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Antineoplastons (ANP) are naturally-occurring peptides and amino acid derivatives which are used to control the growth of cancer.

In 1967 Stanislaw Burzynski, M.D., Ph.D. began investigating the use of antineoplastons after noting significant peptide deficiencies in the blood of cancer patients as compared with a control group[1].

Burzynski initially derived antineoplastons from human blood. Since similar peptides had been isolated from urine, in 1970 Burzynski switched to urine as a cheaper source of antinoeplastons. Since 1980 he has been reproducing antineoplastons synthetically[2].

Since his initial discovery, Burzynski has isolated dozens of peptide fractions from urine, some of which have been found to be active against cancer with low toxicity.

The first active peptide fraction identified was called antineoplaston A-10 (3-phenylacetylamino-2,6-piperidinedione). From A-10, antineoplaston AS2-1, a 4:1 mixture of phenylacetate and phenylacetylglutamine, was derived [3]. The active ingredient of antineoplaston A10-I is phenylacetylglutamine [4]. Current research is being conducted using these compounds alone or in combination.

Burzynski Clinic and Research Institute

Today, Burzynski maintains corporate offices and operates a clinic in Houston, Texas where he treats patients with antineoplastons. At a nearby facility in Stafford, Texas he conducts research and manufactures the pharmaceutical ingredients used in the medications and other products that he produces.

Antineoplastons are being used in a line of skin care products and dietary supplements marketed by Aminocare, a division of the Burzynski Research Institute. FDA approval is currently being sought to sell an antineoplaston-derived dietary supplement designed to boost brain function.

Treatment with Antineoplastons

Patients receiving cancer treatment with antineoplastons must first qualify for one of the currently available clinical trials. In order to qualify for most of the trials, a patient must have first failed standard treatment for the condition being treated, or it must be a condition that is unlikely to respond to currently available therapy and for which no curative therapy exists.

Antineoplastons may be administered intravenously or orally. Patients who respond positively to initial treatment with intravenous antineoplastons sometimes transition to the oral form.

Treatment with antineoplastons can be very costly to patients without insurance coverage, exceeding $100,000 for the first year of intravenous treatment. Many insurance companies consider antineoplaston therapy to be investigational and unproven and will not cover the cost [5][6]

Proposed Mechanism of Action

Although the exact mechanism of action of antineoplastons is still not completely understood, there have been several discoveries that may explain their antitumor properties.

One of the factors that allows some cancers to grow out of control is the presence of abnormal enzymes, a byproduct of DNA methylation. In the presence of these enzymes, the normal life cycle of the cells is disrupted and they replicate continuously. Antineoplastons have been shown in the laboratory to inhibit these enzymes [7].

Recent studies have shown that inhibiting histone deacetylase (HDAC) promotes the activation of tumor suppressor genes p21 and p53. The active ingredient of antineoplaston AS2-1 and phenylbutyrate have been shown to be weak HDAC inhibitors[8].

In normal cells, RAS oncogenes express proteins that act as a switch to regulate cell growth. In about 30% of human cancers, RAS oncogenes contain abnormal mutations that cause proteins be overexpressed, giving rise to uncontrolled cell growth. Antineoplaston AS2-10 binds to the cells, preventing them from growing in response to the protein signals [9].

Burzynski explains that antineoplastons A10 and AS2-1 both work by inhibiting oncogenes, promoting apoptosis, and activating tumor suppressor genes [4].


  1. S.R. Burzynski, Antineoplastons: History of the Research (I)., Drugs Exp Clin Res. 1986;12 Suppl 1:1-9 PMID 3527634
  2. Ralph Moss (1996), The Cancer Industry ISBN 1881025098
  3. NCI Drug Dictionary, Definitions of antineoplastons A10 and AS2-1
  4. 4.0 4.1 S.R. Burzynski, The Proposed Mechanism of Antitumor Activity of Antineoplastons (ANPs) in High Grade Glioma Pathology (HBSG) Integrative Cancer Therapies 2006; 40-47
  5. Aetna Clinical Policy Bulletin, Antineoplaston Therapy and Sodium Phenylbutyrate
  6. Blue Cross/Blue Shield Medical Policy, Antineoplaston Therapy
  7. Ming C. Liau, S.R. Burzynski, Altered Methylation Complex Isozymes as Selective Targets for Cancer Chemotherapy, Drugs Exp Clin Res. 1986;12 Suppl 1:77-86. PMID 3743383
  8. Manfred Jung, Inhibitors of Histone Deacetylase as New Anticancer Agents], Curr Med Chem. 2001 Oct;8(12):1505-11 PMID 11562279
  9. Terri Mitchell, Unlocking the Mystery of Antineoplastons, Life Extension Magazine, May 2004

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