We are subject to the reporting requirements of the Securities Exchange Act of 1934, or the Exchange Act, the Sarbanes-Oxley Act, the listing requirements of the Nasdaq Capital Market, on which our ordinary shares are traded, and other applicable securities rules and regulations. The Exchange Act requires that we file periodic reports with respect to our business and financial condition and maintain effective disclosure controls and procedures and internal control over financial reporting. In addition, subsequent rules implemented by the SEC and the Nasdaq Capital Market may also impose various additional requirements on public companies. As a result, we incurred and will continue to incur additional legal, accounting and other expenses that we did not incur as a privately-held company, particularly after we are no longer considered an “emerging growth company” as defined in the JOBS Act. Further, the need to establish the corporate infrastructure demanded of a public company may divert management’s attention from implementing our development plans. We have made and will continue to make changes to our corporate governance standards, compensation policy, disclosure controls and financial reporting and accounting systems to meet our reporting obligations and applicable law. The measures we take, however, may not be sufficient to satisfy our obligations as a public company, which could subject us to delisting of our ordinary shares, fines, sanctions and other regulatory action and potentially civil litigation.

Raising additional capital would cause dilution to our existing shareholders, and may restrict our operations or require us to relinquish rights.

P311, a gene that was identified in 1993, has been found to have diverse biological functions in processes such as cell proliferation, migration and differentiation. However, its role in fibrosis is unknown. We previously observed that P311 is highly expressed in skin hypertrophic scars. In this study, P311 over-expression was detected in a subset of tubular epithelial cells in clinical biopsy specimens of renal fibrosis; this over-expression, was found concurrent with α-smooth muscle actin (α-SMA) and transforming growth factor beta1 (TGFβ1) expression. Subsequently, these results were verified in a mouse experimental renal fibrosis model induced by unilateral ureteral obstruction. The interstitial deposition of collagen, α-SMA and TGF-β1 expression, and macrophage infiltration were dramatically decreased when P311 was knocked out. Moreover, TGFβ/Smad signaling had a critical effect on the promotion of renal fibrosis by P311. In conclusion, this study demonstrate that P311 plays a key role in renal fibrosis via TGFβ1/Smad signaling, which could be a novel target for the management of renal fibrosis.

Pursuant to our Articles, subject to the rights of holders of shares with limited or preferred rights, ordinary shares shall confer upon the holders thereof equal rights to receive dividends and to participate in the distribution of the assets of the Company upon its winding-up, in proportion to the amount paid up or credited as paid up on account of the nominal value of the shares held by them respectively and in respect of which such dividends are being paid or such distribution is being made, without regard to any premium paid in excess of the nominal value, if any.

In August 2018, the FASB issued ASU 2018-13, “Changes to Disclosure Requirements for Fair Value Measurements”, which will improve the effectiveness of disclosure requirements for recurring and nonrecurring fair value measurements. The standard removes, modifies, and adds certain disclosure requirements, and is effective for the Company beginning on January 1, 2020. The Company does not expect that this standard will have a material effect on the Company’s consolidated financial statements.

Any debt, equity or structured financing that we may need or desire may not be available on terms favorable to us, or at all. If we obtain funding through a strategic collaboration or licensing arrangement, we may be required to relinquish our rights to certain of our technologies, products or marketing territories. If we are unable to obtain required additional capital, we may have to curtail our growth plans or cut back on existing business, and we may not be able to continue operating if we do not generate sufficient revenues from operations needed to stay in business.

Male Sprague-Dawley (SD) rats, weighing 220–280 g were supplied by the animal research center at Fourth Military Medical University, Xi’an, China. The experiments were performed in adherence with the National Institutes of Health Guidelines for the Use of Laboratory Animals and were approved by the Fourth Military Medical University Committee on Animal Care. β-BA (purity >98%) were purchased from the Chinese National Institute for the Control of Pharmaceutical and Biological Products (Beijing, China).

The expressions of 6 enzymes (ALDOA, ENOα, ENOβ, ECH1, HIF1, HSP70) related to energy metabolism were assessed by western blot in different groups. As shown in Fig. 5, AAS challenge led to an increase in the expression of 4 enzymes, including ALDOA, ENOα, HIF1, and HSP70, while a decrease in the expression of ENOβ and ECH1, with AAS2M impairing these proteins more than AAS1M except ECH1 and HSP70. QSYQ restored all the AAS-induced alterations significantly. Mono and combination therapies affected the expression of energy metabolism-related proteins differently depending on the enzyme concerned. For example, ASIV mono-therapy and the ASIV containing combinations inhibited the elevation of ALDOA after AAS, which was intensified by combination with DLA or DLA+R1, while DLA, R1, DO alone and their combinations showed no effect on ALDOA (Fig. 5b). On the other hand, mono-therapy ASIV, DLA or R1 and all the combination therapies showed nearly equally beneficial role for ENOα (Fig. 5c). ASIV, DLA alone and all the combination therapies displayed a beneficial role, but R1 and DO had no effect, in the case of ENOβ (Fig. 5d). ASIV, R1 alone and all combinations except ASIV+DLA increased the expression of ECH1 (Fig. 5e). Interestingly, R1 alone and all the combination therapies showed significant inhibition on HIF1 and HSP70 (Fig. 5f,g). Of notice, in any case, DO alone did not show any effect while QSYQ was always among the most effective treatments.

Before we can submit an NDA to the FDA or a similar approval application to other regulatory authorities, as applicable, we (or our commercialization partner, as the case may be) must conduct one or more clinical trials that will be substantially broader than our ARREST study. We will also need to agree on a protocol with the FDA, EMA or any other regulatory authorities for any clinical trial(s) before commencing any such trial. Clinical trials frequently produce unsatisfactory results even though prior clinical trials were successful. Therefore, the results of the ARREST Study or any future clinical trials that we may conduct may or may not be successful. The applicable regulatory agencies may suspend all clinical trials or require that we conduct additional clinical, pre-clinical, manufacturing, validation or drug product quality studies and submit data from these additional studies before considering or reconsidering the NDA or similar regulatory application. Depending on the extent of these, or any other studies, approval of any applications that we submit may be delayed by several years, or may require us to expend more resources than we have available. It is also possible that additional studies, if performed and completed, may not be considered sufficient by the applicable regulatory agencies to provide regulatory approval. If any of these outcomes occur, we would not receive approval for Aramchol and may be forced to cease operations.

Biovail Corporation (TSX:BVF.TO) is a specialty pharmaceutical company engaged in the formulation, clinical testing, registration, manufacture, and commercialization of pharmaceutical products. The Company is focused on the development and commercialization of medicines that address unmet medical needs in niche specialty central nervous system (CNS) markets.

Great ideas about IF vs. CR. We know that with chronic low energy intake that the body responds with an equal degree of decreased energy expenditure, in other words a drop in metabolic rate , which does not occur with IF. Also IF leads to a pronounced decrease in PCSK-9 which dramatically lowers LDL cholesterol and is the mechanism of the new monoclonal antibodies to prevent heart attacks. IF is safer and cheaper than the new drugs, and even more effective.

That is interesting and I’ll have to read the paper, but I think the key thing to remember is that TERT is like a growth hormone. So its expression will be correlated with MTOR. Think of high MTOR spurring proliferation of new cells and you get the point.