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I was trying to be charitable
The things I have written are so obvious and simple that they stand on their own. First p21 data not v good BUT not expected to be good at low doses. How is that possibly controversial?
The bigger question for the board is why any sentiment other than this drug K is so great meets with sullen disapproval
The real DD we need: get into the Letai lab at Dana Farber with APR-246 and K for a comparison with the new tool BDG. This assumes BDG really works, and that there is a known K dose to compare.
here is the problem.
K will not be first in class. PiSARRO, the APR-246 study with ovarian CA is already farther along, and if safety is ok and the drug works with the trial combo it will beat K to market.
That of course does not matter at all if K works better than APR-246.
Gee whiz- I think I made the same point in every post....Duh.
We are just talking past each other.
p21 may well be important. All I meant is that phase 1 so far has yet to demonstrate any big impact
Sorry guys.
Half of the pts showing little change is unimpressive. or maybe you'd like to address the other half that presumably showed no change.
And how can there be a home run for data that has yet to be presented ....
Maybe we can talk about data that counts-how the later cohorts did-when we know more about it.
Huh? Original poster presentation for K shows p21 increases, dose dependent ,that were large. Cannot recall percentages off top of head but a lot. Easy to look up.
All this likely means is that cohort doses must be higher to see an impact on p21/PUMA etc. (Not at all a surprise)
But it does mean that reported changes in p21 are unimpressive for early cohorts.
Is there any other poster argue that would otherwise?
The relative importance of all of this- rise of p21, PUMA MDM2 ratios- is certainly up for debate.
Would love to know about what actual patients are experiencing.
In one of the articles referenced by KMBJN an asco one about aprea, the article does mention upregulation of PUMA and NOXA by Aprea 246, far down in the article. ? significance
It is very generous for you to take the time to point out those posts, which are very interesting and helpful. I would only say that the more I read about p53 p21 PUMA etc the less clear it all seems.
It is also interesting that Phase 1 for the Aprea drug was not impressive, and yet in combo with Cisplat it may be a winner.
That suggests of course that less than sterling phase 1 for Kevetrin is not the be all or end all, just a beginning.
Thanks again.
ctix yes. aprea maybe private, don't even know.
As I said in same post, next sentence, would not expect much fr early cohorts. And I agree that putting eggs in p21 basket maybe not wise since patient survival is what counts.
Let's see, a direct answer: half of pts increasing by 10%? What could be better than that? How about 2/3 increasing by 20 %? Or 3/4 increasing by 25% Or.......
None of it matters. All that matters is what is to come.
Aprea 246 little impact on ovarian Ca itself but excellent synergy with Cisplatinum. Maybe Kevetrin is simply a better drug. Will be nice to finally get more info.
What are we laughing about? Sorry, don't get it.
Agree with you of course that what really counts is patient survival, and not p21 levels, and that the whole apoptosis thing is very complex.
Did not mean to dredge up Aprea if already discussed well prev, but had not been through that thread. Still trying to understand the whole thing, and I would imagine the science and mechanism of kevetrin-in full- is prob not even understood.
Will K be efficacious in human trials on its own, or only on combo? Interesting that Aprea 246 is in combo trials right up front, from the beginning.
apr 246 and PISARRO trial- very interesting reading. Combo therapy for advanced ovarian CA using in part the Aprea p53 drug. ( I wonder- can I call a rival company product chemo? I realize that word is banned on this board)
Sorry not good enough computer skills to post the links, but website is pretty helpful, easy to find
search Aprea and p53 and you will find a competitor to Kevetrin.
I am glad to be able to buy CTIX after a positive phase 2 for B, which ultimately should make current share prices look good- however long that takes.
I realize that many of you bought in very early on the promise of K. I have joined you in that hope.
In memory of Spock- hey, Nimoy was from Boston!-live long and prosper.
3.141592653
The big question: how far will stock sink with so so Kevetrin news, or not so good news. Yeah I know, posters say CTIX says it is working "as expected" but early cohort p21 data is not impressive at all. I know, I know: so what ? There is not supposed to be an impressive increase in p21 at those doses, is the answer, certainly . Have to wait and see. For later cohorts, who knows, as there is no data reported. Cannot assume "as expected" means that the new numbers will be good, I don't think. The new numbers for p21 and patient response may turn out not to be as expected, since this info and territory is unknown. I know some of you disagree.
Are they holding back data until move to NASDAQ?
