|Industry||Pharmaceuticals, Life Sciences|
|Founder||Professor Claude Wischik|
Dr K. M. Seng
Number of locations
|Singapore and Aberdeen, Scotland|
|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 research into tau pathology and protein aggregation inhibition. In 2002, the company was formed as a spin-out of the University of Aberdeen.
Methylthioninium chloride – a first generation tau aggregation inhibitor (TAI) was used in Phase 2 clinical trials in Alzheimer's. The Phase 2 compared 3 dosages of methylthioninium chloride).
In 2012, Phase 3 clinical trials were starting with leucomethylthioninium salts (LMTX) for mild and moderate Alzheimer's disease and behavioral variant FTD (bvFTD).
LMTX is a stable anhydrous reduced form of methylthioninium chloride.:fig 1A (Chloride is replaced by bromide or methanesulfonate.) One of these is undergoing a phase 3 clinical trial for safety and efficacy in mild AD as "TRx0237". The results of the trial were released in July 2016. As a whole, patients who participated in the trial did not show significant benefits from receiving the LMTX.
TauRx has presented a post-hoc subgroup analysis suggesting that a small group of patients in the trial, who were taking only LMTX without any other Alzheimer's medication, did show significant improvement. However, this characterization of the secondary analysis results has been challenged on statistical grounds, and based on the fact that an inappropriate placebo group was used in the comparison.
- Whalen, Jeanne (2012-11-09). "An outcast among peers gains traction on Alzheimer's cure". Wall Street Journal. Retrieved 2013-03-27. CS1 maint: discouraged parameter (link)
- Marchione, Marilynn (2008-07-30). "Experimental Alzheimer's drug shows early promise". Associated Press. Retrieved 2008-07-31. CS1 maint: discouraged parameter (link)[permanent dead link]
- Wischik CM, Edwards PC, Lai RY, Roth M, Harrington CR (October 1996). "Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines". Proceedings of the National Academy of Sciences of the United States of America. 93 (20): 11213–8. doi:10.1073/pnas.93.20.11213. PMC 38310. PMID 8855335.
- Wischik CM, Lai RY, Harrington CR (1997). "Modelling prion-like processing of tau protein in Alzheimer's disease for pharmaceutical development". In Brandt R, Avila J, Kosik KS (eds.). Brain Microtubule Associated Proteins: Modifications in Disease. Amsterdam: Harwood Acad. Publ. pp. 185–241. ISBN 978-90-5702-173-2.
- Wischik CM, Wischik DJ, Storey JM, Harrington CR (2010). "Beta-Amyloid, Tau Protein and Glucose Metabolism". In Martinez A (ed.). Emerging Drugs and Targets for Alzheimer's Disease. 1. Cambridge: Royal Society of Chemistry. pp. 210–232. ISBN 978-1-84973-064-8.
- Taniguchi S, Suzuki N, Masuda M, Hisanaga S, Iwatsubo T, Goedert M, Hasegawa M (March 2005). "Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins". The Journal of Biological Chemistry. 280 (9): 7614–23. doi:10.1074/jbc.M408714200. PMID 15611092.
- Wischik CM, Bentham P, Wischik DJ, Seng KM (2008). "Tau aggregation inhibitor (TAI) therapy slows disease progression in mild and moderate Alzheimer's disease over 50 weeks". Alzheimer's and Dementia. 4: T167. doi:10.1016/j.jalz.2008.05.438. Retrieved 2012-10-01. CS1 maint: discouraged parameter (link)
- Wilkinson, Emma (2006-07-29). "Alzheimer's drug 'halts' decline". BBC. Retrieved 2008-07-29. CS1 maint: discouraged parameter (link)
- Wischik CM, Staff RT, Wischik DJ, Bentham P, Murray AD, Storey JM, Kook KA, Harrington CR (2015). "Tau aggregation inhibitor therapy: an exploratory phase 2 study in mild or moderate Alzheimer's disease". Journal of Alzheimer's Disease. 44 (2): 705–20. doi:10.3233/JAD-142874. PMID 25550228.
- Complex Disposition of Methylthioninium Redox Forms Determines Efficacy in Tau Aggregation Inhibitor Therapy for Alzheimer’s Disease
- "Safety and efficacy study evaluating TRx0237 in subjects with mild Alzheimer's disease". ClinicalTrials.gov. 2 November 2015. Retrieved 2 November 2015. CS1 maint: discouraged parameter (link)
- Coghlan, Andy (28 July 2016). "Alzheimer's drug that failed trial may still slow disease". New Scientist. Retrieved 29 July 2016.
- Fagan, Tom (29 July 2016). "In First Phase 3 Trial, the Tau Drug LMTM Did Not Work. Period". Alzforum. Retrieved 31 July 2016.