Aa
New drug Nov-205 drug
It says here they were starting clinical trials is Sep 06. Anybody know anything about it? It seems to be already approved in Russia.
NOV-205, Hepatitis
NOV-205 is being developed to treat chronic hepatitis C in the U.S. NOV-205 acts as a hepatoprotective agent with immunomodulating and antiinflammatory properties. The FDA accepted Novelos' Investigational New Drug Application (IND) for NOV-205. The initial U.S.-based Phase 1b trial will evaluate NOV-205 as monotherapy for chronic hepatitis C genotype 1 patients who have failed pegylated interferon plus ribavirin therapy. The trial commenced in September 2006.
NOV-205 is approved for use in the Russian Federation under the trade name Molixan
NOV-205, Hepatitis
NOV-205 is being developed to treat chronic hepatitis C in the U.S. NOV-205 acts as a hepatoprotective agent with immunomodulating and antiinflammatory properties. The FDA accepted Novelos' Investigational New Drug Application (IND) for NOV-205. The initial U.S.-based Phase 1b trial will evaluate NOV-205 as monotherapy for chronic hepatitis C genotype 1 patients who have failed pegylated interferon plus ribavirin therapy. The trial commenced in September 2006.
NOV-205 is approved for use in the Russian Federation under the trade name Molixan
Thank you for your replay,
According to FDA it`s in Phase 1 , the last up date was in 12-2007.
The Q is Whose manufacturing the BAM-205(Molixan) this time?
Where can I get this Drug?
Best Regards
According to FDA it`s in Phase 1 , the last up date was in 12-2007.
The Q is Whose manufacturing the BAM-205(Molixan) this time?
Where can I get this Drug?
Best Regards
According to this it is still in FDA trials phase 1. I wonder if it died there since Phase one trials are often very short lived; usually days and a few weeks. The trial completed, I know that. I see very little about the drug now.
Willy
Willy
Please note this post is 2 and 1/2 years old.
I have not heard of this drug lately. It may not have moved forward in trials. Several have been dropped since this posted.
I would google the drug and/ or check it at clinical trials.gov
best,
Willy
I have not heard of this drug lately. It may not have moved forward in trials. Several have been dropped since this posted.
I would google the drug and/ or check it at clinical trials.gov
best,
Willy
Thank you for your information!
Do you have any new info about NOV-205(Molixan)? And what is the last update of manufacturing this Drug in Russia?
I would appreciate any info you will explain and tell us.
Do you have any new info about NOV-205(Molixan)? And what is the last update of manufacturing this Drug in Russia?
I would appreciate any info you will explain and tell us.
Thank you very much, HR, for that explanation. I have needed that concise explanation more than you can imagine, and I appreciate your time and input so much.
Thanks, too, for the info on the NOV-205.
Have a great day!
Thanks, too, for the info on the NOV-205.
Have a great day!
Thank you, HR, for your explanation. Last night my excitement was somewhat reduced after I could not find any info about viral genotyping or percentages of
I can't see notes on this thread anymore. I see where HR has said something here, but I can't see the note (or any notes) The only thing I see is the first note. I have refreshed the browser, gone out and come back in, and I still cant see anything but the original note.
HR - if you see this note (if it makes it on the forum) and if you have time to respond) can you please explain to me "viral variants" (or viral load increases) and the significance of "drug resistance". I have tried to figure this out by reading notes on MEdHelp (such as in the Alina thread and several others), but I'm still unclear as to what it means.
For example, on the VX-950 study report, it says:
"findings suggest that combination telaprevir treatment with peginterferon alfa-2a *may* prevent the development of clinically significant resistance to HCV protease inhibitors in treatment-naive patients."
On the HCV 796 study report, it says:
The speaker addressed the fact that peak viral load reduction of -1.4 log occurred on day 4 but viral load decline started to increase. The issue of drug resistance was discussed by the speaker as a possible reason and said that the resistance testing results analysis is ongoing and will be presented later this year at another conference.
http://www.natap.org/2006/DDW/DDW_18.htm
Question: I have been offered the trial with HCV 796. I don't really like the looks of it, much, and I'm also wondering if I did say yes to it - could I be setting myself up for "drug resistance" if I'm one whose viral load goes up and keeps going up (and I'm taken off the HCV 796?) If that DID happen, would I possibly then be resistance to all polymerase inhibitors?
Sorry if I sound so *dumb* on this (I can barely figure out how to ask the question), but I have had concerns about drug resistance for a few months now. Thanks if you have time and understand what I'm asking (or if anyone has time and understands what I'm asking.) I'd appreciate any input.
And another question (for anyone). Has anyone out there heard that HCV 796 has already had a Phase II that didn't go well as far as following protocol?
