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Yes, the FAP inhibitors aim to stop FAP working and hence to prevent the tumour growing.

pre|CISION makes use of the FAP enzyme to release cytotoxins directly into the tumour microenvironmnet..

Avacta is not involved with FAP inhibitors. AVA6000 and the other AVAs do not any of them inhibit the activity of FAP. Quite the contrary.

She'll be talking about why Avacta chose that method ("the rationale for model selection") and how they use it to characterise the drug candidates ("sharing best practices for developing co-cultures of tumour cells and human primary FAP+ fibroblasts to assess bystander activity of PDCs in physiologically relevant systems").

Yes, that's right, Mr Ripley.

Was he also Epping or was that someone else?

Epping. That was his later moniker.

There was a Matt Damon (sp) who disappeared and then briefly reappeared maybe 2-3 years ago as a very antagonistic twat. Can't remember his name but do remember he played around whilst people tried to identify him. He was very proud of his accounts being banned by LSE.

You remember the details of the fracas better than I do Craig!

ODX now goes by the name Cambridge Nutritional Sciences (CNSL) and is bumping along at something between 2p to 4p (£5m+ MCap).

There was also that academia business that was being incubated by a portfolio company on AIM and had a lead scientist who used to like to argue publicly with anyone who criticized him! PL75 will remember the details as it was mainly him that the Prof was arguing with!😂😂😂

It's like the rivalry arguments with the Omega Diagnostics folk. What was they rally cry? I forget now. Something like King Colin or Colin is King?

Ah, happy days!

Definitely time to double down on that short now treasureisland.

Good luck!

Yeah. It was actually two sentences, or rather it was one.

You can't understand that you need gravy on turkey?

It would be absolute dedication on CC's part if there were to be an RNS tomorrow or Friday.

Difficult to say what the trend is with news of Phase 1b for SGC expected before year end, so really by 19 Dec, and really, really by 12 Dec. Will the 'Good News' be in the share price by then? Will the share price crash back if there's no announcement of the data by then? Would th efirst full week of January be too late to maintain trust in CC's timelines?

My reading of the trend - for what it's worth, and I'm working on 7 waves - would be 90p by 12 Dec, with 90p being the resistance level. Much higher, probably with a spike, if the 'Good News' is really good and much, much higher if we get credible funding news of some kind.

Q: Is MMAE still under patent?

Google:

Monomethyl auristatin E (MMAE) as a compound is likely no longer under a primary composition of matter patent, but its use in specific antibody-drug conjugates (ADCs) is protected by various active patents.

Here is a breakdown of the patent situation:

The MMAE compound itself: The core technology and structure of MMAE and its common linker combination (vedotin) were disclosed in patents such as US Patent No. 7,659,241. These patents were filed around the early 2000s and would have a standard term of 20 years from the filing date, suggesting their primary protection has expired.

Specific ADC therapies using MMAE: The key to intellectual property protection in this area lies in the specific, innovative way MMAE is used in combination with a targeted antibody and a unique linker technology. Several FDA-approved ADCs that use the MMAE/vedotin system are still protected by their own separate patents:

Adcetris® (Brentuximab vedotin)

Polivy® (Polatuzumab vedotin)

Padcev® (Enfortumab vedotin)

Tivdak® (Tisotumab vedotin)

Newer Patents: Companies are continuously developing new ADCs, formulations, and manufacturing processes involving MMAE, and these innovations are subject to new patents with later expiration dates. For example, patents relating to specific antibody-drug conjugate compositions have adjusted expiration dates as far out as September 2036.

In summary, while the basic molecule may be off-patent, any commercial or research use of MMAE in an ADC context would likely require a thorough freedom-to-operate (FTO) analysis to avoid infringing the numerous active patents held by companies like Seagen (now part of Pfizer) and Astellas.

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Apologies for what will be horrible Google+LSE text formatting. 🙄

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The real question is whether the 'ADC' patents also claim use in PDCs.

Admittedly, not all of them are as verbose and downright mind-numbingly boring as our pub bore!

Ah, but you're not a naive investor are you, you're in the cult.

Happy chanting

Ummmm

There is a cult of 'Hemogenyx can do no wrong' here. Cults are Bad News. They only favour the cult leaders.

Beware! ...Or you'll get fleeced by traders.

Of course it isn't. It's just a 'type' or two. Go to any BB and you'll likely find the same or similar with varying degrees of intelligence and sophistication

$14m upfront for a preclinical compound 'with promise' and possibility to have it made up to $400 in milestones.

Bella, was that person given Autolus's obe-cel (obecabtagene autoleucel, Aucatzyl)? Autolus is designed theirs to minimise CRS by using a rapid binding and release within seconds.

https://www.google.com/search?q=how+does+the+obe-cel+"fast-off"+work%3F

The "fast-off" mechanism in obe-cel is a modification of the CAR T-cell's design that allows it to bind and release target cancer cells more quickly, mimicking natural T-cell interactions. This rapid on/off binding cycle prevents over-stimulation of the T-cells, which reduces T-cell exhaustion, minimizes the risk of severe cytokine release syndrome (CRS) and neurotoxicity, and increases T-cell persistence, leading to potentially deeper and more durable remissions.

How it works

• Rapid binding and unbinding: The chimeric antigen receptor (CAR) on the obe-cel therapy is engineered to have a fast off-rate. This means that after it binds to and kills a target cancer cell, the T-cell quickly detaches and moves on to the next cell.

• Reduced over-stimulation: Unlike traditional CAR T-cells with slower off-rates that can keep the T-cells over-activated for longer periods, the fast-off mechanism limits excessive and prolonged activation.

• Prevention of exhaustion: By preventing over-stimulation, the T-cells are less likely to become "exhausted," a state where they lose their effectiveness over time.

• Lowered toxicity: The reduced over-activation and over-stimulation lead to a decrease in the release of inflammatory cytokines, which in turn results in lower rates of severe cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS).

• Improved persistence and durability: The "fast-off" kinetic allows the T-cells to remain active and persistent in the body for a longer period, which is associated with a higher chance of achieving durable, long-term remissions.

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"According to the researchers, 74.7% of patients enjoyed a remission after the treatment. They estimated nearly half would be alive and disease free after a year.

"Just 2.4% of patients suffered severe cytokine release syndrome. This compares favourably to the approved UK treatment brexu-cel, with around 24% of patients experiencing severe cytokine release syndrome.

"Researcher Dr Claire Roddie, from the UCL Cancer Institute, said: “While we have a licensed CAR-T therapy to treat r/r B-ALL in the UK, high toxicity is an issue in around a quarter of patients and lack of CAR-T persistence in the blood can lead to relapse and the requirement for more lines of therapy, including stem cell transplant.

“In contrast, our results from the FELIX study demonstrate that obe-cel can induce durable remissions with substantially fewer toxicity issues, which is great news for patients with what has historically been a very difficult cancer to treat.”

https://b-s-h.org.uk/about-us/news/second-generation-car-t-shows-promise-for-all