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Share Name | Share Symbol | Market | Type | Share ISIN | Share Description |
---|---|---|---|---|---|
Proteome Sciences Plc | LSE:PRM | London | Ordinary Share | GB0003104196 | ORD 1P |
Price Change | % Change | Share Price | Bid Price | Offer Price | High Price | Low Price | Open Price | Shares Traded | Last Trade | |
---|---|---|---|---|---|---|---|---|---|---|
0.64 | 18.23% | 4.15 | 3.50 | 4.80 | - | 423,867 | 16:35:28 |
Industry Sector | Turnover | Profit | EPS - Basic | PE Ratio | Market Cap |
---|---|---|---|---|---|
Biological Pds,ex Diagnstics | 7.78M | 1.33M | 0.0045 | 7.80 | 10.36M |
Date | Subject | Author | Discuss |
---|---|---|---|
27/1/2024 14:16 | I've got "methinks" just in case anyone was thinking of using it to appear avec wisdom. | small crow | |
27/1/2024 14:01 | Excuse me! I believe I own the copyright to 'wait and see what happens'. Royalty cheques addressed to me, please. | bluemango | |
27/1/2024 13:05 | Aye, I waited and saw my tens of thousands of £2 shares shrink to 5p | dominiccummings | |
27/1/2024 09:07 | I have heard that is the Company’s entire business strategy, although they have been ‘waiting and seeing’ for decades now without much happening. | monte1 | |
27/1/2024 08:58 | Guess we will "wait and see" | coldale1 | |
26/1/2024 21:08 | In the past week, there were two items of news relating to blood based biomarkers that made it news headlines. One of these concerned Tau biomarkers in Alzheimers. Neither of these discoveries were connected to PRM, but ,they were considered significant insofar as they allowed doctors to make accurate diagnosis using a simple blood test.Of course, this might just mean nothing for us long-suffering shareholders ,or it might well mean that there is considerable interest in early diagnosis of disease with simple blood tests... | 049balt | |
25/1/2024 11:28 | Search in "Proteome Sciences leading Alzheimer's technology." - (PRM) Search for: godot Poster Post Found 19 results: | james japp | |
25/1/2024 11:21 | isnt that the used car salesman model, simply waiting...for a customer to arrive | elpirata | |
24/1/2024 20:05 | What about the 'Test for Patience'? | dominiccummings | |
24/1/2024 19:59 | Nor enough money to defend any patent infringements.As for the American venture,it smacks of last chance saloon and 10 years too late.You are the eternal optimist Richard,but your optimism is misplaced with PRM.Where is this Stroke test and all the other tests touted over the years on which your guesstimates were based.One minute we are too early,now you say we can't do it given finances,make your mind up. | peverill | |
24/1/2024 19:55 | I think Goatherd is a paid ramper, he's gotta be on the payroll... | coldale1 | |
24/1/2024 19:04 | #92660 Not directionless. They are enjoying Californian sunshine. Go West!!! | dominiccummings | |
24/1/2024 18:22 | No, actually. The opening of labs in America is hardly "no direction" is it? Apart from that the main company strategy is, I believe, simply waiting to see when other companies launch projects base don biomarkers on which we hold patents. We can't really develop anything much ourselves, can we? We simply have not got enough money. | goatherd | |
24/1/2024 17:43 | Where is it going Richard,they are just floating and paying wages,no direction,even you must shake your head at times. | peverill | |
24/1/2024 17:00 | What a perspicacious post, peverill. For you, that is. :-) | goatherd | |
24/1/2024 10:50 | Who would want the gig? Sure, the money is good whilst it lasts, but it is a dead end when it comes to future ambitions. | james japp | |
24/1/2024 10:45 | This is dire!!.Mrs S isn't much cop is she,where does he find them.? | peverill | |
23/1/2024 13:42 | As that was over 8 years ago & Dr Pike remains in situ -I would have hoped we may have been closer to monetising our ‘discoveryR | base7 | |
23/1/2024 12:27 | Thanks small crow and consider yourself unlucky. | james japp | |
23/1/2024 12:24 | Well done. Have a sweetie. | small crow | |
23/1/2024 12:17 | ...from PRM history .... November 05, 2015 From the 8th Clinical Trials on Alzheimer’s Disease (CTAD) in Barcelona, Proteome Sciences is pleased to announce that a recently completed study testing its proprietary inhibitors of casein kinase 1 delta (CK1d) reduced the level of tau phosphorylation in a second in vivo model of Alzheimer’s disease (AD) tauopathy. Compounds were given orally for five days and the level of tau phosphorylation in the brain cortex was reduced compared to the control group. These results confirmed and are consistent with the previous in vivo study in a different AD model that revealed reduced tau phosphorylation when the compounds were given daily for 8 weeks. Commenting on the results of the study, Dr. Ian Pike, Chief Operating Officer at Proteome Sciences said: “We now have compelling evidence that both acute and chronic dosing of our CK1d inhibitors is reducing levels of phosphorylated tau in the brains of two different models of AD. Surprisingly, the effect of acute dosing on phosphorylated tau was nearly as potent as the chronic administration. Using our SysQuant global phosphoproteomic workflow we also saw that acute dosing resulted in some early changes in many of the downstream pathways we have previously identified that are affected by tau toxicity in human AD and were responsive to chronic CK1d inhibitor dosing. The data from the two in-vivo studies provides excellent support for the beneficial effects of our compounds PS 110 and PS 278-05 and their translation to human disease and adds further substance to our partnering discussions.” and .... Volume 282, Issue 32, 10 August 2007, Pages 23645-23654 Journal home page for Journal of Biological Chemistry Protein Synthesis, Post-Translational Modification, and Degradation Novel Phosphorylation Sites in Tau from Alzheimer Brain Support a Role for Casein Kinase 1 in Disease Pathogenesis* Author links open overlay panelDiane P. Hanger ‡ 1, Helen L. Byers § 1, Selina Wray ‡, Kit-Yi Leung § 3, Malcolm J. Saxton ‡, Anjan Seereeram ‡, C. Hugh Reynolds ‡, Malcolm A. Ward §, Brian H. Anderton ‡ Our findings therefore support the view that PKA and CK1δ might be important for subsequent Tau phosphorylation by GSK-3β. Taken together with the roles of CK1 in the regulation of the intracellular trafficking of β-site amyloid precursor protein cleaving enzyme (72, 73) and in phosphorylation of presenilin (74), our data suggest that CK1 could have a role in the pathogenesis of Alzheimer disease. It remains to be determined which sites on PHF-tau prove to be unique determinants of Alzheimer pathology, but one possibility is that phosphorylation of some or all of these orphan sites requires the concerted action of several different protein kinases to generate all of the known phosphorylation sites on PHF-tau. | small crow |
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