|Industry||Pharmaceuticals, Life Sciences|
|Founders||Professor Claude Wischik
Dr K. M. Seng
|Number of locations||Singapore and Aberdeen, Scotland|
|Key people||Professor Claude Wischik, Executive Chairman
Dr Shay Way Seng, Managing Director
The company was co-founded in 2002 by the late gynecologist, surgeon and venture capitalist K. M. Seng and Claude Wischik, Professor of Old Age Psychiatry at the University of Aberdeen, Scotland, who is currently the company's Executive Chairman.
The company's protein aggregation inhibitors target the underlying pathology of dementia, with the aim of modifying or halting disease progression. Their lead compound, LMTX™, targets aggregation of tau and is believed to act on synuclein, TDP-43 and huntingtin protein. Its primary development in Alzheimer's disease is focused in its activity as a Tau Aggregation Inhibitor (TAI).
In 1988, while at Cambridge University, Wischik and coworkers discovered that abnormal fibres of tau protein form inside nerve cells in patients with Alzheimer's disease, and that their aggregation into tau tangles correlates to the development of dementia. In 1997, Wischik and his team moved to the University of Aberdeen, where they continued their pioneering research into tau pathology and protein aggregation inhibition. In 2002, the company was formed as a spin-out of the University of Aberdeen.
Rember - a first generation TAI - was used in Phase 2 clinical trials in Alzheimer's, with encouraging results announced by Wischik and colleagues in July 2008 at the Alzheimer's Association's International Conference on Alzheimer's Disease (ICAD 2008) in Chicago.
In the latter part of 2012, the company announced that it had initiated Phase 3 clinical trials with LMTXTM for mild and moderate Alzheimer's disease and behavioral variant FTD (bvFTD).
- Whalen, Jeanne (2012-11-09). "An outcast among peers gains traction on Alzheimer's cure". Wall Street Journal. Retrieved 2013-03-27.
- Marchione, Marilynn (2008-07-30). "Experimental Alzheimer's drug shows early promise". Associated Press. Retrieved 2008-07-31.
- Wischik CM, Edwards PC, Lai RYK, Roth M, Harrington CR (1996). "Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines.". Proc Natl Acad Sci USA 93. pp. 11213–11218. Retrieved 2012-10-01.
- Wischik CM, Lai RYK, Harrington CR. Modelling prion-like processing of tau protein in Alzheimer’s disease for pharmaceutical development. In: Brain Microtubule Associated Proteins: Modifications in Disease, eds. Avila J, Brandt R, Kosik KS. (1997) pp. 185-241. Amsterdam: Harwood Academic Publishers.
- Wischik CM, Wischik DJ, Storey JMD, Harrington CR. Rationale for tau-aggregation inhibitor therapy in Alzheimer's disease and other tauopathies. In: Emerging Drugs and Targets for Alzheimer's Disease. Volume 1: Beta-Amyloid, Tau Protein and Glucose Metabolism, ed. Martinez A. (2010) pp. 210-232. Cambridge: RSC Publishing.
- Taniguchi S, Suzuki N, Masuda M, Hisanaga S, Iwatsubo T, Goedert M, et al. (2005). "Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins.". J Biol Chem 280. pp. 7614–7623. Retrieved 2012-10-01.
- Wischik CM, Bentham P, Wischik DJ, Seng KM (2008). "Tau aggregation inhibitor (TAI) therapy with remberTM arrests disease progression in mild and moderate Alzheimer's disease over 50 weeks.". Alzheimer's and Dementia 4. p. T167. Retrieved 2012-10-01.
- Wilkinson, Emma (2006-07-29). "Alzheimer's drug 'halts' decline". BBC. Retrieved 2008-07-29.