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""" Well, I've bought my ticket I know its potential worth I also know it could be a no show ... that's the risk/reward it's not for everyone """

thats a lot of No Shows

No Avidmab
no Mab2811
No Homocitrulline
No Citrullination
No Scib1
No Scib2

any of which paying off would lead to A value way higher than current ...

Scancell is very skilled in the Art of "Binding" ...

have faith ... its the way T cells talk ...

Further to my posts on Scancells level of involvement in the BioNtech Collaboration . had further thoughts on the HSE involvement in the Viral vectors (mentioned by Bermuda) ........ why did they not do it in Germany ? the German site is geared up after all for TCR and safe control of the Vector .... I feel the majority of the work to build this form of moditope delivery again is reliant on the skill set of Scancell because of the CD4 involvement rather than a CD8 ... it really does bode well if BioNtech do a deal as this skill set will be rewarded

Just IMHO

soon Know ...........

what that article is describing ... is the Helper T cells that support cytotoxic CD8 T cells ............ ie our generals ..

have dropped the cd8 ............. and gone cytotoxic themselves .. !!!

Nature always has a reason ............ !

as Time goes on Ray the potency of the CD4 going cytotoxic is observed by others .............. and every report indicates "potency"

https://www.jimmunol.org/content/202/1_Supplement/140.4

For Reference ... CD4+ T cells with cytotoxic activity = (CD4 CTL)

We therefore investigated if viral infections lead to the generation of reprogrammed CD4 CTL and moreover if these reprogrammed CD4 CTL play essential roles for the organism’s protection. Using the well-defined lymphocytic choriomeningitis virus (LCMV) acute (strain LCMV-Amstrong) versus chronic (LCMV-Clone 13) infection model, we observed that solely chronic infection enables activated CD4 T helper cells to lose ThPOK and convert to CTL with potent killer activity. Moreover, viral-induced CD4 CTL precursors produce various cytokines, notably Il-10, which is required for the induction of the reprogramming process. Finally, we engineered two unique mouse model systems, in which either all the CD4 T cells are forced to reprogram to CTL (gain of function) or else, prevented from reprogramming to CTL (loss of function). Using these models, we show that the reprogrammed CD4 CTL generated under chronic infection conditions, play critical roles in protective immunity.

Good spot Bermuda i see the new GMP manufacturing facility also comes on line for personal vaccines this year they certainly are gearing up ...

AGM poster
"""Building internal expertise
in TCR identification """
(BioNTech collaboration)

strikes me Scancell is far more involved in building the """Cd4""" T cell TCR program considering BioNtechs own statements on its website (listed below)

mentioned this before that a CD4 is far more complex because of this differentiation and selection and i believe if BioNtech had gone it alone on a deal for the epitopes, it would have struggled without Lindy's input ... so the resultant commercial value seems to be building in Scancells favor ..

"" ? Lenti-viral transduction of T cells now working in the lab""""
? 40 TCRs recognising citrullinated/homocitrullinated epitopes to screen

I really do hope that the MAB 2811 is involved and that Scancell design input is recognized

BioNtech statement

Our TCR discovery and validation platform will tackle key challenges
We have developed an integrated technology platform for the systematic identification of functional, fully human TCRs from single antigen-reactive T cells. This technology consists of a proprietary high-throughput approach for the fast retrieval, cloning and rapid validation of novel paired T cell receptor sequences. Our approach facilitates the isolation of tumor cell-specific TCRs against multiple antigens and various Human Leukocyte Antigen (HLA) class I and II alleles.

We believe our TCR discovery technology has the potential to unlock an array of patient and tumor specific TCRs suitable for clinical use. We believe this technology has potential utility for:

Therapeutic TCR products encompassing single TCRs for targeting a specific antigen
A therapeutic TCR warehouse encompassing multiple TCRs for targeting of one or more tumor antigens
Individualized T cell therapy involving on-demand identification and timely manufacturing of customized, engineered T cells with autologous TCRs against neoepitopes for adoptive transfer.

at least we will get some sort of update shortly

But lets assume that with BioNtechs new found ""listing value"" that the potential to fully explore Moditope TCR across discovered epitopes Homocitruline and citrullinated is expanded to the full ... the value could be mind blowing if our input is high

found this example

Thymic-derived, regulatory T cells (Treg) represent a subset of CD4(+) T cells that are required for normal immune homeostasis and suppression of unwanted responses against self-antigens (Ags) that prevent autoimmunity. Their role as immune regulators and potent ability to suppress T cell responses has been the focus of intense investigations aimed at utilizing these cells therapeutically, particularly in the settings of autoimmunity and transplantation. Many methods for expanding Treg have been described; however, efforts to generate large numbers of Treg for use in vivo often compromise their suppressor function or rely on the induction of Treg rather than their expansion. Our recent studies have focused on the barrier tissue-derived cytokine IL-33, a recently described IL-1 family member. IL-33 has emerged as a multifunctional protein, with reported roles in driving potent Type 1 and Type 2 immunity, as well as facilitating profound Treg expansion in vitro and in vivo. IL-33-expanded Treg express the IL-33 receptor (R) ST2, and express classical markers associated with Treg phenotype and suppressor function. They suppress both CD4(+) and CD8(+) T cell proliferation and effector functions in vitro, and Treg expressing ST2 have been identified as important regulators of detrimental immune responses in vivo. In the present chapter, we detail methods for expanding significant numbers of Treg using IL-33 both in vitro and in vivo that may potentially be used to promote/maintain organ transplant tolerance or suppress autoimmunity.

https://www.ncbi.nlm.nih.gov/pubmed/26530793

https://www.jimmunol.org/content/200/3/909

Now i am NOT suggesting that Scancell gets involved in TCR for Autoimmune ...

