Hello again, I saw my post earlier got spread on other platforms so now that I've had time to sit down to investigate more I'm finding things to answer general questions and concerns I've seen. Please share because I do not have accounts on Yahoo or anywhere besides here :) 

1) For those wanting a proper description of things that can elevate transaminases: https://www.aafp.org/afp/2017/1201/p709.html

- "Mild, asymptomatic elevations (less than five times the upper limit of normal) of alanine transaminase and aspartate transaminase levels are common in primary care. It is estimated that approximately 10% of the U.S. population has elevated transaminase levels."

- "In a two-year prospective study in the United Kingdom that included nearly 1,300 primary care patients with abnormal transaminase levels, excluding fatty liver disease (38% of patients), less than 5% of diagnostic workups revealed significant liver disease, and only 17 persons (1.3%) had serious liver disease that required immediate treatment."

2) Placebos in Phase I trials can have elevated ALTs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014876/

- In one study (Figure 1), two subjects had values greater than three times ULN during treatment, which was predefined as the criterion for withdrawing subjects on a blind basis. During screening, these subjects had values slightly above the ULN, and should have been excluded, although baseline values were within the normal range.

- You can see a clear trend that for whatever reason, the ALT levels of those two patients increases over the 14 days as if a compound was building up in the body. Something to think about and why Antibe with all the scientists are so worried about placebo controls. 

3) From Page 5 of Antibe's MD&A filed on June 28th (search on SEDAR) and I think this is the clearest hint in Antibe's release today that it was elevated in three patients who completed the trial, not in any other or patients still at Day 21:

"Adverse events typically associated with NSAID use, such as dyspepsia, acid reflux and dizziness, were comparable across placebo and all three treatment arms of otenaproxesul. There were very few serious adverse events or events leading to withdrawal of treatment. Only 1 out of 318 patients administered otenaproxesul had clinically significant, temporary liver transaminase elevations (LTEs) during the 14-day treatment period. At the post-treatment assessment (day 24), patients in the 250 mg, 200 mg and 150 mg treatment arms had clinically significant, temporary LTE incidences of 12.9%, 7.2% and 9.8%, respectively. It is standard for pain trials to allow the use of other medications, commonly acetaminophen. Acetaminophen use, particularly in the post treatment assessment period, along with pre-existing liver conditions and concomitant statin use were associated with a majority of the LTE incidents. Accounting for these factors yields clinically significant, temporary LTE incidence rates of 4.5%, 3.2% and 3.3%, respectively, suggesting a liver safety profile for otenaproxesul comparable to commonly prescribed NSAIDs and well below that observed with acetaminophen (39% clinically significant LTE incidence rate; National Institutes of Health). The clinical study was conducted by Veristat, LLC in 39 sites across Canada."

4) Another good read related to Point #1 and #3: Special Considerations in Interpreting Liver Function Tests https://www.aafp.org/afp/1999/0415/p2223.html

- My main takeway from this is ALT levels rise rapidly due to liver damage, it would not slowly increase. Another great point to Antibe pointing to the three patients being done the trial already. 

5) I do not see anything about hydrogen sulfide increasing aminotransferase enzymes.

- I can't cite anything to prove that, but mainly because Antibe says the other liver functions were normal you can't say it's liver failure. Aminotransferases get released by the liver when the cells are damaged making the membranes permeable, and ALT leaks out. Everything I'm reading talks about toxic symptoms of hydrogen sulfide when it's inhaled so symptoms wouldn't perfectly translate I believe, but still, if you're inhibiting mitochondria function in the liver it's going to die. 

- Roughtly, if the molecular weight of Naproxen is 230g/mol and a mole is 6.02x10^23 (big number), if a healthy liver has 240 billion cells then: when patients were given 250mg of Otenaproxesul you would be giving EACH liver cell 2.5 TRILLION molecules of hydrogen sulfide PER DAY to inhibit the the cytochrome c in the mitochondria. 1 cubic metre contains 44.64 moles of gas and hydrogen sulfide is instantly toxic at 500-1000 ppm so you're giving the body approximately 5.6 cubic centimeters of hydrogen sulfide gas at atmospheric pressure to each individual cell. If the 250mg doses in Phase 2 did not detect the toxicity then this is not the cause... you can argue orders of magnitude of dilution through an entire body and over time or only 1% needs to dissociate but you won't convince me. There's no way even all 3 patients neatly fit into this 100mg trial for longer duration but the 75mg group would not have toxicity.