What are CERTIFIED results. So far they have given top line result for AD. The HD results were pretty good according to the HSG docs, who would know.
That is a good idea to go back 30 days and look at the price.
Back then they had the HD results in the bag and a tiny AD trial running. The company had indicated a pivotal p3 trial in HD as the fastest way to market. The AD trial didn't prove or disprove much, but the extension of that trial is still running and could identify cognition gains as well as continued plaque reduction.
Now the HD trial is still on track, they are working on an Orphan drug application, and two new preclinical drugs are close to the clinic. They will then also add value.
An 80% drop is way overdone and this stock represents reasonable chance of a 10 bagger again.
Sentiment: Strong Buy
"adding value". HUH? The stock is down 80% and new 52 week low? The ONLY value here is the cash they have and at 1.89 Pran is OVERVALUED. Folks go back 30 days and read about all the information posted here. Then look at the stock chart. LOL. You have been warned about the pumpers here. MAYBE there is a buck over cash value for the R&D. ONLY when they post CERTIFIED results don't pay anything over 2.25 a share for this dog.
You have any later paper on MPACs and cancer I would be glad to read it. Oh hang on I forgot, you have no infomation in any of your posts, just stupid slogans and insults.Right now only PBT2 is adding value to Prana, but in several months that will change when PBT434 and 519 emerge from preclinicals. The movement disorder drug PBT434 and HD raise an obvious combination possibility.
The Lindquist paper identified strong synergies between MPACs and several combination options will open up with the emergence of these two new MPACs
Sentiment: Strong Buy
Considering the best results were seen in early HD patients with no plaques that early ageing market of normal agers must be a possible next step.
Remember we have still not seen Barnhams work on excitotoxicity yet.
Sentiment: Strong Buy
Hard to say Pivalde, with 20 times the BBB penetration PBT2 may be different from CQ, even being an analog of CQ. They only tested to 800mg a day without reaching dose limiting toxicity in the early PBT2 trial, nowhere near the 3200mg where they found toxicity in that CQ trial in Canada.
You have to think that with the effect on iron of PBT434, ,maybe there could be a role in cancer prevention there considering research that has emerged over recent years regarding iron damage to P57.
Sentiment: Strong Buy
Not really. The reason I was happy to take the gamble, was because there was some nice backup from the Parkinsons and Brain Cancer drugs. Stated that before trial results.
As it turned out the backup was not needed because HD results were good enough to progress PBT2 to phase 3 trials for approval, but regardless the PD and cancer applications progress and it is worth comment.
Sentiment: Strong Buy
stock is DOWN 80% in a month. All technicals say SELL. It is amazing that it took this long to get a dead cat bounce. That is NOT a good sign. The dropping of VOLUME is the good sign as when we get down below 250K trades with a few under 100K trades is when we will the real bottom. Thus we should see a final bottom from .50-1.50 PM
This paper below gives some understanding about the mechanism of neuronal loss. The toxic oligomers are in a very essential role. PBT2 helps to get rid of them and most likely that is the why hippocampus artrophy was reduced by 35% in the Imagine study (trend ).
Neurobiol Dis. 2014 Feb;62:273-85. doi: 10.1016/j.nbd.2013.10.007. Epub 2013 Oct 17.
Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events.
Bhaskar K1, Maphis N2, Xu G3, Varvel NH4, Kokiko-Cochran ON5, Weick JP6, Staugaitis SM7, Cardona A8, Ransohoff RM9, Herrup K10, Lamb BT11.
Massive neuronal loss is a key pathological hallmark of Alzheimer's disease (AD). However, the mechanisms are still unclear. Here we demonstrate that neuroinflammation, cell autonomous to microglia, is capable of inducing neuronal cell cycle events (CCEs), which are toxic for terminally differentiated neurons. First, oligomeric amyloid-beta peptide (AβO)-mediated microglial activation induced neuronal CCEs via the tumor-necrosis factor-α (TNFα) and the c-Jun Kinase (JNK) signaling pathway. Second, adoptive transfer of CD11b+ microglia from AD transgenic mice (R1.40) induced neuronal cyclin D1 expression via TNFα signaling pathway. Third, genetic deficiency of TNFα in R1.40 mice (R1.40-Tnfα(-/-)) failed to induce neuronal CCEs. Finally, the mitotically active neurons spatially co-exist with F4/80+ activated microglia in the human AD brain and that a portion of these neurons are apoptotic. Together our data suggest a cell-autonomous role of microglia, and identify TNFα as the responsible cytokine, in promoting neuronal CCEs in the pathogenesis of AD.
