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the vaccine is a primer of the immune system .............

the vaccine itself has no clinical interaction with the cancer

Only "natural generated T cells" are activated by the cancer

Keytruda and CTL4 ............ target the T cells not the cancer so they block the ligands that could be turned off by the cancer

however you can lock onto the cancer Ligand .,.. Roche does it this way

Tecentriq is a monoclonal antibody designed to bind with a protein called PD-L1 expressed on tumour cells

this is why Keytruda will work on T cells activated by SCIB1 ...

The Genius of Scancell .... and how they got around this potential problem ( this problem would not be in all patients)

One of the most notable ways of inhibiting
MHC-II expression is Transforming growth factor (TGF)
ß inhibition of CIITA but methylation of the CIITA pIV
and post-transcriptional control of CIITA have also been
identified.17 19 A more effective cancer vaccine could
therefore be generated using multiple epitopes derived
from various antigens that show restriction through
multiple HLA alleles. Many tumors switch to glycolysis,
even when oxygen is not limiting, in a process known
as the ‘Warburg effect’.20 Glycolytic enzymes, including
a-enolase, are widely expressed and are preferred targets
for autophagy. We have recently shown that citrullinated
a-enolase is an excellent target for anti-tumor immunity.21 T cell responses to citrullinated vimentin and
enolase epitopes are documented in RA patients and we
and others have shown these to be restricted through
the HLA-DR*0401 (DR4) allele.6 7 10 21 In addition we
have shown that responses to three peptides can also
be restricted through the HLA-DP*0401 (DP4) allele22
and can stimulate strong anti-tumor immunity in HLA
transgenic mice.10 21 22 Thus, combining two citrullinated
vimentin peptides with a citrullinated enolase peptide
should minimize tumor escape, these three peptides
have been selected for inclusion in the Modi-1 vaccine.
Combining epitopes can lead to dominant responses to
at least one of the included epitopes with subdominant
or absent responses to others.23–27 Thus, it is important to
carefully select appropriate epitope combinations.

""" should minimize tumor escape,"""

excited ...

Modi1 ............

can the cancer escape the vaccine .......... (cancer becomes dangerous when it escapes the immune system)

so Modi1 and Scib1 is trying to tip the balance back in-favor of the immune system

but in this instance ... moditope

this is why ongoing "understanding" from research is not a delay .. and one of the reasons why "Enolase" was added was to stop the cancer editing out single antigens ... thus turning off access to our CD4 killer cells ....

from Scancell

However, due to the heterogeneity of tumors, targeting of
only one antigen has the potential to lead to the selection
of HLA loss, antigen or epitope loss variants and subsequent tumor escape.13–16 HLA loss is more commonly
documented than antigen loss as a result of immune pressure, although most reports are for specific MHC class
I allele loss to avoid recognition by natural killer cells.13
Constitutive expression of MHC-II is largely restricted to
antigen presenting cells (APCs) (dendritic cells, B cell
and macrophages), thymic epithelia cells and activated
T cells.17 In most other cells including epithelia, endothelia, fibroblasts and astrocytes, MHC-II can be induced
by interferon-gamma (IFN?). MHC-II expression is
controlled by Class II Major Histocompatibility complex
transactivator (CIITA) which is regulated by four different
promoters. Promoter I is active in myeloid cells, promoter
III in lymphocytes and promoter IV is essential for responsiveness to IFN?.
18 Therefore most tumors can be induced
to express MHC-II unless they immune edit to prevent its
expression.

mechanism of failure ........... """ unless they immune edit to prevent its
expression. """

you need a Strong Cd4 t cell to signal the B cells to generate the antibodies .. as they also are activated via the MHC 11 pathway .. remember the second signal..

the immune system uses two signals to block "error" ... so that self is not attacked

"""T cell receptors (TCR) on T helper cells bind to the antigen-complexed class II MHC molecule on the B cell surface resulting in T cell activation. The activated T cell then provides a second activation signal to the B cell, which can occur through a variety of proteins. """

its all checks and balances

the system works regardless .......... virus or cancer ............ activation has to be done correctly .

https://www.astrazeneca.com/media-centre/press-releases/2019/astrazeneca-and-daiichi-sankyo-enter-collaboration-for-novel-her-2-targeting-antibody-drug-conjugate.html

another deal
https://www.glycotope.com/daiichi-sankyo-enters-worldwide-licensing-agreement-with-glycotope-for-gatipotuzumab-antibody-drug-conjugate/

that's getting close to the size of a cronovirus ..

https://www.chopharma.com/en/product.php

efficacy efficacy efficacy ..............

that is what sells .......

the one thing i have always found ... those that can corner the market tend to gain the most from it ....

or if we get it right send our stock Soaring .......... !!

i think they have consolidated twice since Rats .. maybe we should ask the Val experts ..

while i am growing up .. Drac

perhaps you could inform us how many times in the last 12 months you have repeated this post ....

Dracula1

Posts: 2,083

Price: 6.25

No Opinion

As of the where Sclp stands today with their Compounds.Today 09:10
What's the chances of. Any of Sclp's compounds In say the Next year getting a far better response from Pharmas than SCIB1 got . IMO

if more than once it would Kinda indicate a Pea for a Brain something akin to a parrot ... maybe you should read your own history as a reminder

nothing has changed ... if the sp today was 45p i would still rec Buy

I believe Bermuda and myself gave you a reality check on VAL at 7p ... ref VAL401 etc

ATB

Under the terms of the agreement, BioNTech will receive a $30 million signing fee. For each potential medicine, BioNTech could receive over $300 million in development, regulatory and commercial milestones. If successfully commercialized, BioNTech would also be eligible for tiered royalty payments up to double-digits. In addition, subject to the terms of the agreement, Lilly will make a $30 million equity investment in BioNTech's subsidiary, Cell & Gene Therapies GmbH, which specializes in the research and development of TCR and chimeric antigen receptor immunotherapeutics. Further financial terms were not disclosed.

fair enough but it would be difficult i feel for BioNtech to undercut there own deal which they accepted

so what value are you ascribing Bermuda for Modi1 peptides out of interest

I would also add the adjuvant market which was wide open in 2010 got competition when the checkpoints took over this area ...
But of course we are still synergistic ... if it works in this trial (late stage) it stands to reason that we can regain access to the adjuvant setting ... we do NOT have to compete head to head

That is really well written ..... well done post Rec. Cars

Konar ... look the dates

05/11/2015
Download PDF
INDIANAPOLIS and MAINZ, Germany, May 11, 2015 /PRNewswire/ -- Eli Lilly and Company (NYSE:LLY) and BioNTech AG today announced they have entered into a research collaboration to discover novel cancer immunotherapies. The companies will seek to use the power of the body's own immune system to attack cancer cells and create possible new treatment options for cancer patients.

Leveraging the scientific expertise between the two organizations, Lilly and BioNTech will collaborate to identify and validate novel tumor targets and their corresponding T cell receptors (TCRs) in one or more types of cancer. These tumor targets and TCRs may then be engineered and developed into potent and selective cancer therapies.