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Healthy Mitichondria could stop Alzheimer's
http://bit.ly/2BYurxR
c'mon Missling...c'mon Gottlieb...
hslauch, I second ITT's call to do a comp with HALO's approach - here's a note of relevance...
Key Opinion Leader Manuel Hidalgo, MD, PhD Harvard Medical School and Beth Israel Deaconess Medical Center-"Pegylated hyaluronidase, may, at the end of the day, make the tumor hot for immunotherapy."
http://bit.ly/2ndzUyB
Awesome terms for a preclinical pipeline. IMO an incredibly dimwitted move by Abbvie in such a tough indication unless they have been shown incontrovertible evidence, (I can't start to imagine what might qualify as such.) My sense is they haven't as the protagonists are talking in high-level conceptual terms like "immuno-oncology of the brain." Something that doesn't seem revolutionary enough not to have been considered for postulation, ages ago.
Broadly speaking, to the extent Alzheimers arises from insults to the brain rather than fully endogenous reasons, focusing on the gatekeepers to the brain (in microglia) may be a worthy approach to slow down and keep away any onset. Don't think they are addressing mitochondrial repair and any receptor restoration that is essential for any reversal of the condition.
Haven't looked into the backgrounds of the 2 main protagonists but I get scared off when I see someone describe oneself as a serial-entrepreneur esp. if the person is primarily a medical researcher. I prefer the Tasos Zografidis types who confine themselves to research and leave profit-seeking motivation as a responsibility for someone else organizationally.
Never a bright move to buy in so early on an indication that's presented such remote a chance in clinically effective treatment. Could be totally wrong but my gut says it had a lot to do with connections.
Say hello to Alector...
http://bit.ly/2i1eumb
With new approach to Alzheimer's, Peninsula company seals $225M deal with drug giant AbbVie
By Ron Leuty – Reporter, San Francisco Business Times
Oct 24, 2017, 4:00am
With a new collaboration and funding from AbbVie Inc., a young Peninsula company hopes to attack memory-robbing Alzheimer's disease in much the same way a new generation of cancer drugs are trying to eliminate tumor cells.
Alector LLC of South San Francisco will receive $205 million upfront and a potential equity investment of up to $20 million from AbbVie (NYSE: ABBV) as part of a deal to research, develop and eventually sell drugs targeting dementia, particularly in Alzheimer's patients, the companies said Tuesday.
As the baby boom generation adds significantly to the number of people with Alzheimer's — by some calculations, the number of Alzheimer's patients in the United States will triple by 2050 from 5 million to 16 million — drug companies have been stymied in developing drugs for the disease. Just last month, former Medivation Inc. CEO David Hung's latest company, Axovant Sciences Inc., said its late-stage clinical trial to treat patients with mild to moderate Alzheimer's failed.
But Alector thinks it can reactivate the immune system in the brains of people with Alzheimer's and other forms of dementia, Parkinson's Disease, multiple sclerosis and amyotrophic lateral sclerosis, or Lou Gehrig's disease. It borrows from discoveries in cancer, where companies are starting to unleash immunotherapy drugs that in various ways target certain proteins to rev up the immune system to uncloak and attack tumor cells.
More specifically, company cofounder and CEO Arnon Rosenthal said, Alector's drugs aim at stimulating, multiplying, moving and directing brain cells called microglia. Those cells account for roughly 15 percent of all brain cells, providing a first line of defense for the central nervous system against foreign invaders and acting as a sort of gray-matter garbage disposal.
The sorts of things that microglial cells should be dumping at the metaphorical curb are amyloid beta and tau, sticky proteins that clump together in the brains of Alzheimer's patients, disrupting the sharing of messages between neurons. Amyloid beta and tau have been the preferred targets of companies trying to disrupt Alzheimer's.
By stimulating microglia, Rosenthal said, Alector's drugs in preclinical models indicate that they can block Alzheimer's on their own or, potentially, in combination with antibody drugs that so far haven't demonstrated efficacy.
