We have derived all of our revenue to date from the Merck Agreement, which we entered into in April 2013. Under the Merck Agreement, we collaborated with Merck and used our proprietary drug discovery technology platform to identify orally available cyclic peptides for non-complement targets nominated by Merck and provided specific research and development services. At the signing, Merck paid us an upfront, non-refundable, license fee payment of $4.5 million. In addition, during the research term, which ended in April 2016, Merck reimbursed us for research and development services provided by us in accordance with a pre-specified number of our full-time equivalent employees ("FTEs") working under the Merck Agreement. At the conclusion of the research term, Merck elected to continue the development of a non-complement cardiovascular program target with a large market opportunity, for which we had received $6.0 million in pre-clinical milestone payments as of December 31, 2018. We are also entitled to receive future aggregate milestone payments of up to $59.0 million and low-to-mid single digit percentage royalties on any future sales for this program target. For additional information about the Merck Agreement, see Item 8, "Financial Statements and Supplementary Data" within this Annual Report on Form 10-K.

We are a clinical-stage biopharmaceutical company focused on the development of the liver targeted stearoyl-coenzyme A desaturase-1, or SCD1, modulator Aramchol, a first in class, novel, oral therapy for the treatment of NASH for variable populations, as well as other liver associated disorders. We believe that our product candidate, Aramchol, has the potential to be a disease modifying treatment for fatty liver disorders, including NASH, which is a chronic disease that constitutes a large unmet medical need.

The Blood Stasis Syndrome model was produced as described previously48. Briefly, rats were kept in plastic cages at 22 ± 2 °C with free access to pellet food and water and on a 12 h light/dark cycle. Rats were randomly divided into four groups (control group, model group, model +β-BA100 mg/kg and model +β-BA 200 mg/kg group) with eight animals in each. Rats were given blank solvent as the vehicle at the same volume for control group. Rats were given blank solvent at the same volume for model group. In the model +β-BA (100 mg/kg) group, rats were given 100 mg/kg β-BA. In the model +β-BA (200 mg/kg) group, rats were given 200 mg/kg β-BA. All treatments were performed by gavage and were administered seven times with an interval of 12 h. After the fifth administration, the model rats except those in control group with blood stasis were established by being placed in ice-cold water (0–2 °C) for 5 min, during the interval between two injections of adrenaline hydrochloride (0.8 mg/kg). Rats were fasted overnight and administration continued after performing the model. Blood samples and carotid artery were collected 30 min after the last administration on the following day.

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RSUs. We have granted RSUs to certain of our Office Holders. Such award agreements may contain acceleration provisions upon certain merger, acquisition, or change of control transactions. See also “Item 6. Directors, Senior Management and Employees—E. Share Ownership.” We describe our 2013 Plan under “Item 6. Directors, Senior Management and Employees—B. Compensation—2013 Incentive Share Option Plan.” If the relationship between us and an Office Holder is terminated, RSUs that are vested shall be settled in accordance with the settlement schedule set forth in the applicable award agreement.

Our financial income consists mainly of interest income from marketable debt securities and short-term deposits, as well as gains from realization of marketable debt securities and foreign currency gains. Our financial expense consists of fees associated with banking activities and losses from realization of marketable debt securities.

The primary endpoint of the study was the change from baseline to end of study in liver triglycerides ratio as measured by magnetic resonance spectroscopy, or MRS (Aramchol 600mg vs. placebo). Secondary endpoints, demonstrated through biopsy, included fibrosis improvement by at least one stage or more without worsening of NASH (defined by an increase of inflammation and or ballooning) and NASH resolution (defined by ballooning score 0 and inflammation score 0-1 at termination) without worsening of fibrosis. Other secondary endpoints included improvement (2 points or more) in NASH activity index, as measured by NAS or SAF, without worsening fibrosis and change in baseline to week 52/termination in ALT (U/L).

Incidentally, BioViva has in its pipeline several other potential therapies (than telomerase). I am wondering if they have the funds to really explore all of these. Part of it could be marketing but I really don’t know.

I was also glad to find Paul Rivas suggestions regarding IP6 and the suggested proper ratio of the Inositol to Inositol hexaphosphate.

hi aldebaran My ferritin level was 88 at last checked. I want it as low as I can get it without having iron deficiency anemia. My Hct is 48 with a normal MCH and MCHC. As long as those are ok then you’re fine , though some include a TIBC which I find redundant to the ferritin level which I feel is best. If you’re over 200 donate blood and start IP6.

I started collecting notes on GHK glycyl-L-histidyl-L-lysine after Broad Institute (collaboration of Harvard and MIT) singled it for resetting of genes to a more healthier state. In human plasma, the level of GHK-Cu is about 200 µg/ml at age 20. By the age of 60, the level drops to 80 µg/ml. I am unable to quote study titles so please Google GHK and Broad Institute. Sharing some part of a research article by Loren Pickett published in BioMed Research International – it’s open access: numerous studies over the course of four decades demonstrated that this simple molecule improves wound healing and tissue regeneration (skin, hair follicles, bones, stomach, intestinal linings, and liver), increases collagen and glycosaminoglycans, stimulates synthesis of decorin, increases angiogenesis, and nerve outgrowth; possesses antioxidant and anti-inflammatory effects, and increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells. GHK’s actions on gene expression were determined by the Broad Institute and, using their data, we determined that GHK increased or decreased gene expression (UP or DOWN more than 50%) in 32.1% of the human genes. In a recent gene study, the Broad Institute’s Connectivity Map was used to find potential therapeutic agents for aggressive, metastatic colon cancer. The gene analysis computer program selected GHK from 1,309 bioactive molecules as the best choice to reset the diseased gene patterns to a healthier pattern. Another study says GHK, abundantly available at low cost in bulk quantities, is a potential treatment for a variety of disease conditions associated with aging. The molecule is very safe and no issues have ever arisen during its use as a skin cosmetic or in human wound healing studies. Thus, GHK would be expected to influence the cells’ gene expression to be more similar to that of a person of age 20–25, an age when the afflictions of aging are very rare. Based on our studies, in which GHK was injected intraperitoneally once daily to induce systemic wound healing throughout the body, we estimate about 100–200 mgs of GHK will produce therapeutic actions in humans. But even this may overestimate the necessary effective dosage of the molecule. Most cultured cells respond maximally to GHK at 1 nanoM. GHK has a half-life of about 0.5 to 1 hour in plasma and two subsequent tissue repair studies in rats found that injecting GHK intraperitoneally 10 times daily lowered the necessary dosage by approximately 100-fold in contrast to our earlier studies. This should get you started.