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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
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.
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