AbbVie has its own tau-targeting experimental Alzheimer's drug, ABBV-8E12, in the second of the three-phase clinical trial process.
"Even for targeted therapeutics, you need an active and robust immune system to get effective therapy," said Rosenthal, a cofounder of Rinat Neuroscience before that South San Francisco company was bought by Pfizer Inc. (NYSE: PFE) in 2006 for $500 million.
"We think there will be significant efficacy as a standalone (therapy)," Rosenthal said.
Forty-employee Alector, a graduate of the QB3@953 incubator and Johnson & Johnson's (NYSE: JNJ) JLabs in South San Francisco, expects to start its first human clinical trial within a year in frontotemporal dementia, where the loss of nerve cells causes behavioral changes in people in their 40s or younger.
Four other Alector drugs could follow into the clinic over the next two years, Rosenthal said.
In all, Alector, founded by Rosenthal, Columbia University associate professor Asa Abeliovich and serial entrepreneur and Dartmouth College bioengineering professor Tillman Gerngross, has raised more than $80 million in four years. Those investors include Orbimed and Polaris Ventures, Google-associated GV, Mission Bay Capital, Merck & Co. (NYSE: MRK), Amgen Inc. (NASDAQ: AMGN), Dementia Discovery Fund and AbbVie.
Alector's deal with AbbVie gives the Chicago-area company an option to global development and commercial rights to two targets. Alector will lead exploratory research, drug discovery and development for lead programs up to proof-of-concept studies. If AbbVie exercises its option, it will lead development and commercialization, but the companies will split drug profits, if drugs get to that point.
"The success of immuno-oncology helps us understand the field," Rosenthal said. "People understand that we are doing immuno-oncology in the brain."
AXON intepirdine post-mortem...
ADAS-cog, p=.22
ADCS-ADL, p=.83
OUCH!!!
Anyone shorting AXON for dementia w/ lewy body readout shortly?
AVXL: Fasten your seatbelts folks...
In case the following hasn't been reported...
Medicinova's SPRINT-MS: Ibudilast Shows Unprecedented Slowing of Brain Atrophy in Progressive MS
Paves way for phase 3 testing of novel treatment approach
An investigational therapy for progressive forms of multiple sclerosis (MS) with a novel mechanism of action slowed progression of brain atrophy by nearly half relative to placebo over two years of follow-up. So reported investigators with SPRINT-MS, a multicenter phase 2 study presented as a late-breaking trial at the 7th Joint ECTRIMS-ACTRIMS Meeting in Paris Oct. 28, 2017.
The 48 percent reduction in brain atrophy with the oral therapy, ibudilast, compares favorably with the 18 percent reduction in brain atrophy reported with ocrelizumab, which earlier this year became the first therapy approved by the FDA for treatment of progressive MS.
“The results of SPRINT-MS are very encouraging,” says Robert Fox, MD, Vice Chairman for Research in Cleveland Clinic’s Neurological Institute and the study’s principal investigator. “Our hope is that ibudilast’s benefit in slowing brain volume loss will translate to slowed progression of physical disabilities as well. That would address a significant unmet need for people with progressive forms of MS.”
These findings will likely pave the way for larger phase 3 studies of ibudilast in progressive MS, which are needed before the drug can be considered for marketing approval for this use.
A novel approach to progressive MS
Ibudilast is a small-molecule compound that acts on three pathways that may be involved in progressive MS: macrophage migration inhibitory factor (MIF), phosphodiesterase-4 (PDE-4) and PDE-10, and toll-like receptor 4 (TLR4).
The agent has been approved in Japan since 1989 for use in asthma and cerebrovascular disorders and is also currently being studied in the U.S. for potential treatment of amyotrophic lateral sclerosis and drug addiction. Animal models suggest that it may be neuroprotective.
