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Effect on glucose/nucleic acid metabolism
One of the most characteristic features of cancer cell biochemistry is the use of glucose primarily for ribose synthesis, a key element of the nucleotides needed for DNA and RNA synthesis, whereas normal cells use glucose primarily for energy consumption processes. The key enzyme in this process is transketolase; changes in its activity have a regulating effect on cancer cell proliferation.
Avemar has a strong, specific and dose-dependent inhibitory effect on nucleotide/nucleic acid synthesis from glucose, forcing the cancer cells to use glucose for the synthesis of non-essential fatty acids and lipids as normal cells do.
As a result, the spread of malignant disease will be slowed or arrested and the performance status and global health of patients taking Avemar will be improved, leading also to an increase in body mass. While the majority of cytostatic drugs such as radiotherapy have a direct inhibitory effect on nucleic acid synthesis, Avemar has an indirect effect on it; this may explain the synergism between the anti-metastatic effect of Avemar and certain cytostatic drugs.
Avemar decreases the glucose uptake of tumour cells (thereby diminishing their proliferative potential) in a dose-dependent manner and, at the same time, alters the intracellular transformation of glucose. Its inhibition of ribose and deoxyribose synthesis also inhibits the production of messenger and ribosomal RNA, DNA replication and, at the same time, increases fatty acid synthesis. Avemar inhibits the activity of glucose 6 phosphate dehydrogenase and transketolase (the key enzyme in ribose synthesis). All of the above effects are tumor cell-specific: the metabolism of normal cells is not influenced unless the patient takes 50 times the recommended dosage.
Conclusions: Avemar has a very efficient effect on processes characteristic primarily of tumour cells, which helps to explain its tumour selectivity.
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