Angiogenesis inhibitors: a new class of drugs

Judah Folkman1

  • 1Harvard Medical School, Children's Hospital; Boston, Massachusetts 02115 USA. jadah.folkman@TCH.Harvard.edu

Cancer Biology & Therapy
|September 26, 2003
PubMed

Insights

Angiogenesis inhibitors are a novel drug class for cancer treatment. This chapter outlines key guidelines for antiangiogenic therapy, differing from conventional chemotherapy, for optimal use in research and clinical settings.

Area of Science:

  • Pharmacology
  • Oncology
  • Drug Development

Background:

  • Angiogenesis inhibitors represent a new class of therapeutic agents.
  • These drugs are increasingly utilized in cancer treatment, with many in clinical trials and some FDA-approved.
  • Their mechanisms differ significantly from traditional cytotoxic chemotherapies.

Purpose of the Study:

  • To compile and discuss significant guidelines for antiangiogenic therapy.
  • To provide a scientific basis for these guidelines.
  • To address the unique requirements for using angiogenesis inhibitors in animal models and human patients.

Main Methods:

  • Review and synthesis of existing literature on angiogenesis inhibitors.
  • Assembly of significant guidelines for antiangiogenic therapy.
  • Discussion of the scientific rationale underpinning these guidelines.

Main Results:

  • Identification of key differences in mechanism and application compared to cytotoxic drugs.
  • Compilation of essential guidelines for the effective use of antiangiogenic therapies.
  • Explanation of the scientific basis for recommended guidelines.

Conclusions:

  • Angiogenesis inhibitors require distinct guidelines for optimal application.
  • Understanding these guidelines is crucial for effective cancer treatment and research.
  • This chapter provides a foundational resource for researchers and clinicians utilizing antiangiogenic therapies.

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...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...