Actually doctors would choose to prescribe it because of it's positive results concerning it's ability to preserve brain mass and it's ability to improve patients conditions with soluble toxic oligomers.
Not only will pbt2 be viable for HD and AD but these brain images of healthy brains make me want pbt2 right now to reduce aging effects! Yikes!
Once it's on the market for HD off label use will include AD and normal aging. It is just a matter of time.
Kadaicher, thanks! So it will be most likely safe to give 500mg PBT2 (perhaps even 750mg) in HD and AD and so we could expect also better efficacy in treating HD and AD, both deadly diseases as cancers.
J Alzheimers Dis. 2014;38(4):809-22. doi: 10.3233/JAD-131247.
Meta-analysis of serum non-ceruloplasmin copper in Alzheimer's disease.
Squitti R1, Simonelli I, Ventriglia M, Siotto M, Pasqualetti P, Rembach A, Doecke J, Bush AI.
The fraction of copper not bound to ceruloplasmin seems altered in Alzheimer's disease (AD). We have addressed this notion evaluating all the studies carried out from 1996 until March 2013 by means of meta-analysis. We performed our analysis on diverse indices evaluating the relationship between copper and ceruloplasmin in general circulation, namely 'Non-Cp copper', '% Non-Cp copper', and 'Adjusted copper'. For Non-Cp copper and % Non-Cp copper, the correct stoichiometry between copper and ceruloplasmin (6-8 atoms of copper for each ceruloplasmin molecule) in healthy controls has been adopted as criterion for the study to be included in the meta-analysis evaluating data with the canonic Walshe's formula for Non-Cp copper. Copper to ceruloplasmin ratio (Cu:Cp), which is an internal quality control check for ceruloplasmin calibration, was used as an index of the actual stoichiometry in the specimens. Adjusted (Adj-Cp) copper, even though less reliable, was calculated, allowing the evaluation of all the studies selected. An additional meta-analysis of systemic total copper was re-calculated accounting for all the studies carried out from 1983 to March 2013. Ten studies were analyzed in the meta-analysis for Non-Cp copper and % Non-Cp copper reaching a pooled total of 599 AD subjects and 867 controls. For Adj-Cp copper, 14 studies were analyzed with a pooled total of 879 AD and 1,712 controls. 27 studies were considered for systemic total copper meta-analysis, with a pooled total of 1,393 AD and 2,159 controls. All the copper indices analyzed were significantly higher in AD subjects compared to healthy controls.
Ann Neurol. 2014 Mar 13. doi: 10.1002/ana.24136. [Epub ahead of print]
Value of serum nonceruloplasmin copper for prediction of mild cognitive impairment conversion to Alzheimer disease.
Squitti R1, Ghidoni R, Siotto M, Ventriglia M, Benussi L, Paterlini A, Magri M, Binetti G, Cassetta E, Caprara D, Vernieri F, Rossini PM, Pasqualetti P.
Meta-analyses show that nonbound ceruloplasmin (non-Cp) copper (also known as free or labile copper) in serum is higher in patients with Alzheimer disease (AD). It differentiates subjects with mild cognitive impairment (MCI) from healthy controls. However, a longitudinal study on an MCI cohort has not yet been performed to assess the accuracy of non-Cp copper for the prediction of conversion from MCI to AD during a long-term follow-up.
The study included 42 MCI converters and 99 stable MCI subjects. We assessed levels of copper, ceruloplasmin, non-Cp copper, iron, transferrin, ferritin, and APOE genotype. A multiple Cox regression analysis-with age, sex, baseline Mini-Mental State Examination, APOE4, iron, non-Cp copper, transferrin, ferritin, hypercholesterolemia, and hypertension as covariates-was applied to predict the conversion from MCI to AD.
Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ∼20%. Subjects with non-Cp copper levels 1.6μmol/l had a hazard conversion rate (50% of conversion in 4 years) that was ∼3× higher than those with values ≤1.6μmol/l (