19
Views
0
CrossRef citations to date
0
Altmetric
Miscellaneous

Therapeutic potential of TNF-related apoptosis-inducing ligand receptor antibodies

Pages 1081-1086 | Published online: 02 Mar 2005
 

Abstract

TNF-related apoptosis-inducing ligand (TRAIL)/apoptosis-2 ligand (Apo-2L) is a member of the TNF superfamily and has recently been shown to induce apoptosis in transformed and cancer cells. In addition to the cytokine TRAIL, agonist antibodies that activate TRAIL receptors (TRAIL-R1/death receptor 4 [DR4]) and TRAIL-R2/DR5) can also induce apoptosis in receptorbearing cells. Such antibodies can be used in the prevention and treatment of human diseases such as cancer, neurodegenerative, immune and inflammatory disorders and infectious disease. In this patent, Human Genome Sciences presents antibodies and related molecules that immunospecifically bind to TRAIL receptors (TRAIL-R1/DR4 and TRAIL-R2/DR5). The invention also relates to nucleic acid molecules encoding anti-TRAIL receptor antibodies, vectors and host cells containing these nucleic acids and methods for producing the same. The use of TRAIL receptor antibody is very promising and will likely provide useful highly targeted therapeutics in the future. Recent patent activity suggests this is an active area of therapy in the pharmaceutical industry where major attention will be paid to the design, selection and formulation of a range of new antibody-based products.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.