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A low ball bid will not be put to shareholders. You will never hear of it. There is no way that a hostile bid would work, or even be contemplated. What would happen to the shareprice as ever increasing TR1 percentages were reported from a large pharma company ? Would the Avacta management stand idly by ?
If that were the case it would be due to a lack of available active FAP. In which case upping the dose would probably have little effect given the long circulation half life of 6K. The chemistry of cleaving either works or it doesn't.
Here is what Novartis have just paid to bankrupt Clovs for one FAP candidate :
Prior to the Chapter 11 filing, and subject to Bankruptcy Court approval, the Company entered into a āstalking horseā purchase and assignment agreement with Novartis Innovative Therapies AG (āNovartisā) to acquire substantially all of the rights of the Company to its pipeline clinical candidate, FAP-2286, as a therapeutic agent for an upfront payment of $50 million and up to an additional $333.75 million upon the successful achievement of specified development and regulatory milestones and $297 million in later sales milestones.
Noticed that the volume is tiny Groot ? The current value and a takeover value are unconnected here. If a big pharma want it is it because they know it works, in which case it is clearly worth a fortune. And there will not be just the one you can be sure.
The key is going to be how much ACTIVE fap there is in circulation. Fiona has alluded to the difference between FAP expression and FAP activity, and no one knows how that is going to pan out yet. For me, it is the big known unknown.
Yes, the others in the family, human DPP, PREP etc do not cut it, and human FAP does. In vitro. No reason a priori why this should be different in bodies, and if it was we would have heard by now. AS has been very clear on a number of occasions how the specificity is what sets this apart, and is the rock upon which others have failed.
All the 'debate' about does it cleave or not is noise to my mind. Of course it does, all the pre clinical data said it would, and the trial would not have got very far if that was wrong. The unknown is how is it distributed in the body, which in turn is all about the distribution of active FAP in that particular patient, at the time of dosing. There is very little unequivocal data on how that might fall, and that would make the difference between a useful drug and a breakthrough one. I'm confident, based on the company's direction of travel, and await imminent communication.
I find it amazing that people still seem to believe in the fallacy that market cap can only be supported by near term sales. Tech markets are littered with high value companies with zero current revenue. That is a bald FACT.
Absolutely. An earlier attempt to make an activated prodrug of doxarubicin used the acidity in the tumor to execute the cleaving mechanism. Bit crude, but it did get into P2 trials before being dropped. This is a prize long sought.
Lots of benefits touted for Affimers over antibodies, but for me three are significant in therapeutic arena :
1 - Of human not animal origin, wholly developed in bacterial systems
2 - Small size means they can get where antibodies do not. Maybe able to cross blood brain barrier, and can get into smaller pockets on cells and proteins. The dose extension technology being developed with LG overcomes some of the problems of small size.
3 - Ability to be expressed in situ. Longer term this may be the clincher. The AffyXell project is low key for now, but could be yet another giant sized chunk of IP for Avacta
All the things like low cost, speed of development etc are nice to have but not game changers. Look how many antibody therapies were rolled out in double quick time during the pandemic.