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Area Under Curve

Pharmacology · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 6 min read

A statistical means of summarizing information from a series of measurements on one individual.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (1,069 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A statistical means of summarizing information from a series of measurements on one individual. It is frequently used in clinical pharmacology where the AUC from serum levels can be interpreted as the total uptake of whatever has been administered. As a plot of the concentration of a drug against time, after a single dose of medicine, producing a standard shape curve, it is a means of comparing the bioavailability of the same drug made by different companies. (From Winslade, Dictionary of Clinical Research, 1992)

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Area Under Curves; Curve, Area Under; Curves, Area Under; Under Curve, Area; Under Curves, Area; AUC.

Where it fits in the MeSH classification

Broader topics
Statistics as Topic; Pharmacokinetics

Research landscape

PubMed indexes 48,823 records tagged with the MeSH heading “Area Under Curve” (counts retrieved 2026-10-29). 8,351 of them (17.1%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 23,464 records.

Reviews account for 1,616 records (3.3%) and meta-analyses for 592. Randomized controlled trials number 7,791 (16.0%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.

PubMed records by publication periodthrough 1999: 2,136 records; 2000-2009: 14,872 records; 2010-2019: 23,464 records; 2020 onward: 8,351 records2,136through 199914,8722000-200923,4642010-20198,3512020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19992,136
2000-200914,872
2010-201923,464
2020 onward8,351
Share of records by publication typeReviews: 3.3 percent; Meta-analyses: 1.2 percent; Randomized controlled trials: 16.0 percentReviews3.3% (1,616)Meta-analyses1.2% (592)Randomized controlled trials16.0% (7,791)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 48,823 PubMed records
TypeRecordsShare
Reviews1,6163.3%
Meta-analyses5921.2%
Randomized controlled trials7,79116.0%

Method: PubMed query "Area Under Curve"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in pharmacology

Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Time-dependent ROC curve analysis in medical research: current methods and applications
Kamarudin AN, Cox T, Kolamunnage-Dona R
2017Research article
Design not recorded in structured metadata
652cc by
PMID 28388943 · DOI · PMC5384160
The genetic interpretation of area under the ROC curve in genomic profiling
Wray NR, Yang J, Goddard ME, Visscher PM
2010Research article
Design not recorded in structured metadata
280cc by
PMID 20195508 · DOI · PMC2829056
Area under precision-recall curves for weighted and unweighted data
Keilwagen J, Grosse I, Grau J
2014Research article
Design not recorded in structured metadata
125cc by
PMID 24651729 · DOI · PMC3961324
Sample size and power analysis for ROC AUC differences in diagnostic tests: a methodological evaluation of the Obuchowski-McClish and Hanley-McNeil methods
Emir B, Can FE, Kaymaz E, Ozel Z, Efgan MG, Tekindal MA, et al.
2026Research article
Design not recorded in structured metadata
7cc by
PMID 41606502 · DOI · PMC12924612

Time-dependent ROC curve analysis in medical research: current methods and applications [1]

Research article Kamarudin AN, Cox T, Kolamunnage-Dona R · · 2017 · cited 652 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundROC (receiver operating characteristic) curve analysis is well established for assessing how well a marker is capable of discriminating between individuals who experience disease onset and individuals who do not.
Closing excerpt
We have illustrated the methods in practice using currently available software and made some recommendations for future research.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (274 words)

