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If I had a 20% chance of developing OM, I would gladly take a swish-and-spit drug with no side effects to drop that percentage down to somewhere around 5% (rough guess). I think the potential patient population could be quite large since IPIX is developing this as a preventive treatment and not reactive.
Please provide your source for this information.
Anyone else excited for a K update? Trial started 2/10. 3 weeks of treatment plus 3 week follow up.
Dr. B-
“This will be a small trial that will move quickly with the end goal to provide the critical data necessary to forge a partnership with a large pharmaceutical company interested in co-developing Kevetrin as it makes progress toward possibly becoming the first p53-activating drug approved by the FDA.”
PR quote-
"Cellceutix believes that this clinical trial, using IV dosing, will directly inform how Kevetrin modulates the p53 signaling pathway—one of the key questions asked by multiple pharmaceutical companies we are engaged with under Confidential Disclosure Agreements."
Just to clarify, the 35% was the Per Protocol population which do include investigator non-compliance site. Here are the numbers I'm figuring:
ITT 200mg: 7/27 (25.9%)
PP 200mg: 7/20 (35%)
Subtract Site non-compliance: 7/16 (43.8%) - this is my assumption based on the stats. Company did not provide the actual numbers to my knowledge.
We still don't know why those 7 patients did not meet the protocol criteria, but I don't believe it has anything to do with investigator non-compliance that the company mentioned (based on stats above).
Gotcha. Thanks for the clarification. Interesting that the Ph2b had better efficacy stats than Ph3. I guess we'll compare our results to all of Otezla's trials and see where we stand.
Actually their graph shows 26.3% PASI75 for Otezla. I'll spend time on this later.
I have been referring to another report that shows 33%. Here are the two reports though:
33%: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2014/206088Orig1s000StatR.pdf
40%:
http://ir.celgene.com/releasedetail.cfm?releaseid=902701
I don't have time to look into the differences between the trials, but it's interesting that IPIX posted Otezla's graph of 33% on their Corporate Overview (which is what I thought we were aiming to beat). I'll look into it later tonight.
6 months - $6.50 (guessing a P partnership)
12 months - $20.00 (guessing OM results won't be delivered until early 2018, followed shortly by a B partnership)
If K gains interest from this study, then add $5 to both of the above.
Something I thought about the other day is that If P has zero clinical effect, then there are equal odds the beneficial difference noticed in the Ph2a trial results between arms could have been seen in placebo, 50mg, 100mg, or 200mg. In my opinion, the fact that the slight improvement over the other arms happened in the 200mg group (highest dosage) and the fact that we have excellent preclinical results, I believe there are good odds it's due to P and didn't just occur by chance.
I understand this. I was originally commenting on the post that you reposted from another person, which said "To summarize: Prurisol met the primary endpoint (2 pt reduction) in 35% of ALL patients who received a 200mg dose per day."
The "ALL" was even capitalized as if to stress this factor. However, there are 7 people who were assigned to the 200mg arm that are not included in this percentage; therefore, I believe this statement is false (unless the company reported these 7 individuals did not take 200mg per day, but I don't recall ever seeing/hearing this).
I'm not trying to be difficult, but with a small sample size, I believe we need to be careful with how we analyze the data.
Sorry, I worded that poorly. It was stated that 35% of ALL patients who took 200mg of P achieved the primary endpoint. However, I would argue that 26% of ALL patients who took 200mg of P achieved the endpoint (7/20 vs 7/27).
Yes, I agree. This data, coupled with pre-clinical data, is very encouraging. It will be fun around the end of the year to think back about all this nervous anticipation I've been experiencing haha.
Very good write up. The only thing I would point out is that in the 200mg group, 35% of the Per Protocol population met the primary endpoint. I feel it is misleading to state ALL people met the endpoint that took 200mg of P, especially since we don't know why there was such a difference between total people assigned to 200mg vs. PP population.
I believe the raw data is:
ITT POPULATION
200mg arm: 7/27 patients achieved endpoint
Placebo arm: 4/30 patients achieved endpoint
PP POPULATION
200mg arm: 7/20 patients achieved endpoint
Placebo arm: 3/18 patients achieved endpoint
With a small sample, I think it's helpful to look at the raw data to help put the percentages in perspective. Had our Placebo rate been closer to that of Otezla's placebo rate (about 4% PASI 75), this data would look a lot better.
True, thanks for pointing that out. I like how "Psoriasis" is the only disease that is underlined on their Upcoming Milestone Chart. I'm sure it means nothing, but fun to think management is most excited about it.
