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Can you please explain then the mechanism of action for prurisol in psoriasis?
Sorry at work - v quick read if 28 works as ITT # ok- but they showed ITT 200 mg # as 29 not 28, and I lost interest from there
The numbers work if you use different numbers from the ones they show as ITT?
I will start again tonight
How is any response at just one dose a trend?
My failure to see the mouse SCID stuff- odd then that it has not been borne out in P trials thus far- beautiful murine response and p2a unimpressive
Meaning they somehow got the dosing wrong in 2a? And should've included higher doses?
Still very mysterious- equivalency based on abacavir and abacavir has no activity in psoriasis?
OK, How about actual patient numbers?
That was the assignment
I am interested to read that you are optimistic regarding 2b. How do the very small numbers help you see 2b as glass half full?
Sure maybe it'll work, but it can very easily fail.
Just wondering- have you tried to fit the numbers into the Bertolino decision making slide? Biotech showcase slide 11. Actual patients instead of percentages? It is hard to do based on the numbers provided- When I start to use the provided percentages I get parts of patients, not whole ones
I figure I must be making a simple mistake, but wonder what numbers he uses to derive the percentages
Perhaps you would like to share actual numbers with us to support your conclusions.
You could start by trying to reproduce the famous page 11 Biotech showcase slide using patient numbers and NOT percentages.
How about supporting your conclusions?
Oh yes- back to the mice, right?
What aabout 2aP data
your big chance everyone! It has been suggested I am making mountain out of molehill re P 2a results.
Actually it is precisely the opposite- i am making a molehill of the supposed p2 a results mountain
But, hark: all you have to do is look at the post I sent to KarinCA for questions to ask Bertolino
And you are of course free to prove me wrong and set the record straight.
Thumb back through the posts to alight upon the aforementioned please ask Dr B questions.
Wherein dear readers, one asked: Dr B you have said that sept slide deck #11 was what led you to join the company AND YET, the percentages are misleading when one (1) considers that they are based upon miniscule numbers, where any variance would lead to skewed results, and not only that, (2)using your percentages the patient numbers are not whole integers, but, rather, parts of patients(please refer to prior post for actual multiplication)
Would any MD PhD make his or her decision on that basis? (let me think, umm, no)
Only if no other job offers in sight, nor would I ever say so in public-
please, anyone, explain the discrepancies.
Yes I have written, as I said, to the company, some word back from the CEO, nothing from Dr B. Will KarinCA help clarify in an interview? One expects a glossover, no? No straight reply- No real answer
Can any of you do better? RSVP
time will tell? Of course it will
does 2a inform 2b? Of course it does
and 2a was a just barely made it out of the dugout trial result for P
I see your point
they will measure tumor response for ....how many weeks?
sigh
progression free survival not important? It is of course essential
partner after this safety trial? Seriously?
Gotta prove efficacy- then the drug will be worth something(should I even need to write this down)?
Leo would sell K before demonstrating its value? Only if he thinks it is worthless
what do you suppose the big pharma response was to the stellar trial results you cite?
I would imagine it was on the order of- come back when you have some real data.
Which they have yet to demonstrate. Not even close.
Squeak squeak back to the slides of those mice. Now that's improvement.
no response to 50 and 100mg and that is a positive? what then might a dose response curve be?
Sure maybe they started too low a dose with 2a
And maybe 2b will be a flop
and the statistical significance?
Of 7 vs 4?
sigh
Wake up people- CTIX tells you that its cancer program has scrapped its planned trial-WITH AN ENDPOINT THAT WOULD INCLUDE SURVIVAL-in favor of a small safety study, and you expect a rally?
Gimme a break.
The data are right there for the picking-ITT 7of 27 at 200mg dose responded while 4 of 30 placebo improved. How would the board characterize such data?
Robust? Very informative?
Weak?
I am going with just barely staying afloat for 2b, almost did not survive.....
2a results mean nothing for 2b??
in fact 2a results- which are threadbare, weak, just sneaking by- inform the 2b results in spectacular fashion
they say it is a tossup and failure entirely possible
Major step backward with K ovarian CA trials and everyone is happy?
everyone is excited when we have a new safety study?
The PLANNED study, promised to start last year, was to show efficacy with combo therapy, with some dose adjustment of K as the trial went along
What really happened? FDA would not approve moving forward with the proposed because not enough safety data on frequent dosing? Or not enough money to do the trial they proposed? I wonder which it is. Aprea was able to get their initial combo trial underway and show efficacy even though final dosing was still in doubt. Presumably that is what would have been done with K ovarian 2, diff doses K at trial start plus a chemo agent as they planned. But not now
I suppose I should beglad that anything at all happen with K, and thought maybe nothing would move forward until equivalency studies done with oral K and then use oral K
Some big chance of efficacy with the short trial? I doubt it , but who knows.