Cannot believe start of phase 3 trials with B will move stock, unless partnership announced too. If CTIX goes it alone for phase 3 these results are far off.
Positive K news, on the other hand, I think, would probably mean that some of the crazy share prices that you see bandied about might be reached. But it is still so far away from real later trial data for K. Nonetheless good news for a very small number of patients would still be very good news.
sclimmuno if you come again some time let me know. Do not have private email on ihub. My wife attended meeting- she is a biochemist. We live in Cambridge. Maybe by the time of next meet news with ctix.
Ha! TOLL RIG NOD PAMP. Dude this might as well be lions and tigers and bears. I am regular old emergency doc and not an immunologist or researcher.
Yes, what the article is getting at is how different antibiotics impact a variety of modulators of the inflammatory response in attacking Gm + bacteria. But it is very investigational and preliminary and it is out of my league to comment on.
If TOLLs and PAMPs etc become critical to understanding advantage of Brilacidin vs the others(Vanco, Dapto, Linezolid) I can try to really study up on it.
Thanks. Such was the intent, obv.
I freely admit to stealing the closing line from another board member (etradeedge?)- resistance is futile. Those Borg! You gotta love'em.
Crayons and arrows. OK: I was wrong to say that PR was about Brilacidin and dermatology products, when it was about all those other arrows in the defensin box, or quiver.
And what a threat they are: all in development, all work in the lab , none may ever work in any patient in any trial. Now those are real weapons!
Maybe one day one of those gm negative babies will be America's go to drug for the superbugs. Maybe. That's a long day away.
hey I am a shareholder(paltry), and a believer too, just not to the extent of many of you.
None of this excuses my misreading of Astavakra's original post. I am glad it elicited his graceful response about the crayons, though.
It means that I cannot go see yet another person with an injury from a slipping from his ladder or his snowy roof (endless variations on this theme this winter here in greater Boston)and competently post in quick succession. Will need to pay better attn.
still the same arrow though-Brilacidin
a different target, at least
The topic was bacterial infections, not cancer and psoriasis.
Quiver quibble: is this worthwhile saying? I assume you all would agree that there is a quiver in progress, but no arrows other than Brilacidin currently. All those other compounds in development may never even see the light of day. Or they may be the greatest thing since sliced bread. But none of them have ever been given to a single patient so they do not constitute a quiver.
I do not say this to be argumentative, or mean spirited, just to state the obvious. Maybe too obvious to even post. But there seems to be a sense on the board that because Brilacidin looks good so far, that the other drugs might do well too- but this is not at all a given.
Saying that B is ineffective against some bacteria is not a criticism. It would not be expected to kill every bacteria, right?
I hope you are right. Now if a press release would just confirm it....
First reference: Poster conclusion PMX30063(B)not so good against Pseudomonas, and other gm -. March 2014 discussion of superbugs does not mention B. I think B prob would not work against the CRE, as discussed prev, or we would have heard about this potential from the company.
Which is not to say that other drugs in development may not work.
Also note fr first reference(2011 poster) that B not so effective vs Strep pneumoniae(also gm +), which would have been very nice, given how big a problem that bug is.
The tumor sample reports that you printed are where oncology is headed, as a variety of articles referenced on the board recently have suggested- the one in the NYT about treatment based on genetics, and not based on organ of origin of a tumor, and the other referencing a Cell(I think) article about sorting out possible treatment alternatives in 16 hours(yowza).
Look: the reason for all of the focus on p53 is because if you had the same report on every person with cancer in the US about half would mention p53 as a genetic mutation and therefore a potential target. It is nice to see that they reference Kevetrin as a potential treatment.
Now we just have to wait patiently to see if the mouse data translate into human success
I applaud your ability to track this down and would love to read a link. Thanks, Sam
Flabby post written when tired.
SIRS refers to potential consequences of bacteria floating around in your bloodstream and not staying local, as in a UTI, or pneumonia. The main adverse impact is striking prolonged drops in blood pressure which is a common killer.
Thanks. I look forward to writing about my first chance to order Brilacidin for a pt in the ED.
Yes I can recognize sarcasm, and of course I earned it, because who really cares if I bought the stock or not.
