AR-12
No one needs that much cancer-fighting capability!
“AR-12”..... we simply just can’t have that.
If I recall correctly, the Israelis initially discovered and pursued this. Hope it lives up to expectations.
And this is the last we will ever hear of it.
OSU-03012 - Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/OSU-03012 Proxy Highlight
OSU-03012 (AR-12) is a celecoxib derivative with anticancer and anti-microbial activity. Unlike celecoxib, OSU-03012 does not inhibit COX, but inhibits several other important enzymes instead which may be useful in the treatment of some forms of cancer, while also having antifungal activity via disruption of ... The European Commission has designated AR-12 as an orphan drug for ...
AR-12 - Arno Therapeutics, Inc.
www.arnothera.com/ar12.html Proxy Highlight
AR-12. Drug Description AR-12 is a potentially first-in-class, orally available, targeted anti-cancer agent that has been shown in preclinical studies to inhibit ...
Arno Therapeutics to Inhibit Cancer and Enhance Portfolios: CEO Alexander Zukiwski [ARNI]
TLSR: What can you tell me about Arno’s third compound, AR-12?
AZ: There is evidence that AR-12 hits the glucose-regulated protein 78 (GRP 78) chaperone. This is a master regulator of unfolded protein response. For normal cells, it doesn’t cause any major toxicity, but it has tremendous potential activity against various diseases. In addition, AR-12 inhibits heat shock protein (Hsp) 70 and Hsp 90 chaperones. Our colleagues at OSU demonstrated that AR-12 also induces and enhances autophagy in host effector cells.
“We are optimistic that AR-42 could have activity in different solid tumors.”
Through a series of collaborations, AR-12 was shown to have in vitro activity against various microbial pathogens. What is exciting is that this novel mechanism of action potentially allows for development of a host-targeted antimicrobial agent. By targeting host cells instead of microbes, AR-12 may not be subject to typical drug resistance mechanisms reported for certain antiviral agents and antibiotics. We are currently developing a series of collaborations to further explore the potential of AR-12 in the antimicrobial space.
TLSR: What disease targets are of interest for your first studies?
AZ: AR-12 has published activity against certain fungal species. Furthermore, our colleagues from Virginia Commonwealth University have recently published data demonstrating AR-12 to have activity against a series of viruses and antibiotic-resistant bacteria. Before selecting disease targets, we want to understand the spectrum of activity. Next, we intend to focus development on those areas deemed to have the highest likelihood of success, and where there is a clear medical need.
TLSR: What are the catalysts or milestones that investors should look for with respect to each of your compounds?
AZ: First will be completion of the onapristone Phase 2 study in recurrent and metastatic endometrioid cancer. For AR-42, we are looking for an increasing amount of data from the Phase 2 studies in various tumor types. For AR-12, being at an opportunistic phase, we are determining the best avenue for development in the infectious disease space. All of these are possible over the next two years.
Consider the ramifications of this:
Find a cure for HIV?
The floodgates of unrestrained fudge packers and carpet munchers will be opened wide, and sodomy will be celebrated as just another “healthy life style” choice.
Find a cure for Ebola?
All residents of Ebola-prone African nations will be given a warm, unconditional welcome to visit and STAY in the United States.
Be careful what you wish for.
I hope the drug is indeed as good as initial indications show.
Thanks for posting this.
Careful. This article could be part of a carefully orchestrated pump-and-dump scheme for the stock, which is traded on the OTCBB.
The medicine may well live up to its high expectations. As someone who works in the health care sector, I simply hope that each new clinical trial inches us closer to a good understanding of how to halt and/or prevent diseases.
Company A’s stock price is low. The execs buy up as many shares as possible. Company A announces a new wonder drug that can cure cancer and Ebola and hepatitis and a host of other maladies. Company A’s stock goes through the roof. The execs sell their stocks. Later the research data on the drug is revealed as bogus (just like 50% of all current drug research. The execs and their pals at the FDA retire and move to Cancun.
Rinse and repeat.
HIV. The gift from excrement-eating homosexuals to an unsuspecting populace.
‘Gay Pride’?
I am sure there will be a few more tweaks and iterations to the drug before its totally finalized.
Imagine if libtards are saved by an ar-15.
Cures cancer, will be FDA approved in 50 years.
I hate to burst any bubbles, but actual evidence of this compound being a miracle drug is lacking.
Speaking purely from my PhD-level knowledge of biochemistry, I have strong reservations about any drug whose mechanism of action is to inhibit the functionality of hsp70 and hsp90 (referenced in post 8, this thread). The heat shock proteins play a major role in converting newly made proteins into their functional forms by helping them to fold properly and maintaining them in the correctly folded shapes. Cells, and therefore, organisms, function on properly folded proteins. Some diseases, notably the prion diseases, occur because certain proteins misfold.
The ability to show an anti-microbial or anti-cancer effect in vitro is not very significant. The effect must be shown in a living system, and the effect must be specific to the target without causing significant harm to the host. One of the most effective anti-microbial and anti-cancer agents I know is common household bleach. I haven’t seen a cancer cell yet that does not die upon being bleached. Most microorganisms die within seconds of being bleached. Despite this incredibly high activity of bleach to kill nasty things, it has absolutely no therapeutic value as an anti-cancer or anti-microbial treatment.
I looked for clinical trials of this drug, using the search terms “PDK1 inhibitor AR-12” and “OSU-03012” and found 1 result using the first search term. This was a phase 1 trial, conducted between 2009 and 2013, with no results posted. The fact that the study took 5 years is a red flag, as is the fact that no results are available 3 years after the completion date. The study was also extremely small, with only 35 patients.
In PubMed, the research database, there are only 11 articles published, found using the full chemical name as a search term. The earliest one was in 2006. The fact that there is so little published on this compound is another red flag. Yet another red flag is the fact that the last article published is actually a warning from the editors of a journal that published an article about the compound in 2007. The warning indicates that there is some evidence to believe that the 2007 article was fraudulent. (See:
http://molpharm.aspetjournals.org/content/90/1/61.long.)
My take on this particular UK Express article is that someone is trying to gin up interest in this compound in order to attract investors. The fact that so few scientists are interested in studying the compound is a clue: don’t waste your money on this.
Ping
This is just a derivative of the prescription NSAID Celebrex that has been modified so that it doesn’t block the COX-2 enzyme so to remove the potentially bad side effects of coronary problems and gastrointestinal bleeding that sometimes occur with drugs of that class. Not likely a “miracle cancer cure” by any means (any more than celebrex itself, which presumedly acts via a similar mechanism), possibly useful as an adjunct. This is just hype to pump the stock, the sleazy reporter probably got paid to plant it.
On the other hand if I had colon cancer I probably would take an NSAID as an adjuctive treatment, preferably celebrex or sulindac both of which have a slew of studies pointing to efficacy in treating certain cancers, especially of the colon.