The mononitrate looks like this:
Thiamin pyrophosphate (TPP) is a coenzyme for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. The first two of these enzymes function in the metabolism of carbohydrates, while transketolase functions in the pentose phosphate pathway to synthesize NADPH and the pentose sugars deoxyribose and ribose. Systemic thiamin deficiency can lead to myriad problems including neurodegeneration, wasting, and death. Well known syndromes caused by lack of thiamin due to malnutrition or a diet high in thiaminase-rich foods include Wernicke-Korsakoff syndrome and beriberi, diseases also common in chronic abusers of alcohol.
Genetic diseases of thiamin transport are rare but serious. Thiamin Responsive Megaloblastic Anemia with diabetes mellitus and sensorineural deafness (TRMA) (http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=249270) is an autosomal recessive disorder caused by mutations in the gene SLC19A2 (http://www.ncbi.nlm.nih.gov:80/entrez/dispomim.cgi?id=603941), a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamin deficiency, suggesting redundancy in the thiamin transport system. This has led to the discovery of a second high affinity thiamin transporter, SLC19A3 (http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=606152).
Thiamin was first discovered Umetaro Suzuki in Japan when researching how rice bran cured patients of beriberi. He named it aberic acid.