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Angiogenesis (blood vessel growth), lymphangiogenesis (lymph system growth) are all intrinsically connected with lymphedema and share many of the same genes. We have several pages on both processes.

Pat O'Connor

May 23, 2008

Angiogenesis Inhibitors in the Treatment of Cancer

Angiogenesis means the formation of new blood vessels. Angiogenesis is a process controlled by certain chemicals produced in the body. These chemicals stimulate cells to repair damaged blood vessels or form new ones. Other chemicals, called angiogenesis inhibitors, signal the process to stop.

Angiogenesis plays an important role in the growth and spread of cancer. New blood vessels "feed" the cancer cells with oxygen and nutrients, allowing these cells to grow, invade nearby tissue, spread to other parts of the body, and form new colonies of cancer cells.

Because cancer cannot grow or spread without the formation of new blood vessels, scientists are trying to find ways to stop angiogenesis. They are studying natural and synthetic angiogenesis inhibitors, also called anti-angiogenesis agents, in the hope that these chemicals will prevent the growth of cancer by blocking the formation of new blood vessels. In animal studies, angiogenesis inhibitors have successfully stopped the formation of new blood vessels, causing the cancer to shrink and die.

Whether angiogenesis inhibitors will be effective against cancer in humans is not yet known. Various angiogenesis inhibitors are currently being evaluated in clinical trials (research studies in humans). These studies include patients with cancers of the breast, prostate, brain, pancreas, lung, stomach, ovary, and cervix; some leukemias and lymphomas; and AIDS-related Kaposi’s sarcoma. If the results of clinical trials show that angiogenesis inhibitors are both safe and effective in treating cancer in humans, these agents may be approved by the Food and Drug Administration (FDA) and made available for widespread use. The process of producing and testing angiogenesis inhibitors is likely to take several years.

Detailed information about ongoing clinical trials evaluating angiogenesis inhibitors and other promising new treatments is available from the Cancer Information Service (CIS) -

.The CIS, a national information and education network, is a free public service of the National Cancer Institute (NCI) , the Nation’s primary agency for cancer research. The CIS meets the information needs of patients, the public, and health professionals. The toll-free phone number is 1–800–4–CANCER (1–800–422–6237). For callers with TTY equipment, the number is 1–800–332–8615. The NCI’s Web site also provides a listing of NCI-sponsored clinical trials at on the Internet.

# # #

Sources of National Cancer Institute Information

Cancer Information Service
Toll-free: 1–800–4–CANCER (1–800–422–6237)
TTY (for deaf and hard of hearing callers): 1–800–332–8615
NCI Online
Use to reach NCI's Web site.
Cancer Information Specialists offer online assistance through the LiveHelp link on the NCI's Web site.



This page is intended as an overview of some of the active trials of antiangiogenesis agents. It is not a comprehensive summary of all of the clinical trials ongoing with drugs that inhibit angiogenesis. Therefore, there may be additional trials not represented here.

All of the studies listed here are drawn from NCI's clinical trials database. (See the user's guide for information on how to search the database yourself.) For more information about the NCI database and other matters related to cancer, call the NCI Cancer Information Service at 1-800-4-CANCER.

All sponsors and investigators with antiangiogenesis trials are invited to submit their trials to the NCI database so that they will be included in this table. See Questions and Answers about Submitting Trials to PDQ for further information and links to an electronic submission form and checklist.

Drugs that block matrix breakdown:
Drug List of Active Clinical Trials
BMS-275291 List of BMS-275291 trials

List of dalteparin trials


List of suramin trials

Drugs that inhibit endothelial cells directly:
Drug List of Active Clinical Trials
List of 2-ME trials
(Thalidomide Analog)

List of CC-5013 trials

Combretastatin A4 Phosphate

List of combretastatin A4 phosphate trials

(Protein Kinase C Beta Inhibitor)

List of LY317615 trials

Soy Isoflavone
(Genistein; Soy Protein Isolate)

List of soy isoflavone trials


List of thalidomide trials

Drugs that block activators of angiogenesis:
Drug List of Active Clinical Trials
(Neovastat™; GW786034)

