Member Info for RayPointer

I mean this really is a double whammy.
Not only has Lindy found a product that makes Scancell's own glycans targeting MABs more potent, this same product has the potential to be used on any therapeutic MAB.

IMO Lindy is so clever at learning from other companies. I wouldn't be surprised if she started on this track when she saw what Amplivant could do.

I've been driving all day so I missed the fun.

"AvidiMab™ has broad potential to increase the avidity or potency of any therapeutic monoclonal antibody including those being developed for autoimmune diseases, as well as cancer. A patent application has been filed that seeks broad protection for the AvidiMab technology. This is Scancell's third proprietary platform technology, after ImmunoBody and Moditope, in the field of immunotherapy."

That could be massive. All CIs are MABs for a start. How many more are out there? Anybody care to hazard a guess.
Avidity is so important whatever you are targeting and has always been stressed by Lindy. Remember that article by Lindy's colleagues that mentioned avidity no less than 52 times.
Not bad for a part-time CSO in a lifestyle company!

Archer v Smith resumes tomorrow

Nom

Achilles have just received £100 million of funding.
It is worth looking at this from another angle.

Scancell have had a number of placings and kept 100% of their IP
Achilles have just had a huge cash injection, but what percentage of their IP do they still hold?
We may never know the answer to that since they are a private company.

So, a valid question is - Is it better to beg, steal and borrow and retain 100% of IP OR sacrifice a large share for the IP for a big cash injection? A hard question to answer when you don't know the full facts.

Then we have the relative merits of the two sciences. I think you could probably say Scancell is in the lead there with so much interest from other scientists outside the company. But again it is debatable - so let's debate it.

Then we have the speed to the clinic. Well Achilles definitely have the lead there - 3 years is impressive for what looks like a complex process.

So the score stands at 1-1 with a VAR decision pending

You must be man and wife. Come on, kiss and make up

No problem Drac.
There is obvious synergy between SCIB1 and Keytruda and that is why the trial is going forward.

SCIB1 proved excellent in the adjuvant setting (resected tumours) but less so when tumours were unable to be removed by surgery. So this combo trial is for patients with inoperable tumours. Keytruda blocks off PD1 on TCells and this hopefully gives SCIB1 a much better chance at attacking the tumours.

As to why there was no deal on the back of the SCIB1 results

Take your pick
1) RG no good as a salesman
2) Cancer vaccines out of favour with big pharma (there is good evidence for this)
3) Big pharma thinking the results were due to biased patient selection (I believe David Evans put this forward as a possible reason)
4) The excitement of CIs producing good trial results
5) Bias towards newer sciences such as TCR or Car-T

Any discussion on a competing science is useful IMO
In fact I would say essential

I'm all for allowing and discussing positive and negative posts.
But I'm a bit puzzled about what the distraction is in this case.
I personally think that
a) The Achilles science is very interesting and novel
b) Scancell are poor at attracting investment in the amounts needed to prove their products in the clinic. Achilles on the other hand appear to be good at this.

But the question I would ask is:
"Have Achillies retained 100% of their IP?"

Thanks nom

Here's another
https://www.newscientist.com/article/mg24032000-200-fasting-power-can-going-without-food-really-make-you-healthier/

It's logical that fasting promotes autophagy as this article points out.
So perhaps the Modi1 trial patients will be asked to fast.

Quote from C7:

"Logic and AIM are a deadly mix, with such a buyer the SP should be much higher, but we have a seller and the MMs have struck an agreed trading level at 7p to match seller to buyer, not only that we are experiencing a very low volume of PI buys, even sells to hold that trading range.ah an interesting week, lets see who blinks first. Night Ray."

Quote from Knowlesi

"They have now created a "buyer" to try and create a ramp frenzy - they try it day in, day out - the above quote is a perfect example of the level of ignorance here by regular "expert" posters. MM's have apparently agreed a trading limit - nope - they are matching buys and sells. There is a big buyer - maybe - put the share price hasnt moved so there must be an equally sized seller. "

Aren't these 2 quotes saying the same thing?

