Antineoplaston

From Wikipedia, the free encyclopedia

Antineoplaston (ANP) is a name coined by Stanislaw Burzynski for a group of peptides, derivatives, and mixtures for which he claims anti-cancer activity. These compounds have been administered by Burzynski to cancer patients since 1976. The clinical efficacy of antineoplastons combinations for various diseases are the current subject of numerous FDA Phase II trials by Burzynski and his associates. Antineoplastons are manufactured at a facility in Stafford, Texas for investigational use by the Burzynski Clinic, a public company that trades as a penny stock on the OTC Bulletin Board (BZYR).

Contents

[edit] Background

In 1967 Stanislaw Burzynski began investigating the use of antineoplastons after noting significant peptide deficiencies in the blood of cancer patients as compared with a control group[1][1]. Burzynski first identified antineoplastons from human blood. Since similar peptides had been isolated from urine, in 1970 Burzynski initially purified urine as a bulk source of antinoeplastons. Since 1980 he has been reproducing his compounds synthetically.[2] Since his initial discovery, Burzynski has isolated dozens of peptide and derivatives, some of which have been reportedly 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 phenylacetic acid and phenylacetylglutamine, was derived [3]. The active ingredient of antineoplaston A10-I is phenylacetylglutamine [4].

Phenylacetic acid is a toxic compound that the body produces during normal metabolism. It is detoxified in the liver to phenylacetyl glutamine. The "antineoplaston A-10" compound is an isolation artifact resulting from heating the urine under acidic conditions. The "antineoplaston AS2-1" mixture is the result of an alkaline hydrolysis of "antineoplaston A-10". All compounds are widely available cheap chemicals.

[edit] Treatment

For legal reasons Burzynski currently sells his treatments only in the context of clinical trials. 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. Intravenous antineoplastons are administered continuously with a portable programmable pump that the patient carries on a shoulder strap in a canvas bag.

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 do not cover the cost.[5][6]

The "antineoplastons," natural peptides and metabolites, are not generally cytotoxic like many historical (and current) antineoplastic agents; rather the highest usage levels carry a very high sodium load that require careful attention to fluid and electrolyte balance.

[edit] Proposed mechanisms

Antineoplastons, being investigational drugs, have never been FDA approved as "safe and effective" in treating human cancer. Independent tests at at the National Cancer Institute have never been positive.[7] The Japanese National Cancer Institute has reported that antineoplastons did not work in their studies.[citation needed]

Burzynski suggests that antineoplastons A10 and AS2-1 both work by inhibiting oncogenes, promoting apoptosis, and activating tumor suppressor genes [4]. Several other mechanism of action have been proposed.

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 [8].

Recent studies have shown that inhibiting histone deacetylase (HDAC) promotes the activation of tumor suppressor genes p21 and p53. Phenylacetic acid contained in the AS2-1 mixture has been shown to be a weak HDAC inhibitor[9].

[edit] References

  1. ^ Burzynski SR (1986). "Antineoplastons: history of the research (I)". Drugs under experimental and clinical research 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. ^ a b 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. ^ Burzynski SR (1999). "Efficacy of antineoplastons A10 and AS2-1". Mayo Clin. Proc. 74 (6): 641–2. PMID 10377942. 
  8. ^ Liau MC, Burzynski SR (1986). "Altered methylation complex isozymes as selective targets for cancer chemotherapy". Drugs under experimental and clinical research 12 Suppl 1: 77–86. PMID 3743383. 
  9. ^ Jung M (2001). "Inhibitors of histone deacetylase as new anticancer agents". Curr. Med. Chem. 8 (12): 1505–11. PMID 11562279. 

[edit] External links

Languages