Hope I don't come off as countering your points too aggressively. I'm glad you posted and are thinking through the data, and my intent has just been to give my own version of what you already laid out for us very usefully.
4. I think you are assigning way too much weight to the lack of statistical significance, especially given that 2-73 is showing substantially positive data in almost every single measure of this trial. A 3+ point improvement in ADCS-ADL is very meaningful despite not achieving statistical significance, which was never a reasonable expectation of a 32-patient trial that was not designed to achieve that. As you point out, 11 of 14 responding positively is also very encouraging.
5. Cogstate alone would not be grounds for FDA approval, and I'm not sure it will be included in P3 (as it is sort of a stand-in for the more traditionally accepted ADAS-Cog test, though Cogstate may ultimately prove a superior test) -- however, the fact that Cogstate lends yet another voice to the choir of positive results for 2-73 in every testing category is meaningful.
I don't see how anyone could reasonably ask for any better data than what Anavex just reported -- I had high expectations and they were exceeded. The data fully supports moving 2-73 into a pivotal double-blind, placebo-controlled trial, and makes a good argument for fast-tracking that trial as well. I now fully believe that 2-73 works, and my only remaining question is how long it can sustain its benefit to the patients.
Couldn't care less what the market does Monday or even the next few weeks -- this drug will go to market with a BP partner. It's only a matter of how soon. I can't wait for the next batch of data on the Part B extension.
1. This is great, not at all disappointing -- only reason percentage is lower is because baseline for 30 was higher than the 7/22 baseline for 12 (meaning merely that the first 12 tended to have more severe AD than the next 18); what matters is that 2-73 appears to be restoring patients almost all the way to healthy control level after just 5 weeks of on-off-on dosing
2. This isn't the P300 latency electrode measure that supposedly carries more weight than amplitude (but that is contradicted by recent Neuronetrix study that uses better technology and systemic method than older ways of measuring P300) -- this is an addendum to the electrode measures, a three-pronged target exercise that does measure latency via button-press activity and actually was more statistically significant in the Neuronetrix study than the P300 electrode measure that some people claim is the be-all end-all of EEG/ERP (incorrectly in my opinion); Anavex's data here is very encouraging, especially (as you point out) the statistically significant result in Reaction Time, one of the three button-press latency tests
3. The important point, which you mention but wrongly (in my opinion) subordinate to the uneducated opinion of the market (or what you believe will be the opinion of the market on Monday), is that even after 5 weeks of suboptimal dosing 2-73 doubles the typical effect of donepezil over a similar time period and already matches the typical peak of what donepezil can achieve in MMSE at any point -- this is a similar result to what was observed on 7/22 for P300 amp, where 2-73 bested donepezil over same time frame and already matched the peak of what donepezil ever achieves (validating the PR comment on 7/22 that MMSE scores were "consistent with the observed trend" in P300 amp). The reason data was not stat sig is because the study is not powered (enrolling enough patients) to achieve that, nor was it intended to be. Some measures accommodate stat sig more readily than others.
never was intended to be statistically significant -- exploratory efficacy
it's a great result for 5 weeks of on-off-on dosing and meshes nicely with all the other great results in Cogstate, EEG/ERP, and ADCS-ADL
Wrong again. Per the 10/7 PR, the Nov 7CTAD presentation will give full Part A data for all 32 patients, and preliminary Part B data (most likely the 12-wk data for those same 12 patients whose Part A data was reported on 7/22).
No, Part A is 36 days and there is no MMSE assessment during those 36 days except to take the baseline measure right when the patient first begins the trial. Comparative MMSE data is not collected until Part B. It's all right there on clinicaltrials dot gov website.
MMSE measured in Part B only (just read trial details on clinicaltrials dot gov website) -- the July 22nd data release was for Part A
Still referred to MMSE because they had some Part B data at that point, and what they had "was consistent with the observed trend" for the P300 data revealed for 12 patients in Part A, but did not release MMSE data at that time, presumably since it was only from a few patients (less than 12)
Now on 11/7 we will find out what MacFarlane meant by "Clincal Cognitive Improvement observed in MMSE and other Cognitive Markers"
Given that Agora reserves buy recommendations for its subscribers, and bases its recommendations on the science rather than price targets and the like (at least that was the case when Patrick Cox was there), I believe the Twitter rumor is false. Even if true, wouldn't bother me a bit.
preliminary data that made a significant difference in 10 of the 12 and registered a mean P300 amplitude benefit 4x greater than donepezil's, data consistent with what the study investigator was seeing in MMSE and Cogstate scores as well and with the feedback he was getting from caregivers and patients/families
Maybe that's all just a coincidence -- would be one holy heck of a coincidence, though
because AXON's IPO was arranged by its hedge-fund owner who has lots of connections and knew how to manipulate the company's launch so as to keep a high valuation -- AXON's market cap has nothing to do with anyone actually believing in its drug (except for true suckers) and everything to do with Ramaswamy being a savvy financial guy. Ultimately the stock is doomed, but I'm sure Ramaswamy, his family, and other cronies will come out of it with profits all around.
They won't do and already haven't done nearly as well (percentage-wise) as the retail owners of AVXL, though.
scottrade and nasdaq only show institutional ownership as reported on 13-K forms
Institutions are generally not required to report their ownership of OTC stocks on 13-K forms
We know AVXL's institutional ownership (at least as of earlier in 2015) because of the S-1 form filed regarding the warrants
Institutions do invest in OTC stocks but generally are not required to report those investments on 13-K forms (which is why institutional ownership of OTC stocks is not reflected on sites like nasdaq and scottrade since they rely on 13-K forms)
The 54% number comes from an S-1 form related to the warrants from earlier in 2015
He does have a million shares already, so plenty of incentive to make him want to see the share price rise, and not a whole lot of need to add more (seeing as his holding is already worth about $14M today)
He may not have had oodles of cash lying around before becoming CEO
With the right trial results Missling can negotiate a highly beneficial partnership (because there will be a surge of competing suitors) that will get 2-73 to market (and revenues) much faster than Anavex could accomplish on its own. Patents only last a certain number of years, so extra years of revenue early on are very important. Missling has stated in interviews (SNN one is on Youtube) that the company will partner 2-73 for AD and I expect he means what he says.
Right, MacFarlane as Principal Investigator is the one who knows the data, and he is also the one who worded the initial presentation title as "Clinical Cognitive Improvement observed"
Note that Missling told Street Sweeper on Oct 14 or so that he did not know "what the data will be"
Regardless, the preponderance of evidence (preclinicals, July 22nd, CTAD initial title) tells us that we will be happy with the 11/7 interim data.
Lincoln Park's reputation is fine -- detractors have ulterior motives and no credibility. Anavex gets access to $50M that will accelerate its ability to establish a new SOC in Alzheimer's.