GENTICEL’s proprietary vector platform, the recombinant Adenylate Cyclase protein vector (CyaA), on which we build our therapeutic HPV vaccines, has the potential to be used for a broad range of other vaccine applications.

Over the last decade, the Institut Pasteur and its collaborators have provided preclinical proof of concept for the use of CyaA in vaccines for:

• Viral diseases such as Lymphocytic Choriomeningitis Virus (LCMV) and HIV (Fayolle C. et al., 1996; Saron et al, 1997; Mascarell L. et al., 2005). The potency of some of these vaccine candidates has been demonstrated in non-human primates (Mascarell L. et al., 2006)
• Chronic bacterial diseases such as tuberculosis (Hervas-Stubbs S et al, 2006, Majlessi et al, 2006).
• Melanoma (Dadaglio et al, 2003).

Genticel has worked with the teams of Prof Claude Leclerc and Dr Daniel Ladant at the Institut Pasteur, demonstrating proof of concept for:

• HPV-induced cervical cancer (Préville et al., Cancer Research, 2005; Berraondo et al., Cancer Research, 2007).

Genticel has also provided preclinical POC in other cancer models, using human tumour antigens (BT PHARMA, unpublished data).

Based on these positive results, obtained in distinct diseases, the CyaA platform is an attractive option for new therapeutic vaccines applied to other indications, including:

• Chronic viral diseases such as HIV, HBV, HCV, EPV, CMV, Herpes simplex & Varicella zoster.
• Chronic bacterial diseases such as those caused by Mycobacterium tuberculosis, Chlamydia trachomatis and zoögnostic Chlamydophyla species.
• Other HPV-induced cancers besides cervical cancer such as other ano-genital cancers (vulva, vagina, anus, penis), and head and neck cancers (oral cavity, tonsil, pharynx, larynx), and possibly some breast adenocarcinoma’s. (IARC Monograph Working Group, 2007; Cogliano et al, 2005; Bouvard et al, 2009; Heng et al 2009)
• Other early-detectable or resectable pre-cancers (vulva, vagina, anus, penis, intraepithelial neoplasia of the oral cavity).
• Other diseases involving cellular dysfunction associated with the over-expression or accumulation of autologous proteins e.g. certain neurodegenerative diseases.