Innovation Pharmaceuticals Inc (IPIX)

[wsbc]

Just going by these posted mentions:

http://www.ipharminc.com/new-blog/2017/12/27/kevetrins-effect-on-the-p53-signaling-pathway-in-a-broader-scientific-context

'Preliminary results show modulation of the p53 protein, as well the activated form of the protein, phospho-p53, in response to the administration of Kevetrin. Pathways analyses also point to concomitant cell cycle modulation at the level of gene expression. Importantly, these data directly support Kevetrin's ability, in ovarian cancer patient tumors, to affect p53 and associated molecular pathways -- the central gene signaling network involved in regulating cell growth and the cell cycle, helping to prevent cancer. '

I don't think they can say this in any sort of PR w/o coming under significant legal pressure (liability) for misrepresentation?



further: https://static1.squarespace.com/static/5715352e20c647639137f992/t/58e38969ff7c50817178cbe0/1491306863482/AACR+2017+complete+poster++FINAL+2017MAR30.pdf

Results summary:

•Kevetrin induced apoptosis in wild type p53, mutant p53 and
partially deleted p53 ovarian cancer cell lines as assayed by
cleavage of PARP.
•p53 and p21 increased protein levels were seen in A2780 cells (p53
wild type) after 24 to 48 hr exposure to Kevetrin. Depletion of p53
by SiRNA reduced the p21 expression as assayed by FACS.
•Kevetrin downregulated oncogenic mutant p53 in OVCAR-3 and
OV-90 (p53 mutant)
•Increase in p21 mRNA in response to Kevetrin was observed in all
OC cell lines.
•No significant changes were observed in p53 mRNA.
•In xenograft models, Kevetrin inhibited A2780 tumor growth, and
increased SKOV-3 animal survival.
•Transcriptomic analyses demonstrated that Kevetrin modulates p53
signaling pathways and induces apoptosis and cell cycle arrest in
ovarian cancer cell lines as well as xenograft tumors as shown by
RNAseq data. KEGG pathway analysis was used for these studies.
• Altered expression of miRNA-27a, miRNA-1274b, miRNA-25
(known to be dysregulated in ovarian cancer) in a time-dependent
manner in OVCAR-3 cells provides possible biomarkers for
Kevetrin response.
•In tumors where p53 is partially deleted (SKOV-3), Kevetrin
modulates p53 pathways and induces apoptosis. Further detailed
mechanism studies are ongoing.


Certainly not trying to take George's copy/paste approach here and beating the IPIX-drum over the deafening noise of burning corporate fundamentals (not to mention a broad history of missed deadlines, a P2 failure, gibberish PR's etc), but there seems to be supporting data to the effect of them being onto something with K.

I think ultimately BP will determine what our products are worth based on them putting their dollars on the table. Things are only worth what the market is willing to pay.

I'm also certainly not blind to the risk in BioTech. Lord knows I'm stuck holding a pretty significant bag here, and have ridden a ridiculously large position all the way down to where we currently sit.

I would like to see things change, but not purely for selfish reasons. Bringing B-OM to market will address a significant unmet need and alleviate suffering. That's the best we could hope for. Not to mention funding IPIX and getting us off the floor where we're currently laying... bloody and battered.

Kevetrin possibly in concert with other treatment tandem-options, could possibly do wonders for addressing one of the more serious health-concerns we currently face as a species.

I don't think we're getting a 'New Year's deal-message' because they're not 'there yet'. Maybe end of Jan, or a week or two sooner perhaps.

No, it didn't. It showed that there is hope that the MOA is valid and that K could be effective. The P failure should be a fresh reminder of the risk in biotech research. There was indeed a comprehension failure, but ya pointed the finger in the wrong direction.

The market is right to be skeptical of our pipeline. K could go the way of P very easily.

Let's see it we get a New Year's message from the company that gives indication about a B deal. GLTA smile
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