List of AE-941 trials

Anti-VEGF Antibody
(Bevacizumab; Avastin™)
List of anti-VEGF antibody trials

List of interferon-alpha trials

PTK787/ZK 222584

List of PTK787/ZK 222584 trials


List of VEGF-Trap trials


List of ZD6474 trials

Drugs that inhibit endothelial-specific integrin/survival signaling:
Drug List of Active Clinical Trials
EMD 121974

List of EMD 121974 trials

Drugs with non-specific mechanism of action:
Drug List of Active Clinical Trials
List of CAI trials
List of celecoxib trials
Halofuginone Hydrobromide

List of halofuginone hydrobromide trials

Interleukin-12 List of interleukin-12 trials
llink no longer available


Fighting Cancer with Angiogenesis Inhibitors

Once a nest of cancer cells reaches a certain size (1–2 mm in diameter), it must develop a blood supply in order to grow larger. Diffusion is no longer adequate to supply the cells with oxygen and nutrients and to take away wastes.

Cancer cells (probably like all tissues) secrete substances that promote the formation of new blood vessels - a process called angiogenesis.

Over a dozen substances have been identified that promote angiogenesis. A few examples are: Curiously, some tumors also secrete substances that inhibit angiogenesis. This explains a clinical phenomenon that has been known for decades:

This phenomenon caused Dr. Judah Folkman of Children's Hospital and the Harvard Medical School in Boston to hypothesize that a large primary tumor secretes not only stimulators of its own angiogenesis but angiogenesis inhibitors that are released into the circulation and inhibit angiogenesis - and thus further growth - of any metastases of the primary tumor.

A number of inhibitors of angiogenesis have been discovered.


Angiostatin is a polypeptide of approximately 200 amino acids. It is produced by the cleavage of plasminogen, a plasma protein that is important for dissolving blood clots. Angiostatin binds to subunits of ATP synthase exposed at the surface of the cell embedded in the plasma membrane. (Before this recent discovery, ATP synthase was known only as a mitochondrial protein.)


Endostatin is a polypeptide of 184 amino acids. It is the globular domain found at the C-terminal of Type XVIII (18) collagen (a collagen found in blood vessels) cut off from the parent molecule.

Biological effects of angiostatin and endostatin in mice

In mice,

Other Angiogenesis Inhibitors

Epithelial cells express transmembrane proteins on their surface — called integrins — by which they anchor themselves to the extracellular matrix.

It turns out that the new blood vessels in tumors express a vascular integrin — designated alpha-v/beta-3 — that is not found on the old blood vessels of normal tissues.

Vitaxin®, a monoclonal antibody directed against the alpha-v/beta-3 vascular integrin, shrinks tumors in mice without harming them. In Phase II clinical trials in humans, Vitaxin has shown some promise in shrinking solid tumors without harmful side effects.

What does the future hold for angiogenesis inhibitors?

Although Phase II clinical trials of endostatin have begun (manufactured by recombinant DNA technology), there is some doubt whether any company is willing to invest in its continued development.

Phase I and Phase II trials are now complete for Vitaxin®, a humanized monoclonal antibody against the vascular integrin anb3 (see section above). It has shown some promise at shrinking solid tumors and only minor side effects.

Bevacizumab (Avastin®). This is a humanized monoclonal antibody that blocks the action of VEGF. Approved by the US FDA in February 2004 for the treatment of colorectal cancers.

Trials are also scheduled to begin on a synthetic ribozyme that blocks synthesis of the VEGF receptor.

These are only a few examples of the ~60 antiangiogenesis drugs now in clinical trials.



Angiogenesis is the medical term for the production of new blood vessels (from Greek angeion, a vessel), so an angiogenesis inhibitor is one that stops them forming. They’ve been studied in the laboratory for many years in the hope that one will be found that chokes off the blood supply to cancers in the body and so makes them shrink. A great advantage of such drugs is that they are likely to be much less toxic than the existing chemotherapy agents. The first drug to treat a cancer by this means has recently been approved by the US Food and Drug Administration. It is now suggested that they might also be useful in treating obesity, since the stores of fat in the body are served by active blood supplies. However, fears have been expressed that they might damage immune reactions in the body and they are a long way from being a practical therapy for this purpose.