Here is the Phase II that is recruiting now, but I can't find any previous Phase II studies.
http://www.clinicaltrials.gov/ct/show/NCT00367887?order=1
Thanks.
HR - if you see this note (if it makes it on the forum) and if you have time to respond) can you please explain to me "viral variants" (or viral load increases) and the significance of "drug resistance". I have tried to figure this out by reading notes on MEdHelp (such as in the Alina thread and several others), but I'm still unclear as to what it means.
For example, on the VX-950 study report, it says:
"findings suggest that combination telaprevir treatment with peginterferon alfa-2a *may* prevent the development of clinically significant resistance to HCV protease inhibitors in treatment-naive patients."
On the HCV 796 study report, it says:
The speaker addressed the fact that peak viral load reduction of -1.4 log occurred on day 4 but viral load decline started to increase. The issue of drug resistance was discussed by the speaker as a possible reason and said that the resistance testing results analysis is ongoing and will be presented later this year at another conference.
http://www.natap.org/2006/DDW/DDW_18.htm
Question: I have been offered the trial with HCV 796. I don't really like the looks of it, much, and I'm also wondering if I did say yes to it - could I be setting myself up for "drug resistance" if I'm one whose viral load goes up and keeps going up (and I'm taken off the HCV 796?) If that DID happen, would I possibly then be resistance to all polymerase inhibitors?
Sorry if I sound so *dumb* on this (I can barely figure out how to ask the question), but I have had concerns about drug resistance for a few months now. Thanks if you have time and understand what I'm asking (or if anyone has time and understands what I'm asking.) I'd appreciate any input.
And another question (for anyone). Has anyone out there heard that HCV 796 has already had a Phase II that didn't go well as far as following protocol?
Here is the Phase II that is recruiting now, but I can't find any previous Phase II studies.
http://www.clinicaltrials.gov/ct/show/NCT00367887?order=1
Thanks.
d*** doctors! d**** research centers. I'm sorry - it has stopped snowing, and I guess I'm just in a bad mood (thank God for the laughter I get off Med Help :)
Yeah... let's invade Russia!
Yeah... let's invade Russia!
Molotov cocktail?
Sure sounds too good to believe!
1. Monotherapy
2. 1 to 2 months tx.
3. Apparently no sx's.
So that
Sure sounds too good to believe!
1. Monotherapy
2. 1 to 2 months tx.
3. Apparently no sx's.
So that
I'm getting very excited about this drug (Glutoxim & Monixan)! Basically, group of Russian scientists was working on its development last decade. Unscientific description of this product: basically combination of modified amino acids (building blocks of protein) for "immunomodulation or immune stimulation". It ultimately increases Th1/Th2 response (HR was explaining this well in prior threads) and shifts it in right direction. Production of Interleukins (sp?), WBC, RBC, etc. is increased... So, the possibilities of this product application are endless!
Russian company
Russian company
My Primary care Dr. is from Russia. I'm going to run these sites by him.
Thanks for the info.
Thanks for the info.
MEDICAL PROFESSIONAL
We are aware of this drug for a while and have made numerous specific inquiries.
There are two versions: The "Glutoxim" which is basically two glutathione molecules joined together. It likely works by improving extracellular glutathione status. It cannot easily pass into the intracellular space (cytosol). This drug is available in Russia, can also be shipped to anywhere by some international pharmacies.
We have contacted Dr. Castello, the Italian Dr. that generated the Italien website re Glutoxim and Molixan.
He can only get Glutoxim and he treated HCV patients with it. He has seen drops in ALT levels but never achieved HCV PCR negativity.
The Bam 205 - Molixan- is the same double Glutathione molecule, but has an additional small molecule attached to it, that enables reportedly its transfer across the cell membrane. Presumably this will lead to an increase of intracellular glutathione levels and other effects.
The Bam 205 or Nov 205 that is now in US trial is not available anywhere, including Russia. It is approved in Russia, but is not produced/available since there is a fight going on re the financial and patent rights.
We also spoke with Novelos, the US company that pursues Molixan - Nov 205 (BAM-205)here. The info re the 180 patients treated in Russia for HBV or HCV was not very complete, we could not determine how many HCV or HBV patients were involved and there was no clear info on VL responses. There were definitely reductions in LFTs reported.
There are two versions: The "Glutoxim" which is basically two glutathione molecules joined together. It likely works by improving extracellular glutathione status. It cannot easily pass into the intracellular space (cytosol). This drug is available in Russia, can also be shipped to anywhere by some international pharmacies.
We have contacted Dr. Castello, the Italian Dr. that generated the Italien website re Glutoxim and Molixan.