Bought because Brilacidin ought to be worth a lot some day-1 year? 2 years? And if Kevetrin has some good late cohort info CTIX really will climb I realize this is nothing new to any reader here. As a new person to CTIX and its products it took me a bit of time and reading to be convinced
SIRS is just a new name for fairly severe and severe sepsis , meaning bacteria cultured from blood, in patients with a wide variety of infections, like pneumonia, or pyelonephritis, or UTI, or cellulitis. In other words, many types of infections can make you sick enough to qualify as SIRS. To the extent that Brilacidin can establish itself as a gm + treatment of choice, it will be a go to drug. The gm- part will be harder. There would need to be studies showing that it can beat, or do as well as the usual gm negative drugs, in the same way it did so well against Daptomycin.
Slow response.
Drove from Boston to NC today, 13 hrs in the car....
woops meant to say partner after phase 3 not before/during
No longer shareless after today, but still view this as much more of a gamble than many of you do. Also see this as a very long term investment. Suppose CTIX wants to partner after phase 3, and before, for Brilacidin? Suppose end of phase 1 is promising for Kevetrin but not so exciting that everyone will jump in, and phase 2 results needed? Then we are looking a sideways for a long time. I still agree the stock looks like a winner, but prepared for a long wait.
I will be just one of many who will thank you for this amazing link. Impossible to watch without tears. Even harder to ponder all of the other patients who did not qualify for the trials and did not make it. And then to think of those in similar ground-breaking trials who died (someone referenced JUNO experience) Very moving to see the patients/families.
Cannot tell if you are joking, since this was discussed before. For those who view this as blasphemy, put me on IGNORE
Ladies and gentlemen- I hope you have all read this article carefully because IF it iturns out to be valid- and this is just the first report about this approach to cancer treatment- it will change everything.
AGAIN- any oncologists reading, please weigh in here.
But, this finding, that in LESS THAN A DAY you can predict the best chemo for a given pt, is astounding, and revolutionary.
Once the MTD is known then Kevetrin can be added to the mix somewhere in a Dana Farber lab. Yeah, yeah I know, these are for the FDA approved drugs- that makes perfect sense. But you can bet that once you have a completed Phase 1 that shows no horrible toxicity that anyone would want to know if Kevetrin- and all the other new chemo agents - will work, and they will be doing comparisons of newer drugs, unofficially or not.
It is a big IF. Will these results hold up?
It is also quite scary: I was reading about Aprea and their p53 drug, now in an ovarian cancer trial. Let's say they send over a sample of their new drug to Dana Farber. (Or maybe they can run the same tests in many labs around the world. How tricky, and how easily reproducible, is the process) And you know in a day how good K is, or how good the Aprea drug is, etc!?!!
First I have ever heard of anything like this. If this type of testing pans out it will be a total game changer for trials and treatment. Almost beyond belief.
NYT article this morning about treating cancer based on genetic mutations rather than organ of origin; sorry not able to link. Will need to work on basic computer skills.
More about Brilacidin.
OK recall the curve posted by ?sclimmuno- it showed what you would expect- big pharma pays more for drugs as they are farther along in trials.(duh) If CTIX has enough money for phase 3 why not hold out for more money from a big company? When they are further down the road, and not n the near future? Better for shareholders, ultimately , if they do.
More applications for Brilacidin- I do not have the ability to search prev posts- not a paying ihub customer. Has much been written about non cellulitis applications of the drug?
If not, I can try to add more- and I will gladly defer to any infectious disease docs who follow this board- are there any, by the way?
Any pt with pneumonia admitted to any US hospital who comes from a nursing center or rehab center must be covered for Gm positives, esp MRSA. ALWAYS two drugs, never one drug. Almost automatically this is Vancomycin(plus another antibiotic to cover gm - etc) Here is another potential big market for Brilacidin- so much simpler, as has been detailed, vs Vanco
Yes I am considering buying in a bit, but with 3 daughters in college(and another to come) little to invest. I am sure you know how it goes. Still shareless.
Fair enough.
Case closed.
Unsure if you meant to describe the Jarisch-Herxheimer reaction, well known effect of antimicrobial treatment of say lyme disease, where the pt feels worse for a while as many bacteria are killed off. If I were more computer savvy I would post links, but I am not. Easy to look up. Describes toxicity from rapid cell death- syphilis Lyme etc.
But remember: this is a post from someone just masquerading as a physician, who describes this very reaction to many many pts who get Lyme disease in the Boston area, as he discusses their treatment,,,
Oh yeah- is it ok on the board to say Brilacidin is an antibiotic? Since you cannot call Kevetrin chemo?
All right, I will drop it