"They have the money to buy innovation when their own begins to slip"
Roche is a fine example this morning, and they were considering Gantenerumab in compbination with a BACE Inhibitor, an already failed approach in the eyes of many, but big pharma companies are still pushing BACE inhibitors into new trials...
Headline today from the other thread:
Roche scuttles PhIII Alzheimer's study in yet another setback for the field
December 19, 2014 | By John Carroll
Yet another big Phase III test of an experimental Alzheimer's drug has flopped. And this time it's Roche's turn to admit defeat.
Gantenerumab is a fully human IgG1 antibody designed to bind with subnanomolar affinity to a conformational epitope on Aβ fibrils. It encompasses both N-terminal and central amino acids of Aβ. The therapeutic rationale for this antibody is that it acts centrally to disassemble and degrade amyloid plaques by recruiting microglia and activating phagocytosis. Gantenerumab preferentially interacts with aggregated brain Aβ, both parenchymal and vascular. The antibody elicits phagocytosis of human Aβ deposits in AD brain slices co-cultured with human macrophages. It also neutralizes oligomeric Aβ42-mediated inhibitory effects on long-term potentiation in rat brains. In APP/PS-1 transgenic mice, gantenerumab binds to cerebral Aβ, reduces small plaques by recruiting microglia, and prevents new plaque formation. Gantenerumab does not alter plasma Aβ (see Bohrmann et al., 2012). It is being studied as a potential combination therapy with the Roche BACE inhibitor RG7129 in mouse models of Aβ amyloidosis (see Apr 2013 news story).
Yep, AB reduction is not the whole story. I have been sitting on some AVXL for quite some time and almost doubled my holdings of it today. I'm not betting the farm, but from this price level a double could happen with any inkling of a positive trend, and any significant news could bring a five or ten multiple. I took my chances at least to build at least a little nest egg at this level.
You should try citing studies from this decade versus going back to the aluminum frying pan scare where you are still trying to discredit Iron, Copper, Zinc's potential role in AD based upon the successful campaign to discredit science of that decade. There is a lot of independent studies supporting the MOA of Prana's PBT2, and wiki is just another biased forum, driven by whatever bully wants to stuff it full of drivel.
I know Prana's metals theory, but that's still based on the AB theory of AB reduction. I still think it has legs, and hopefully PBT2 does as well.
I would be putting my money here long before investing in a BACE inhibitor, but I'm not knocking the AB reduction MOA at this point. I still have some coins in PRAN also.
I dropped more coins here today. The timing is ripe and the upside is huge for this one.
The complimentary nature of their compound with donepezil gives this company a natural partner. Plus the fact they are testing it standalone, and in a complimentary nature gives the company higher odds of success, and room for both surprise and mitigation. This also gives them potential leverage in partnering negotiations.
First patient now enrolled means first patient about to be dosed.
Open Label trial means announcements or partnerships could be announced anytime, and good indications are going to go public sooner.
Partnering conference announced today for Jan 12th in San Francisco, so a little publicity possibly in the wings.
This is a high risk but also a high reward stock. The timing to me looks s pretty good for an upside run from here. Just my opinion only.
Thanks for sharing this, I also read it earlier and we must remember that it was this yeast model that screened Prana's compounds and many others coming up with only a small number of potential drugs. Wasn't it also the Lindquist group that came out in support of Prana's trial, and based upon their own trial disappointment in the drug that was sold to Pfizer, via the FoldRX transaction they advised that a longer dosing period may be required to determine significance, but that the approach was sound. They more/less predicted eventual success of Prana's drug PBT2. Susan and Rudy shower each other w/love within their profession.
I see on the slide listing B-Amyloid (Anti-Abeta Therapies) it lists GSMs, Immune, PBT2
As he just now mentions PBT2 again in talking of "targeting metals is as good a strategy as ANY out there"!!!
I have been sucking wind on this stock for along time, but added more today. Good news fed into a bad market is ok by me. Nice to get an opportunity to buy more before this news sinks in. I like the options incentives in tranches requiring a 2.50 & 3.50 shareprice. That is how companies should always do it, but most just give away options to execs anymore without requiring shareprice performance. This is truly how it should always be done. Now I know the CEO will be working hard to make things happen, and he appears to have the experience to get it done.
It's obvious you are back here to make up your tremendous losses on the two stocks you were pumping - Mankind and EDAP, both of which completely tanked. If you think you have any credibility whatsoever on this board, think again.
Maybe you can buy into Pran and recoup some of your losses.
Go read the normal aged mouse study results, and the findings show are quite promising for PBT2 and HD.
The aforementioned result is from the normal aged mouse study - not ZNT3 knock-out AD mice....so might be different w/AD...
Here it is...glad they are doing further research...
I found the mention I was thinking of in this excerpt from the normal aged mouse study in aging cell:
PBT2 increases VGLUT1 and glutamate levels
Whether the increase in cellular zinc levels directly translates to an increased availability of zinc specifically at the synapse is unclear. To this end, we examined the levels of the zinc transporter 3 (ZnT3) protein in the hippocampus. ZnT3 is primarily localized to glutamatergic synapses (Palmiter et al., 1996) and is essential for loading zinc into synaptic vesicles (Cole et al., 1999). We have previously shown that the ablation of ZnT3 results in a profound age-dependent cognitive phenotype and that there is an age-related decline in this protein in both normal mice and healthy older adults and a further exaggerated decline in AD (Adlard et al., 2010). Thus, in addition to an increase in zinc levels, a plausible mechanistic pathway to account for the restored cognitive function following PBT2 treatment observed in this study would require an upregulation of a synaptic vesicle zinc transporter such as ZnT3 (PBT2 itself may also be acting as a surrogate vesicular/synaptic zinc transporter, which is the subject of ongoing investigations). This would ensure the correct localization of zinc that would then facilitate the cellular signalling pathways required for cognition. Surprisingly however, there was a significant decrease in total hippocampal ZnT3 levels following PBT2 treatment [PBT2 (−33%), P = 0.01] (Fig. 4a), suggesting that another zinc transporter may be activated following PBT2 treatment. Thus, we examined the levels of the vesicular glutamate transporter 1 (VGLUT1) in the hippocampus
I am pretty sure that an early Adlard paper conjectured that znt3 was an anticipated MOA of PBT2, but that later evidence suggested otherwise in one study. I'll search and come back with the reference. Was PBT2 mentioned at all in this study?