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Meds, Mind, Body & Benefits => Research News & Studies => Topic started by: J220 on July 15, 2006, 10:39:54 pm

Title: BIT 225
Post by: J220 on July 15, 2006, 10:39:54 pm
I just read this over at lilachat.it (thanks goldrake!), has anyone heard anything about this???

http://www.biotron.com.au/ftp/11July06.pdf

BIT225 represents a novel, first in class approach to the treatment of HIV. BIT225 has a new mode of action against HIV compared to existing anti-HIV therapies, targeting the Vpu protein of HIV. By blocking a new pathway in HIV infectivity, Biotron’s Vpu inhibitors have the potential to combat drug-resistant viral strains, in combination with highly active antiretroviral therapies ('HAART') and in monotherapy. Unlike existing drugs, BIT225 is active in the viral reservoir in the body, and complete elimination of HIV from infected patients is not possible unless these underlying reservoirs of infection can be cleared. BIT225 represents an opportunity to eliminate the underlying seat of infection, potentially leading to a cure for HIV.
Title: Re: BIT 225
Post by: J220 on July 16, 2006, 12:42:02 am
Some more info from the website:

"The HIV/Vpu program is the most advanced [within Biotron's projects] , with a lead compound currently in preclinical safety tests. Vpu represents a new drug target in the fight against HIV. The protein plays an important role in the budding and release of newly formed viruses from infected cells, a process that is crucial for the progression of infection.

Existing HIV therapeutics are directed at one of three stages in viral replication: reverse transcription, protease activity and receptor binding to facilitate viral entry into the host cell. As a result of the limited range of drug targets, the emergence of drug resistant viral strains has become a significant issue. By blocking a new pathway in HIV infectivity, Vpu inhibitors have the potential to combat drug-resistant viral strains, in combination with highly active antiretroviral therapies (HAART) and in monotherapy.

Biotron's Vpu inhibitors differ to existing therapies in that they are particularly effective against monocytes and macrophages, both of which are cell types that current regimens of HAART fail to target successfully. Recent research has highlighted the importance of these cells in HIV infection by demonstrating that they can act as reservoirs of virus in HIV-infected individuals. Phase I/IIa clinical trials for Biotron's lead HIV therapeutic will be initiated at the conclusion of preclinical safety tests."
Title: Re: BIT 225
Post by: HIVworker on July 16, 2006, 09:42:13 am
It's an interesting idea. One thing that isn't clear to me is how the drug clears virus from reservoirs? That's not a drug target problem but a PK problem. Do they list where the drug goes that current therapy fails?

R
Title: Re: BIT 225
Post by: HIVworker on July 16, 2006, 09:48:01 am
Oh...I found something interesting. It works well in macrophages! We should keep an eye on these clinical trials! That's an interesting finding - I'd like to know how well, but that might offer some hope.

http://www.biotron.com.au/virion.htm (http://www.biotron.com.au/virion.htm)

R
Title: Re: BIT 225
Post by: J220 on July 16, 2006, 01:11:19 pm
It works well in macrophages!

No doubt, that's the key element to this being truly significant (if true and applicable in vivo). Apparently they are getting ready to start phase I, although it is not clear where or when exactly. By the way, is there anything significant you see offhand from the chemical formula of the compound (see image below, assuming this is close to the BIT225 version?

(http://www.biotron.com.au/images/Macrophage2.jpg)

J.
Title: Re: BIT 225
Post by: HIVworker on July 16, 2006, 09:48:49 pm
I don't see anything significant in it, but that isn't a shock as it depends on what it does to Vpu. I had a think today about the macrophage thing. There are many NNRTIs that reach macrophages, its nukes that have the biggest problem I understand (because of the way they are taken up). I guess the key for this drug is like that of any other - does it reach macrophages in the correct places where current drugs can not reach? That's a pharmacokinetics question that we don't have the answer to. My question to them is do they have information that it goes to places not touched or are they saying that because it can reach macrophages it has the potential to do better than current therapy? I'd be more excited if it were the former, as the latter would sound like salesmanship.

I await their phase II study results in a year..

R