Look: CTIX had already planned to use K in combo with a standard agent for efficacy. That was scrapped for reasons no one knows, and now we take a step backward-
Now we will lose even more time!!
CTIX announces big disappointment with progress ovarian cancer trial and people are pleased? I do not get it
here is what to expect from 2b P:
maybe success maybe not
too close to call
just look at the 2 a numbers, for a sober dose of reality
they may have been used but what is proven correlation.? The Sonis date for hamsters was pretty darn close in 3 human trials- if I recall correctly.
Look- just on the data we have now NO SUCH correlation P mice with P people- on human data P just barely squeaked (sorry)by into 2b.
Again: rat data just perfect(hey, how great are those results) human data, barely any hint of efficacy.
Are you positive? That no protocol changes can ever occur? I doubt that.
Prev already found an example where the protocol for K was changed, in a conversation with Kahuna
we have already covered this ground, when you asserted no changes could be made in a protocol, and I offered an example of change in protocol to our very own Kevetrin.
Protocols NEVER change, you wish to assert?
They focus instead on a drug whose trial would have ended in failure, and dismissal, if there were just 2 or 3 less responders.
You might have heard of that $10 billion dollar, guaranteed success, Otezla slayer. It managed to reach a 2b next trial round ONLY BY THE SKIN OF ITS TEETH.
It's called Prurisol
what is your answer to the question?
If you are aware of lots of data from trials of rats- done the way that CTIX did the P trial in rats- that correlate closely with human trials please advise.
Sonis hamster trials showed good correlation in 3 human trials- that is how I recall it without looking it up again
It begs the question: are there other unreported Sonis hamster trials ? That did not correlate?
Prurisol exceptional results?
In reality: with a change in the response of 2 or 3 patients there would be no phase 2 b
Prurisol would be in the rear view mirror
Statiscally speaking, it could still easily end up there in short order
what do you know
I have been whining for many months now about the need for a safety study with different dosing.
They should have done this A YEAR AGO, at least.
The results of the P 2a trial are based on such small numbers that 2 or 3 patients with different responses would have meant the end of P- bye bye
It is that close
It means that the next time the trial is done that the results might be very different.
At least this time there will be larger sample sizes
how about 500 out of 800
for a clinical trial
you know- sufficient power to provide actual results
as lacking by p2a
summary- i am a believer in B OM (Sonis hamster studies correlate well prev with actual human studies)and that has led me to average down
the example you give refers to larger sized trials
I think any reasonable person would conclude that using percentages for reporting trial results where there are very small numbers of patients is unhelpful
we agree about a small trial and inability to predict dose response
my original points were about bogus reporting of tiny response as percentages, even though those percentages would be drastically skewed by diff results in 2 or 3 patients
as if Bertolino does not understand this is NOT the way to present data. We can all grasp this I think
only that is not the active agent
and there is a new salt
new mode of action, new drug in some ways for certain
oh sure, no problem- only I would not be so sure when they explain it to the FDA
my recent posts are about the science, and not about buying and selling
From time to time here one comes across "it's all about the science" Right?
perhaps someone would like to explain how the percentages of patients at 200mg ITT do not even add up to whole numbers? From the very famous slide #11, the Bertolino career move slide??
Yes I did ask CTIX/Bertolino. We shall see. Maybe karin will ask too
However the two drugs work differently.
Maybe not so simple to say the salts allow 505-
1) You understand perfectly well the purpose of a control group, and if the course of the disease, without treatment shows lots of people getting better, then how much better is Prurisol? Dropping one of 4 patients whose skin got better is important.
2) see above.
3)Unsure about your point here. You mean the pK data on the INACTIVE agent abacavir? Seriously? What did Bertolino just say?
No curve of improvement from 50 to 100 to 200 to suggest any such response. Bertolino specifically said no benefit at 50 and 100. No way to predict better results at 300 or 400.
We can all hope for good news, but that is it.
Hope, based on very small numbers
Predicting responses based on very small numbers is not rational.
Tell me, what happened to the 4th placebo responder at 200mg? Why was that patient dropped when move from ITT to PP? What happens to your lovely percentages when the responders at 200 mg had been 5 or 6 instead of 7?
NO WAY to extrapolate limited data
I did not say there is no potential benefit. I said the data are sparse and presenting info as percentages ignores the fact that the actual numbers of responders is so small.
