In addition to patents, we rely on trade secrets and know-how to develop and maintain our competitive position. Trade secrets and know-how can be difficult to protect. We seek to protect our proprietary processes, in part, by confidentiality agreements and invention assignment agreements with our employees, consultants, scientific advisors, contractors and commercial partners. These agreements are designed to protect our proprietary information. We also seek to preserve the integrity and confidentiality of our data, trade secrets and know-how by maintaining physical security of our premises and physical and electronic security of our information technology systems. While we have confidence in these individuals, organizations and systems, such agreements or security measures may be breached, and we may not have adequate remedies for any breach. In addition, our trade secrets may otherwise become known or be independently discovered by competitors or others.

Aramchol is a synthetic conjugate of cholic acid, or a type of bile acid, and arachidic acid, or a type of saturated fatty acid, both of which, in their non-synthetic forms, are naturally occurring. The conjugated molecule acts upon important metabolic pathways, reducing fat accumulation in the liver, improving fatty acid oxidation and regulating the transport of cholesterol. The ability of Aramchol to decrease liver fat content may also reduce the inflammation and fibrosis in the liver and the risk of cardiovascular complications associated with NASH. Pre-clinical studies suggest Aramchol effect on fibrosis is also direct via collagen production from human hepatic stellate cells. We believe that Aramchol’s ability to reduce liver fat and liver fibrosis and the safety profile observed to date will enable it to be a safe and effective treatment for all stages of NASH in patients who are overweight or obese and have pre diabetes or type II diabetes mellitus and prevent the hepatic complications associated therewith.

Certain distributions treated as dividends that are received by an individual U.S. Holder from a “qualified foreign corporation” may be classified as “qualified dividend income,” — which is generally taxed at the lower applicable long term capital gains rates provided certain holding period and other requirements are satisfied. A non-U.S. corporation (other than a PFIC for the taxable year in which the dividend is paid or the preceding taxable year) generally will be considered to be a qualified foreign corporation (i) if it is eligible for the benefits of a comprehensive tax treaty with the United States which the Secretary of Treasury of the United States determines is satisfactory for purposes of this provision and which includes an exchange of information program, or (ii) with respect to any dividend it pays on stock which is readily tradable on an established securities market in the United States. As discussed below under “Passive Foreign Investment Company,” we believe that we were not a PFIC for our 2018 taxable year. However, we do expect to be a PFIC for the 2019 taxable year. Because the PFIC determination is highly fact intensive, there can be no assurance that we will be a PFIC in 2019 or for any other taxable year. Our ordinary shares will generally be considered to be readily tradable on an established securities market in the United States if they are listed on the Nasdaq Capital Market, as we intend our ordinary shares will be. U.S. Holders should consult their own tax advisors regarding the availability of the lower rate for dividends paid with respect to our ordinary shares.

Ariad Pharmaceuticals Inc. (NasdaqGM: ARIA ) ARIAD is engaged in the discovery and development of breakthrough medicines to treat cancer by regulating cell signaling with small molecules. ARIAD is developing a comprehensive approach to patients with cancer that addresses the greatest medical need – aggressive and advanced-stage cancers for which current treatments are inadequate. ARIAD has a global partnership with Merck & Co., Inc. to develop and commercialize deforolimus, ARIAD’s lead cancer product candidate, which is in Phase 3 clinical development. ARIAD’s second oncology product candidate, oral AP24534, is a novel multi-targeted kinase inhibitor in Phase 1 clinical development in hematological cancers.

This seems like it’s not an actual problem(doesn’t cause real world issues) and is purely related to how they calculate the extra cancer burden. low level genotoxicity would be concerning for children or people of child bearing age, but it seems unlikely for someone to actually develop cancer from it if they take it for the last 15 years of life. Does the FDA factor in some latency in development of the cancer when the do the calculations?

drug product on the market. Other member states allow companies to fix their own prices for drug products, but monitor and control company profits. The downward pressure on health care costs in general, particularly prescription drugs, has become intense. As a result, increasingly high barriers are being erected to the entry of new products. In addition, in some countries, cross-border imports from low-priced markets exert competitive pressure that may reduce pricing within a country. Any country that has price controls or reimbursement limitations for drug products may not allow favorable reimbursement and pricing arrangements.

If we encounter difficulties enrolling patients in our clinical trials, our clinical development activities could be delayed or otherwise adversely affected.

I don’t think the brain of a naked mole rat is slower than the brain of a typical rat but the naked mole rat live for about 30 years while the typical rat live for 3 years.

That isn’t good, because N-nitrosoamines are definitely genotoxic, at least at high levels. We’re stepping off into a big toxicology argument at this point, because the genotoxicity of these things at lower levels is a matter for (heated) debate. It all depends on how the high-dose animal studies can be extrapolated down, how both high- and low-dose animal studies can be extrapolated to humans in general, and how to interpret human observational data (on, for example, the consumption of cured meats, which contain low levels of nitrosamines) in the presence of multiple other factors. Not least among these is the problem that some of the N-nitroso compounds are in foodstuffs themselves, while others are produced by gut bacteria. Everyone can agree, though, that large amounts of N-nitroso compounds are bad news, for some value of “large”. And everyone can agree that exposing yourself to such compounds for no reason at all is senseless.

W.Z. and N.L. made equal contributions in this study. W.Z. conceived the experimental plan, performed material preparation and all data analysis, and co-wrote the manuscript. N.L. performed the animal experiments, identification of cell characterizations and biomedical analysis, and wrote the draft manuscript. H.G.S. and B.Z. performed molecular experiments and the analysis. J.L., L.X.S. and H.Y.W. performed materials characterization. J.H.J. and P.K.C. conceived the experimental plan and finalized the manuscript. All authors reviewed and approved the final manuscript.

Regarding resveratrol, i don’t think it is the best candidate for sirtuin activation, it only activates sirtuin1 and it has a awful bioavailability (did they inject the mouse or did they feed them orally?) further more we see that there is other problems too like rapid metabolism and elimination.

        We currently engage third-party manufacturers to provide non-clinical services, as well as fill-finish and secondary package and labeling services, for clinical supplies for zilucoplan.