Anti-VEGF

Anti-VEGF
Specialtyoncology

Anti–vascular endothelial growth factor therapy, also known as anti-VEGF (/vɛdʒˈɛf/) therapy or medication, is the use of medications that block vascular endothelial growth factor. This is done in the treatment of certain cancers and in age-related macular degeneration. They can involve monoclonal antibodies such as bevacizumab, antibody derivatives such as ranibizumab (Lucentis), or orally-available small molecules that inhibit the tyrosine kinases stimulated by VEGF: sunitinib, sorafenib, axitinib, and pazopanib (some of these therapies target VEGF receptors rather than the VEGFs).

Both antibody-based compounds and the first three orally available compounds are commercialized. The latter two, axitinib and pazopanib, are in clinical trials.[clarification needed]

Bergers and Hanahan concluded in 2008 that anti-VEGF drugs can show therapeutic efficacy in mouse models of cancer and in an increasing number of human cancers. But, "the benefits are at best transitory and are followed by a restoration of tumour growth and progression."[1]

Later studies into the consequences of VEGF inhibitor use have shown that, although they can reduce the growth of primary tumours, VEGF inhibitors can concomitantly promote invasiveness and metastasis of tumours.[2][3]

AZ2171 (cediranib), a multi-targeted tyrosine kinase inhibitor has been shown to have anti-edema effects by reducing the permeability and aiding in vascular normalization.[4]

A 2014 Cochrane Systematic Review studied the effectiveness of ranibizumab and pegaptanib, on patients who have macular edema caused by central retinal vein occlusion.[5] Participants in both treatment groups showed improvement in visual acuity measures and a reduction in macular edema symptoms over six months.[5]

  1. ^ Bergers G, Hanahan D (August 2008). "Modes of resistance to anti-angiogenic therapy". Nature Reviews. Cancer. 8 (8): 592–603. doi:10.1038/nrc2442. PMC 2874834. PMID 18650835.
  2. ^ Ebos JM, Lee CR, Cruz-Munoz W, Bjarnason GA, Christensen JG, Kerbel RS (March 2009). "Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis". Cancer Cell. 15 (3): 232–9. doi:10.1016/j.ccr.2009.01.021. PMC 4540346. PMID 19249681.
  3. ^ Pàez-Ribes M, Allen E, Hudock J, Takeda T, Okuyama H, Viñals F, Inoue M, Bergers G, Hanahan D, Casanovas O (March 2009). "Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis". Cancer Cell. 15 (3): 220–31. doi:10.1016/j.ccr.2009.01.027. PMC 2874829. PMID 19249680.
  4. ^ Ledermann JA, Embleton AC, Raja F, Perren TJ, Jayson GC, Rustin GJ, Kaye SB, Hirte H, Eisenhauer E, Vaughan M, Friedlander M, González-Martín A, Stark D, Clark E, Farrelly L, Swart AM, Cook A, Kaplan RS, Parmar MK (March 2016). "Cediranib in patients with relapsed platinum-sensitive ovarian cancer (ICON6): a randomised, double-blind, placebo-controlled phase 3 trial". Lancet. 387 (10023): 1066–1074. doi:10.1016/S0140-6736(15)01167-8. PMID 27025186.
  5. ^ a b Braithwaite T, Nanji AA, Lindsley K, Greenberg PB (May 2014). "Anti-vascular endothelial growth factor for macular oedema secondary to central retinal vein occlusion". The Cochrane Database of Systematic Reviews. 2014 (5): CD007325. doi:10.1002/14651858.CD007325.pub3. PMC 4292843. PMID 24788977.