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I read the following on wikipedia:

There is, however, no agent known that can break down the most common AGE, glucosepane, which appears 10 to 1,000 times more common in human tissue than any other cross-linking AGE.

(AGEs are related to oxidative stress, aging and chronic diseases.)

I was wondering maybe the article is out of date, and there is a glucosepane cross-link breaker available. Do you know anything of that, or a current research which aims to find that?

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Unfortunately at this time, there are no known glucosepane breakers which can feasibly be used in a living organism. There is a small (very small) amount of research being done on the topic by Yale university in cooperation with the SENS foundation, but the focus is extremely early stage - nothing more than synthesis and detection of artifical glucosepane and precursors.

It is a rather frustrating situation, as there are very good arguments indicating glucosepane as an almost universal 'bad thing that should be fixed', and the molecule itself isn't particularly complicated. It seems that this would be a low effort/high reward research area.

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    $\begingroup$ Welcome to Bio SE and thanks for your interesting answer! Could you add some resources (web links, or preferably citations to articles) to this answer? $\endgroup$ – AliceD Jan 22 '15 at 2:40
  • $\begingroup$ I accepted the answer, because I have found nothing after a few days of search either. You should add references to your answer especially about the research on Yale university you mentioned. $\endgroup$ – inf3rno Jan 22 '15 at 22:37
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You may want to look at Chebulic Acid as a potential inhibitor of AGE cross linking AND a breaker of AGE cross-linking.

Review this article: http://biofoundations.org/?p=1004

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  • $\begingroup$ Thanks, it is interesting! :-) It is hard to find anything relevant, but according to this it is unlikely that CA breaks glucosepane. quora.com/… Ofc. there is still hope, I think we need more experiments. $\endgroup$ – inf3rno Mar 2 '16 at 23:09
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The problem is the glucosepane bond is very strong, hence the molecules which would break this bond need be necessarily toxic and damaging to other molecules in the body. Glucosepane breakers already exist, but they are too toxic, and perhaps all will necessarily be that way. All hope is not lost however. Other very effective medical drugs (like clot breaking agents) are extremely toxic although life saving if applied in a local fashion via angiography under controlled conditions. My hunch is that the same will need to be done for the known glucosepane breakers. Glucosepane is extracellular, so the problem is really to avoid liver and renal toxicity. Animal studies should concentrate on delivering known glucosepane breakers under special conditions of renal, liver, and cardiovascular and respiratory support and though hyper-hydration, hypothermia, ECMO, dialysis, metabolic blocking agents, etc, to limit systemic toxicities. It won't be easy, but it could be well worth the effort if such single shot therapies could be developed which might then have long lasting effects as glucosepane would take many years to decades to build up again.

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I came across this new research from Yale University:

We are currently in the process of evaluating the enzyme’s mechanisms of action and identifying other metabolites generated. This is the first demonstration that glucosepane can be broken down enzymatically.

http://diabetes.diabetesjournals.org/content/67/Supplement_1/1229-P

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  • $\begingroup$ The link is broken. Probably just server malfunction and they will restore later. $\endgroup$ – inf3rno Sep 28 '18 at 22:04

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