Member Info for inanaco

depends on liquidity Bob ... if they have very few shares and the buying pressure continues ..

Knowlesi the Pinstripe comes good in a Rally ... .... love 15 ....... 2 sets down 5 -1 down in set 3 ... market is winning

https://youtu.be/rLDm254jtZA

Knowlesi missed the Buy ...
now we can expect his Mumbles and Grumbles all the way up ..

Glycans

"""" Potential targets for redirected T cell and CAR-T therapy """"

acts like an Immtac ?

links a T cell or a Car T cell with a cancer cell

no idea, but the market was changing big time at that with the introduction of Pd-1 .. as its turned out we are now going to see the benefit of combining with the market leader ...
as i already explained when the original trial was started the adjuvant setting had now standard of care other than wait and see, its changed a lot since the PD-1 came on the scene as they are now the standard of care in that area. hence it pays to show synergy with it.

scib1 was not left on the shelf ... Ichor over shot the time lines for the implementation of TriGrid 2 ... now delay by the FDA is the issue despite TriGrid 2 approval in Europe ..

Get your facts right

If you study the science of the way the PD-1 Mab engages T cells which "Turns then On" and blocks the cancers ability to turn them off. Then you look at all the data from the Trials involving 35 patients on the SCIB1 trial which have seen efficacy from the High Avidity T cells targeting the GP100 and TPR" antigen .. then "believe" should be changed to "Expect"

Because any mechanism of failure to engage cancer would have been identified in the 35 patients treated .. Now the vaccine induced T cells were never expected to engage solid tumors, indeed it was developed for adjuvant melanoma (after surgery) but it did because it was better than predicted which is why the Authorities agreed to extend the trial for a 5 year period .............. but that was the failure point as the attack on the cancer was thwarted by the cancer cloaking itself with the PD-1 ligand as Lindy has already stated ...... SCIB1 t cells when confronted with a PD-1 ligand are turned off .......... however in some patients SCIB1 still managed to clear solid tumors without PD-1 which is why Scancell is so excited with the approval of keytruda .

Cancer Research UK has completed Due Diligence on the SCIB2 using the same platform but using a different form of delivery so this is a Second third party to agree Immunobody is worth pursuing commercially , the First being the Trial investigators of SCIB1

now Diggles has just completed 12 months due Diligence resulting in a £4m investment ........

what is not to like ....

even without Moditope Scancell has the products which are becoming highly valued in the market place because of Keytruda and Opdivo

its now a Tick Tock ... for results

Has SCIB1 failed Ruck ?
Has Keytruda failed ruck ?

as they compliment each other which is proven now .... what is the mechanism of failure ?

between a T cell and a Pd-1 ...

which is why i keep posting

what is the mechanism of Failure for SCIB1 and Keytruda

when all the evidence points to a big success ....

including a cell-penetrating peptide the biotech thinks will promote the efficient cross presentation of epitopes to cytotoxic T cells.

"thinks will"

Scancell ... does

as a foot note ...

keytruda approved Sept 2014 ...
that's 4.5 years ago
Scancell announces synergy 12 Aug 2014
http://www.scancell.co.uk/news/latest-news/synergy-of-scib1-with-checkpoint-inhibitors
so we would need to look at posts from 2013 ?

really

Tf .... I dont recall any one on this BB dismissing Check point inhibitors apart from they have no place currently with Moditope .. possibly CTl4 might assist but then how do you show the mouse data when moditope is already 100% ... Its ok Goosed posting Paul Rennert etc but he is not backing up the posts with copies of the "dismissed out of hand." posts ?

so the post maybe interesting ... but is it factual ?

........ Super Vaccine coming ..... Over to Scancell

look at Immunocore ........... Immtacs ... are Go between T cell and Antigen to create the link .....

of course this is very simplistic posting ... making it sound like that you can build a car t or an immtac in a week .......... if only ....

Chester Car T
Its a designer "TCR" ..........

Biomarkers are an integral part of cancer management due to their use in risk assessment, screening, differential diagnosis, prognosis, prediction of response to treatment, and monitoring progress of disease. Recently, with the advent of Chimeric Antigen Receptor (CAR) T cell therapy, a new category of targetable biomarkers has emerged. These biomarkers are associated with the surface of malignant cells and serve as targets for directing cytotoxic T cells. The first biomarker target used for CAR T cell therapy was CD19, a B cell marker expressed highly on malignant B cells. With the success of CD19, the last decade has shown an explosion of new targetable biomarkers on a range of human malignancies. These surface targets have made it possible to provide directed, specific therapy that reduces healthy tissue destruction and preserves the patient’s immune system during treatment. As of May 2018, there are over 100 clinical trials underway that target over 25 different surface biomarkers in almost every human tissue. This expansion has led to not only promising results in terms of patient outcome, but has also led to an exponential growth in the investigation of new biomarkers that could potentially be utilized in CAR T cell therapy for treating patients. In this review, we discuss the biomarkers currently under investigation and point out several promising biomarkers in the preclinical stage of development that may be useful as targets.

just think of everything as a code ........ 12345678910

012345678910 ... so a zero in front the immune system can see it .... you dont need a designer TCR

but 12345678910 ..... cannot be seen by the immune system .......... so make a T cell that can ... Car T ...

You had best follow the premier league then .. Ruck ..

I would point out no premier league poster is a research scientist and post there own work ...

indeed we learn by reading the work of others .. so that we don't get confused between Car T and TCR

what like yours .... confused about Car T and TCR ...

Your problem Ruck is your attempt, yet again of challenging my credibility without any of your own ..

why you do it is beyond me ? this comes from your attempts at valuations with all the drivel you posted on ADFVN right through to current ... give it a rest .. enjoy the coming Sport feast

its a good doc that Wild, but its important that folks understand the action takes place on the cell surface not internal to the cell.
Human Leukocyte Antigen, or HLA, is a class of protein which is often found on the surface membrane of cells, and which serves the purpose of "presenting" possible antigen to T and B cells. There are different sorts of HLA - class I HLA and class II HLA - and they each work slightly differently.

Both do essentially the same job though. They sit inside a cell, and have a groove in which they can attach little bits of protein. (These bits of protein will have come from outside the cell or could be products of the cell's own genes.) Once a bit of protein (or other possible antigen) is attached, the HLA moves out and sits on the outside of the cell, so that a T cell can come along and check the molecule that is being presented. The T cells, in their turn, check whether the molecule is "self" or foreign, and will either pass over it or react to its presence (either destroying the cell, or raising the alarm about the foreign substance by emitting cytokines">cytokines).

its so complex

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2632691/

look at it like this .... the designer car T can bind to antigens that are NOT recognized by the immune system