Study essentials
SPRINT-MS was conducted at 28 U.S. sites, with Cleveland Clinic’s Mellen Center for Multiple Sclerosis as lead center. The study randomized 255 patients (mean age, 56 years) with primary or secondary progressive MS to 96 weeks of ibudilast (up to 100 mg/day orally) or placebo. Patients were permitted to continue existing therapy with glatiramer acetate or interferon beta-1 agents. All had evidence of disability progression during the prior two years.
One primary end point was change in brain atrophy — which is associated with physical and cognitive disability in MS — as measured by the MRI analysis technique known as brain parenchymal fraction. The other primary end point was safety and tolerability.
Secondary outcomes included changes in magnetization transfer ratio (MTR) and diffusion tensor imaging (DTI), two measures of brain tissue integrity. Optical coherence tomography (OCT) studies, cortical atrophy evaluations and clinical assessments were also conducted but have not yet been analyzed.
The intention-to-treat analysis included 244 patients, and the trial had an 86 percent retention rate.
On the primary efficacy end point, ibudilast showed a 48 percent relative reduction in brain atrophy rate versus placebo (P = .04). On the secondary end point of MTR, ibudilast was associated with a 77 to 82 percent reduction in rate of decline versus placebo, with superior outcomes for normal-appearing overall brain tissue as well as gray matter. In contrast, there was no significant difference from placebo in DTI findings.
In safety analyses, ibudilast was associated with higher rates of gastrointestinal side effects, rash, depression and fatigue relative to placebo. But there were no differences from placebo in overall tolerability, discontinuation rates or rates of serious adverse events. “The drug appears to be quite safe,” Dr. Fox observes.
What lies ahead
He notes that although SPRINT-MS was not powered to detect differences in clinical effects, measures of disability and quality of life will be forthcoming in a future full-length publication of study results. “Our hope is that this substantial 48 percent slowing in brain atrophy progression will translate to a slowing in disability progression too,” he says.
But phase 3 testing in larger numbers of patients is needed to determine ibudilast’s effects on clinical disability and confirm its safety profile. Dr. Fox says those results are likely about five years off.
“In the meantime, these results are promising,” he says, adding that SPRINT-MS is also helping shape the design of future phase 2 trials in progressive MS. “By evaluating for the first time the longitudinal change in multiple imaging measures and their correlation with disability, we hope to refine our understanding of the best biomarkers for future progressive MS trials.” Publication of the full study will include the OTC and cortical atrophy findings as well as effects on clinical progression, he notes.
“It looks like with this study, not only have we caught a good fish, but we’ve also learned how to fish better,” Dr. Fox says. “This should help us develop more therapies for progressive MS, and do so more quickly and efficiently.”
The study is principally funded by the NeuroNEXT Network, a clinical trials initiative of the National Institutes of Health.
Happy Halloween - AZ Koolaid (article below) for us AVXL holders...
... 99.6% failure rate because all past co's ran their compounds through the standard clinical trial sausage factory without asking the tough questions AVXL is asking - on trial design, selection criteria, biomarkers, optimized dosage, etc. They did so more out of hope and didn't look into the different causes of AD. Co's like VTVT run trials on a patient population comprising of MCI and (believe it or not) "probable" AD (as identified only on MRI) and with a placebo control arm instead of SOC - all in hopes of beating/cheating the system.
In the event we fail, we cannot fault Missling for having left any stone unturned.
-------------------
This nutrient-rich drink may help treat the root cause of Alzheimer's
Updated: Oct 31, 2017, 05.22 PM IST
NEW YORK: Researchers from the Massachusetts Institute of Technology (MIT) have developed a nutrient mix that has shown potential to slow down cognitive impairment in the early stages of Alzheimer's disease.
The drink, called Souvenaid is aimed at treating "the root cause" of Alzheimer's, which is the loss of brain synapses.
