Drug Discovery · eve-bio
drug-target-activity
Interaction and potency measurements for 1,397 mostly FDA-approved small molecule drugs across three target classes.
What drug-target-activity is
This dataset provides experimental drug-target interaction and potency measurements produced by EvE Bio. It systematically profiles a compound library containing 1,397 small molecule drugs, primarily FDA-approved therapeutics, across nuclear receptors, 7-transmembrane receptors (7TMs, also known as G-protein coupled receptors), and protein kinases. Measurements are reported for all target-compound combinations, capturing both active interactions and inactive results.
Systematic profiling across broad target panels is essential for clarifying compound selectivity, identifying off-target mechanisms, and uncovering opportunities for drug repurposing. Because drug activity is sparse (typically around 1%), testing entire panels under consistent conditions enables researchers to identify true pharmacological hits while tracking assay artifacts and cytotoxicity.
Data updates are added every other month for newly screened targets. The dataset includes cell viability measurements alongside live-cell 7TM assays, flags for compound interference, and multiple identifiers for chemical entities and biological targets.
How it was made
Measurements are acquired using a two-phase quantitative screening workflow. In the initial screening phase, all compound and assay pairs are evaluated in two replicates across three concentrations. A rules-based progression algorithm selects active compounds to advance to the profiling phase, which employs an 11-point concentration curve spanning 10 pM to 10 μM. Potency is estimated from four-parameter logistic curve fits as pXC50 (the negative logarithm of the IC50 or EC50, where 5 is the lowest quantifiable value). Compounds that exhibit activity below the quantifiable potency threshold remain recorded as active but unquantified.
Assay modalities vary by target class. Nuclear receptors are assessed via cell-free time-resolved fluorescence energy transfer (TR-FRET) assays measuring co-activator/co-repressor recruitment or RXR heterodimerisation in agonist and antagonist modes. Protein kinases are evaluated in a binding mode using cell-free competitive binding assays on wild-type and mutant enzymes. 7TM receptors are screened in cell-based assays across both G-protein activation and β-arrestin2 recruitment pathways (using FRET or luminescence) in agonist and antagonist modes, complemented by cell viability assays matched by cell line and incubation period.
Key facts
- Curator
- EvE Bio
- Compound library size
- 1,397 compounds (primarily FDA-approved small molecules)
- Target classes
- Nuclear receptors (NRs), 7-transmembrane receptors (7TMs/GPCRs), and protein kinases (PKs)
- Screening concentration range
- 10 pM to 10 μM (11-point profiling phase)
- Assay technologies
- TR-FRET, FRET, and Luminescence
- Assay modes
- Agonist, Antagonist, Inhibition, and Binding
- Potency metric
- pXC50 (negative log of IC50 or EC50; minimum quantifiable value 5)
- Compound identifiers
- SMILES, InChIKey, CAS registry number, UNII, and DrugBank ID
- Target identifiers
- Gene name, UniProt ID, ChEMBL target ID, PubChem target ID, and Ensembl transcript names for isoforms
- File format
- Parquet
What you can use it for
- Drug repurposing analysis
- Identify secondary target activities and unexpected affinities for FDA-approved therapeutics across kinase, GPCR, and nuclear receptor panels.
- GPCR pathway bias evaluation
- Assess whether 7TM agonists preferentially drive signalling through G-protein pathways versus β-arrestin2 recruitment.
- Kinase mutant selectivity profiling
- Compare compound binding affinities across matched wild-type and mutant kinase variants using target wild-type linkers.
- Assay interference and cytotoxicity filtering
- Distinguish genuine GPCR antagonism from cell death using paired cell viability readouts, or model compound assay interference using hit-frequency flags.
Explore the data
This dataset is gated
Its authors require their terms to be accepted before the data can be read. Accept them on the original dataset page. The platform does not accept terms on your behalf, so the rows are not shown here.Strengths and limits
Good at
- Reports complete negative and positive experimental results for every compound-target combination, avoiding publication bias toward active hits.
- Evaluates 7TM receptors across both G-protein activation and β-arrestin2 pathways to give dual-pathway pharmacological coverage.
- Includes dedicated cell viability assays and interference flags to detect false positives caused by cytotoxicity or assay promiscuity.
Watch out for
- Full concentration-response curves are capped between 10 pM and 10 μM, leaving compounds with weak potency active but unquantified.
- Cell death can mimic GPCR antagonism in cell-based assays, requiring cross-referencing against cell viability controls to avoid false positives.
Questions
Can I look inside drug-target-activity without downloading it?
Not here: its authors gate it behind terms each user must accept on the original page. Its description and statistics are still shown.
What licence is drug-target-activity under?
Its authors declare cc-by-nc-sa-4.0. Read the terms on the original page before reusing the data.
What does pXC50 represent in this dataset?
pXC50 is the negative log of the half-maximal inhibitory concentration (IC50) or half-maximal effective concentration (EC50) determined by four-parameter logistic curve fitting. Higher numbers indicate higher potency, with 5 representing the lowest quantifiable potency within the tested range.
Why are some active compound results unquantified?
Compounds advance to an 11-point profiling phase spanning 10 pM to 10 μM only if they pass a rules-based screening threshold. If a compound shows activity but its potency is too weak to reach half-maximal response within the 10 μM ceiling, it is designated as active but lacks a quantified pXC50.
How should cell viability be factored into 7TM receptor analysis?
Because 7TM receptors are measured using live-cell assays, cytotoxic compounds can produce false-positive antagonism signals. Researchers should inspect the viability flag and link corresponding viability assay identifiers to verify whether cell killing explains observed receptor inhibition.
What is indicated by the frequency flag?
The frequency flag marks compounds that register as hits more than 20 times within a given target class, mechanism, and mode. These compounds may reflect promiscuous binders or non-specific assay interferers.
How to cite it
EvE Bio, LLC (2026). Data Releases #1-#14. https://huggingface.co/datasets/eve-bio/drug-target-activity. Accessed yyyy-mm-dd.
Written from drug-target-activity's own dataset card. Statements citing a figure that does not appear there are removed before publication. Licence and running details come from our registry.