OSU-03012 not only inhibits a variety of tumors, but also inhibits many bacteria and many viruses such as HIV, HAV, HBV, HCV, etc.
July 25, 2016 Source: Bio Valley
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)]; Celecoxib is a newly marketed non-steroidal anti-inflammatory drug (NSAID) in recent years. It is a selective COX2 inhibitor mainly used for antipyretic analgesia and anti-rheumatic treatment. It has been approved in the United States. Used in the treatment of familial polyps.
OSU-03012 is a celecoxib derivative, also known as AR-12, which is a potent recombinant PDK-1 inhibitor. Its anticancer activity is higher than celecoxib, but it does not inhibit COX2.
In 2004, Jiuxiang Zhu et al found that OSU-03012 inhibits the growth of a variety of tumor cells, such as it can induce apoptosis in human prostate cancer cell line PC-3 with an IC50 of 5 μM.
In 2006, Adly Yacoub et al found that OSU-03012 is more effective in promoting cell death than glioma cells compared to normal glial cells.
In 2007, Leonardo M. Porchia et al found that OSU-03012 inhibited the proliferation and migration of thyroid cancer cells (NPA, WRO and ARO cell lines) and induced apoptosis, resulting in an increase in S phase cells and no increase in G2 phase cells. OSU-03012 is an ATP competitive inhibitor that acts on thyroid cancer cells and inhibits p21-activated kinase (PAK) activity and serine/threonine kinase (AKT) phosphorylation.
In 2008, Ming Gao et al found that OSU-03012 inhibited the growth of hepatocellular carcinoma cell lines (including Huh7, Hep3B and HepG2) with IC50 <1 μM. OSU-03012 acts on Huh7 cells, does not inhibit 3-phosphoinositide-dependent protein kinase 1 (PDK1) or AKT activity, and does not induce apoptosis, but induces autophagy. Moreover, after treatment with OSU-03012, active oxygen accumulation is caused.
In animal models, some found that OSU-03012 acts on Huh7 xenografts at a dose of 200 mg/kg, inhibiting 57.59% of tumor growth. It has also been found that OSU-03012 acts on MDA-MB-435/LCC6 xenografts, significantly reducing EGFR protein expression, down about 48%, and also prevents YB-1 from binding to the EGFR promoter. In addition, oral OSU-03012 has been found to inhibit the growth of HMS-97 nerve sheath xenografts by up to 55%.
However, if we think that OSU-03012 can only inhibit a variety of tumor growth, then we feel that there is nothing remarkable. However, in fact, scientists have found that OSU-03012 is amazing, it can also inhibit many viral and bacterial infections, including the multi-drug resistant HIV strains that people talk about.
In July 2015, a federally-acquired study from the University of Virginia in the United States confirmed a chaperone protein called GRP78, which may be a universal target for the treatment of human diseases, including brain cancer, Ebola. Viral infections, influenza virus infections, hepatitis virus infections and super bacteria - such as methicillin-resistant Staphylococcus epidermidis (MRSE) and methicillin-resistant Staphylococcus aureus (MRSA) - infection. The task of a companion protein is to keep the enzyme and the viral coat protein in their correct three-dimensional shape. If an enzyme or coat protein has the wrong three-dimensional shape, the enzyme will not work properly and the capsid protein will not become part of the new virus.
By using OSU-03012 (also known as AR-12, a potent recombinant PDK-1 inhibitor) for clinical testing and obtaining FDA-approved phosphodiesterase type 5 (PDE5) Inhibitors, such as Viagra and Cialis, which target the chaperone protein GRP78, are used in combination to target GRP78 and related proteins, and researchers have blocked various major viruses in infected cells. The internal replication makes antibiotic-resistant bacteria vulnerable to attack by common antibiotics, and they also found evidence that brain cancer stem cells are killed by this combination of drugs.
The researchers used a variety of brain cancer stem cell types, influenza virus, mumps virus, measles virus, rubella virus, respiratory syncytial virus, cytomegalovirus,
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