Hydroxyurea is a drug that inhibits the synthesis of DNA and so is classified as an antimetabolite. Hydroxyurea is used to treat a number of diseases, including chronic myeloid leukemia (CML), polycythemia vera, carcinoma of the head and neck, ovary, and cervix, melanoma, and sickle cell disease. Hydroxyurea is used to treat melanoma (a type of skin cancer), chronic myelocytic leukemia (CML), cancer of the ovary, and primary squamous cell (skin) cancer of the head and neck. Hydroxyurea is also used in the treatment of sickle cell anemia.
Hydroxyurea is a chemically simple antimetabolite that inhibits the enzyme ribonucleotide reductase. It has been in clinical use since the 1960s and is widely used for the treatment of severe sickle-cell disease, chronic myeloid leukaemia, myeloproliferative disorders such as polycythaemia vera and essential thrombocythaemia and, increasingly, in combination with didanosine in HIV infection. Hydroxyurea is sometimes used for the treatment of psoriasis and various solid tumours.
Hydroxyurea blocks an enzyme produced by human cells. This enzyme makes building blocks used by cells that are multiplying. Cancer cells multiply very quickly, so when hydroxyurea blocks this enzyme, the cancer grows more slowly. These building blocks are also used by HIV when it multiplies. Some of the drugs used against HIV (the nucleoside analog reverse transcriptase inhibitors) are "fake" versions of these same building blocks. When HIV uses the fake materials, it can't multiply. When hydroxyurea reduces the amount of "real" building blocks, then HIV is forced to use more of the "fake" versions: the anti-HIV drugs. Even though hydroxyurea does not attack HIV directly, it can make some anti-HIV drugs work better. Hydroxyurea works very well with the drugs ddI and d4T. Researchers are studying how Hydroxyurea works with other anti-HIV drugs.
Hydroxyurea is converted to a free radical nitroxide. In psoriasis, it is thought to work by reducing the replication of DNA within the basal cell of the epidermis. A response is noted in about half of treated patients, sometimes in those resistant to other therapies such as methotrexate, acitretin or phototherapy. Improvement usually begins about two weeks after starting treatment, and is maximum after about eight weeks.