Replies to post #94400 on Innovation Pharmaceuticals Inc (IPIX)

[havendale]

Infinity, those are all fair points (but be prepared to be attacked anyway)

In 4-5 months, all of your questions and many other questions will be answered, and we will all see the direction that Leo is going to take the company.

For what its worth I still maintain that starting in 2 weeks, we should start to see some answers and that it will continue for the next 4-5 months (that doesn't mean a news release everyday)but a few each month, with a shareholder update, etc.

Although I have never been a proponent of the mothership theory with a stock price of 200. to 300., I still maintain a price target of 18 to 20 by years end, and then lets see what develops before we start thinking about 2016 and beyond.

By September/2015 a lot more of what we need to know should be known.(good, bad or ugly) but I'm very optimistic.

Great weekend all.

[biodoc]

In that you found the 'early cohort p21 data' not impressive, what would you consider impressive p21 data? I do not know. It's complicated- more p21 may not be better for the patient. Patient response and tumor markers are easier for me to understand.

[frrol]

I've voiced the same opinion on Kevetrin and some people here have pointed to management's statements that recent Phase 1 results are going as expected, e.g. with respect to P21 correlation. I don't know how this is really known unless management is privvy to early test results. That seems strange to me but I choose to believe them.

As for Brilacidin, I don't think announcement of the Phase 3 would itself would move the stock, but the conditions of the Phase 3 may be a catalyst, e.g. fast track approval.

[Amatuer17]

Good questions and are valid. You have been raising them since you joined.

But here is the thing - people on this board are not newbees - they have invested in this stock for more than a year and most are in black - many of them have decent appreciation.

Also mist of the group here know the risk of investing in bio-tech and have decent level of appetite for risk (one of my bio-tech stock dropped from 26 to 8 in 3 days)

Howver CTIX provides an opportunity that IMO that allows multi-bagger potential against maybe 60-70% loss from current price if all results are adverse as you mention.

This is one of the reasons I am so much invested in this stock - many other have same view as well

[Whoops]

And here I was very impressed with the low dose p21 results. The 10% threshold they put on it removes natural variations one might see so what is raising p21 levels then? We are now dosing 8x the dose from the first p21 test. And mind you they will also test this on tumor types that may not even have mutated p53. All signs have looked very good...but then I am a fool I still think spleen lesion in a stage 4 cancer patient is very encouraging. Remember this is mainly a safety study and has already become a success we are moving on to multiple phase2's. As far as stock price and potential drops what is the company currently valued for??? My answer at these prices is how smashing Leo looks with a yellow tie!

[TheHound]

Holy Pessimistic Vibes penetrating my CTIX soul.

[govorchin]

i should leave this for BK to answer but he has been busy as of late i think.

dr kumar is credited with proving the MOA of kevetrin. he noticed that p21 expression increased as the dosage escalated in the mice trials. p21 kills cancer cells. so since the scientists at CTIX receive the PD and PK results from the trial weekly they see the P21 expression. dr menon says it increases with the dosage increase. tumors were stabilized at dosage of 10 to 30. tumor shrunk at 75 or lower and pancreatic cancer stabilized. at 315 one tumor disappeared.

as expected means GREAT news because we know what dr menon was expecting from the mice studies.

leo recently said they were told to gather materials for a publication.

it is impossible for you rain on the parade. imo

gov

[slcimmuno]

P53/P21-PUMA -- I'm largely a Kevetrin novice but the cites below might be of interest to the onc-informed on the Board, particularly as we await news out of Dana Farber.

The U of Colorado 2013 study adds a wrinkle to the claim more p21 expressed the better. It also seems to reinforce the idea that, if K pans out, it could be used as a combo therapy and not just as a standalone (what Georgi advances).

That D Farber apoptosis tool also came to mind -- so in an ideal world you'd first have screened patients genetic profile (per the Colorado rsch) then screened the drug/drug cocktail to assess if it is working, causing apoptosis (per the D Farber rsch)...

To the Precision Medicine idea: the Future of Medicine.

DANA FARBER
http://www.dana-farber.org/Newsroom/News-Releases/novel-precision-medicine-tool-could-help-personalize-cancer-treatments.aspx

Xx

U OF COLORADO
Study details genes that control whether tumors adapt or die when faced with p53 activating drugs

EXCERPT
When turned on, the gene p53 turns off cancer. However, when existing drugs boost p53, only a few tumors die – the rest resist the challenge.

A studypublished in the journal Cell Reports shows how: tumors that live even in the face of p53 reactivation create more of the protein p21 than the protein PUMA; tumors that die have more PUMA than p21. And, for the first time, the current study shows a handful of genes that control this ratio.

“The gene p53 is one of the most commonly mutated cancer genes. Tumors turn it off and then they can avoid controls that should kill them. Fine: we have drugs that can reactivate p53. But the bad news is when we go into the clinic with these drugs, only maybe one in ten tumors actually dies. We wanted to know what genes fine-tune this p53 effectiveness,” says Joaquin Espinosa, PhD, investigator at the University of Colorado Cancer Center, associate professor in the Department of Molecular, Cellular and Developmental Biology at CU Boulder, and the paper’s senior author.

[...]

The hope is that in addition to drugs that reactivate the tumor-suppressor gene p53, patients could be given a second drug targeting genes that control this p21/PUMA ratio, thus making first drug more effective. Likewise, in cases in which toxicity in healthy tissue limits the use of p53 activating drugs, Espinosa’s research could lead to new drugs that thumb the scale of the p21/PUMA ratio toward survival in these healthy tissues. Up or down: learning to adjust the ratio has immense promise.

The group’s next step is likely repeating the genetic screen with additional tumor and healthy cell lines to discover which of their newly discovered candidate genes are common controllers of the p21/PUMA ratio across cancer types. And, interestingly, the same technique could be used to make many existing drugs more effective.

“With many of these molecularly targeted therapies, you want one effect but then you end up with many other possible effects,” Espinosa says. (An example is the recently-reported side effect of low testosterone in male lung cancer patient taking the molecularly targeted drug crizotinib.) The genetic screening technique used in the Espinosa lab could help disentangle effect from side effect – showing which secondary genes regulate the desired, tumor-killing response and which secondary genes lead to undesirable side-effects.

“Not only could this technique lead to drugs that decrease the side effects of targeted therapies, but if you’re not limited by these side effects, you can simply give more drug, perhaps making existing drugs much more powerful,” Espinosa says.

http://www.coloradocancerblogs.org/study-details-genes-that-control-whether-tumors-adapt-or-die-when-faced-with-p53-activating-drugs/
FULL STUDY
http://www.cell.com/cell-reports/pdf/S2211-1247(13)00196-4.pdf

P53/P21 TUTORIAL
(still clear as mud to me)