The irony, says Li, is that many of us already take angiogenesis inhibitors every day without even knowing it, and they could be protecting us from cancer and keeping us thin into the bargain. A long list of dietary factors strongly inhibit blood vessel growth, among them resveratrol in red wine, as well as genistein in soya, catechins in green tea and brassinin in Chinese cabbage.

[New Scientist, 10 Apr. 2004]

Novartis ... Bayer, and Pfizer are among the big companies with angiogenesis inhibitors in final testing for colon, kidney, and gastrointestinal cancers, among others.

[Knight Ridder/Tribune Business News, 26 Feb. 2004]



Dr. Tobey J. MacDonald


Angiogenesis Inhibitors

Like all cells, cancer cells require a constant supply of nutrients and oxygen in order to grow and divide. Without an adequate blood supply tumors will not grow. Tumors produce factors that stimulate the formation of blood vessels to provide them with the food and oxygen they need. More details on this process.

The process of blood vessel formation is termed angiogenesis.This process is a very active area of research in cancer treatment for several reasons. 1. The treatments should have low toxicity. Angiogenesis occurs at high levels during fetal development, the menstrual cycle and in wound healing. The treatments might be expected to interfere with these processes but should not harm most normal dividing cells. 2.The treatments are not designed to directly attack the cancer cells. The targets of several of these treatments are normal processes controlled by normal cells (such as the cells that form blood vessels), not the tumor cells themselves. The high mutation rates of cancer cells that often render chemotherapy ineffective will not interfere with these drugs.

There are a couple of naturally occuring proteins that are being examined as potential treatments for different types of cancer. See the Current Research section for information about these experimental treatment options.

There are also three other approaches to the inhibition of angiogenesis:

  1. Matrix Metalloproteinases Inhibitors: The degradation of the extracellular matrix that surrounds all cells is an important process in the in the formation of new blood vessels. As described in detail in the subsection on metastasis, this process is also integral to the spread of tumor cells to distant locations in the body.Growing blood vessel cells secrete enzymes called matrix metalloproteinases (MMPs) that are able to digest the extracellular matrix and allow blood vessels to invade the area and supply the tumor with nutrients. Inhibition of this process is the target of several drugs.
    See the Current Research section for information on experimental treatments of this type.

  2. Endothelial Cell Inhibitors: Several different drugs are under investigation that inhibit angiogenesis by acting to prevent the growth or activities of the endothelial cells that form the blood vessels.
    See the Current Research section for information on experimental treatments of this type.

  3. Inhibitors of Angiogenesis Activation: The drugs in this class of angiogenesis inhibitors work by blocking the cascade of events that cause blood vessels to form. One drug is currently approved in this category: Avastin®
    See the Current Research section for information on experimental treatments of this type.

Current Research on Angiogenesis Inhibitors: Activation Inhibitors

This is a naturally occuring protein. It inhibits the production of the endothelial cell growth factors bFGF and VEGF, preventing the initiation of cell division and blood vessel formation. Anti-angiogenic effects of this drug as a cancer therapy are currently being investigated.

Anti-VEGF Antibody
This antibody binds to VEGF preventing it from interacting with its receptor on endothelial (blood vessel) cells.

One anti-VEGF antibody currently in trials is bevacizumab (Avastin™) by Genentech. In trials on colorectal cancer results have been promising and trials are ongoing for colorectal, kidney and breast cancers.


Angiogenesis Inhibitors: An Update - Can Iressa and Thalomid Rejuvenate the Angiogenesis Inhibitor Class?

Despite dozens of angiogenesis inhibitors being investigated in clinical trials, they have failed to live up to expectations and the class has suffered a number of high profile failures. However, there are several promising angiogenesis inhibitors in late stage development, in particular, AstraZeneca's Iressa and Celgene's Thalomid. This brief examines the key angiogenesis inhibitors, the problems encountered by the class and what pharmaceutical companies need to do to avoid these pitfalls.

Scope of this report
Research and analysis highlights

Angiogenesis inhibitors have been beset with problems. To date, only one agent has been approved in just one market. One of the main reasons for poor performance of the drug class has been poor clinical trial design. With increased understanding of the role of angiogenesis in cancer, these problems are generally avoidable and pharmaceutical companies can increase the chance of gaining approval for angiogenesis inhibitors by following Datamonitor's key recommendations.

