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Sorry, but this is rubbish Floretin. We are not talking about slowing aging. Certainly that is what many current interventions do. But we are looking to epigenetic reprogramming, telomere lengthening, senescent cell removal, etc, which we have on the horizon now. These are all rejuvenating treatments because they are rewinding the clock or removing damage that has accumulated through the action of our metabolism over the years. These treatments will in some sense reverse aging and leave you in a younger state than your were before. You will likely continue to age from that point, but from a younger starting point, hence extending your life. This is well established by numerous papers, many of Josh’s blog posts, and our previous discussions. Your perception of time will not change, as your brain will be a young brain, so you woukd not have issues keeping up with change, as old people do now, although your perspective will be that of a person who has been alive longer than your appearance would suggest. This, I imagine will lead to a wiser, more humane world.

The Company’s financial assets are measured at fair value on a recurring basis by level within the fair value hierarchy. All of the Company’s marketable securities are classified as Level 1. Other than the marketable debt securities, the Company doesn’t have any other financial assets or financial liabilities marked to market at fair value.

        For the purposes of accelerated approval, a surrogate endpoint is a marker, such as a laboratory measurement, radiographic image, physical sign, or other measure that is thought to predict clinical benefit but is not itself a measure of clinical benefit. Surrogate endpoints can often be measured more easily or more rapidly than clinical endpoints. An intermediate clinical endpoint is a measurement of a therapeutic effect that is considered reasonably likely to predict the clinical benefit of a product, such as an effect on IMM. The FDA has limited experience with accelerated approvals based on intermediate clinical endpoints but has indicated that such endpoints generally may support accelerated approval where the therapeutic effect measured by the endpoint is not itself a clinical benefit and basis for traditional approval, if there is a basis for concluding that the therapeutic effect is reasonably likely to predict the ultimate clinical benefit of a product.

This makes sense Paul, i am all in for inhibiting mTOR in a intermittent fashion. I was merely pointing out that based on the study we see:

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Shiraishi, T., Hiraiwa, M. & Uda, Y. Effects of cyclodextrins on the hydrolysis of ganglioside GM1 by acid beta-galactosidases. Glycoconj J 10, 170–4 (1993).

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During early times, laboratories had to make their own PLG polymers and monomers. These polymers, especially polymers with high glycolide content (e.g., 50:50 lactide:glycolide polymers) had solubility challenges due to their long glycolide blocks. Also, polymer solubility varied from batch to batch, making it difficult to perform robust formulation processing and achieve reproducible drug-delivery performance from microparticles and implants. Resomer polymers offer more consistent properties with better and reproducible solubility. 

        The terms of the Merck Agreement contain multiple promised goods and services, which include licenses, research and development activities and participation on the joint steering committee. Payments under the agreement include: (i) an upfront nonrefundable license fee; (ii) payments for research and development services performed by us, including reimbursement for certain lab supplies and reagents; (iii) payments based upon the achievement of certain development (pre-clinical and clinical), regulatory and commercial milestones; and (iv) royalties on net product sales, if any.

Our operating loss for the year ended December 31, 2017 was approximately $12.4 million, representing a decrease in our operating loss of approximately $4.5 million, or approximately 27%, compared to approximately $16.9 million for the year ended December 31, 2016.

One-millimeter ring segments of the mesenteric artery were dissected and mounted in individual organ chambers filled with Krebs buffer (composition in mM: NaCl 118, KCl 4.75, NaHCO3 25, MgSO4 1.2, CaCl2 2, KH2PO4 1.2, glucose 11). The Krebs solution was continuously gassed with a 95% O2 and 5% CO2 mixture and kept at 37 °C. Rings were stretched to 2 g of resting tension by means of two L-shaped stainless-steel wires, which were inserted into the lumen and attached to the chamber and to an isometric force-displacement transducer, as previously described50. Rings were equilibrated for 60 to 90 min, and during this period, tissues were restretched and washed every 30 min with warm Krebs solution. Endothelial-dependent relaxation were assessed in response to increasing doses of acetylcholine (ACh) endothelium-dependent, after precontracted by 10−6 M phenylephrine. To evaluate the formation of basal NO, the contraction induced by 10−6 M phenylephrine was obtained in rings incubated for 30 min with the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10−4 M).


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