J Korean Med Assoc.  2011 Nov;54(11):1191-1198.

Oral chemotherapeutic agents in current use

Affiliations
  • 1Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, Korea. mdnslee@schmc.ac.kr

Abstract

Currently, 10% of cancer chemotherapy is provided to patients by oral formulation; however, by 2013 this percentage is predicted to increase to 25%. Chemotherapy is traditionally given by injection. Oral chemotherapy has been developed as a more convenient method for treating patients. Oral chemotherapy offers many advantages including the elimination of pain often caused by injections, the lack of fees for administering intravenous drugs, more time at home for patients, and a patient's increased sense of autonomy. The role of oral chemotherapy has been expanding because of the potential advantages in convenience and better quality of life for patients, and in the cost-effectiveness of treatment as compared to intravenous chemotherapy. A number of novel oral targeted and cytotoxic chemotherapeutic agents are entering the market or are in development. Many of the agents display significant clinical activity against various cancers. The growing availability of effective oral chemotherapy treatments, especially the new class of 'targeted biologic therapies', is one of the wonderful recent advances in cancer care. This manuscript describes the progress of clinical development and efficacy of these newly developed chemotherapeutic agents.

Keyword

Neoplasms; Drug therapy; Oral administration

MeSH Terms

Administration, Oral
Fees and Charges
Humans
Quality of Life

Figure

  • Figure 1 Metabolism of capecitabine. 5'-DFCR, 5'-deoxy-5-fluorocytidine; dThdPase, thymidine phosphorylase; 5'-DFUR, 5'-deoxy-5-fluorouridine; 5-FU, 5-fluorouracil.

  • Figure 2 Mode of action of imatinib on BCR-ABL. ADP, adenosine diphosphate; ATP, adenosine triphosphate; P, phosphate.

  • Figure 3 ErbB2 cellular signaling pathways and lapatinib mechanism of action. PI3K, phosphatidylinositol 3-kinase; IGFIR, insulin-like growth factor receptor; EGFR, epidermal growth factor receptor; mTOR, mammalian target of rapamycin; PTEN, phosphatase and tensin homolog (From Vogel C, et al. Jpn J Clin Oncol 2010;40:999-1013, with permission from Oxford University Press) [14].

  • Figure 4 Mode of action of everolimus. PI3K, phosphatidylinositol 3-kinase; PTEN, phosphatase and tensin homolog; mTOR, mammalian target of rapamycin (From Atkins MB, et al. Nat Rev Drug Discov 2009;8:535-536, with permission from Nature) [19].


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