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kykkern

06/15/18 3:35 PM

#44855 RE: Waitforit53 #44854

10-q is depressing news; only about raising capital and dilution of shareholders:

"The Company has sustained losses in all reporting periods since inception, with an inception-to date-loss of $121.6 million as of April 30, 2018. Further, the Company has never generated any cash from its operations, does not expect to generate such cash in the near term, and does not presently have any firm commitments for future capital. Consequently, the Company will need additional capital to continue operating its business#

".....its stockholders could lose all of their investment in the Company...."

But the disasteous COE Punit gets a bonus: "We have entered into a separation agreement with Mr. Dhillon that triggers the compensation provisions pursuant to his Amended and Restated Executive Employment Agreement, dated November 7, 2017"

"....As a result, none of our product candidates are near commercial availability..."

A never ending cycle of bad news about dilution of shareholders
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hschlauch

06/15/18 6:01 PM

#44857 RE: Waitforit53 #44854

Great, thanks Wait.

I continue to believe in this company's disruptive potential. In my opinion, there is nothing discouraging in the company's filings, its finances, its data, its researchers, its clinical investigators, its patent applications, its leadership, or its partners.

I would certainly like to learn more about their multigene products, but I'm sure information will be delivered on that front this year. The PIIM construct that includes encoded flt3-ligand and antigen is truly ingenious; this is one way to overwhelm Tregs with mature dendritic cells and allow priming to occur through the expansion of dendritic cell populations. It is essentially a diversion.

The convergence of their key technologies and approaches - tissue adaptive electroporation, deep tissue applicator, intratumoral-administered treatments, multigene plasmid constructs, and improved gene expression - should facilitate cancer antigen-specific immune responses across multiple solid tumor cancers. They may even have the capacity to directly treat most visceral lesions locally using their technology.

The key to anti-PD-1 drug success is having adequate numbers of cancer antigen-specific CD8 T cells intratumorally. And cancer patients won't achieve adequate thresholds if there are too many Tregs preventing immune responses during the priming phase. I am not a medical doctor, but I spend exorbitant amounts of time researching immunotherapy; it has become an obsession. Sometimes, spectators can see more than the players on the field. Medical doctors are the skilled players, but they don't always have an opportunity to scan the entire field at any given moment. And immuno oncology is a rapidly evolving game. If there is one thing I am absolutely sure about, it is that intratumoral Tregs and Tregs in TDLs are preventing immune responses in so many of these patients who are failing anti-PD-1 therapies. Immune privileged sites and organs that require substantial immune tolerance, are locations where cancer, if found, cannot be easily eliminated by anti-PD-1 monotherapy.