We could not find any results for:
Make sure your spelling is correct or try broadening your search.
Share Name | Share Symbol | Market | Type | Share ISIN | Share Description |
---|---|---|---|---|---|
Scancell Holdings Plc | LSE:SCLP | London | Ordinary Share | GB00B63D3314 | ORD 0.1P |
Price Change | % Change | Share Price | Bid Price | Offer Price | High Price | Low Price | Open Price | Shares Traded | Last Trade | |
---|---|---|---|---|---|---|---|---|---|---|
0.00 | 0.00% | 9.75 | 9.50 | 10.00 | 9.85 | 9.75 | 9.75 | 436,098 | 08:00:10 |
Industry Sector | Turnover | Profit | EPS - Basic | PE Ratio | Market Cap |
---|---|---|---|---|---|
Pharmaceutical Preparations | 0 | -5.86M | -0.0057 | -17.11 | 101.09M |
Date | Subject | Author | Discuss |
---|---|---|---|
12/1/2025 11:59 | most on here have got wise to you Ruck .... I hope Ivy has and takes my post as intended which was critical of investors expectation not Scancells | inanaco | |
12/1/2025 11:48 | keep it simple We have synergy and a low SP its a blessing !! if you make the most of it but if your scared of investing or not sure of yourself that is OK ... just take it easy | inanaco | |
12/1/2025 11:44 | you argue with yourself Ruck .... Bermuda used to do it a lot usually starting with Do you mean ? than translates my post into something i didn't mean than argues against his own misunderstanding its horrendous to try and follow his Drivel same applies to you ... | inanaco | |
12/1/2025 11:40 | it explains Investor expectation was higher than Scancells expectation are you so Stupid .... that you cannot read that ???????????????????? | inanaco | |
12/1/2025 11:38 | ruck read the posts again ............ | inanaco | |
12/1/2025 11:38 | "i am not debating you ruck its like dealing with a 6 year old you just do not read the posts correctly"Surely that's the point of a debate - make a statement, give the opportunity for an alternative viewpoint then clarify any misunderstanding? | ruckrover | |
12/1/2025 11:38 | other people agree chester18 Posts: 3,443 Price: 9.75 No Opinion RE: Cancer VaccinesToday 11:30 Morning Ruckrover Thank you for miss quoting me. | inanaco | |
12/1/2025 11:37 | Inan, "can you show us the RNS ruck"No, this was not the official line from the company but the over hyped drivel propagated on these boards by the over enthusiastic happy clappers (many of whom have since sold up and moved on) | ruckrover | |
12/1/2025 11:35 | i am not debating you ruck its like dealing with a 6 year old you just do not read the posts correctly | inanaco | |
12/1/2025 11:34 | Inan, Your 15962 suggest that Modi as a mono therapy works as expectedYour 15963 suggests Scancell didn't expect to work as expected (hence the combo trials)Which is it? | ruckrover | |
12/1/2025 11:34 | can you show us the RNS ruck It will be 90% effective It will totally disrupt the cancer drug market It will work totally stand alone many thanks | inanaco | |
12/1/2025 11:32 | i have replied to Ivy .... are you a ventriloquist now as well, with an Ivy Puppet on your lap | inanaco | |
12/1/2025 11:30 | so there it is ................. 1.7m says i am Right probably buy some more tomorrow that will send Nigel Mental | inanaco | |
12/1/2025 11:30 | Inan, "so the check points are a failure because they don't work very well in Ovarian ?"You need to read posts a little more careful. Ivy specifically said NOT a failure. His point is that Modi has not lived up to expectations which, just to remind you were:It will be 90% effective It will totally disrupt the cancer drug marketIt will work totally stand aloneThe above will result in a £8 per share price (£3.75 with dilution)I think everyone now accepts that just isn't going to happen. | ruckrover | |
12/1/2025 11:26 | Ruck is already off on one ........... | inanaco | |
12/1/2025 11:25 | Moditope Needs inflammation to work .. without that signal Moditope Does NOT FUNCTION its in all the pre-clinical Data ............. so Yervoy Ctl-4 blocking MAB can reverse the enviroment for Moditope to work CTLA-4 is a critical regulator in the inflammatory response. It is expressed in activated T cells and is constitutively expressed on Tregs. and This is why i am Here ... otherwise you have Ivy and Ruck talking absolute nonsense | inanaco | |
