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Santaris Pharma presents positive preclinical data on SPC2996 at,the American Association for Cancer Research

>The protein Bcl-2, first identified in B-cell lymphoma/leukaemia cells from which its name derives, is one of a family of intracellular proteins regulating cell survival and cell death. Some types of cells in the body, for example blood cells, are programmed to die after a few weeks of life, in the case of blood cells to be replaced in the circulation by fresh cells produced in the bone marrow. This process of programmed cell death is known as apoptosis. Bcl-2 is an apoptosis suppressor protein, i.e. it extends the lifespan of the cell in the presence of normal apoptosis stimuli. The levels of Bcl-2 within the cell are frequently over-expressed in malignant cancers, and this is particularly the case in human chronic lymphocytic leukaemia and lymphoma where it acts to prolong the life of malignant white blood cells. Drugs which lower the concentration of Bcl-2 or inhibit its function may therefore have therapeutic benefit by inducing cancer cell death and removal without resorting to chemotherapy.

About SPC2966

SPC2996 is the first of a portfolio of novel experimental drugs blocking harmful gene expression being designed and developed by Santaris Pharma. The drug belongs to a new class of drugs called RNA Antagonists, proprietary to Santaris Pharma, based on the novel three-dimensional analogue of RNA known as Locked Nucleic Acid (LNA). The drug binds with high potency and specificity to the messenger RNA for Bcl-2 and destroys it within the cell, resulting in a reduction in Bcl-2 protein concentration. SPC2996 is an investigational product which has not yet been approved by any regulatory agency as effective or safe for patient use but the novel agent is currently being evaluated in international Phase I/II studies in human CLL in centres in Denmark, France, UK and the USA.

AACR Abstract

An Abstract of the work described in this release can be found on the American Association for Cancer Research (AACR) 2007 Annual Meeting database at th
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