Major Technical Innovation in Drug And Tumour Modelling Results in Partial Vesting of Share Options
Oxford, UK 25th October 2005 Physiomics (AIM: PYC), a European systems biology simulation company, has developed a sophisticated addition to its core cell growth model showing why different cancer cells respond in different ways to an innovative new class of anti-cancer drugs. The simulation
work also shows how some time-consuming laboratory work to grow cancer cells could now be modelled quickly in a computer rather than taking significantly longer in a laboratory. The utility of 1.2 Physiomics’ computer simulation approach was discussed at the International Conference on
Systems Biology meeting in Boston, USA, 19 -21 October 2005.
The technical innovation shows, using Physiomics’ SystemCell® software, complex virtual cells “growing” in the computer to mimic the experimental behaviour of many cancer cells and their responses to drugs. This important development paves the way for realistic and predictive models of tumours’ drug responses. It also meets the criteria laid down by Physiomics’ Remuneration Committee on key technical criteria such that 25% of the unapproved options granted on 26 June 2005 are now available for exercise.
A better predictive system for testing cancer therapeutics is expected to be enormously valuable to pharmaceutical companies and could confer significant patient benefit through better treatment. Currently, only 5% of all cancer drugs that are tested in clinical trials are approved for patient use, half the industry norm 3. The new work on cell growth examines why small genetic differences between cancer cells mean that some die when treated whereas others survive and grow. This is not obvious from standard cell biology work, and it opens up the possibility of optimising treatment using appropriate drug combinations depending on patient profiles.
The data used to develop this model is from the scientific literature and focuses specifically on an aurora kinase inhibitor drug candidate, VX-680, developed by Vertex Pharmaceuticals Inc. and licensed to Merck & Co. Inc4. Published data on an aurora kinase inhibitor being developed by AstraZeneca has also been used. Aurora kinase inhibitors are a new type of therapeutic that has shown excellent cancer killing ability in preclinical studies. Some 16 aurora kinase inhibitors are under development by companies such as Astex Therapeutics Ltd, Chroma Therapeutics, Cyclacel Ltd, Millennium Pharmaceuticals Inc, Rigel Pharmaceuticals Inc and Serenex, in addition to Merck & Co and Vertex.
Physiomics believes that computer simulations could help to optimise the transition from preclinical to clinical development and help in the optimisation of dose scheduling, one of the major problems in clinical trials. Studies5 have shown that improving the drug development success rate by 10% overall could save $242m per drug. Physiomics and Bayer Technology Services collaborate on Clinical Response Prediction in the area of cancer.
“For the pharmaceutical industry the virtual approach could represent huge savings in time and money by predicting the effective drug dose and schedule for different cell types. This currently is done step by step in the laboratory, or in inflexible clinical trials.” said Dr John Savin, CEO of Physiomics. “Our technology is also very relevant for working out how best to use the new generation of targeted therapeutics and for reducing their clinical development risks.”
1) Cell Cycle Simulations for Examining the Effects of Drugs inhibiting Aurora Kinase According to Cancer Cell Phenotype, Chassagnole et al, Poster at ICSB 2005
2) Cell Cycle Lab: Using SystemCell® Technology for Multiple-Cell Simulations, Finney et al, Poster at ICSB 2005
3) Can the pharmaceutical industry reduce attrition rates? Kola, I. and Landis, J. Nature Reviews Drug Discovery, 3 (2004) 711-715
4) VX-680, a small molecule inhibitor of Aurora Kinases induces endoreplication and apoptosis preferentially in p53 and p21 deficient cells, Gizatullin, F,, et al, Poster LB-238 AACR Meeting 2004.
5) Tufts Center Impact Report 2002