I guess you didn't read the part right before your quote that reads "has given very strong signals"
Obviously more confirmation is needed, but you can't show me an Alzheimer's trial with better data.
In any case, the point is that the science will drive the success or failure of this company, not the source of its funding.
and was at $2.32 (split-adjusted) when the first one happened in July 2013.
Obviously the stock price has not suffered from the time of those deals until now, and the reason why is that what matters is whether the drug works, not where the money to test it comes from. The decline from $2.32 to $0.79 had nothing to do with Lincoln Park and everything to do with the fact that no one knew whether 2-73 could show efficacy in humans or not, because that had never been tested as of Oct 2014. The appreciation from $2.32 to today's $7-range price had nothing to do with Lincoln Park either, and everything to do with the fact that human testing has given very strong signals in 2015 that Anavex 2-73 works better on Alzheimer's than any other drug out there.
Right, good analogy w/ lithium -- eventually we'll catch up to exactly how and why 2-73 and 3-71 are working. In the meantime, kudos to the scientists (Vamvakides, Fisher, etc) who found their way to effective drugs by a combination of study, reasoning, and good old-fashioned trial and error.
Remember though that the sigma-1 receptor is only part of the equation--muscarinic receptors are indispensable to the 2-73 and 3-71 MOAs. The basic idea behind molecules like 2-73 and 3-71 is "to simultaneously activate a neuroprotective pathway, eg, the M1/PLC/PKC pathway, and amplify it, through a concomitant activation of the sigma-1 protein (Vamvakides, 2002a, b; Espallergues, et al, 2007; Villard, et al, 2009, 2011)."
Anavex never left the sigma-1 receptor -- that's been its raison d'etre from the beginning in 2007. As you know, however, not all sigma-1 agonists do so in the same way. So far, no one has found a sigma-1 agonist to generate the quality of preclinical and clinical data that 2-73 and 3-71 have produced so far, and of course those two operate differently from each other as well. And yes, even though there are many scientific publications on sigma-1 receptor over the past 15 years, there is still much to learn about why 2-73 and 3-71 are working. To some extent, it's a case of form following function, as often happens with new discoveries.
Zero credibility -- have seen Sierra do this sort of thing many times over the past few years and never once prove correct.
Yep, daily living (ADCS-ADL) is where the rubber meets the road in Alzheimer's testing -- no drug besides 2-73 (and no placebo effect) has ever before produced sustained improvement in that measure.
Unlike you, I'm not so narcissistic as to believe I'm the smartest person in every room. Anavex is obviously doing just fine without me. Anyone can learn the science, and that's what I've done over the past four years, and that's why I'm invested along with many other smart people on this board to whom you love to condescend and bloviate.
Yes, and understanding point 1a renders the rest of minor consideration (but I understand those, too). BP and its billions keep getting wasted on the failed Abeta hypothesis.
In fairness .17 a few months back would be a split-adjusted .68, still pretty great obviously. My lowest buy was .19 (.76 sa) and average cost .47 (1.88 sa), so I didn't make the genius/lucky cutoff at .17, alas.
Nope, I've been in the stock since early 2012. What about the percentage gain since Missling took over do you not understand? Please come join us in late 2015, as a lot has happened since early 2015 thanks to the funding from Lincoln Park and others, which Missling used to enable the current phase 2a trial.
Anavex has had a business relationship with Lincoln Park since July 8, 2013. Since then, the share price has increased in value by 223% as of today's close. The second deal was struck on October 27, 2014. Since then, the share price is up 275%.
Making deals with Lincoln Park is nothing new for Anavex, and it has thrived in that relationship for the past two and a half years.
Don't worry, I have no interest in debating you, as I see right through your disingenuous persona. I'm just pointing out for others how wrong you are in certain particulars. And give me a break on not understanding something as elementary as clinical research methods. I am well aware that the current trial is not placebo-controlled and that the next trial, the pivotal one for FDA approval, will need to be. That does not change the fact that 2-73 has already demonstrated statistically significant efficacy in humans according to certain Cogstate and ERP measures, despite the low power of the present trial. I am not claiming 2-73 will receive FDA approval purely on the basis of that demonstrated efficacy, only the inarguable fact that it has established statistically significant efficacy in a trial design accepted by the FDA.
The placebo effect is not a major concern where cognitive deficits are concerned, because patients with impaired thinking and memory will find it very difficult to imagine better thinking. Please point me to an Alzheimer's trial where the placebo arm has produced efficacy data to rival the 2-73 data. You can't do it, nor can you do it for any other Alzheimer's drug.