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I've been surprised so many times in th epast, I'm not going to predict what's 'in th epipeline' nor when we'll get to hear about it. I just think that it is far, far more likely to be positive news than negative.

It's important to bear in mind that there is a paradigm shift going on here: the rules of small molecule chemo have been completely upended and the extremely toxic preclinical, and earlier, candidates that would kill patients' organs before killing tumours can potentially now be used to attack just the tumours. Companies developing anticancer therapies are in a unique position within the industry because they want to find compounds that actually ARE the most toxic and what had been the hard problem of differential toxicity has just got a whole lot easier.

Pharma companies everywhere will have shelves and shelves in their fridges full of samples of highly toxic candidates that failed even in early animal testing, let alone preclinical. The question now is maybe "Which is the best target to go for in order to fully kill the cancer?"

I think "another oncology drug in a potential partner's pipeline" is clearly drug X and could be anything with any company!

Yes, doxorubicin, and for TNBC, as he had said in an earlier video. He also talked about 22 weeks of 3-weekly chemo, so I guess 8 cycles of 60mg/m² if Alan was to be believed that 60 was a standard dose.

Top publication, Scrip, so this is excellent exposure for CC and Avacta in their 'preview' of the year.

Yes, the pre|CISION pie can be cut many ways: by drugs, indications and territories, and all with or without exclusivity. People might say that faridox, with its boring old doxorubicin, will be overtaken by newer, more powerful pre|CISION drugs but the fact is it is here and now and not far off its first approved indication, salivary gland cancer, if the data released so far is to be believed.

So with all that, why would any company want to license it when there could be better options in the future? Well, if the offer was a global exclusive licence to develop faridox for SGC, plus the option to have first dibs on any future Avacta pre|CISION drug for SGC, plus the rights to develop their own pre|CISION drugs for SGC—essentially an exclusive licence agreement to control the global pre|CISION SGC market—then that would surely be of great interest.

If it's taking Simon a long time to get that first deal, well the licensing possibilities are nearly endless and newly revealed data and developments are moving the goal posts in Avacta's favour all the time as conclusive evidence proves the platform (I'll call it that now already).

$4bn would be 668p a share. Not enough for me. I'd be looking for at least 1,000p a share, a $6bn buyout. At least.

I did indeed make a terminological error though. I used 'receptor site' rather than the broader 'binding site'. FAP binds its substrate (protein or pre|CISION dipeptide) at the binding site and then cleaves it.

If AVA6103 can be fairly strongly bound to FAP but not easy to cleave due to its flexible 3D structure (everything is on a spectrum), then it could be said to be partially inhibiting FAP, meaning hindering FAP in doing its job of cleaving proteins as part of the process of cancer growth (or more generally tissue remodelling). This is all supposition as Avacta haven't yet divulged the struture of AVA6103 nor how it is retained within the TME but they are talking about a small molecule.

Anyway, I can quickly knock the 'exatecan from AVA6103 behaves differently' idea on the head.

How long does exatecan stay in the tumour microenvironment? https://www.google.com/search?q=How+long+does+exatecan+stay+in+the+tumour+microenvironment%3F

You get different text/presentations with each running of this query but the essence is:

"The retention time of exatecan in the tumor microenvironment (TME) depends heavily on how it is delivered (free drug vs. conjugate/ADC), but it is designed to be highly retained, particularly when released from carriers, with active effects lasting for days to weeks.

"... [AVA6103 is often mentioned as an example of slow release]

"In summary, via specialized delivery, exatecan can maintain active concentrations in the tumor for several days, with therapeutic effects extending for weeks."

Note that the summary does not mean that the SAME exatecan molecules are retained, rather that the exatecan concentration is maintained due to the slow release from the prodrug.

I don't remember that quote but it sounds like what I might have written as it rings true, although context is important re the inhibitor part. If someone can find the thread it comes from- I couldn't back to put-Xmas - that would give the context.

Most here just seen to want happy clappy you'll-be-rich-soon posts but if anyone is interested in a deeper understanding of the chemistry I'd be happy to try to give it (its complexity does require a certain basic level of chemistry knowledge or a LOT of explanation) when I'm on my laptop.

Maybe the rate of cleavage for AVA6103 is slower than for AVA6000 as AVA6103 is almost acting like an inhibitor, occupying the FAP receptor (aka cleavage) site?

I agree with the comments to the OP but Wmsjames, can you explain why AVA6103 hangs around in the TME for so long in animal models without being cleaved, when the same is not true of AVA6000?

I believe most on the board would have understood what I meant.😂😂😂

A note in the RNS about the size of the current anthracyclines market (I assume faridox could do a better job than all the currently available anthracyclines?), together with a listing of the issues with anthracyclines, might have been an idea.

Yes, faridox may not be available for a while but the maximum cumulative lifetime dose removal news could be sold as a British biopharma success story, particularly if the additional chemistry of AVA6103 and AVA6207 get a mention.

It's a pity Avacta couldn't have piggy-backed this with a little mention in the news services and dailies about the removal of the doxorubicin lifetime limit.

Call it pedantic all you wish if you don't care about truth and just want to think happy thoughts, which many here obviously do. "Killing cancer cells kills cancer" is factually incorrect unless ALL the cancer cells are killed, which doxorubicin has not been proven to do - as you like to say, FACT! 😁

Yes, the statement “doxorubicin kills cancer cells” is scientifically and clinically correct but you stated "doxorubicin ... kills cancer" which is factually not correct. There is a significant difference between cancer cells and cancer the disease. I will accept that you were not using precise terminology.

What do you mean by "kills cancer"? Which cancers are you referring to?

Https://www.youtube.com/watch?v=moNHrJweepg

Time will tell for sure...