmark of cancer and neurodegeneration, the lack of standardized, drug-perturbed datasets has hindered the development of predictive models capable of capturing context-dependent PTM responses. Effective predictive modeling must therefore integrate multidimensional data, including the specific drug, dosage, treatment duration, cellular background, and the modified site. However, existing PTM resources remain largely static and fail to capture drug-induced regulation across these critical dimensions. To address this gap, we present DrugPTM-Bench, a curated, large-scale benchmark derived from decryptM-derived dose-dependent PTM measurements, standardizing site-level drug response across 7 cancer cell lines, 27 drugs, and 11,167 proteins. Comprising 99.5% phosphorylation events, the dataset includes six time points, 16 dosage levels, and pEC50 potency values (half-maximal effective concentration). We formulate a classification task to identify upregulated, downregulated, or unchanged PTM sites (following a drug treatment), a critical step in deciphering drug Mechanism of Action (MoA) and target engagement. Our evaluation reveals that in protein-disjoint out-of-distribution (OOD) setting, baseline machine learning and deep learning models struggle to recover minority regulation classes, while standard rebalancing strategies improve recall only at the cost of precision and overall F1-score. These results indicate that current methods do not learn robust decision boundaries between regulated and unchanged PTM events. DrugPTM-Bench provides a phosphoproteomics benchmark for modeling drug-induced PTM regulation in imbalanced biological settings. Beyond classification, DrugPTM-Bench's retention of pEC50 values, drug perturbation profiles, and site-level sequence context enables additional predictive tasks including drug potency regression, mechanism-of-action prediction from PTM fingerprints, and drug-specific PTM site sensitivity ranking, establishing a multi-task benchmark for PTM-centric drug discovery. Ultimately, DrugPTM-Bench establishes a rigorous framework for developing robust, context-aware models to elucidate drug MoA and signaling dynamics.

Identifiers

PMID42094496
PMCPMC13142332

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.