He can only get Glutoxim and he treated HCV patients with it. He has seen drops in ALT levels but never achieved HCV PCR negativity.
The Bam 205 - Molixan- is the same double Glutathione molecule, but has an additional small molecule attached to it, that enables reportedly its transfer across the cell membrane. Presumably this will lead to an increase of intracellular glutathione levels and other effects.
The Bam 205 or Nov 205 that is now in US trial is not available anywhere, including Russia. It is approved in Russia, but is not produced/available since there is a fight going on re the financial and patent rights.
We also spoke with Novelos, the US company that pursues Molixan - Nov 205 (BAM-205)here. The info re the 180 patients treated in Russia for HBV or HCV was not very complete, we could not determine how many HCV or HBV patients were involved and there was no clear info on VL responses. There were definitely reductions in LFTs reported.
Let's invade Russia and grab the NOV-205.
This seemingly has it all and close to a vaccine.
1. Monotherapy
2. 1 to 2 months tx.
3. Apparently no sx's.
This seemingly has it all and close to a vaccine.
1. Monotherapy
2. 1 to 2 months tx.
3. Apparently no sx's.
Thanks for the insight and info on the Bam/Nov 205.
Do you happen to know if the patent/financial fight is internal in Russia or are other outside companies involved? The patent rights struggle Sounds like it is going to take awhile(yrs?)to settle.
Do you happen to know if the patent/financial fight is internal in Russia or are other outside companies involved? The patent rights struggle Sounds like it is going to take awhile(yrs?)to settle.
If it has antinflammitory effects then it may have hope for improving fibrosis wouldn't it?
MEDICAL PROFESSIONAL
Yes, resistance was discussed frequently.
In a resistance mutation the genetic code of the variant is changed such that the molecular shape of , for example, the HCV polymerase is altered in a fashion that the inhibitor does not attach or inhibit effectively anymore. A nonnucleoside inhibitor such as HCV 796 snuggles close to the shape of the wild type protein, blocking its molecular movements and functions. When even a single amino acid is exchanged in the area of the protein, where the inhibitor binds, it does not fit tightly anymore, without substantial alterations in the functionality of the polymerase function itself. Here you have a quick mutant that is still fit. Thats why this drug was effective after 4 days and completely mutated against after 14 days under continued dosing.
Such a mutant would not however typically make you resistant against most other drugs, only against some, having a similar target site. This is called cross resistance. Certainly resistance against a HCV nunnuke polymerase inhibitor has no effect on Proteinase inhibitors. Within the same class however, cross resistance is not unlikely, hard to predict however. Often there is partial resistance generated under these circumstances, just like LAM (YMDD)resistance against HBV causes partial resistance against entecavir/baraclude and almost complete resistance against telbivudine/Tyzeka.
The nucleoside polymerase inhibitors are harder to muate against, since the mutation is close to the natural binding site of the natural substrate and alterations to reject the drug often make the protein unfit to bind the natural nucleotide. However if valopicitabine is fully effective against an HCV 796 resistance mutant needs to be seen.
In combo with IFN/Riba even a superquick resistance prone drug /+ not so strong inhibitor like HCV796 might provide enough helper function - reduction of viral adaptive power- to make a decent difference in SVR rates. Only trials can unveil this. Vertex950 had a substantial higher primary inhibitory power (log VL reduction in monotrials initially), however and chances for SVR %improvements therefore seem to be better.
In a resistance mutation the genetic code of the variant is changed such that the molecular shape of , for example, the HCV polymerase is altered in a fashion that the inhibitor does not attach or inhibit effectively anymore. A nonnucleoside inhibitor such as HCV 796 snuggles close to the shape of the wild type protein, blocking its molecular movements and functions. When even a single amino acid is exchanged in the area of the protein, where the inhibitor binds, it does not fit tightly anymore, without substantial alterations in the functionality of the polymerase function itself. Here you have a quick mutant that is still fit. Thats why this drug was effective after 4 days and completely mutated against after 14 days under continued dosing.
Such a mutant would not however typically make you resistant against most other drugs, only against some, having a similar target site. This is called cross resistance. Certainly resistance against a HCV nunnuke polymerase inhibitor has no effect on Proteinase inhibitors. Within the same class however, cross resistance is not unlikely, hard to predict however. Often there is partial resistance generated under these circumstances, just like LAM (YMDD)resistance against HBV causes partial resistance against entecavir/baraclude and almost complete resistance against telbivudine/Tyzeka.
The nucleoside polymerase inhibitors are harder to muate against, since the mutation is close to the natural binding site of the natural substrate and alterations to reject the drug often make the protein unfit to bind the natural nucleotide. However if valopicitabine is fully effective against an HCV 796 resistance mutant needs to be seen.
