There is no evidence to support the anticancer effects of antineoplastons in humans.
Antineoplastons are compounds that were first isolated from human urine and blood by Stanislaw Burzynski. He claims that they promote the body’s natural defenses against cancer. However, there is insufficient evidence to support this theory. Adverse reactions from antineoplaston treatment include confusion, sleepiness, and exacerbation of seizures, headache, vomiting, and fatigue.
Antineoplastons refer to mixtures of peptides, amino acids, and other organic substances that were first isolated from human urine and blood by Stanislaw Burzynski. He claims to have used antineoplastons to treat a variety of cancers based on the belief that they promote the body’s natural defenses against cancer.
In 1993, the National Cancer Institute sponsored clinical trials to investigate the antitumor potential of antineoplastons in patients with brain tumors (4). The trials were closed two years later as poor patient accrual precluded conclusions about the efficacy of the treatment. A Mayo clinic study found no benefit (1).
Antineoplastons have also been tested in patients with glioma (6)(7)(8), but the lack of a rigid scientific approach in these studies is being questioned (9).
Status of clinical trials using antineoplastons as investigational drugs for various cancers remains unknown (5).
Adverse reactions observed include confusion, sleepiness, and exacerbation of underlying seizures, headache, vomiting, and fatigue.
The proposed mechanisms for the anticancer activity of antineoplastons include activation of the tumor suppressor gene p53 by phenylacetate (PN) and AS2-1, metabolites of A10 (3-phenyl-acetylamino-2, 6-peperidinedione) (2). Phenylacetylglutamine (PG), the main component of A10-I, is thought to inhibit uptake of amino acids that are essential for cancer cell growth (2). A10 was shown in a study to inhibit neutrophil apoptosis in breast cancer cells. Since depletion of neutrophils is associated with development of cancer, researchers suggest a role for A10 as an adjuvant therapy for breast cancer (3).