stealth accumulation is going on.No one was ready to sell below 6$.Now they have to raise bid to buy in more shares
This one could be making a big move soon, unfortunately it could be down. I still wonder if the drug has any use, but the company may not be the right one. $3 has held since mid-Nov 2015, but this descending triangle/wedge now looms. Watch which way it breaks.
Currently under $3, but 10% off its lows today (went down to $2.65). It seems like it cannot push lower than that. There was a volume explosion 3 weeks ago (see box in chart), and then a virtual desert of buyers/sellers. Today it pushed lower, but then quickly bounced back.
Yeah I still look at this stock. Biotechs (IBB) fought back nicely today, still need to overtake the 20 ma. This one has been able to hold above 50 ma support.
Triple-topped around $4, then pulled back and held $2.40. Looks like it wants to make one more run this year.
New ATH, gives me hope that something really is happening with their Alzheimer's treatment. It works in a different way from all the other ones that have failed; everyone keeps trying to remove amyloid plaques, and that has always failed. Seems those drugs can remove (part of) the plaque the first time, but the plaque comes back and then the drug isn't effective anymore.
Anavex Life Sciences' Alzheimer's Candidate Mechanism Of Action Explained In Medical Journal https://finance.yahoo.com/news/anavex-life-sciences-reports-publication-110000181.html Scientific Paper Highlights: Sigma-1 receptor (SIGMAR1)’s expression increases with age, however in Alzheimer’s disease (AD) it decreases The decrease in SIGMAR1 expression during AD coincides with an age-related decrease in autophagy The SIGMAR1 may compensate for loss of receptors and autophagic machinery during healthy aging SIGMAR1 is activated by ANAVEX-compounds ANAVEX®2-73 has been shown to induce autophagy Activation of the SIGMAR1 can induce cytoprotective autophagic pathways Spoiler The authors of the paper point out that studies using positron emission tomography (PET) have shown that in healthy aging, there is no loss of the SIGMAR1; in fact, there is a possible increase in SIGMAR1 expression2 that coincides with the age-related loss of the M1/M4 muscarinic receptors3, D1/D2 dopamine receptors4, and serotonin (5HT2A) receptors5. The increase in SIGMAR1 expression may be a compensatory mechanism for the loss of the other receptors6. However, PET scans of patients with a recent AD diagnosis show a reduction of SIGMAR1 expression7. SIGMAR1 also promotes autophagy and results in the degradation of amyloid-beta precursor protein (APP) thereby inhibiting Aβ production8. The publication explains that AD is a multifactorial disease, where several pathways interlink with each other and cause cognitive impairments. The available drugs only tend to target a single pathway and mitigate the symptoms of AD without slowing the disease progression. Combinatorial therapy has been suggested as a treatment strategy; however, the existence of drug-drug interaction is a concern. Hence, there is a need for the development of drug molecules that can target multiple pathways to halt disease progression and improve the memory function. SIGMAR1 has emerged as one of the prominent targets in treating neurodegeneration. It is involved in the modulation of glutamate levels, maintaining endoplasmic reticulum (ER) function, and calcium regulation, promoting neurogenesis, reducing reactive oxygen species (ROS) formation, suppressing neuroinflammation and ameliorating Aβ toxicity9. Recent studies with ANAVEX®2-73 show that SIGMAR1 activation is also involved in autophagy, an intricate phenomenon that clears damaged cellular organelles and misfolded proteins10. SIGMAR1 agonists, including ANAVEX®2-73 and ANAVEX®3-71 have been reported to block toxic Aβ, tau and neuroinflammation. Autophagy and the cellular machinery involved are essential to homeostasis and cell survival. Autophagy has been shown to be important for axonal health and homeostasis as autophagy inhibition leads to axonal wasting12. During the early stages of AD, it has been noted that there is an accumulation of Aβ and tau protein in the dystrophic or swollen neurites of AD patients’ brains. Furthermore, it is well known that autophagy plays a key role in the management of Aβ and tau protein levels, and that some of the key proteins involved in the autophagy mechanism disappear with age, resulting in decreased autophagy in older brains13. At the same time the SIGMAR1 is upregulated, possibly compensating for the reduction in autophagy, and reduction in other receptors, such as muscarinic receptors14, dopamine receptors15, and serotonin receptors16, in an attempt to protect the neuron cells. Since it has been observed that a number of SIGMAR1 agonists, including ANAVEX®2-73, is able to upregulate SIGMAR1 expression in the brain, it is possible that these drugs could help the cells to compensate for the loss of other receptors and autophagy machinery. The authors conclude, that in the future it may be the case that SIGMAR1 ligands (or drug combinations) targeting the activation of autophagy, and other SIGMAR1 related neuroprotective pathways, are prescribed prophylactically, in much the same way as with statins for the prevention of heart disease today in an effort to prevent the loss of the SIGMAR1 receptor seen during AD. “This independent paper highlights the understanding of the relevance of utilizing sigma-1 receptor activation as compensatory mechanism to chronic CNS diseases, currently tested in late-stage placebo-controlled ANAVEX®2-73 Phase 2b/3 clinical Alzheimer's disease study, which recently completed enrollment, as well as in Parkinson’s disease dementia (ANAVEX2-73-PDD-001) and ongoing Rett syndrome program (ANAVEX2-73-RS-001/002/003)”, said Christopher U Missling, PhD, President and Chief Executive Officer of Anavex. ANAVEX®2-73 activates the sigma-1 receptor (SIGMAR1). Data suggests that activation of SIGMAR1 results in the restoration of complete housekeeping function within the body and is pivotal to restoring neural cell homeostasis and promoting neuroplasticity.17 Anavex Life Sciences’ product portfolio platform includes small molecule drug lead candidate ANAVEX®2-73 for the treatment of Alzheimer’s disease, Parkinson’s disease and Rett syndrome and ANAVEX®3-71 for frontotemporal dementia. I copy/pasta a lot so put it in spoiler tag. But here's the take home: available drugs only tend to target a single pathway and mitigate the symptoms of AD (Alzheimer's Disease) They do nothing to the actual disease. AD is more than just amyloid plaques.
The company’s Alzheimer’s disease treatment, Anavex 2-73, is currently in use for a Phase 3 clinical trial.
