The information below summarizes an overview of the use of antineoplastons as treatments for people with cancer. Antineoplastons are experimental/cancer therapy developed by S.R.Burzynski, M.D, Ph.D. Chemically, antineoplastons are a mixture of amino acid derivates, peptides, and amino acids found in human blood and urine. Initially, antineoplastons were isolated from human blood and subsequently synthesized from commercially available chemicals at Burzynski Research Institute.

According to them, antineoplastons are a part of the body's biochemical surveillance system and work as 'molecular switches". For the developer, cell differentiation is the key to cancer therapy. At the molecular level, abnormal cells that are potential cancer cells need to be "switched" to normal code. Antineoplastons are the surveillance system that directs cancer cells into normal channels of differentiation. According to the developer's statements, people with cancer lack this surveillance system because they do not have an adequate supply of antineoplastons. The notion of controlling tumor growth through a naturally occurring biochemical mechanism in the body that directs cancer cells into normal channels of differentiation is one of the theoretical foundations of antineoplaston therapy.

In our bodies, cells are continuously differentiating and regenerating. Abnormal cell phenomenon usually occurs under the influence of carcinogenic factors from outside or inside bodies such as smoking, alcohol, drugs, medication, stress, and more. Our body must have a mechanism to deal with these abnormal cell growth, called apoptosis. The developer has given the body's proposed components that correct abnormal cells' differentiation problems and send them into normal pathways named "antineoplastons."

They define antineoplastons as "substances produced by the living organism that protect it against the development of neoplastic growth by a non-immunological process which does not significantly inhibit the growth of normal tissues.

A theoretical mechanism of action proposes that antineoplaston is specifically capable of intercalating with DNA at specific base pairs and thereby might interfere with carcinogens binding to the DNA helix. This interweaving may be capable of interfering with DNA replication, transcription, or translation. Antineoplastons have been proposed to bind to chromatin and relate to other anticancer drugs such as doxorubicin that interact directly with DNA. Two additional mechanisms of action have been proposed at the cellular level to explain tumor growth inhibition. One theory involves a component of some antineoplastons to compete with glutamine for access to the glutamine membrane transporter and may inhibit glutamine into the proteins of neoplastic cells.

Glutamine is essential for the cell cycle transition where DNA replication occurs; antineoplastons may arrest cell cycle progression and stop cell division. Another theory proposes that phenylacetic acid, also a component of several antineoplastons, inhibits methylation of nucleic acids in cancer cells. The hypomethylation of DNA in cancer cells may lead to terminal differentiation and tumor growth or progression prevention. In conclusion, all theory explains the prevention of tumor progression and tumor growth.