 Hi Marcus
Thanks .. so my communicating skills are at least reasonable
Triads
is basically the system of how the immune system functions
with the Professional antigen presenting cell at its heart
in fact Moditope is reliant on the Professional APC that resides inside the tumour because that has already been flagged by Autophagy but the cancer is suppressing it
so no T cells can see it
unless activated with first signal from the moditope vaccine
which activates a Professional antigen presenting cells in your arm but not fully
when the ist signal t cells migrate into the tumor ...they go fully active inside the cancer because they see second signal ...
a Professional APC can engage simultaneously with CD4 and CD8
indeed the "plasmid" that encodes Cd4 and CD8 using ISCib1 are forced into (transfected) a Professional Antigen presenting cells
but the same plasmid creates a MAB when transfected into other cells
these mab's engage the Professional antigen presenting cell that has already received first signal from the plasmid transfection and with Avidmab they Cluster around the CD64 receptor by non covalent links activating second signal
of both Cd4 T cell and CD8 t cell ... and without an adjuvant because the "transfection ie high speed transfer via gun" creates a little bit of inflammation thus enhancing activation and i am pretty sure 2 APC's can do this with each one receiving one side of the signal ... but i would have to check with Lindy on that one
that is why its such a clever vaccine ... |
"for those that have not read my posts fully"
Nobody reads your posts fully. They are far too long, repetitive and too crypic.
What I'd really like you to explain in a single paragraph is how big pharma calculate actual risk as you asserted earlier? |
Inan,
which post are you talking about? I understand a lot of it but am not a scientist.
Cancer and the immune system is incredibly complicated and we are learning all the time.
Doublet seems to have a great synergy with Scancell`s vaccines and I am very hopeful of good results in RCC.
Cold tumours lack the attributes to support robust anti-cancer immune responses, for example because they are surrounded by cells that stop T cells from attacking. Immunotherapies have limited efficacy in such cancers, creating interest in how to turn cold tumours hot and allow more patients to benefit from the powerful drug class
T cells at the tumour site are often of poor quality or exhausted.
Check points protect our vaccines.
Anti-CTLA-4 immunotherapy creates new T cells while freeing them to fight
“Our findings tell us that we may be creating entirely new T cells with CTLA-4 inhibition, not just expanding existing cells,”
The secretion of IFN-ϒ and the resultant inflammation could alter the nature of the TME, effectively converting “cold” tumours into “hot” ones, and so make a tumour visible to other elements of the immune system. Hence, Moditope stimulates the production of killer CD4 T cells which overcome the immune suppression induced by tumours, allowing activated T cells to seek out and kill tumour cells that would otherwise remain hidden from the immune system.
Volrustomig looks interesting.
Did you know about immune triads Inan, see bottom, fascinating?
Immune triads contain tumour-specific cytotoxic CD8 T cells, CD4 T cells, and antigen-presenting dendritic cells – all engaged together. The location of immune triads within the tumour is crucial for effectively combating cancer, outweighing the importance of their quantity within the tumour.
Volrustomig (MEDI5752) is a monovalent, PD-1/CTLA-4 bispecific, humanized IgG1 monoclonal antibody engineered to specifically inhibit PD-1, with increased CTLA-4 blockade on PD-1+ activated T cells compared to PD-1– resting peripheral T cells. This mode of action may facilitate enhanced CTLA-4 inhibition at tolerable doses beyond those achievable with current PD-1/CTLA-4 combinations. Data from the first-in-human phase 1/2 study (NCT03530397) showed encouraging antitumor activity and acceptable tolerability with 1L volrustomig plus carboplatin/pemetrexed (CP) in NSCLC, particularly in pts with PD-L1 TC <1%.
July 17, 2024 Ajit Muley
The Cancer Research Institute (CRI) is excited to share the latest study from CRI Lloyd J. Old STAR Andrea Schietinger, PhD, from Memorial Sloan Kettering Cancer Center, published in Cancer Cell. The study focuses on the interaction between different immune cells to eliminate tumors.
Dr. Schietinger and her team found that CD4 T cells play a unique role in helping cytotoxic CD8 T cells fight against solid tumors in adoptive T cell therapy (ACT).
CD4 T cells, commonly known as ’T helper cells,’ have long been acknowledged for their vital role in initiating the activation of CD8 T cells through cytokine secretion and antigen presentation. The activated CD8 T cells alone are established frontline effectors of the immune response aimed at eliminating tumor cells in ACT.