Souvenaid contains omega-3 fatty acids found in oily fish like salmon and mackerel along with high doses of Vitamin B13, B, C and E.
The mixture increases production of new synapses and restores connectivity between brain regions, improving memory and other cognitive functions, the researchers reported, in the MIT Technology Review.
In the new clinical trial, published in the journal Lancet Neurology, the team conducted a 24-month trial, where more than 300 patients with prodromal Alzheimer's -- the predementia stage of Alzheimer's with mild symptoms -- were randomly assigned Souvenaid or a placebo.
Patients who drank Souvenaid showed less worsening in everyday cognitive and functional performance and improvement in verbal-memory performance.
"It feels like science-fiction, where you can take a drink of Souvenaid and you get more synapses...for improved cognitive function. But it works," said Richard Wurtman, Professor at the Massachusetts Institute of Technology in Boston.
Importantly, Souvenaid led to a 26 per cent reduction in the loss of hippocampal volume, which is caused early in Alzheimer's by brain tissue loss.
The results indicate that Souvenaid may be able to slow or stop full progression of very early Alzheimer's into a full-blown disease, Wurtman noted.
The findings could encourage more researchers to view synapse restoration as a treatment for Alzheimer's.
"Everyone who writes about Alzheimer's knows there's a synapse deficiency, and this impairs connections between brain regions. Even if the amyloid or another problem gets solved, one way or another, you'll have to replace these synapses," Wurtman said.
------------
[Fresh from their success in patenting/copywriting their combo salmon+mackerel+Centrum oil MIT researchers say they are running snake oil through preclinicals and they are very optimistic.]
A few interesting articles on:
The importance of the patient caregiver in AZ clinical trial outcomes
http://newsroom.ucla.edu/releases/in-alzheimer-s-clinical-trials-241844
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842422/
The APoE-4 gene and AZ
https://stories.abbvie.com/stories/finding-hope-for-alzheimers-in-little-gene-that-could.htm
Biogen going all in with Aducanumab
biogen-commits-an-extra-500m-to-alzheimers-blockbuster-hopeful-aducanumab
We have to remember, this to an extent a vote of what they think of their partnership/takeover-eligible competition and their respective stages of development, currently. IMO we are much too early in dev stage and without data that blows the roof off (to overcome early stage doubts.)
yes, while that stock price headed for (a)equinox-ian levels my portfolio, in its absence, stayed in solstice.
Wasn't aware of the connection - thanks for the tip!
F1ash, useful DD. Another one would be VTVT's compound currently in a late P3 and the next one on deck for readout in AZ space. Their approach of modulation of the RAGE pathway may improve mitochondrial damage. (Not your typical targeting of abeta aggregation or tau tangles.)
I haven't done enough digging to have a stake in this. Ron Perelman is a huge stakeholder. (PS: Moderators, I'm long & strong AVXL & not looking to get bashed / deleted.)
http://www.sciencedirect.com/science/article/pii/S0891584917307281
F1ash, Thanks for sharing. BTW what 'statistical rules' is he talking about (which you seemed to pick up on earlier from the call)? All I see is raw data averaged up (while somehow accounting for the dropouts.)
This wait has been incredibly unbelievable (bested only by IPIX)!
I mean, if anyone forks up $ for the entire P2b/P3 trial, they should need more than Part B results and a promise that Ariana based incl/excl criteria will work.
Instead, I think, a Part C validation of Ariana's KEM based subgroup selection for 7 pts and possibly dose escalation for some of the remaining 25 pts for a full 12 months is what would be the minimum necessary for the funding.
I believe this is why Missling "delayed" the start of Alz P2b/3 until Nov/Dec. He had to because he needed 12mo data for Ariana-driven Part C for funding. Otherwise sitting on Part B data for a year is unjustified. The idea that computing PK/PD results and Ariana's KEM analysis of the data CAUSED the delay NEVER rang true to me.
