Heisenburger:
"...since Alagebrium has turned out to be a dead end and there’s pretty much nothing we can do about AGEs right now..."
Are we sure about that?
Chelation: A Fundamental Mechanism of Action of AGE Inhibitors, AGE Breakers, and Other Inhibitors of Diabetes Complications
...The original AGE breaker...alagebrium (ALT)-711...and recently described pyridinium analogs TRC4186 and TRC4149 ... were designed to cleave AGE cross-links in tissue proteins. As support for their mechanism of action, these compounds 1) released AGE albumin from preformed AGE-albumin-collagen complexes, 2) released immunoglobulins bound to red cells of diabetic rats, and 3) reversed or decreased collagen cross-linking in diabetic rats. Despite these observations, not a single AGE cross-link structure identified in tissue proteins to date...contains a dicarbonyl structure susceptible to the proposed mechanism of action of AGE breakers. Indeed, the proposed target of AGE breakers, dicarbonyl cross-links, would be reactive carbonyl compounds, which are unlikely to accumulate in protein...
...Despite the lack of evidence for their AGE-breaking activity, AGE breakers are potent chelators, and their hydrolysis products have even stronger chelating activity than the intact compounds (23) (Table 1)...
...Administration of triethylenetetramine for 6 months caused a significant ∼5% reversion of left ventricular mass toward normal...
http://www.ncbi.nlm....les/PMC3282805/
Perhaps the the much sought after AGE breaking solution has been right under our noses in the form of a combination of chelation therapies selected to simultaneously/synergistically? 'attack' the different types of AGEs?
I note that the Major Mouse Testing program plans to test age breakers...
http://www.majormouse.org/?q=node/57
I would add Chebulic Acid to the combinations of chelators tried:
Effects of Chebulic Acid on Advanced Glycation Endproducts-induced Collagen Cross-links
...Also, the breaking activity on collagen cross-links induced by glycol-BSA was potent with CA (IC50 = 1.46 ± 0.05 mM), exhibiting 50-fold stronger breaking activity than with ALT-711, a well-known cross-link breaker (IC50 = 72.2 ± 2.4 mM).
https://www.jstage.j...-00034/_article
Suppression of the onset and progression of collagen-induced arthritis by chebulagic acid screened from a natural product library.
...all clinical scores, serum levels of total and anticollagen IgG, and levels of interleukin-10 (IL-10) and IL-6 were reduced, while serum levels of transforming growth factor beta (TGFbeta) were markedly elevated. The number of granulocytes was reduced, but the proportion of CD4+,CD25+ T cells was greater in the knee joints of CHE-treated CIA mice. Expression of Foxp3 and TGFbeta messenger RNA was also augmented significantly in the knee joints of CHE-treated CIA mice in the therapeutic dosing model.
http://www.ncbi.nlm....pubmed/15641090
NB:
I assume the above study is referring to TGF-β3 and not TGF-β1 & TGF-β2 which you DON'T want elevated!
The other cause of increased TGF-β1 & 2 and TNF-α and (bad) NF-kB (= less telomerase = epigenetically older phenotype), is low level, chronic infection.
DRACO looks very promising, but Bavituximab is much closer to production.
Solutions available right now are ... 
Edited by Logic, 28 January 2016 - 07:24 PM.