I like your discoure a lot more than mine, KB. I think we align...

I like your discoure a lot more than mine, KB. I think we align on many things.

I didn't realise you couldn't use a biomarker as a screening target until it had been determined in a clinical trial. What a shame that the original Sheba 1 tumors weren't available for further biochemical analysis. Well, I guess having clinical and biochemical data to better define causation is enough to get me moderately excited.

I'm pretty confident that the salvage therapy theory can be laid to rest, but time will tell.

The market can view the data however they want, but they will probably be looking at it through the wrong lense. You only have to look as far as IMU to see that investors do not understand the science that underpins their investment. Merck has clearly seen straight through it.

You probably already understand my point, but I'll try to explain myself further. Let's say the data is indeed average and we get no clinical responses from Zantrene in this trial. Does that mean the drug doesn't work as an FTO inhibitor? No, it doesn't. I'm invested because of the FTO-inhibitory nature of Zantrene, so a trial that does not answer that question does not get a lot of interest from me. It all gets a little bit more interesting with the biochemical and post-hoc analysis that they are doing. I guess I am just trying to temper peoples expectations from this trial and put a more realistic spin on things. I said it before, but it really is like throwing darts at a dartboard blindfolded, and I do not like that approach for a drug that requires a specific patient population. Of course, the difference and bonus is the biochemical analysis to determine why patients did or did not respond.

I agree with your points of optimism I am impartial about the RAC share price movements. If it goes up, I get wealthier. If it goes down, I buy more.

@IndexInvestor
I don't agree with "We know Zantrene requires a specific patient population". We have a hypothesis that Zantrene will be most effective against cancers with over-expressed FTO. But we don't know that Zantrene will be useless in other cases.

You can disagree if you would like to, but I think it is pretty clear Zantrene requires a specific patient population. I don't really care if a tumor is over-expressing Zantrene, it is whether the FTO component of the cancer is driving tumorigenesis and would therefore be sensitive to an FTO inhibitor. Tumors that are driven by the hyper-demethylation of m6A as a result of FTO expression, and are sensitive to inhibition of FTO by a compound are exactly the type of patients we want included in the trial. Additionally, tumors that increase FTO expression as a result of chemotherapy, immunotherapy, or radiotherapy, and are therefore sensitive to inhibition of FTO by a compound are also the patients that we want to include. All of the accumulated preclinical data that is either testing Zantrene as an anthracycline or FTO inhibitor, or testing FTO inhibitors in general is pointing in this direction. Also, there is already a small accumulation of evidence that screening participants to the sensitivity of Zantrene and including only patients who are sensitive at low concentrations improves the likelihood of clinical responses (3 in 4 patients). Put this into context with the the 25 or so other historic solid tumor clinical trials where there are limited or no clinical responses with sub-optimal dosing regimens. You could also use the Phase 3 Breast cancer clinical trial as another reference for the need of a specific patient population. The fact that Zantrene works in some and not others highlights the precision field in which it lives.

I agree with you that we don't know Zantrene won't be useless in other cases.