Evidence map›Paper›PMID 21246315›Full record

ReviewThe AAPS journal2011

The pharmacokinetic/pharmacodynamic pipeline: translating anticancer drug pharmacology to the clinic.

Qingyu Zhou, James M Gallo

Abstract readReview
In one paragraph

Review in The AAPS journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Array of translational systems pharmacodynamic models of anti-cancer drugs.Journal of pharmacokinetics and pharmacodynamics · 2016
    Review
  9. Review
  10. Pharmacokinetics and Pharmacodynamics in Breast Cancer Animal Models.Methods in molecular biology (Clifton, N.J.) · 2016
    Article
  11. Article
  12. Article
  13. Non-invasive, real-time reporting drug release in vitro and in vivo.Chemical communications (Cambridge, England) · 2015
    Article
  14. Integrated PK-PD and agent-based modeling in oncology.Journal of pharmacokinetics and pharmacodynamics · 2015
    Review
  15. Translational PK-PD modeling in pain.Journal of pharmacokinetics and pharmacodynamics · 2013
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

2 authors.

Qingyu ZhouDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York 10029, USA.
James M Gallo

Funding

INTERACTIONS BETWEEN CYTOTOXIC AND ANTIANGIOGENIC DRUGSR01CA072937 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI GALLO, JAMES M. · 1998 to 2015
$2.3M
Development of Targeted Anticancer DrugsR01CA127963 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI GALLO, JAMES M. · 2008 to 2012
$2.0M
NCI NIH HHS CA072937NCI NIH HHS CA127963NCI NIH HHS CA127963-S1NCI NIH HHS R01 CA072937NCI NIH HHS R01 CA127963
6 · The paper itself

Abstract

Progress in an understanding of the genetic basis of cancer coupled to molecular pharmacology of potential new anticancer drugs calls for new approaches that are able to address key issues in the drug development process, including pharmacokinetic (PK) and pharmacodynamic (PD) relationships. The incorporation of predictive preclinical PK/PD models into rationally designed early-stage clinical trials offers a promising way to relieve a significant bottleneck in the drug discovery pipeline. The aim of the current review is to discuss some considerations for how quantitative PK and PD analyses for anticancer drugs may be conducted and integrated into a global translational effort, and the importance of examining drug disposition and dynamics in target tissues to support the development of preclinical PK/PD models that can be subsequently extrapolated to predict pharmacologic characteristics in patients. In this article, we describe three different physiologically based (PB) PK modeling approaches, i.e., the whole-body PBPK model, the hybrid PBPK model, and the two-pore model for macromolecules, as well as their applications. General conclusions are that greater effort should be made to generate more clinical data that could validate scaled preclinical PB-PK/PD tumor-based models and, thus, stimulate a framework for preclinical to clinical translation. Finally, given the innovative techniques to measure tissue drug concentrations and associated biomarkers of drug responses, development of predictive PK/PD models will become a standard approach for drug discovery and development.

Indexed as

Translational Research, BiomedicalAntineoplastic AgentsBiomarkersDrug DesignHumansModels, StatisticalNeoplasmsSystems BiologyAntineoplastic AgentsBiomarkers

Identifiers

PMID21246315
PMCPMC3032092

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.