Aldophosphamide is a tautomer of the main active metabolite of the alkylating antineoplastic agent cyclophosphamide - the 4-hydroxycyclophosphamide. Some of the aldophosphamide is then intracellularly hydrolyzed by the enzyme phosphatase to the of the two directly cytotoxically active metabolites - phosphoramide mustard and acrolein - in the metabolic activation pathway of the cyclophosphamide. But most of the aldophosphamide undergoes metabolic inactivation, catalyzed by another enzyme, ALDH, which gives rise to carboxycyclophosphamide.
Aldophosphamide residue is a component in molecules of some new oxazaphosphorine anticancer drugs that are now underway in clinical and preclinical testing: the NSC 612567 (aldophosphamide perhydrothiazine) and NSC 613060 (aldophosphamide thiazolidine).
Affects one in three adults
Affecting about 35 percent of all adults in the United States according to the CDC, metabolic syndrome contributes to weight gain, by causing a state of internal starvation called metabolic starvation. This in turn leads to increases hunger, sugar cravings and increased portions leading to overeating and weight gain.
Cause and effect misunderstood
Since we traditionally thought that the portion control (which in turn was attributed wrongly to poor will power)is the cause of weight gain, rather than the effect of this metabolic starvation, all our traditional ideas about cause and effect of obesity were not only wrong but lead to the “blame the victim” attitude when it comes to obesity.
Secret of weight gain revealed
Secret of weight gain, and metabolic syndrome revealed - it has been recently proven that metabolic syndrome, and the weight gain itself are caused by a process called insulin resistance. Check your metabolic syndrome risk using the free Metabolic syndrome meter. Watch this amazing Ted Med video that reveals the secret of weight loss - Stop blaming the victim for obesity
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Search for other drug names not listed above Portions of content adapted from Wikipedias article on Aldophosphamide licensed under GNU FDL.
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