Key reasons to read this report

Reference Code: BFHC0506


Inhibitors of angiogenesis

Marc A. Lafleur, Madeleine M. Handsley and Dylan R. Edwards

Author contact details

Table 1. Inhibitors of angiogenesis
Process inhibited Synthetic/exogenous inhibitors Endogenous inhibitors
EC proliferation or migration TNP470 (synthetic derivative of fumagillin, a product of the fungus Aspergillus fumigatus) (Ref. 272)
Squalamine (an aminosterol, originally isolated from the dogfish shark Squalus acanthias) (Ref. 273)
Captopril (inhibitor of angiotensin-I-converting enzyme) (Ref. 274)
Combretastatin-A4 (tubulin-binding agent) (Ref. 275)
Thrombospondin 1 (Ref. 276) IFN-a (Ref. 277)
Angiostatin (a fragment of plasminogen) (Ref. 278)
Endostatin (a fragment of collagen XVIII) (Ref. 279)
Arresten, canstatin and tumstatin (fragments of type IV collagen) (Refs 182, 280)

Propagation of angiogenic stimuli

Antibodies targeted to proteins involved in the angiogenic process (e.g.VEGF, VEGFR), or small peptides that interfere with receptor–ligand binding and signalling (e.g. SU5416 inhibits the tyrosine kinase activity of VEGFR-2) (Refs 38, 281) Inhibitors of gene expression (e.g. angiozyme, a ribozyme that selectively cleaves the mRNA for VEGFR-1) (Ref. 282) Platelet factor 4 (prevents binding of FGF-2 and VEGF to their corresponding receptors) (Ref. 283)
EC adhesion (through induction of apoptosis) Vitaxin (humanised monoclonal antibody against the integrin avb3 present on the surface of ‘activated’ ECs) (Ref. 284)
EMD121974 (a cyclic RGD-penta-peptide that binds av integrins) (Ref. 285)

Thrombospondin 1 (Ref. 276)
Canstatin and tumstatin (Refs 182, 280)

ECM proteolysis and EC invasion Synthetic MMP inhibitors: marimastat, AG-3340, COL-3 and neovastat (Refs 132, 236, 239, 286) TIMPs (Refs 130, 134, 140, 141, 142)
Arresten and canstatin (inhibit migration and tube formation) (Ref. 280)
Abbreviations: EC, endothelial cell; FGF, fibroblast growth factor; IFN, interferon; VEGF, vascular endothelial growth factor; TIMP, tissue inhibitor of metalloproteinases; VEGFR, VEGF receptor.

References cited in Table 1

38 Yancopoulos, G.D. et al. (2000) Vascular-specific growth factors and blood vessel formation. Nature 407, 242-248, PubMed

130 Anand-Apte, B. et al. (1997) Inhibition of angiogenesis by tissue inhibitor of metalloproteinase-3. Invest Ophthalmol Vis Sci 38, 817-823, PubMed

132 Shalinsky, D.R. et al. (1999) Broad antitumor and antiangiogenic activities of AG3340, a potent and selective MMP inhibitor undergoing advanced oncology clinical trials. Ann N Y Acad Sci 878, 236-270, PubMed

134 Li, H. et al. (2001) AdTIMP-2 inhibits tumor growth, angiogenesis, and metastasis, and prolongs survival in mice. Hum Gene Ther 12, 515-526, PubMed

140 Collen, A. et al. (2003) Membrane-type matrix metalloproteinase-mediated angiogenesis in a fibrin-collagen matrix. Blood 101, 1810-1817, PubMed

141 Lafleur, M.A. et al. (2002) Endothelial tubulogenesis within fibrin gels specifically requires the activity of membrane-type-matrix metalloproteinases (MT-MMPs). J Cell Sci 115, 3427-3438, PubMed

142 Ikenaka, Y. et al. (2003) Tissue inhibitor of metalloproteinases-1 (TIMP-1) inhibits tumor growth and angiogenesis in the TIMP-1 transgenic mouse model. Int J Cancer 105, 340-346, PubMed

182 Maeshima, Y. et al. (2002) Tumstatin, an endothelial cell-specific inhibitor of protein synthesis. Science 295, 140-143, PubMed

236 Drummond, A.H. et al. (1999) Preclinical and clinical studies of MMP inhibitors in cancer. Ann N Y Acad Sci 878, 228-235, PubMed