But think of that MAB .......... 2811

so how can the science of Scancell be transfered ....

this is only my own thoughts ......

but if you can build a "cytotoxic cd 4 t cell" and expand them outside the body using patients CD4 and swapping out the TCR

BioNtech

You can build a regulatory Cd4 ........... expand them out of the body and reintroduce ...

the technology is the same ....

autoimmune decease ............

Effector T Cells in Multiple Sclerosis.
Kaskow BJ1, Baecher-Allan C2.
Author information
1
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
2
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Abstract
Multiple sclerosis (MS) has long been considered a CD4 T-cell disease, primarily because of the findings that the strongest genetic risk for MS is the major histocompatibility complex (MHC) class II locus, and that T cells play a central role in directing the immune response. The importance that the T helper (Th)1 cytokine, interferon ? (IFN-?), and the Th17 cytokine, interleukin (IL)-17, play in MS pathogenesis is indicated by recent clinical trial data by the enhanced presence of Th1/Th17 cells in central nervous system (CNS) tissue, cerebrospinal fluid (CSF), and blood, and by research on animal models of MS, such as experimental autoimmune encephalomyelitis (EAE). Although the majority of research on MS pathogenesis has centered on the role of effector CD4 T cells, accumulating data suggests that CD8 T cells may play a significant role in the human disease. In fact, in contrast to most animal models, the primary T cell found in the CNS in patients with MS, is the CD8 T cell. As patient-derived effector T cells are also resistant to mechanisms of dominant tolerance such as that induced by interaction with regulatory T cells (Tregs), their reduced response to regulation may also contribute to the unchecked effector T-cell activity in patients with MS. These concepts will be discussed below.

https://www.ncbi.nlm.nih.gov/pubmed/29358315

Try and look at this as the opposite to the issues Scancell discovered over the period of development of the Modi1 vaccine

The issue most cannot understand is that Cd4 T cells are so diverse and to understand the process of Autophagy, Cd4 activation, differential changes etc etc ..... was and still is massive

so we need to make it simple ....

Cd4 Helper T cells are helping a Cd8 attack
so they are in effect .... effector cells

To control the response the CD4 then have the opposite "Regulatory T cells" ... so these guys calm the response

so in RA etc ... your trying to calm the response ......... "more regulatory t cells"

in cancer you want the opposite ....... "more effector t cells"

you can read about this in Scancells research ... why so indepth ... well the first thing a regulator will ask ...

How does it work

So what Lindy has presented here (bermuda's link) is the Compressed science of all the work they have done consolidated into one report with additions of unpublished work ...

so i suspect this is part of the move to the clinic and the preparation of the science which is to be presented to the regulators
for the Modi1 vaccine

"within 4 days " an easy read ........ that is striking ....

If That Translates ..........

As yet unpublished data from our group shows a single immunization with the combination of citrullinated vimentin and enolase peptides was sufficient to induce significant regression of established B16 melanoma within 4 days of vaccination

Overall, it is clear that the potential of CD4+ CAR T cells to mediate multiple target cell killing could further potentiate the efficacy of CAR T cell therapy. Moving forward, there is a need to identify and deliver optimal CAR T cell subset compositions, an area which is already in focus for current clinical research [105].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6470706/

they also note that "Cytotoxic cd4 Killer T cells " are potent and effective .... indeed just as effective as a modified Car T Cd8

"""anti-CD19 4-1BB/CD28/CD3? (CD19-BB-28-3z) CAR-T cells at the systems level [41] upon antigen-specific activation. CD4+ and CD8+ CAR-T cells are found to be equally effective in direct killing of target tumor cells """

which is why Mab 2811 could be very valuable addition to those 3rd or 4th generation Car T ...

""MAB 2811 identifies the most potent and robust Cd4 Subsets ""

IMHO

BioNtech RNS coming soon i hope ........
Assuming it has all gone well .........
I expect multiple agreements the first could be regardless of the moditope collaboration but is also part of it ...
That involves FG2811 Mab because its such a useful tool for TCR and Cart T i would be very surprised if that was not licensed on a non exclusive basis by BioNtech ... regardless

but watch the value of FG2811 .............. because it can be used in other BioNtech research so an RNS could appear even before the collaboration is finished and with other Cart T and TCR developers ...

I think over time you will see that little Mab appear as another Jewel in the crown ..... IMHO

I thought that DE had inspired you ......

""" I’d still take what he says over you all day long."""

excellent ... so it does not inspire you !

maybe your so impressed by the "struggle" posts your a little overwhelmed

then you should expect a bid Ruck ... after all DE states scancell is vulnerable and you should start buying anything below 22p ..

in fact bermuda ...reply was

Bermudashorts5 Jan '20 - 17:11 - 26584 of 26701
0 2 0
NXC - I sincerely hope you're wrong.

so the power and the decision making at that time was the Joint CEO of lindy and Richard

just to put things into perspective, now i am not saying he had no influence however by the very nature of being not in the day to day running of the company .. the role played was a figure head

Ruck ... i have replied to that post ... by the way

DE was a "Non" executive chairman "

A non-executive chairman of the board does not occupy a management position in the company. The chair operates independently from the company, receives plans and proposals from the CEO, through the corporate secretary, and presents these to the board for approval.

well u don't need to leave the champagne on ice ............

I do like this

https://www.bbc.co.uk/news/av/technology-51028494/ces-2020-juno-reverse-microwave-oven-cools-drinks-in-seconds

""erroneous ""

David Evans words

One could argue that dosing of a first patient is more RNS Reach than RNS but I do not have all the facts nor do I have the view of the Nomad which is crucial.