BackgroundROC (receiver operating characteristic) curve analysis is well established for assessing how well a marker is capable of discriminating between individuals who experience disease onset and individuals who do not. The classical (standard) approach of ROC curve analysis considers event (disease) status and marker value for an individual as fixed over time, however in practice, both the disease status and marker value change over time. Individuals who are disease-free earlier may develop the disease later due to longer study follow-up, and also their marker value may change from baseline during follow-up. Thus, an ROC curve as a function of time is more appropriate. However, many researchers still use the standard ROC curve approach to determine the marker capability ignoring the time dependency of the disease status or the marker.MethodsWe comprehensively review currently proposed methodologies of time-dependent ROC curves which use single or longitudinal marker measurements, aiming to provide clarity in each methodology, identify software tools to carry out such analysis in practice and illustrate several applications of the methodology. We have also extended some methods to incorporate a longitudinal marker and illustrated the methodologies using a sequential dataset from the Mayo Clinic trial in primary biliary cirrhosis (PBC) of the liver.ResultsFrom our methodological review, we have identified 18 estimation methods of time-dependent ROC curve analyses for censored event times and three other methods can only deal with non-censored event times. Despite the considerable numbers of estimation methods, applications of the methodology in clinical studies are still lacking.ConclusionsThe value of time-dependent ROC curve methods has been re-established. We have illustrated the methods in practice using currently available software and made some recommendations for future research.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28388943 · DOI · PMC5384160

The genetic interpretation of area under the ROC curve in genomic profiling [2]

Research article Wray NR, Yang J, Goddard ME, Visscher PM · · 2010 · cited 280 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Genome-wide association studies in human populations have facilitated the creation of genomic profiles which combine the effects of many associated genetic variants to predict risk of disease.
Closing excerpt
We provide a strategy to estimate proportion of genetic variance explained on the liability scale from estimates of AUC, disease prevalence, and heritability (or sibling recurrence risk) available as an online calculator.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (244 words)

Genome-wide association studies in human populations have facilitated the creation of genomic profiles which combine the effects of many associated genetic variants to predict risk of disease. The area under the receiver operator characteristic (ROC) curve is a well established measure for determining the efficacy of tests in correctly classifying diseased and non-diseased individuals. We use quantitative genetics theory to provide insight into the genetic interpretation of the area under the ROC curve (AUC) when the test classifier is a predictor of genetic risk. Even when the proportion of genetic variance explained by the test is 100%, there is a maximum value for AUC that depends on the genetic epidemiology of the disease, i.e. either the sibling recurrence risk or heritability and disease prevalence. We derive an equation relating maximum AUC to heritability and disease prevalence. The expression can be reversed to calculate the proportion of genetic variance explained given AUC, disease prevalence, and heritability. We use published estimates of disease prevalence and sibling recurrence risk for 17 complex genetic diseases to calculate the proportion of genetic variance that a test must explain to achieve AUC = 0.75; this varied from 0.10 to 0.74. We provide a genetic interpretation of AUC for use with predictors of genetic risk based on genomic profiles. We provide a strategy to estimate proportion of genetic variance explained on the liability scale from estimates of AUC, disease prevalence, and heritability (or sibling recurrence risk) available as an online calculator.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20195508 · DOI · PMC2829056

Area under precision-recall curves for weighted and unweighted data [3]

Research article Keilwagen J, Grosse I, Grau J · · 2014 · cited 125 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Precision-recall curves are highly informative about the performance of binary classifiers, and the area under these curves is a popular scalar performance measure for comparing different classifiers.
Closing excerpt
We investigate accordances and differences of the proposed interpolation and previous ones, and we demonstrate that taking into account existing weights of test data is important for the comparison of classifiers.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)

Precision-recall curves are highly informative about the performance of binary classifiers, and the area under these curves is a popular scalar performance measure for comparing different classifiers. However, for many applications class labels are not provided with absolute certainty, but with some degree of confidence, often reflected by weights or soft labels assigned to data points. Computing the area under the precision-recall curve requires interpolating between adjacent supporting points, but previous interpolation schemes are not directly applicable to weighted data. Hence, even in cases where weights were available, they had to be neglected for assessing classifiers using precision-recall curves. Here, we propose an interpolation for precision-recall curves that can also be used for weighted data, and we derive conditions for classification scores yielding the maximum and minimum area under the precision-recall curve. We investigate accordances and differences of the proposed interpolation and previous ones, and we demonstrate that taking into account existing weights of test data is important for the comparison of classifiers.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24651729 · DOI · PMC3961324