239 Coussens, L.M., Fingleton, B. and Matrisian, L.M. (2002) Matrix metalloproteinase inhibitors and cancer: trials and tribulations. Science 295, 2387-2392, PubMed

272 Yanase, T. et al. (1993) Inhibitory effect of angiogenesis inhibitor TNP-470 on tumor growth and metastasis of human cell lines in vitro and in vivo. Cancer Res 53, 2566-2570, PubMed

273 Sills, A.K., Jr. et al. (1998) Squalamine inhibits angiogenesis and solid tumor growth in vivo and perturbs embryonic vasculature. Cancer Res 58, 2784-2792, PubMed

274 Volpert, O.V. et al. (1996) Captopril inhibits angiogenesis and slows the growth of experimental tumors in rats. J Clin Invest 98, 671-679, PubMed

275 Griggs, J. et al. (2002) Inhibition of proliferative retinopathy by the anti-vascular agent combretastatin-A4. Am J Pathol 160, 1097-1103, PubMed

276 Sargiannidou, I., Zhou, J. and Tuszynski, G.P. (2001) The role of thrombospondin-1 in tumor progression. Exp Biol Med (Maywood) 226, 726-733, PubMed

277 Indraccolo, S. et al. (2002) Differential effects of angiostatin, endostatin and interferon-alpha(1) gene transfer on in vivo growth of human breast cancer cells. Gene Ther 9, 867-878, PubMed

278 O’Reilly, M.S. et al. (1996) Angiostatin induces and sustains dormancy of human primary tumors in mice. Nat Med 2, 689-692, PubMed

279 Colorado, P.C. et al. (2000) Anti-angiogenic cues from vascular basement membrane collagen. Cancer Res 60, 2520-2526, PubMed

280 Kamphaus, G.D. et al. (2000) Canstatin, a novel matrix-derived inhibitor of angiogenesis and tumor growth. J Biol Chem 275, 1209-1215, PubMed

281 Mendel, D.B. et al. (2000) The angiogenesis inhibitor SU5416 has long-lasting effects on vascular endothelial growth factor receptor phosphorylation and function. Clin Cancer Res 6, 4848-4858, PubMed

282 Sandberg, J.A. et al. (1999) Pharmacokinetics of an antiangiogenic ribozyme (ANGIOZYME) in the mouse. Antisense Nucleic Acid Drug Dev 9, 271-277, PubMed

283 Jouan, V. et al. (1999) Inhibition of in vitro angiogenesis by platelet factor-4-derived peptides and mechanism of action. Blood 94, 984-993, PubMed

284 Gutheil, J.C. et al. (2000) Targeted antiangiogenic therapy for cancer using Vitaxin: a humanized monoclonal antibody to the integrin alphavbeta3. Clin Cancer Res 6, 3056-3061, PubMed

285 Taga, T. et al. (2002) alpha v-Integrin antagonist EMD 121974 induces apoptosis in brain tumor cells growing on vitronectin and tenascin. Int J Cancer 98, 690-697, PubMed

286 Gingras, D. et al. (2003) Neovastat-a novel antiangiogenic drug for cancer therapy. Anticancer Drugs 14, 91-96, PubMed

Link no longer available


Angiogenesis Inhibitors - Information & News


Calvin J Kuo, MD, PhD

UpToDate performs a continuous review of over 330 journals and other resources. Updates are added as important new information is published. The literature review for version 12.3 is current through August 2004; this topic was last changed on March 24, 2004. The next version of UpToDate (13.1) will be released in February 2005.

INTRODUCTION — As the embryo develops, mesodermal precursors differentiate into endothelial cells and assemble into primitive vascular networks in a process called vasculogenesis. These networks undergo extensive budding and branching, and associate themselves with vascular smooth muscle elements in a process termed angiogenesis, thus yielding an extensive vasculature capable of responding to systemic as well as local tissue needs. The end result is that each cell is supported by a capillary network that enables it to receive necessary nutrients and oxygen, and export its cellular products (eg, hormones, vasoactive materials, metabolic waste products).