In Scancell's case the big rise came on the announcement of Moditope which also coincided with a rising SP with expectation of good results from the SCIB1 trial - so a double whammy. So the herd arrived but soon lost interest.

The irony of it is that Scancell has now started a 2nd trial for SCIB1, and is within about 9 months of starting a Modi1 trial, and then a 3rd trial (SCIB2) on the horizon. On top of that we have the BionTech collaboration and so many scientists awaiting the Modi1 trial. Then we also have the Vulpes investment.

Logic would dictate that the MCAP of Scancell should be much higher. Instead we are seeing a slow trickle of steers, the main herd is still waiting.

"Dr Richard Goodfellow, CEO of Scancell added: "If this preliminary data is confirmed in a larger clinical study, it has the potential to improve the design of future clinical trials using SCIB1 by selecting patients most likely to positively respond to our novel treatment and thereby increase the chances of a successful outcome.""

Looks like it is one for the future, perhaps after a P3 trial.

The discussion about autophagy, on the other hand, is all about Moditope.
So we have a lot of scientists trying to inhibit autophagy simply because it is important for the survival and proliferation of cancer cells.
Lindy, being a contrarian, has found a way of exploiting the consequences of autophagy. Autophagy is essential for the working of Moditope and far from supressing it, she wants to encourage it.

The obsession now with a lot of cancer research seems to be finding molecular structures to inhibit rather than finding ways of strengthening the immune response. All down to the success of Keytruda and other CIs IMO.

Hi C7

As I understand it the thymus creates the TCells early in life and then gradually ceases to function

https://www.endocrineweb.com/endocrinology/overview-thymus

The low avidity of TCells is, as Inan says, because the immune system does not want to create something too reactive. So the thymus deletes TCells deemed to be too powerful (too high an avidity).

So IMHO, it is highly significant that Immunobody is able to activate TCells and give them a high avidity.

I wonder if the high avidity of the CD4/CD8 TCells Immunobody activates is important.

https://www.researchgate.net/publication/309713639_SCIB1_a_huIgG1_antibody_DNA_vaccination_combined_with_PD-1_blockade_induced_efficient_therapy_of_poorly_immunogenic_tumors

Well the word "avidity" occurs 52 times in this article LOL.

The article below stresses the importance of high avidity when attacking cancer

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4150879/

But the high avidity cells are actually deleted in the thymus

"High avidity T cells that react to these self-proteins are deleted in the thymus during development, leaving predominantly low avidity T cells that recognize tumor antigens. Self-reactive T cells that survive negative selection in the thymus are also regulated by peripheral tolerance, which further reduces the anti-tumor T cell response. "

I mean that's what makes Moditope so interesting and diametrically opposed to many approaches.
It actively exploits something (Autophagy) that allows cancer to survive and prosper.

141 references at the end of that article but I am willing to bet that none of them talk about encouraging Autophagy as a means of attacking cancer.

The success of CIs has lead numerous researchers to look for the expression of other molecular structures to inhibit.
Lindy is apparently in a different race. A race that nobody else is allowed to compete (at least as far as citrullination and homocitrullination is concerned)

But isn't this article about trying to inhibit autophagy since cancer cells survive and grow with the help of autophagy?

Moditope in contrast works by using the consequences of autophagy - PAD expression and consequent conversion of arginine/lysine to citcrulline/homocitrulline. So for Moditope the more the autophagy the better it works.

https://en.wikipedia.org/wiki/Cancer_stem_cell#Targeting

What was that guy with the electric guitar doing in Ugur's presentation LOL?

It's not so much the TCR platform. Biontech already have that. It comes down to those Moditope targets.

And also there is the fact that BionTech and Genetech also have an important collaboration.
Here's Ugur Sahin talking about the technology behind that collaboration

https://www.youtube.com/watch?v=5mijZw6Nss4

It's a fascinating situation to say the least. 2 companies in collaboration but both companies willing to join Lindy's project blueprint. We all know that project blueprint is officially dead but unofficially who knows what conversations are still going on.