Date: 2013-07-23
Type of information: Licensing agreement
Compound: VPM1002
Company: Serum Institute of India (India) Vakzine Projekt Management GmbH (Germany)
Therapeutic area: Infectious diseases
Type agreement: licensing
Action mechanism: VPM1002 is based on the Mycobacterium bovis (M.bovis) Bacille Calmette Guérin (BCG) strain. As BCG is not sufficiently effective to stop the spread of TB,2 modifications have been implemented in VPM1002 to improve its immunogenicity. First, a gene of Listeria monocytogenes (L.monocytogenes) coding for listeriolysin (Hly) has been integrated into the genome of BCG. This protein is responsible for the formation of pores in the phagosome after endocytotic uptake of the bacterium, enabling the bacterium to move into the cytosol. This principle was utilized in VPM1002. In contrast to BCG, which is trapped inside the phagosome and thus is conducted towards the MHC II pathway, VPM1002 moves from the phagosome via listeriolysin formed pores into the cytosol, ultimately leading to MHC I presentation of bacterium derived peptides. MHC I presentation and subsequent induction of CD8+ T cells resembles the natural mechanism of protection against M. tuberculosis, more closely and is thus believed to be the appropriate means for improving the induction of immunity. Second, BCG’s gene for urease C (ureC) has beeninactivated. Urease C catalyzes the hydrolysis of urea into carbon dioxide and ammonia, thus creating a basic environment. Its inactivation was necessary as aforementioned listeriolysin is optimally active under acidic conditions. Stefan Kaufmann, founding director of the Max Planck Institute for Infection Biology in Berlin, developed the scientific basis for VPM1002. VPM then developed the new vaccine after licensing it from the technology transfer organization Max Planck Innovation and with support from Helmholtz Centre for Infection Research basic science research, ultimately taking it to the clinical trial stage.
Disease: tuberculosis
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