In the mature organism, the processes of vasculogenesis and angiogenesis are repeated during tissue repair (eg, wound healing) and overall growth of the organism. They are highly coordinated with hemostasis [1], as well as during certain specialized situations, such as during the menstrual cycle and implantation of the embryo during pregnancy. Alterations in normal or newly-formed vascular networks can also be associated with disease, as illustrated by the following situations:

  • Occlusion of blood vessels can result in tissue hypoxia and damage (eg, peripheral vascular disease, myocardial infarction, stroke, vasoocclusive crises of sickle cell disease).
  • Interference with the action of vascular endothelial growth factor and placental growth factor may play a central role in the placental hypoperfusion seen in preeclampsia. (See "Pathogenesis of preeclampsia", section on Systemic endothelial dysfunction).
  • Inappropriate growth of blood vessels plays a causative role in certain disorders (eg, diabetic retinopathy, macular degeneration). Furthermore, the induction of angiogenesis (neovascularization) is an important mechanism by which tumors promote their own continued growth and metastasis [2].

Because of the central role that angiogenesis plays in tumor growth, it represents an attractive therapeutic target for patients with cancer, particularly those with chemotherapy-resistant tumors. The general approaches for inhibiting angiogenesis in the treatment of malignancy will be discussed here. Applications of the many angiogenesis inhibitors now in clinical trials are discussed in more detail under the specific tumor being treated, including:

GENERAL REVIEW OF ANGIOGENESIS — Angiogenesis is a complex process that is under both positive and negative control [3-11]. Many, but not all of the growth factors that stimulate angiogenesis are heparin-binding. The biologic counterpart of this property is the ability to bind to the cell surface and extracellular matrix (ECM) heparan sulfates. Such binding typically stabilizes the growth factor, prolongs its tissue half-life, and may facilitate binding to specific high affinity receptors.

All growth factors are presumed to induce neovascularization by stimulation of endothelial cell proliferation and migration. Other contributory factors include stimulation of ECM breakdown, attraction of pericytes and macrophages, stimulation of smooth muscle cell proliferation and migration, formation and "sealing" of new vascular structures, and deposition of new matrix.


Nurse Directories on: The Nurse Friendly
Anti Angiogenesis, Angiogenesis Inhibitors,
Chemotherapy Research Links


Angiogenesis Inhibbitors for Cancer


PubMed Search Page for  Angiogenesis


Angiogenesis Inhibitors for Cancer


Local Delivery of Chitosan/VEGF siRNA Nanoplexes Reduces Angiogenesis and Growth of BreastCancer In Vivo. 

Jan. 2012


Cancer Drugs: Study Sheds Light On Angiogenesis Inhibitors, Points To Limitations, Solutions


Exosomes released by K562 chronic myeloid leukemia cells promote angiogenesis in a src-dependent fashion. 

Dec. 2011

Keywords  Exosomes – Nanotubes – Chronic myeloid leukemia – Endothelial cells – Tyrosine kinase inhibitors


Limitation of in vivo models investigating angiogenesis in breast cancer

Jan. 2011

Keywords Mesenchymal stem cells, tumor angiogenesis, breast cancer, migration, immunsystem


Lymphedema People Angiogenesis Related Pages:


Angiogenesis and Cancer

Angiogenesis and Cancer Control

Angiogenesis Inhibitors and Cancer


Lymphedema People Lymphangiogenesis Related Pages:

The Formation of Lymphatic Vessels and Its Importance in the Setting of Malignancy

Lymphangiogenesis Lymphedema and Cancer

Lymphangiogenesis and Gastric Cancer

Lymphangiogenesis in Head and Neck Cancer

Lymphangiogenesis and Kaposi's Sarcoma VEGF-C

Lymphangiogenesis in Wound Healing

A model for gene therapy of human hereditary lymphedema

VEGFR-3 Ligands and Lymphangiogenesis (1)

VEGFR-3 Ligands and Lymphangiogenesis (2)

VEGFR-3 Ligands and Lymphangiogenesis (3)

Vascular Endothelial Growth Factor; VEGF


VEGF-D is the strongest angiogenic and lymphangiogenic effector

Inhibition of Lymphatic Regeneration by VEGFR3

VEGFR3 and Metastasis in Prostate Cancer


Lymphedema People Genetics, Research, Lymphangiogenesis, Angiogenesis Forum


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