In combo with IFN/Riba even a superquick resistance prone drug /+ not so strong inhibitor like HCV796 might provide enough helper function - reduction of viral adaptive power- to make a decent difference in SVR rates. Only trials can unveil this. Vertex950 had a substantial higher primary inhibitory power (log VL reduction in monotrials initially), however and chances for SVR %improvements therefore seem to be better.
MEDICAL PROFESSIONAL
It seems to be a candidate on the antibrotic drug list. But currently, considering the need to inject and the difficulty to get one might think of replenishing the intracellular glutathione levels with NAC, that works without question very well in that effect.
Notwithstanding the above , there might be more to this double glutathione than just the glutathione effect. But since it worked against HBV and HCV - probably by decreasing hepatic injury- it is not very likely to encompass a direct inhibitory effect upon the HCV machinery, but rather an indirect effect - if any- against HCV VL by enhancing immune functions.
Notwithstanding the above , there might be more to this double glutathione than just the glutathione effect. But since it worked against HBV and HCV - probably by decreasing hepatic injury- it is not very likely to encompass a direct inhibitory effect upon the HCV machinery, but rather an indirect effect - if any- against HCV VL by enhancing immune functions.
So what you are saying is that it may be a candidate to replace interferon in combo treatment also?
MEDICAL PROFESSIONAL
If it indeed has an immunomodulatory effect - that remains to be seen- I would doubt it would be of such a strength that it could replace inteferon.
sounds interesting here are a couple more sites to look at
www.tiopoietine.info/Molixengl.htm
Risultati del molixan nella terapia dell'epatite cronica attiva
this should come up hit translate (unless you read russian ) the text should appear in english the graphs dont seem to transulate
this chemical seems to be composed of 3 amino acids non essential and ribofuranozil hypoxanthine the amino acids are needed for cytokine formation regulation (modulate immune response)some xanthine drugs seem to inhibit or decrease liver fibrosis ( caffine,pentoxifylline (trental)
the ribofuranozil who knows maybe some structural similarities to riba . will have to watch this trial
www.tiopoietine.info/Molixengl.htm
Risultati del molixan nella terapia dell'epatite cronica attiva
this should come up hit translate (unless you read russian ) the text should appear in english the graphs dont seem to transulate
this chemical seems to be composed of 3 amino acids non essential and ribofuranozil hypoxanthine the amino acids are needed for cytokine formation regulation (modulate immune response)some xanthine drugs seem to inhibit or decrease liver fibrosis ( caffine,pentoxifylline (trental)
the ribofuranozil who knows maybe some structural similarities to riba . will have to watch this trial
So You'd "THINK"... But it certainly doesn't appear that way... but hey.. maybe we're not supossed to THINK...
My old Dr Quack, Quack use to get insulted when I'd read something in here & bring it to his attention, or question him on certain things... He took it as a personal assault on his authority, then tell me that we get information quicker on the net than THEY do because it takes them awhile to get the newsletters with studies & read up on them!!! LoL...
I suppose that could be true, but seems to me IF they were truley interrested they would be consistantly on "TOP" of the latest & greatest! I don't get it....
This particular bit of info totally BLINDSIDED me... like it was suddenly pulled out of a hat! Had No Clue!
Well, you're right... leaves lots of questions... but I guess it just gives us something else to look forward to, & watch for.....more competition has got to be a good thing... Right!!!
;)
My old Dr Quack, Quack use to get insulted when I'd read something in here & bring it to his attention, or question him on certain things... He took it as a personal assault on his authority, then tell me that we get information quicker on the net than THEY do because it takes them awhile to get the newsletters with studies & read up on them!!! LoL...
I suppose that could be true, but seems to me IF they were truley interrested they would be consistantly on "TOP" of the latest & greatest! I don't get it....
This particular bit of info totally BLINDSIDED me... like it was suddenly pulled out of a hat! Had No Clue!
Well, you're right... leaves lots of questions... but I guess it just gives us something else to look forward to, & watch for.....more competition has got to be a good thing... Right!!!
;)
Have an Answer?
You are reading content posted in the Hepatitis C Community
Learn about this treatable virus.
Getting tested for this viral infection.
3 key steps to getting on treatment.
4 steps to getting on therapy.
What you need to know about Hep C drugs.
How the drugs might affect you.
These tips may up your chances of a cure.
A list of national and international resources and hotlines to help connect you to needed health and medical services.
Herpes sores blister, then burst, scab and heal.
Herpes spreads by oral, vaginal and anal sex.
STIs are the most common cause of genital sores.
Condoms are the most effective way to prevent HIV and STDs.
PrEP is used by people with high risk to prevent HIV infection.