Bertolino questions:(1)
Back to pivotal slide 11, the one that explains why he took the job. What patient numbers are even used? The ITT 200mg population is listed at the top of the slide, with 67.9% considered to start with moderate disease, and 32.1 with mild.
ITT 200mg : n = 27, so 67.9% is 18.333 patients. Ad 32.1% is 8.667 patients.
What then are the real numbers and why doesn't the mulitplication even work on this life-changing slide?
(2)Why represent very small numbers of patient responses as percentages? At the 200mg dose: If 7 people responded in one group and 4 placebo patients also responded, is that really a great victory? And why was one placebo responder dropped in final data-4 down to 3?
(3)Advantages for Prusrisol in FDA approval relate to 505 pathway, and yet you have stated that abacavir has no impact on psoriasis. How then does 505 apply to Prurisol?
Please be sure that he provides the actual exact numbers from the trial, and NOT the percentages, which are BASELESS. Misleading, really, to be honest.
It matters not that in the end P may prove to be a winner. The real point is manipulation of data, and he should know that much better than the average board member.
And yes, I will continue to ask the company for more information in this regard.
My guess is they will say: of course the numbers are small, but we are optimistic.
Nonetheless- it is still not the right way to present data.
Or, do you disagree?
Of course there is more data to come- thank goodness. Our only hope But how good can we feel about it all?
But you understand Bertolino's point right? That one slide justifies his decision to sign on-
Totally bogus.
He is an MD? and a PhD?
and a decision is based of 2 or 3 or 4 patients? In a subjective measure.
Yikes....
sort of
the question is why try to sell it based on little data as a big challenge to Otzela etc etc hype hype hype
Bertolino says, right, I based my decision to join CTIX on that slide!
Sticky worthy-
"But it is your post."
Not only that, it casts doubt on Prurisol results. You know , the 10 billion dollar drug.
"Of all the nerve..."
I just wrote the company about the problem of raising hopes using percentages with TINY numbers. I will post a response if I get one and it is allowed. Not to mention, again the abacavir /505 bit .
It would be great if you can ask him directly.
The question is precisely how many patients is he using to come up with these response curves. From what they say the numbers are 1-2-3-4 total patients - responding versus nonresponding - including eliminating one responder from ITT to PP.
Does this seem right to anyone?
Squeak squeak: what about the mice?
Mesdames et messieurs: OK Bertolino has said that he based his decision to join the ctix bandwagon based on data from a slide from the presentation to a conf in Jan of this year, prev referred to in Sept this year, and prior to that.
This is the slide where 67.9 ITT pts go from moderate disease(score #3) to 25 %: source Biotech showcase 1/9/17 page 11, the very pivotal page.
Bertolino is an MD PhD, right? So what is he smoking?
Look at the numbers- you CANNOT, I repeat CANNOT rely on percentages when total numbers are so small, right? Can we agree on this? So when you report percentages of pts responding, when you are discussing the results of a few people whose skin condition you can count ON ONE HAND, can you generalize with percentages? Of course you cannot.
ok data from CTIX PR 9/19/2016 : recent P trial, 2a as it turns out: Placebo (no P) 30 pts: 3/18(PP) are responders and 4/30 (ITT) respond. 200mg dose 7/20 (PP) respond and 7/27 (ITT)do ok .
They took out one responder from placebo--WHY!!?? That would have made results close, exclusion on what basis? BioShowcase data , page 11
So what do we see? We see a percentage trend that is an emperor with NO CLOTHES because the numbers are too small. 7 people get better while 3- or is it 4- got better in placebo??!!? What if the numbers are off by 1 or 2? What happened to that 4th responder from placebo- there is no explanation . They are quoting these big percentage changes based on 3 or 4 people!!!! It just does not cut it.
Bertolino signed on to CTIX because of 3 or 4 more responders- at the very most!!- out of 10 with good results?
You gotta be kidding me.
He must know something else. He better know something else.
All this over the top hoopla over CTIX may or may not prove ot, but THE NUMBERS ARE TOO SMALL TO RELY ON if you are paying any attention.
Nota bene folks: 505 advantage is based on abacavir - and Bertolino just told us that abacavir is not the active agent!!!?! Is anyone paying attn to this?
OK, taking a deep breath, and that is most certainly in order if one wishes to peruse the almost baseless trial data favoring Prurisol, and admit that the antiinflammatory platform for Brilacidin is promising. Well thank goodness because the rest of the pipeline is going nowhere fast.
Oh yes- squeak squeak.
what about the pretty pictures in the mice who did so well with Prurisol? Can we just put up those slides again. Sure why not, if it makes you feel better....