However, Dr. Schietinger and her team’s latest research challenges this conventional wisdom.
Their new discovery has revealed an uncharted aspect of CD4 T cells’ function: their direct involvement in the effector phase of CD8 T cells, thereby aiding in tumor eradication. This process relies on the formation of specialized three-cell complexes known as ’immune triads.’
These immune triads contain tumor-specific cytotoxic CD8 T cells, CD4 T cells, and antigen-presenting dendritic cells – all engaged together. Dendritic cells are special immune cells that act like messengers in the body and play a key role in triggering the immune system’s response to fight off infections and diseases. The location of immune triads within the tumor is crucial for effectively combating cancer, outweighing the importance of their quantity within the tumor.
This is the first time CD4 cells have been shown to be directly involved in the effector phase of anti-tumor immune responses. The study notes CD4 T cells do not directly attack cancer cells in this process. Instead, they help reprogram cytotoxic CD8 T cells through cytokine signals and direct interactions between the two types of T cells in the effector phase.
These findings are significant for their role in ACT and for their potential application in multiple therapeutic approaches. These strategies can be utilized for treating cancers through diverse approaches such as immune checkpoint blockade (ICB) therapies and cancer vaccines.
Overall, Dr. Schietinger’s innovative approach sheds new light on the dynamics of immune cell interactions with the tumor microenvironment and their implications for developing effective cancer immunotherapies. |
for those that have not read my posts fully
""""Please let me know where the status of SCLP ID Vax Platform is now.?"""
its being used in ISCIB1 and SCIB1 |
I'm thinking more genmab and 300m. We'll see. I'd be delighted. |
by the way "WE" refer's to Bermuda |
tell you why nobody asks you a question Ivy ...
you claim so much but deliver so little
an example post .... one that is ruled by stupidity
Ivyspivey - 31 Jan 2025 - 11:56:49 - 16927 of 17121 Scancell - Pot of Gold or POS? - SCLP
You know perfectly well that we were both referring to an Infectious disease Vax platform not oncology.
Please let me know where the status of SCLP ID Vax Platform is now.? |
i see the Prat is at it again sci
scib1 (which is not even scancell's invention)
so who's invention is it ? |
what is also interesting
why has Nobody asked Ivy for His thoughts !!
how sad is that !! |
as Chester has now reminded you Ivy .....
you really need to keep up with whats already posted ! |
then you have SC102 ... who is convinced that Lindy has been around longer than Global warming and Queen Victoria !! |
Nigel,True and a good price for both parties would be £1.50. Glad you came round in the end :) |
2tyke,Investment funds and pension funds have to have a way of "valuing" companies they invest in. They do this using fairly industry standard methods based on yield. In order to apply that to Scancell who do not have any revenue or yield you have to try and work out what that might be if ever they got to a position of earning revenue what that yield might be. Not perfect, but you have to start somewhere don't you? |
You've not grasped that big pharma don't just chuck money about for fun either. They'll evaluate and pay a good price for them. |
Which one has failed?
Well, keytruda is successful beyond any doubt. SCIB1 has been in clinical development for 355 years more or less, to the point where patents have expired. So yeah, scib1 is infinitely closer to failure than Keytruda, why don't you stop asking that stupid question already? |
and surely if you are smart Ivy why can't you answer it yourself
rather than using Ask the Audience
creating an "average answer"
because nobody can be definitive |
Ivy .... problem for you, nobody is interested in you
Bermuda even left you hanging yourself |
again No business Acumen
ATB
you can't think for others Ruck
if you have no business acumen |
Yep very happy for Marcus to answer specifically why does he think SCLP have gone for Cohort 4.Only interested in that response not the other stuff. |
"and you want to sell your share at ?1.5"I'd LOVE to sell my shares for £1.50 yes, so would 99% of investors. |
"Ruck what is the royalty per year at 17.5% of $9 billion"$1.575 billion. |
and you want to sell your share at £1.5 |
Nigel,You don't seem to have grasped the fact that just because some investors are prepared to sell for a few pennies that this has no bearing on the future or potential value. A PI may think 9p is a good buy if they can sell for 15p in a few weeks. A big pharma may think £1 is a good price if it opens up a $3.5B market. Chalk and cheese. |
Rucks maths ....
Ruck what is the royalty per year at 17.5% of $9 billion |
Many of us think that x10 or more is very achievable.
Hang on. That's a very different point. Even I believe that is achievable!
My point was simply that a RNS landing at some point with a knock out bid at > 10x the current price is NOT going to happen. |
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