Sample size and power analysis for ROC AUC differences in diagnostic tests: a methodological evaluation of the Obuchowski-McClish and Hanley-McNeil methods [4]

Research article Emir B, Can FE, Kaymaz E, Ozel Z, Efgan MG, Tekindal MA, et al. · · 2026 · cited 7 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BACKGROUND: Sample size determination for area under the curve (AUC) comparisons in diagnostic accuracy studies requires the consideration of multiple methodological parameters.
Closing excerpt
These results provide evidence-based guidance for efficient planning of diagnostic accuracy studies and underscore the critical importance of methodological considerations in study design optimization.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (388 words)

BACKGROUND: Sample size determination for area under the curve (AUC) comparisons in diagnostic accuracy studies requires the consideration of multiple methodological parameters. The type of diagnostic test, the nature of the data (discrete or continuous), the correlation structure between tests, and the degree of AUC differences all influence optimal study design and planning. To address these factors, this study provides comprehensive sample size and power calculations for comparing AUCs between diagnostic tests across clinically relevant scenarios. METHODS: We conducted a comprehensive evaluation of sample size and power analysis for AUC comparisons under varying correlation levels (ρ = 0.30, 0.50, 0.80), data types (discrete vs. continuous), and AUC differences (ΔAUC = 0.02–0.10). The Obuchowski–McClish method was applied for discrete data, and the Hanley–McNeil approach was applied for continuous data, assuming balanced case-control allocation and two-sided testing (α = 0.05). Sample sizes were calculated to achieve 80% statistical power based on established methodological approaches and adjusted for a 20% anticipated attrition rate. Power curves were generated to illustrate the relationship between sample size and statistical power across the evaluated scenarios. RESULTS: The required sample sizes varied substantially across scenarios, ranging from 36 − 3,709 participants per group to achieve 80% power. The degree of difference in the area under the curve (AUC) was the primary determinant: ΔAUC = 0.02 required 909-3,709 participants, whereas a ΔAUC = 0.10 required only 36–142 participants. Inter-test correlation also had a marked impact on efficiency, with a strong correlation (ρ = 0.8) reducing sample sizes by 49% in discrete models and 68% in continuous models compared with a weak correlation (ρ = 0.3). Continuous data models consistently outperformed discrete models, requiring 24–53% fewer participants across all the scenarios. The most demanding scenario (ΔAUC = 0.02, discrete data, ρ = 0.3) required 3,709 participants per group, whereas the most efficient scenario (ΔAUC = 0.10, continuous data, ρ = 0.8) required only 36 participants, representing a 103-fold difference. CONCLUSIONS: Methodological choices lead to substantial variations in sample size requirements for diagnostic accuracy studies. Optimal parameter selection, particularly the use of continuous data models and accounting for strong inter-test correlations, can reduce the required sample sizes by up to 68% compared with suboptimal combinations. These results provide evidence-based guidance for efficient planning of diagnostic accuracy studies and underscore the critical importance of methodological considerations in study design optimization.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41606502 · DOI · PMC12924612

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Drug-drug interactions for UDP-glucuronosyltransferase substrates: a pharmacokinetic explanation for typically observed low exposure (AUCi/AUC) ratios [5]
    Williams JA, Hyland R, Jones BC, Smith DA, Hurst S, Goosen TC, et al. · Drug Metab Dispos · 2004 · cited 618 times (Europe PMC)
  • Research article Application of fluoroquinolone pharmacodynamics [6]
    Wright DH, Brown GH, Peterson ML, Rotschafer JC · J Antimicrob Chemother · 2000 · cited 242 times (Europe PMC)
  • Research article Predicting death: an empirical evaluation of predictive tools for mortality [7]
    Siontis GC, Tzoulaki I, Ioannidis JP · Arch Intern Med · 2011 · cited 92 times (Europe PMC)
  • Research article Reappraisal of Contemporary Pharmacokinetic and Pharmacodynamic Principles for Informing Aminoglycoside Dosing [8]
    Bland CM, Pai MP, Lodise TP · Pharmacotherapy · 2018 · cited 75 times (Europe PMC)
  • Research article Mechanisms and Clinical Significance of Pharmacokinetic-Based Drug-Drug Interactions with Drugs Approved by the U.S. Food and Drug Administration in 2017 [9]
    Yu J, Petrie ID, Levy RH, Ragueneau-Majlessi I · Drug Metab Dispos · 2019 · cited 62 times (Europe PMC)
  • Research article Fluoroquinolone AUIC break points and the link to bacterial killing rates. Part 2: human trials [10]
    Schentag JJ, Meagher AK, Forrest A · Ann Pharmacother · 2003 · cited 54 times (Europe PMC)