Trial started October 31. On May 10, they reported about 70% enrollment. So about 133 patients enrolled in 190 days, or 0.7 people/day. 56 more patients to go, so assuming the same recruitment rate, all patients would be enrolled around July 29.
6 weeks after that would be Sept. 9, so mid September would be a safe bet. I believe recruitment rate improved since trial sites were added, so my bet is mid August, or about 1 month from now.
Sorry for the weird question, but thankfully I'm not familiar with enemas. With the current liquid formulation, does that mean once it's administered that most of the drug drips back out? So with a gel/foam, more of the drug would stay in your system longer, lining the GI tract? Is that the reason we expect improved efficacy with a gel/foam?
Did anyone receive the PR in their email? I'm pretty sure I re-signed up on the IPIX website for alerts, but maybe not...
I agree that they have to be further along in the OM trial; however, IPIX did issue the following statement back in May, so I was hoping to see more data.
"Second, the Company will be presenting topline findings from the Brilacidin-UP/UPS trial as well as additional interim data from its Phase 2 trial of Brilacidin for Oral Mucositis at Drug Discovery and Therapy World Congress 2017, to be held July 10 – 13, 2017, in Boston. More details to come."
http://www.ipharminc.com/press-release/2017/5/10/cellceutix-provides-corporate-update-significant-milestones-ahead-as-multiple-mid-phase-clinical-trials-set-to-conclude
For their study, they had a very very small difference between population sizes of PP and ITT (or what they call FAS - full analysis set). Even the placebo group and a very high rate of people meeting PP. I wonder why our Ph2a study and a large difference between these two groups.
Refer to page 16 of the document you linked to for reference.
Looks like there were 12 patients in the Placebo group that did not meet Per Protocol conditions, which was 40% of overall patients assigned to that group. Meanwhile 7 of 27 patients in the 200mg arm did not meet PP conditions (26%).
Very small sample size, but the optimist in me wants to think that since a larger percentage of people stuck to the protocol in the 200mg group than the Placebo, maybe people were encouraged by their results while taking Prurisol. People who didn't see quick results were discouraged and forgot to take their meds or gave up altogether. Just a guess...
Finally found it, it's in one of their blog posts:
http://www.cellceutix.com/new-blog/2017/6/1/prurisol-for-psoriasisan-overview
I need to do some research to determine what exactly this means, although I think I remember a lot of conversation about it way back when the results were first out.
Yes, you're correct. So we know that however 46% was calculated, the numerator (number of patients that achieved end point) has to be 7 or less. We don't know if the denominator is ITT or PP though.
The chart on slide #22 states that 7/27 in ITT and 7/20 in PP met the primary endpoint. So how did we get to 13 patients?
https://static1.squarespace.com/static/5715352e20c647639137f992/t/5865318920099e2bc425d577/1483026833173/Cellceutix_Corporate_Slide+Deck_DERMATOLOGY_November+2016+Website+Vers.pdf
Maybe it has something to do with Per Protocol vs. ITT. The only solution I can come up with using normal decimal rounding is 6 of 13 patients.
Or maybe something with the last sentence that is throwing me off:
IPIX: Among patients with the severest form of psoriasis in study, those having a baseline IGA score of 3 (“moderate”), the primary endpoint was met in 46% of patients who received 200 mg per day. These data were derived from analyses of all patients.
Thank you! Wasn't sure if I was missing something.
So 8 of 18 patients is 44.4% and 9 of 18 patients is 50%. How do we get to 46% of 18 patients?
Weren't there 28 people in the 200mg arm? So 46% of 28 people is 12.88 people, which doesn't make sense.
I think this was discussed before, but does anyone know the actual number of patients that equals 46%? 46% of 18 patients is 8.28 people, which obviously doesn't make sense. I can't get any number of people to come out to 46%... Thanks!
Has anyone come across info on likelihood and/or costs associated with farmer's destroying hemp crops for too much THC? I can't seem to find much info on it. It would be interesting to figure out what kind of potential cost savings farmers could encounter by using XXII/Anandia seeds.
We should also have K interim results (Cohort 1), probably in the first half of the year (obviously depending on recruitment/screening speed).
.60 cents = $0.0060
60 cents = $0.60
I don't know what a reasonable charge is, but I do believe the 400,000 was for the US only.
If B-OM is proven to be preventive, then I believe it would be used on a lot more than 400,000 people. I was reading about other cancers in which a portion of the people develop OM (maybe 10-20%). I would think all patients with that cancer would be treated with B to prevent it, whether or not they would actually develop it.
Thanks Karin. Will that have any effect on becoming approved in the US?
