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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Modified-Release Drug Delivery Systems: Site-Targeted01:24

Modified-Release Drug Delivery Systems: Site-Targeted

Site-targeted drug delivery systems enhance therapeutic efficacy while minimizing systemic toxicity and treatment costs. Unlike conventional methods, these systems ensure precise drug delivery, improving bioavailability and reducing side effects. Targeted drug delivery is classified into three levels. First-order targeting directs drugs to the capillary beds of specific organs or tissues. Second-order targets specific cell types, such as tumor cells, using receptor-mediated interactions.
Targets for Drug Action: Overview01:26

Targets for Drug Action: Overview

Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...

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Related Experiment Video

Updated: Jun 10, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
09:29

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model

Published on: March 20, 2020

Beyond Target Occupancy in Triple-Negative Breast Cancer: A Medicinal Chemistry Perspective on Modality-Guided Design

Weikun Zeng1, Yihua Chen2, Nouri Neamati3

  • 1Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education; Yunnan Key Laboratory of Research & Development for Natural Products; School of Chemical Science and Technology; School of Pharmacy, Yunnan University, Kunming650091, China.

Journal of Medicinal Chemistry
|June 9, 2026
PubMed
Summary

Triple-negative breast cancer (TNBC) treatment is challenging due to its adaptive biology. New medicinal chemistry approaches are needed to match chemical modalities with specific TNBC vulnerabilities for durable network control.

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Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?
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Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?

Published on: June 13, 2014

Area of Science:

  • Oncology
  • Medicinal Chemistry
  • Cancer Biology

Background:

  • Triple-negative breast cancer (TNBC) poses significant treatment challenges, with conventional therapies rarely achieving durable responses.
  • The difficulty in treating TNBC stems from its adaptive network biology, which is not adequately addressed by reversible, single-target interventions.
  • Existing treatment strategies often fail to bridge the gap between TNBC's complex biology and the limited scope of current therapeutic interventions.

Purpose of the Study:

  • To reframe the medicinal chemistry challenge in TNBC treatment, focusing on matching chemical modalities to biological vulnerabilities.
  • To explore how understanding TNBC's adaptive network biology can inform the design of more effective therapeutic strategies.
  • To highlight the importance of chemical modality selection in achieving durable control over TNBC's complex biological networks.

Main Methods:

  • Discussion of TNBC vulnerabilities including metabolic coupling, epigenetic scaffold dependence, immune-stromal exclusion, and DNA damage response plasticity.
  • Exploration of targeted protein degradation, molecular glues, covalent inhibition, rational polypharmacology, and prodrug design as potential intervention modalities.
  • Analysis of key factors influencing therapeutic success, such as ternary-complex productivity, linker topology, and isoform selectivity.

Main Results:

  • Specific TNBC vulnerabilities suggest the utility of diverse chemical modalities beyond traditional occupancy-driven inhibition.
  • Factors like ternary-complex productivity, linker topology, and isoform selectivity are critical for durable therapeutic effects.
  • The choice of chemical modality is crucial for effectively intervening in TNBC's adaptive network biology.

Conclusions:

  • Biological vulnerability in TNBC dictates the design of therapeutic interventions.
  • Chemical modality selection is key to defining the logic of intervention for TNBC.
  • Achieving durable network control, rather than just target potency, defines successful TNBC treatment strategies.