References

  1. Kamarudin AN, Cox T, Kolamunnage-Dona R. Time-dependent ROC curve analysis in medical research: current methods and applications. . 2017. PMID 28388943 · DOI · PMC5384160
  2. Wray NR, Yang J, Goddard ME, Visscher PM. The genetic interpretation of area under the ROC curve in genomic profiling. . 2010. PMID 20195508 · DOI · PMC2829056
  3. Keilwagen J, Grosse I, Grau J. Area under precision-recall curves for weighted and unweighted data. . 2014. PMID 24651729 · DOI · PMC3961324
  4. Emir B, Can FE, Kaymaz E, Ozel Z, Efgan MG, Tekindal MA, et al.. Sample size and power analysis for ROC AUC differences in diagnostic tests: a methodological evaluation of the Obuchowski-McClish and Hanley-McNeil methods. . 2026. PMID 41606502 · DOI · PMC12924612
  5. Williams JA, Hyland R, Jones BC, Smith DA, Hurst S, Goosen TC, et al.. Drug-drug interactions for UDP-glucuronosyltransferase substrates: a pharmacokinetic explanation for typically observed low exposure (AUCi/AUC) ratios. Drug Metab Dispos. 2004. PMID 15304429 · DOI
  6. Wright DH, Brown GH, Peterson ML, Rotschafer JC. Application of fluoroquinolone pharmacodynamics. J Antimicrob Chemother. 2000. PMID 11062185 · DOI
  7. Siontis GC, Tzoulaki I, Ioannidis JP. Predicting death: an empirical evaluation of predictive tools for mortality. Arch Intern Med. 2011. PMID 21788535 · DOI
  8. Bland CM, Pai MP, Lodise TP. Reappraisal of Contemporary Pharmacokinetic and Pharmacodynamic Principles for Informing Aminoglycoside Dosing. Pharmacotherapy. 2018. PMID 30403305 · DOI
  9. Yu J, Petrie ID, Levy RH, Ragueneau-Majlessi I. Mechanisms and Clinical Significance of Pharmacokinetic-Based Drug-Drug Interactions with Drugs Approved by the U.S. Food and Drug Administration in 2017. Drug Metab Dispos. 2019. PMID 30442649 · DOI
  10. Schentag JJ, Meagher AK, Forrest A. Fluoroquinolone AUIC break points and the link to bacterial killing rates. Part 2: human trials. Ann Pharmacother. 2003. PMID 14519053 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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Related research topics

  • ROC CurveClinical Research
  • Cardiometabolic Risk FactorsClinical Research
  • Cluster AnalysisClinical Research
  • Confidence IntervalsClinical Research
  • Discriminant AnalysisClinical Research
  • Disease-Free SurvivalClinical Research

All 99 articles in Pharmacology →

At a glance

48,823
PubMed records on this heading
17%
published since 2020
1,616
review articles
7,791
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • ROC CurveClinical Research
  • Cardiometabolic Risk FactorsClinical Research
  • Cluster AnalysisClinical Research
  • Confidence IntervalsClinical Research
  • Discriminant AnalysisClinical Research

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