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its an art to explain the complex in a simple form ..

which is why i Use "generals" and the road network and i always point out .. what i look for in my research is mechanism of failure ...can i find something in others research to cast doubt ...

and I cannot all i find is complementary evidence ..

indeed it worth reading the link i put up yesterday

Stressed Cell + Interferon Gamma = cell expressing the peptides

scancell use these peptides connected to amplivant to program CD4 T cells to Proinflammatory TH1 Killer T cells but unlike normal vaccines ... these are the Generals of the immune system going cytotoxic ..

""""" carbamylated peptides may accumulate during inflammation conditions."""""

Modi-2 ... is the same

which is why its critical Moditope must "induce" a proinflammatory environment ...

that two year delay which crippled the sp is worth BILLIONS ... when its proven ..

which is why i have never been concerned about the delay because if you understand the link between ISA Pharma amplivant

and Moditope ... you would buy more and more because this business is all about "interferon Gamma"

Konar
""" When a tumor cell rapidly grows it uses up all the nutrients that the blood supply can provide. The cells get stressed. They start to consume unwanted proteins and give off proteins in the process. Moditope converts these proteins and when they do, the immune system recognises the tumor and triggers a powerful immune response. Moditope 1 and 2 are just two different ways in which these proteins and converted.""""

Sorry mate this is just not correct ..

Cell under stress consumes unwanted proteins within its cell "recycled " this is autophagy ...

under this condition coupled with an external cytokine induced by inflammation the cell identifies itself by a protein on it outside surface

Its not "giving off proteins

so this is a citrullinated cell displaying an epitope as an identification ..

Modi2 is also an Autophagy event .. Homocitrulline

Autophagy is a homeostatic and physiological process that promotes the turnover of proteins and organelles damaged in conditions of cellular stress. We previously demonstrated that autophagy represents a key processing event creating a substrate for autoreactivity, which is involved in post-translational changes and generation of citrullinated peptides, recognized by the immune system in RA. In this study, we analysed whether autophagy is involved in other post-translational changes that can generate autoantigens, focusing on carbamylation processes. Carbamylation is a nonenzymatic post-translational modification, in which homocitrulline is generated by the reaction of cyanate with the primary amine of lysine residues; carbamylated peptides may accumulate during inflammation conditions.

so Moditope is ......... citrullinated tumour-associated peptide or a Homocitrulline tumour-associated peptide

so moditope does not engage "inside the cell"

hope that explains it better

https://www.ncbi.nlm.nih.gov/pubmed/29982776

Crumbs

"" Cancer cells due to being stressed express molecules that act as a red flag to killer T cells """

only when subjected to inflammation .. the two have to go hand in hand

"interferon Gamma"

think of it as a road network ..

Modi1 and 2 ..

both roads have the same outcome via different routes .. both induce a cd4 cytotoxic t cell ...

then you have variation of Binding and Inflammatory signaling ... which is why they can complement each other ...

when you look at many current forms of personal neo antigen vaccines they are looking to induce CD4/CD8 vaccines and then using the power of a checkpoint like keytruda to gain advantage ..

Moditope does away with all of that .. and works in far more cancers than Checkpoints can cover ..

as time progresses the full impact will hit the market .. when it does watch the share price ..

all about the "response rates from here "

the market has slaughtered the SP because it has looked at the delays as a problem rather than looking at the delays as solving the efficacy issues which is the way Lindy has developed moditope .. (excludes manufacture delay because that was a technical hurdle to overcome)

this efficacy issue is all about Turning "ON" the inflammatory environment ...... because without it Moditope does not work effectively

To date every thing i has seen coming out of scancell supports this correct path .. the market will catch up in due course

Ruck you posted

" I’d be prepared to not make money so long as some cancer cures came out of this"

are you still holding VAL ?

I will leave you to bore the pants off the BB ...

Keytruda is approved ....

ATB

this was my first post on the subject .............. Ruck, ........ you seem to want to make "waffle" posts based on what exactly ?? nothing

and you are desperate to find "concerns" ........

SCLPRE: WFMon 12:15
The dosage is set by the approved drug Keytruda and the experience Oncologists have acquired in the use off ..

as i have stated the link between SCIB1 and Keytruda is not relevant

as its the link between % of t cells engaged by the keytruda Mab and the patients T cells is what is relevant ...

Scancell does not manufacture T cells ........ they are natural t cells programmed to Tpr2 and Gp100 they expand at the site

Keytruda cannot tell the difference

what concen ?

Its an approved treatment ....... i will repeat again

Has the FDA and EMA got it wrong ?

and Ruck has it correct ?

all i can say ....

read bermudas post

You suggested weight was an issue ? your post listed below

""" This means for small people the dose is relatively high and for large people relatively low.
This could mean that efficacy in small people is higher but side-effects also higher.
In large people, efficacy could be lower but side effects also lower. """"

Further to my earlier posts .. IMHO .. the information coming out of scancell points to all three vaccines Modi1/2/3 as a packaged treatment for the 17 mesenchymal cell cancers plus TCR capability and

the decision to add neoantigen personal vaccines (Grand Ch.) as an adjuvant is possible to spark antigen expression of moditope via Interferon gamma release from a neo antigen personal vaccine

TF I believe Bermuda has corrected Ruck ..

pointless me trying ..

its approved .. Ruck .. your making a song and dance about an "approved dosage" FDA has approved, EMA has approved ..

Ruck has not approved ..

Oh well

it's not me making such a fuss about Dosing ,,The Fat Controller's clogged arteries .. or if Vegans gets preferential treatment by the NHS providing they smoke the correct therapeutic thc.

what affects the SP ?

None of the above

any way does it matter, the sp won't be affected . ATB

trial criteria is the

"overlap"

of the acceptance of patients onto the SCIB1 trials to date and the Keytruda approved use

cannot remember seeing a "fat person criteria" ?

most doctors can work out the maths based on 2mg/kg ... so why would you give a 50kg woman 100kg weight equivalent ? just because she is an adult ..

The point i keep making about the trial is that keytruda has proven to be effective with T cells .. and Scancell has proved conclusively that its programmed t cells work .. so synergy has to exist otherwise Keytruda or SCIB1 would have failed in previous trials ..

to disprove that statement and apply risk you would have to show one of the trials has failed ... keytruda or SCIB1 ..

as the mechanism of action is pretty clear ...

now i appreciate its only one part of the immunosuppressive environment SCIB1 has to overcome, however its a key part ...

The dosage is set by the approved drug Keytruda and the experience Oncologists have acquired in the use off ..

as i have stated the link between SCIB1 and Keytruda is not relevant

as its the link between % of t cells engaged by the keytruda Mab and the patients T cells is what is relevant ...

Scancell does not manufacture T cells ........ they are natural t cells programmed to Tpr2 and Gp100 they expand at the site

Keytruda cannot tell the difference

Keytruda binds onto any T cell displaying a PD-1 as such the dosage is relevant to the patient not the vaccine induced t cell .. Keytruda cannot tell the difference

so it's simple if you don't give enough Keytruda you will fail to bind to enough T cells to make it effective.