The latest Investing Matters Podcast episode featuring Jeremy Skillington, CEO of Poolbeg Pharma has just been released. Listen here.
There is a point here, with straight dox at a concentration of say 1 unit, the amount of dox hitting that RA site would be proportional to the size of the area, so maybe 0.1% so 0.001 units. With 6k it would be much higher, both because the dose would be maybe 2.5 and not 1, and it would only be hitting the RA site and the Tumour. Assume that the tumour is expressing 10x more than the RA site and they are similar sizes then maybe 0.2 (ish) hitting the RA site.
This isn't great, BUT it'll still be better than straight dox for the heart, so you'll be alive, have an undamaged heart and worse RA. Maybe there is a way around it, immunosuppressants to downregulate FAP-A at the RA site, choosing patients for those with little/no RA (although a lot of RA might be better as each site would receive less), but this is still a better position to be in financially than either the straight dox market (more cycles, fewer contraindications (age, heart etc. )) and better for most patients.
Everyone here knows that drugs have been approved that only improve things for a small fraction of the population with a disease whilst having bad side effects, this is no different, except that it'll do that, likely for a (much) larger fraction and it'll not have the side effects, so this does not hurt our chances in the slightest.
The cohort doesn't need to be big enough in ph1, it's about tolerance and safety. It's not killing people left right and centre so it's good enough to move on to ph2.
If you had arthritis and cancer would you rather have treatment that gives you lots of side effects and damages the heart, or would you rather have something whose side effect is to damage the arthritic areas some more but nothing else significant.
However, as a side note, and not suggesting that this is likely, RA is an immune response, where the immune system attacks healthy cells, what happens if those healthy cells are killed off? Does the immune response lessen? MS patients (I know one who has been treated like this) have been treated with chemo to kill off the immune system so that it stops attacking the nerve sheath, and it works. Whilst this is the same same effect, stopping the response, by another means removing the target for the immune response could be beneficial. Anyway all of this is fantasy but it shows that it's not necessarily a bad thing.
Yuyu your view on the probability of the results of a match suggest a level of sophistication of thought that's frankly not that great.
But can I say thanks for exposing those thoughts so that I know to temper your words with that knowledge.
Precision in that case may mean something different, more akin to personalised medicine, ie gaining a precise understanding of the particulars of the disease that the patient has and tailoring something precisely for their disease.
Matml, it apparently matters because it wasn't invented here.
It could have been invented here, you could have asked, they could have said yes or no, but there's too much bickering, one-upmanship, talking about size buyers and NY opening, saying 'I'm an astronaut', never mind reams of tech analysis which really only applies in the absence of news, calling AS a liar, barely literate posters who don't know the difference between Million and Billion. But you need to have a coherent view to go to them and say we want to know more, we want more flavour. If this board wants to be taken seriously it needs moderating, and people that are here to solely talk the company down need to go, especially when most of what they say is 'wrong' is factually incorrect.
Someone else does something that will end up benefiting all, it reminds AS that we exist, and we can behave like adults, and the response here proves why they would not entertain talking to representation from this group.
You can hide behind 'it's banter' or 'It's another opinion', but that's all BS. There is the occasional nugget, but it's constantly hidden behind drivel.
In part this is the fault of LSE, and the lack of moderation mechanisms, but that's why other mechanisms exist, you might shout echo chamber (people have), but they want the same things those that shout that want, so what's the problem. Ditto the comments about 'a bunch of rampers' so what, they aren't, but if they were what's the problem, they aren't turning from ramp to deramp, so what's the problem with a group that is positive.
I won't trust that you called and/or emailed Avacta.
'Managed to obtain a copy' that's hilarious, i.e. they are in the group, that's all it took.
Nice shiny new account from someone.
You missed out
1. LSE un moderated disruption from certain members.
So approach Alistair yourself? They put the effort in to create and moderate a group, make contact, with though how it might work. Who would you invite from here? Would want him to see the conversations here?
They organised it, so why shouldn't it be there?
So they weren't real people? You'll never ever get all members of a group to recognise representation.
Ophidians nose is out of joint as he got kicked from that group for exposing personal financial information about members of that group, he did this, imo, because he wasn't invited and that hurt his ego, he's toxic as we found out here ages ago, and doesn't know everything he professes to.
Hey just reporting on the most vocal member of that debate
The ***** is q-u-i-n-t no idea why that is blocked.
not quite, one member 'cue' claims to be ex pharma but constantly refers to the fca and not the fda, he's in intensity, similar position to us, (risk in fact), old drug new targeted delivery mechanism, they'll need ph3, have merck involved but no offers etc. therefore counselling its a risk. his position of more likely to fail than not is still wrong, and that wrongness probably applies to intensity too (as he explained it), perhaps it's not the high 90%'s that some of us here think, but it's certainly >50% imo if you understand, not sure that he does or wants to.
there was stuff before that that i've not looked at, he's the one carrying on, doubt he's tw, more like the old *****, my bio is better than yours with prtg.
I popped in there, seems to be someone saying lots of trials fail, and someone saying this is different. At least that was the tail end of it, and if the 'fails' poster hadn't realised why that was less likely (he still thinks fail is more more likely than sucdess) then no points were taken on board.
Thanks for copying and pasting something that's been highlighted with a red dot just above your post.
Ticino, the outside of the tumour contains FAP-a, for those cancer types that over express it, so the warhead is delivered to the right place and attacks the shell, it does not work on a cell by cell basis.
There are cancer types that do not express much FAP-a, these have been highlighted in many of the documents from avacta, so there are plenty of types of cancer to work on.
Ph2 would be a few tens of millions, not hundreds of millions.
At that point it will require Ph3 testing, to ensure that it hasn't effected the action of the drug. But it's not like there isn't enough to get started on.
It's a platform that can deliver any drug with an appropriate structure that can be attached to the linker, to a FAP-alpha rich target. If the target is not FAP-a expressing or thedrug cannot be linked to (hence velacde analogue not straight velcade) then it cannot be pro'd.
There may be other linkers that hit other targets, or can attach to other dugs but this is what we have for now.