The study is very new so I can’t get access to its full contents yet, but I wanted to post about it ASAP as it is one of the first studies in a major journal that specifically targets cancer’s redox nature – i.e. “cancer” cells are in a highly reduced state and administering pro-oxidant therapy (i.e. oxidizing agents or NAD+ precursors) is likely to be therapeutic. As my readers know quite well, quinone molecules are some of the most widely used for basic research and redox modulation, and the naphthoquinone family has been studied extensively specifically for cancer. Vitamin K and its analogs are napththoquinones that have been getting a lot of attention lately, culminating in the FDA approval of a cancer drug called Apatone (combination of vitamin K3 and vitamin C), which works exclusively through redox\/metabolic mechanisms. Well, the study below used just vitamin K3 specifically for its pro-oxidant effects and found that it greatly diminished prostate cancer growth. The mechanism of action was generic (i.e. redox state) and applicable to every cell, healthy or “cancerous” alike. The study had an in-vivo component, and since most prostate cancer mouse models are done with xenograft models (human tumor hosted by another organism), the findings of study suggests that the effects of vitamin K(3) are relevant for human cancer. Since I cannot get access to the full study, I don’t know what dose they used and for how long the administration lasted. However, most human studies with the closely-related vitamin K2 (MK-4) typically use 30mg-45mg for cancer, and there are already highly promising human cancer trials with vitamin K2 (MK-4). In fact, the rumor is that vitamin K2 (MK-4) may soon be approved as a prescription drug for preventing\/treating liver cancer, as well as various blood cancers (leukemias, lymphomas, etc). So, it looks like medicine is finally waking up from its “slumber” and recognizing that metabolism and redox state sit at the very core of “cancer” and should be primary targets for its treatment.<\/p>\n