Posted 14 February 2013 - 08:52 PM

Abnormal MET activation in cancer correlates with poor prognosis, where aberrantly active MET triggers tumor growth, formation of new blood vessels (angiogenesis) that supply the tumor with nutrients, and cancer spread to other organs (metastasis). MET is deregulated in many types of human malignancies, including cancers of kidney, liver, stomach, breast, and brain. Normally, only stem cells and progenitor cellsexpress MET, which allows these cells to grow invasively in order to generate new tissues in an embryo or regenerate damaged tissues in an adult. However, cancer stem cells are thought to hijack the ability of normal stem cells to express MET, and thus become the cause of cancer persistence and spread to other sites in the body.

And here is where the problem in my mind lies. I am by no means saying that Dihexa absolutely has the potential to cause cancerous growth, all I am saying is that it seems that overactivation of the c-Met receptor is implicated in the sustenance and growth of tumors. This of course, is why I'm waiting to see what comes from their tests. The person I talked to said that their tests have all come out incredibly well, and their tests have shown drastic cognitive improvement in scopolamine-induced mice alzheimer's dementia model. We just need to see the tests that come after it's been tested on thousands of rats, to see the result. Side-note: they are also reportedly preparing for IND enabling studies, so we'll see this tested on human subjects sometime soon.



That said, I would ABSOLUTELY NOT recommend testing this one on yourself until more test results come out.



Lastly worth mentioning, I made the mistake of mentioning the c-Met issue in my followup email, and after that never got any more responses. For obvious reasons.

I have some very unfortunate news for you all. I was hesitant about posting this, as it's potentially libel, however it's the truth coming from the horse's mouth so-to-speak. I want to make it very clear: my following statement is by NO MEANS my way of saying that the aforementioned product (Dihexa) ABSOLUTELY CAUSES said effects I am about to list, I am merely theorizing. It is up to further testing to confirm whether or not the following statement will be an issue.Anyway. That said, I spoke with the CEO of M3 Biotechnology (manufacturer of Dihexa) over email about a month or two back. I inquired as to the direct mechanism of action, how it worked, etc etc, as I was curious if it was simply some kind of positive allosteric modulator of the TrkB receptor, or something else. I will not copy and paste the emails, however I will paraphrase to give the general gist:It was stated to me that Dihexa is a "small molecule agonist of HGF (hepatocyte growth factor)" HGF is the obligate ligand of the c-Met receptor, a tyrosine kinase receptor similar to TrkB, and a receptor that Angiotensin IV seems implicated in activating. To quote part of the email, "c-Met is localized in dendrites and HGF activation seems to result in synaptogenesis, neuritegenesis and neurogenesis."Now this all sounds fine and dandy, great potential there. However, this part scares me: quoting WIKIPEDIA, (not always the most pure of authors):

Edited by Rior, 14 February 2013 - 08:54 PM.