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Experimental Anticancer Drug Tested As Antiviral; May be Antibacterial, Antimalarial

Accepted submission by butthurt at 2016-07-14 05:41:11
Science

The drug AR-12, otherwise known as OSU-030124 (presumably for being discovered at the Ohio State University), which has been known for "more than ten years," has been licenced to the American company Arno Therapeutics1 since 2008.2 A company statement says2

In preclinical studies, AR-12 has shown efficacy in a wide range of tumor types, including breast, lung, prostate, pancreatic, brain and hematological cancers, as both a single-agent as well as in combination with leading oncology therapeutics.
[...]
We are currently conducting a multi-centered, two-part, Phase I clinical study of AR-12 in adult patients with advanced or recurrent solid tumors or lymphoma.

Animal testing has shown it has antiviarl properties:1

In animal models, AR12 doubled survival and suppressed liver damage caused by another hemorrhagic fever virus, effectively protected cells from Ebola and suppressed drug-resistant strains of HIV significantly more effectively than any of the approved anti-viral treatments.

The drug is believed to "reduce the expression of multiple chaperone proteins," including GRP78 [wikipedia.org], which are "proteins which facilitate the viral life cycle."4

According to Paul Dent, a researcher who studies the drug,1

Lots of bits of the chaperones change throughout evolution, but the key bits of the chaperones have often stayed almost the same. The result is that AR-12 can nobble malaria just like it can do to bacteria.

The company is said to be "planning its first clinical trial as an antiviral drug in Nottingham."1

[1] The Australian, "Breakthrough cancer therapy destroys drug-resistant superbugs" [theaustralian.com.au]

[2] Arno Therapeutics Web site [arnothera.com]

[3] ReliaWire, "Experimental cancer drug has been found to effectively treat Ebola and drug-resistant HIV" [reliawire.com]

[4] Journal of Cellular Physiology, "AR-12 Inhibits Multiple Chaperones Concomitant With Stimulating Autophagosome Formation Collectively Preventing Virus Replication" (DOI: 10.1002/jcp.25431) [wiley.com]


Original Submission