Do you know why B-UP is being done overseas? I can't seem to remember what the reasoning behind that was. Thanks.
B-OM Predictability Drug Comparisons:
My first long post, so hopefully the formatting turns out ok (this site does not make it easy to format!)
In CTIX's slides, they show three other OM drugs with comparison of pre-clinical and clinical results to validate the Hamster Model. All drugs involved Dr. Sonis, as indicated on the slide, so it would be very encouraging to hear positive feedback from him during interim results since he clearly has a lot of experience with OM. Here is the current state of those drugs (probably been discussed before, but I wanted to look into this and thought I'd share it):
AG013 - Company is studying the drug further before proceeding to a Phase 2.
Phase 1B trial involved 25 patients. They saw a 35% reduction in duration of OM compared to placebo. Close to 30% of patients treated with AG013 were full responders. All placebo patients developed OM (should help us analyze B's interim results).
It looks like this drug was invented by Actogenix, then the company bought out by Intrexon and somehow Oragenics is involved (this made it a little difficult to follow the trail).
http://investors.dna.com/2015-06-10-Intrexon-and-Oragenics-Expand-Collaboration-to-Pursue-Development-of-Biotherapeutics-for-the-Oral-Cavity
http://www.oragenics.com/technology-pipeline/lbp/ag013
SCV-07 - Phase 2B interim results did not meet primary efficacy endpoints, so they discontinued the trial and drug. Below are links to the Phase 2 "successful" trial and Phase 2b failed trial.
http://investor.sciclone.com/releasedetail.cfm?releaseid=455703
http://investor.sciclone.com/releasedetail.cfm?releaseid=653604
hFGF-20 - Phase 2 did not meet efficacy endpoints. A previous study showed their lowest dose to be effective, but I can’t find much info as to why the Phase 2 results were poor (this was from 2006/2007).
Their previous study was for reducing the incidence and duration of OM for treatment of hematologic cancer - which only has a 60% incidence rate of developing severe OM (read the biospace link below for study details). Placebo group had an average duration of 2.4 days for severe OM, so this doesn't seem like the best comparison to B-OM for head/neck cancer. However, if B-OM is effective, safe, and preventive, I could see all hematologic cancer patients taking it as a preventive drug regardless if they were to develop OM (higher sales $).
http://www.biospace.com/News/curagen-corporation-confirms-failed-phase-ii/10334
http://www.reuters.com/article/idUSIN20071011070121CRGN20071011
Just a few more weeks until we see some results!
Thanks BK, that makes sense. With 400,000 cases in the US per year, I'm hoping this trial can wrap up quickly. I think I remember there being a competitive drug in trials that was slowing us down (I think that failed?), but we have 12 sites recruiting, so we just need to average about 5 OM cases per trial site.
Do you know how it is decided which patients get drug vs. placebo? I'm wondering if drug vs. placebo is usually evenly distributed (i.e. we should expect interim results to have about 50% drug 50% placebo). With 80-100% of head and neck cancer patients developing OM, it should be pretty easy to analyze interim data.
Another random question, we say there are 400,000 cases in the US, but once we have an approved drug, is it easy to sell across the world (why just look at number of cases in US)?
I don't have very much experience in biotech investing, but if we saw awesome results in B-OM (let's say reduced number of days of severe OM by 90%+ compared to placebo) with no serious side effects, is there any chance of going straight to market? We have a pretty small sample size, so I wouldn't be too optimistic, but it almost seems unethical not to offer treatment for this condition.
Great info. In one of the articles, Dr. Sylvia Holden commented, "As a stand-alone or combination front-line therapy, the magnitude of the potential of Kevetrin™ is simply unparalleled by anything that I have ever seen in the laboratory before.”
I'm thinking "front-line therapy" would mean the first treatment, then followed by chemo/other treatments, which is what K Ph2 is doing. I don't believe we are following the patients throughout their traditional treatments after K treatment though, so we wouldn't know any long-term effects of K, correct?
Let's hope we see some positive K Ph2 Cohort 1 results in the first half of the year. Things will really get interesting.
Kevetrin Questions
How many subjects in Phase 1 had Ovarian Cancer (I came across this info a while back, but can't seem to find it now)?
On CTIX Fact Sheet for Kevetrin, it states 60% of Ovarian Cancer patients had a 3%-73% increase in p21 biomarker. Was it ever stated if the percentage was correlated with dose? Is the raw data available anywhere that we can see each patient, their dose, and their response?
I'm trying to do a little research on the relationship between p21 and p53, but my non-medical background isn't helping. If anyone has a dumbed down website on it, please feel free to share.
Thanks everyone.