DESIGNED FOR THE EYE

LUCENTIS is designed to have an effect where it matters and clear rapidly from the body

LUCENTIS is specifically designed as an antigen-binding fragment (Fab*) without an Fc region1

*The Fab region is the antigen-binding portion on the antibody.

The clinical significance of the molecular design of LUCENTIS is not established

Fabs lack an Fc region and are not subject to Fc receptor (FcRn) recycling upon entering systemic circulation2

  • FcRn recycling is part of the body’s immune response to retain antibodies3
  • Serum proteins that do not have an Fc region will be degraded in lysosomes

Adapted from Roopenian and Akilesh.3

IMPORTANT DOSING INFORMATION

  • The intravitreal injection procedure should be carried out under controlled aseptic conditions, which include the use of sterile gloves, a sterile drape, and a sterile eyelid speculum (or equivalent). Prior to and 30 minutes following the intravitreal injection, patients should be monitored for elevation in intraocular pressure using tonometry. Monitoring may also consist of a check for perfusion of the optic nerve head immediately after the injection. Patients should also be monitored for and instructed to report any symptoms suggestive of endophthalmitis without delay following the injection.

Based on preclinical studies, Fabs and Fc-containing molecules have demonstrated similar vitreous half-lives2

Adapted from Xu et al.2

Upon entering systemic circulation, LUCENTIS is eliminated with an estimated serum half-life on approximately 2 hours2

The clinical significance of the molecular design of LUCENTIS is not established

  • References:
  • 1. Ferrara N, Damico L, Shams N, Lowman H, Kim R. Development of ranibizumab, an anti–vascular endothelial growth factor antigen binding fragment, as therapy for neovascular age-related macular degeneration. Retina. 2006;26:859-870.
  • 2. Xu L, Lu T, Tuomi L, et al. Pharmacokinetics of ranibizumab in patients with neovascular age-related macular degeneration: a population approach. Invest Ophthalmol Vis Sci. 2013;54:1616-1624.
  • 3. Roopenian DC, Akilesh S. FcRn: the neonatal Fc receptor comes of age. Nat Rev Immunol. 2007;7:715-725.
  • 4. LUCENTIS package insert. South San Francisco, CA: Genentech, Inc; 2013.
  • 5. Chakravarthy U, Harding SP, Rogers CA, et al; IVAN Study Investigators. Ranibizumab versus bevacizumab to treat neovascular age-related macular degeneration: one-year findings from the IVAN randomized trial. Ophthalmology. 2012;119:1399-1411.
  • 6. Chen HX, Cleck JN. Adverse effects of anticancer agents that target the VEGF pathway. Nat Rev Clin Oncol. 2009;6:465-477.
  • 7. Carmeliet P, Jain RK. Molecular mechanisms and clinical applications of angiogenesis. Nature. 2011;473:298-307.
  • 8. Kamba T, Tam BYY, Hashizume H, et al. VEGF-dependent plasticity of fenestrated capillaries in the normal adult microvasculature. Am J Physiol Heart Circ Physiol. 2006;290:H560-H576.
  • 9. Wirostko B, Wong TY, Simó R. Vascular endothelial growth factor and diabetic complications. Prog Retin Eye Res. 2008;27:608-621.
  • 10. Devescovi V, Leonardi E, Ciapetti G, Cenni E. Growth factors in bone repair. Chir Organi Mov. 2008;92:161-168.