This is a bit odd. Both CR and rapamycin will slow proliferation, but end up preserving stem cell function because they reduce senescence. Like you Paul, I can only imagine the rapamycin dose was not intermittent. I’ll watch the video through though, to see what they say.

        In February 2018, we completed a follow-on public offering of 9,660,000 shares of common stock, including the full exercise of the underwriters’ option to purchase an additional 1,260,000 shares, at $6.00 per share and received aggregate net proceeds of $54.1 million, after deducting $3.5 million of underwriting discounts and commissions and approximately $0.4 million of offering expenses.

This should not be done when rapamycin is most active in the system but should also be used in a intermittent manner.

There is growing evidence that microRNAs play important roles in cellular responses to hypoxia and in pulmonary hypertensive vascular remodeling, but the exact molecular mechanisms involved are not fully elucidated. In this study, we identified miR-322 as one of the microRNAs induced in lungs of chronically hypoxic mice and rats. The expression of miR-322 was also upregulated in primary cultured rat pulmonary arterial smooth muscle cells (PASMC) in response to hypoxia. We demonstrated that HIF-1α, but not HIF-2α, transcriptionally upregulates the expression of miR-322 in hypoxia. Furthermore, miR-322 facilitated the accumulation of HIF-1α in the nucleus and promoted hypoxia-induced cell proliferation and migration. Direct targeting BMPR1a and smad5 by miR-322 was demonstrated in PASMCs suggesting that downregulation of BMP-Smad signaling pathway may be mediating the hypoxia-induced PASMC proliferation and migration. Our study implicates miR-322 in the hypoxic proliferative response of PASMCs suggesting that it may be playing a role in pulmonary vascular remodeling associated with pulmonary hypertension.

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NK cell cytotoxicity was assessed as previously described42. Target (T) cells labeled with 5 μM calcein AM (Invitrogen) for 1 h at 37°C and effector (E) cells were co-incubated with 200 μl complete medium in a 96 well plate for 4 h at 37°C. Spontaneous release of calcein was determined by incubating loaded target cells in medium alone, and maximal release was determined by adding 0.1% Triton X-100 to lyse all target cells. After incubation, plates were centrifuged at 300 × g for 5 min, and 100 μl of supernatant from each sample was transferred to a 96-well plate. Fluorescence was measured at 480 nm excitation/538 nm emission wavelengths. Cytotoxicity, measured as a percent specific release of calcein, was calculated using the following formula: percent specific release = (experimental release – spontaneous release)/(maximum release – spontaneous release) × 100.

5.        The Company’s other certifying officer and I have disclosed, based on our most recent evaluation of internal control over financial reporting, to the Company’s auditors and the audit committee of the Company’s board of directors (or persons performing the equivalent function):

We are a clinical-stage biopharmaceutical company with an operating history limited to pre-clinical and clinical drug development and no approved products. To date, we have focused nearly exclusively on developing our product candidate, Aramchol. In addition, we have limited operating experience and have not yet demonstrated an ability to successfully overcome many of the risks and uncertainties frequently encountered by companies in new and rapidly evolving fields, particularly in the pharmaceutical industry. We have funded our research and development programs and operations to date primarily through proceeds from private placements and public offerings. We currently have no products approved for marketing in the United States or any other jurisdiction and have not generated any revenue from product sales to date, although we have generated revenue from our licensing agreement with Samil Pharm. Co., Ltd., or Samil. We have incurred operating losses in each year since the inception of our predecessor in 2000. Our loss attributable to holders of our ordinary shares for the years ended December 31, 2016, 2017, and 2018 was approximately $17.0 million, $12.3 million, and $9.9 million, respectively. As of December 31, 2018, we had an accumulated deficit of $86.5 million. Substantially all of our operating losses resulted from costs incurred in connection with our development program and from general and administrative costs associated with our operations.

        Our share-based compensation programs grant awards which may include stock options, restricted stock awards ("RSAs"), restricted stock units ("RSUs"), and other stock-based awards.

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The table above shows that the primary endpoint of the study was attained. The study demonstrated a statistically significant, dose dependent reduction in fat content in the livers of patients treated with Aramchol, with a 19% difference between the 300 mg dose group and the placebo group, while the difference between the 100 mg dose group and the placebo group was not statistically significant. Notably, the minimal effective dose of Aramchol for fat reduction has been defined.

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