12/1/2025 11:23 | "becareful of trap doors !!"It's OK, if I fall you'll already be down there to break my fall. | ruckrover | |
12/1/2025 11:21 | "can you show workings"There aren't any workings necessary. You posted the article and that has all the figures. The rest is just logic. If 3.4% of cancer drugs starting clinical trials succeed then it is fairly obvious that drugs that have already started trials, have been in trials for a number of years, have data showing tumour shrinkage, have a good safety profile and have passed Simon stage 1/2 MUST have a higher chance. Don't you agree? Even TD have MODI with a 12.5% chance of success and Immunobody between 5 and 10% chance. Do you agree with the TD percentages? Either way, they are higher than 3.4%.Is this the point you were trying to make? | ruckrover | |
12/1/2025 11:21 | just so you understand when reading that if you don 't use a Blocking Mab like Yervoy ... this is the effect T-cell motility CTLA-4 increases T-cell motility and limits their binding to antigen-presenting cells (DCs). This is known as the "reverse-stop signal model". T-cell proliferation | inanaco | |
12/1/2025 11:18 | Cytotoxic T-lymphocyte antigen 4 (CTLA-4) and CD4+ T cells interact in a number of ways, including: T-cell motility CTLA-4 increases T-cell motility and limits their binding to antigen-presenting cells (DCs). This is known as the "reverse-stop signal model". T-cell proliferation CTLA-4 may inhibit T-cell proliferation, similar to its effect on effector T cells. T-cell activation CTLA-4 blockade can increase the number of activated effector CD4+ T cells. Treg expansion CTLA-4 blockade can increase the number of CD4+ FoxP3+ regulatory T cells (Tregs). These expanded Tregs have suppressor function and proliferate with treatment. Treg function CTLA-4 proteins are responsible for all three characteristic Treg functions: suppression, TCR hyposignaling, and anergy. T-cell localization CTLA-4 proteins in Tregs are localized in submembrane vesicles, while in naive Tconv cells they are retained in Golgi vesicles. T-cell function after TCR signaling TCR signaling of Tconv cells releases CTLA-4 proteins from Golgi retention, causing activated Tconv cells to acquire suppressor function. CTLA-4 is a critical regulator in the inflammatory response. It is expressed in activated T cells and is constitutively expressed on Tregs. | inanaco | |
12/1/2025 11:15 | but ................... as i have explained when it comes to CD4 T cells ............... the biggest player in the checkpoint arena ... is Ctl-4 just you wait and see ... | inanaco | |
12/1/2025 11:13 | I will accept that our understanding of the TME 5 years ago was far more limited than today so Expectations where actually higher based on how moditope worked but what we did not do 5 years ago was look at how difficult to treat cold cancers are and the TME what some have learned including me is that the TME is way more complex over that time period Lindy understood that hence getting combo's approved .... so it was our ignorance Ivy .... not Scancells over exuberance of moditope capabilities | inanaco | |
12/1/2025 11:05 | if the expectation that monotherapy alone would be sufficient to work as a standalone treatment Scancell would not have run combination trials ! and applied for approval all at the same time ............ Investor Expectation was higher than Scancells expectation !! that is not Scancells problem it was ours !! | inanaco | |
12/1/2025 10:57 | Dr David Pinato, Principal Investigator at Imperial College, commented: "Advanced ovarian cancer is an aggressive cancer which is hard to treat. A disease control rate of 44% with Modi-1 in patients who have exhausted most treatment options is very encouraging". Ivy commented did not meet expectations IMHO | inanaco |
It looks like you are not logged in. Click the button below to log in and keep track of your recent history.
Support: +44 (0) 203 8794 460 | support@advfn.com
By accessing the services available at ADVFN you are agreeing to be bound by ADVFN's Terms & Conditions