News of full external funding of Alz P2b/3 will be a major factor in popping AVXL stock. I'm reaching a bit here but if at CTAD, Missling shows an additional 7 super-responders for a total of 14 in Part C, I will be ecstatic.
Daniela Semedo was completely off her rocker in writing that - a case of very poor DD. I would expect you to have dismissed it off the bat without blinking and not spent an extra second thinking about it again. Perry's case is cringeworthy and I hope you can estab. contact.
And of course we have 7 remaining who have improved MMSE scores at 12 months. So an equivalent ~20%/ITT to Flurizipan. It hasn't been in contention to my knowledge (I don't read every post.)
F1ash, your quote referencing their poster describes Part B while I was alluding to Part C. I was using your clarification there, that Part C is really a completely new trial to speculate that it would give them the freedom to adjust the lower doses. I assumed that they were constrained from doing so by Part A + Part B protocol and not patient tolerability. If they attempted to titrate up and reached the tolerability bounds earlier then my guess of their flexibility to do so in Part C is redundant.
Separately, I'm not sure why Dr. Perry said that the case of a drug improving or benefiting patients through a long period has never been witnessed before when you have shown results from the Flurizipan study in detailed charts, clearly showing about a good 18% showing retained improvement at the 12 month interval.
I'm not sure why Dr. Perry was on the call (as 3rd party) in the first place. It's as if Missling were implying "if you don't believe in the data or what Anavex is saying then listen to this editor of the Journal of AD". Esp. when he has a galaxy of stars in the Anavex SAB. Beats me.
Could Missling be using Part C as his secret (early) Phase 3 by taking Ariana feedback and confirming Ariana projections on the "current 32?"
ie. at a minimum, he should be able to escalate dosage on the "ongoing 25" to 50mg in case they were below it and didn't optimally respond, to then determine if observed effect matches Ariana's projections.
ie. on top of the "ongoing 25", Missling has the discretion to use Ariana's screening to pick his "new 7" and confirm if ALL of them "super-respond."
He will have almost 12 months of observations on them by now.
I'm sure it's obvious to Anavex & Ariana but it's worth mentioning - I think there are 2 separate analyses on which the explanatory analysis of KEM must be applied: dose response and concentration response.
One answers the question what biological factors hinder/facilitate the absorption of the compound into the CNS and its ease of crossing the blood brain barrier.
The other question of what biological factors hinder facilitate the translation of concentration into measured improvement.
One more - after today's CC do we have clarity on whether AVXL will be successful in statistically proving superiority over SOC in AD? I think it the targeted approach that will get us over the hurdle which would be otherwise hard to cross.
I think the 21st CCA will allow us to attempt a titration of each patient up to 50mg over time if 50mg up front is not immediately suited.
My CC questions/observations:
Wonder what the inclusion/exclusion criteria are and whether they will be revealed at CTAD or at trial commencement. (No mention of the more pertinent biological factors either.) Otherwise this whole exercise still sounds very conceptual and an incomplete exercise after a year of waiting.
Will the same inc/exc criteria be applied for all trials?
Impressive to see them mucking around with 80! different explanatory variables and sussing out 83! rules. Can't believe they said they have "additional data to be incorporated" after all this time and all before start of trials.
Seems like dose response is likely to be the big driver around which KEM is modeling. I would think they have exercised any ability to escalate dosage going into Part C of the trial. There's a bunch in the bottom left quadrant that stand to move diagonally up to the top right and make the overall scatterplot a successful story to tell.
Am I wildly off in thinking, they have just 2 data-points/patients to try and figure out what biological factors may have allowed for an MMSE improvement at a low dose?
Wonder why they chose MMSE slope from baseline as y-axis of scatterplot rather than MMSE delta from baseline (like they did for ADCS-ADL.)
Have INDs been filed/accepted with the FDA at this point for Rett & Fragile-X? I'm guessing they have been filed unannounced as they insist on starting the trials this year.
Overall, I'm optimistic - this may be simplistic thinking but if you were to draw a diagonal on the scatterplot, running from the bottom-left corner to the top-right corner, most of the points on the scatterplot reside on the top-left side of that diagonal. To me they are the super-responders and ones that offer promise. Just 4 patients exist clearly to the bottom-right of that diagonal that may be considered as unlikely to see any benefit.
Alzheimers: Pharma & patient desperation
https://www.statnews.com/2017/10/03/alzheimers-pharma-homeless/
Webpage archive of Anavex Pipeline webpage (from Wayback machine)
July 7, 2017 archive
https://web.archive.org/web/20170707125929/http://www.anavex.com/pipeline/
May 17, 2017 archive
https://web.archive.org/web/20170517144326/http://www.anavex.com/pipeline/
Anavex isn't presenting at ECTRIMS - Wayne State is & it's all pre-clinical findings.
power, my gut wants to believe it. i'll take a 15% cut of revenues to Anavex with appropriate lump-sums at p1/p2/p3 milestones. When Missling throws crumbs, he doesn't throw them for nothing. I roughly cuff the last jump as a 10-bagger - 30c to ~$3.3 ($14 rev.split adj). Can't do a 10-bagger this time but 4x to $14-15 is doable - fingers crossed.
jmvho, hope you're right. TTTav66's post# 113277 was highlighted again today - Wayne State prof. will be presenting A2-73 remyelination at ECTRIMS/ACTRIMS in Paris on 10/27. Tantalizingly BIIB will be talking about RWE & personalized medicine at the conference, a term that Ariana showcases. Why is BIIB suddenly talking RWE & personalized medicine when they have clunky overpowered tests on weak compounds chasing defunct (beta amyloid) theories? So many threads...
fireman pointed out Klamer talking about MS as recently at CNS Partnering and Deal Making on 9/11.
Last but not least, Biostockclub's post# 122112...
Anavex couldn't possibly have dropped the indication from further testing. It makes the other outcome viable.
I hear you re: strong MS pre-clinical results as does jmvho's post# 122089. Very perplexed to say the least on removal of MS development from presentation and website. I still don;t buy the NDA/BIIB hypothesis.
Blu, no need to clutch at straws here, esp. since you're always rational. MS w/ Biogen is gone and more concerning is the MS indication has been taken off the pipeline development chart on pg.4.
AVXL couldn't possibly ignore any ongoing development interest from BIIB. With all the white elephant chasing in Alz by BIIB & big pharma running multi-1000 patient trials, a no-thanks is a genuine source of concern for it's implications in other indications too.
Missling's in/out-licensing statement is a very generic CEO statement in investor forum presentations. I think in-licensing was an inapplicable term he used earlier to begin with - can;t buy much with $20mm in the bank. Now he's trying to gloss over it by stating in/out- and in the next presentation you might see just out-licensing which is what matters to us as far as pipeline drugs are concerned.
I don't mind if they open the door to Roche, Pfizer, etc.
Notes from leafing over the presentation...
Pg 3
* 1st time printed mention of "strong IP (COM to 2033)"
* 54? subjects treated with A2-73 over p1+2a? No one's discussed the 54-32=22 subjects plausibly treated in p1?
* Q4 - PK/PD release & start of 3 trials reiterated
Pg 4
* A-2-73 for MS with Biogen is dead & buried - no mention in remainder of main presentation - leftover in appendix is probably oversight
Pg 14
* 1 page is very little detail on establishing hypothesis & plan forward with Parkinsons
Pg 20 LOVED IT!!!
* Full Genomic Sequencing!!!
* Affirmative validation of Ariana's KEM to estab. "Systematic Responders Hypothesis"!!!
"Actionable optimized p2/3 clinical trial patameters" !!!
Pg 22
"Ongoing in-licensing/out-licensing review to optimize value of pipeline" - still on Missling's mind - consummate (potential) dealmaker!
Pg 28
* While they have said it before, I like them pointing out - "Temporary improvement in P300 amplitude seen with donepezil therapy persists (italics) with ANAVEX 2-73"
OVERALL
Timeline: I still don't think Anavex can effectively commence by EOY2017, esp. trial site id & 1st patient recruitment for Parkinsons and maybe Alzheimers. It leads me to believe we will see a master protocol under 21st Century Cures Act as some have speculated which will allow Anavex to formally claim the start of all 3 trials.
Great to see a mostly NEW slide-deck - the old one was wearing on me. They ought to change the pics on the front & back covers though - I could recognize the 2 ladies on the cover in a mall if I ran into them - seen their mugs so many times now. put Ern Heaven's pic :)
Speculation on a timeline to buyout - the case of Kite Pharma (KITE)
AVXL has been very quiet for very long and has apparently delayed the start of it's next set of trials. The latest speculation on the latter points towards the wait for release of FDA's new design protocols. But that shouldn't stop AVXL from releasing 1.5yr & PK/PD data.
What about the silence? With Missling executing his program buys, I have wondered if it throws cold water on the possibility of an Non-Disclosure Agreement/confidentiality agreement, AVXL may have signed with BIIB (or PFE) to evaluate either an MS (AZ) collaboration (or a buyout.)
However someone on Twitter speculated on the timeline to the ultimate buyout of KITE by GILD starting with NDA signing. If you compare it with insider purchases and sales, many company insiders and their uncles were buying / selling KITE until close to announcement. Granted most of them were out of the loop but the EVP - BizDev sold as recently as Aug 10. It's clear the big chunk of group buys took place after hypothesized NDA agreement date.
Going by this, I'm inclined not to count out deal-making involving AVXL just yet. Only doubt is, it's too early in its clinical stage with very limited data but data-length helps if data is passing good.
One thing's for sure if we were to believe this timeline - deal talks take time and a fruitful outcome to BIIB's MS testing agreement is possible.
Investor, try solving Missling's 1000 share purchases in 2015 with 20/20 hindsight and I promise I'll have a prize for you. This time, Missling wanted to spend about 25K on this exercise and guessed an approx. avg. price of 4.5 - so the 375 shares.
Pls. don't let the few kids running amok on this otherwise useful board bait you into lowering your standards of commentary
Mike, your website rolled up 6/30 & 7/1 (1K each) purchases into ONE entry of 2K recorded for 7/1. It also rolled up 7/6 and 7/7 purchases into 1 entry under 7/7. These in combination give the appearance of 11 purchases.
The SEC website http://bit.ly/2xtQqPe is the best to go by.
Mike, Missling bought 13 times in 2015. See post# 115176 by hess or sec archives.
Bio, look forward to what your bio-patent friend has to say. Until not too long ago (but not lately), Missling kept talking up the phrase "in-licensing" and I felt its definition didn't fit his objective (as I interpreted it.) I felt like out-licensing was the correct term to use which is what you are describing. Always wondered how an ex-investment banker like him would ever make a faux pas like this. Any thoughts?
JG, did you see the following?
Is $AUPH's lupus nephritis hegemony threatened by $GSK's Benlysta? New commentary at http://stockgumshoe.com .
Biostockclub, thanks for the explanation - hadn't quite understood the motivation behind the preferreds earlier. Signal of confidence just like Misslings scheduled share purchase breadcrumbs now. (Not quite sure why he put preferreds to a vote back in 2015 though - too early in hindsight.)
Hoping any earlier dispersion in MMSE or ADCS/ADL or P300 among indiv. patient timeseries have tightened up towards the upside over these 1.5 years.
hess/kld, "MECP2 Reactivation under "Cure" could be Anavex. See presentation link below from Anavex website:
http://www.anavex.com/assessment-of-anavex-2-73-in-a-mecp2-rett-syndrome-mouse-model/