Aa
Something has been changed nowadays
Here is a researcher's opinion from the HBV Knockdown Blog about the EASL 2014 meeting.
"Having attended the EASL European Liver Meeting last week and listened to some of the clinical thought-leaders and companies involved in HBV research and treatment, it confirmed the view that there is a GREAT hunger in the field for new approaches to achieve that elusive finite treatment goal for HBV. For this, all differentiated, potentially high-impact new treatment approaches are welcome, RNAi or not. And yes, following the successes in HCV, the industry now views HBV as an opportunity as big as HCV and is shifting its resources accordingly.
There were numerous, not very imaginative studies about trying various permutations of treating HBV with the old, and tired workhorses interferon and NUCs: treat with NUCs, then come in with interferon or vice versa, trying different interferons (alpha or lambda), trying different treatment times…without much, if anything to show for it to change current standard of care.
Where there was progress in HBV was in better understanding the kinetics of this complex disease and in the development of better animal and tissue culture model systems that I expect to greatly facilitate the development of drugs for HBV. For example, following the discovery of NTCP as the viral entry receptor, it is now possible to have HBV replicate in the petri dish. Similarly, there are now mice with not only human livers, but also human immune systems. This is critical for studying immune-based treatment approaches which are viewed as most promising, including HBsAg gene knockdown.
The fact that HBsAg has emerged as a very important biomarker should aid in garnering support for knockdown approaches, although awareness of them is not great yet. This also showed from the reactions to a talk on the ISIS/GSK antisense candidate that I attended. Although multi-log knockdowns were achieved in certain model systems, I did not see great potency at doses that are clinically relevant. For example, what point is a 3 log HBsAg knockdown when you need 200mg/kg oligos in mice (or don't even show the data)? Granted, Arrowhead Research has also advertised knockdown levels with dosages that will not be used in the clinic, but with 2mg/kg they are close to or even better than something quite potent in humans.
With regard to other new treatment approaches besides HBsAg gene knockdown, there is the HBV entry inhibitor Myrcludex which is receiving more widespread attention, although the downside to that approach is that it has no apparent immune angle and would largely work the way that NUCs do…reduce viral load. Finally, there is the idea of inhibiting the PD-1 pathway as discussed in an earlier blog entry, but I’m quite skeptical about the safety of an antibody/small molecule approach here due to potential toxicity arising from the systemic inhibition of this pathway, including autoimmunity. More interesting would be an RNAi Therapeutics approach that targets thepathway specifically in the liver."
"Having attended the EASL European Liver Meeting last week and listened to some of the clinical thought-leaders and companies involved in HBV research and treatment, it confirmed the view that there is a GREAT hunger in the field for new approaches to achieve that elusive finite treatment goal for HBV. For this, all differentiated, potentially high-impact new treatment approaches are welcome, RNAi or not. And yes, following the successes in HCV, the industry now views HBV as an opportunity as big as HCV and is shifting its resources accordingly.
There were numerous, not very imaginative studies about trying various permutations of treating HBV with the old, and tired workhorses interferon and NUCs: treat with NUCs, then come in with interferon or vice versa, trying different interferons (alpha or lambda), trying different treatment times…without much, if anything to show for it to change current standard of care.
Where there was progress in HBV was in better understanding the kinetics of this complex disease and in the development of better animal and tissue culture model systems that I expect to greatly facilitate the development of drugs for HBV. For example, following the discovery of NTCP as the viral entry receptor, it is now possible to have HBV replicate in the petri dish. Similarly, there are now mice with not only human livers, but also human immune systems. This is critical for studying immune-based treatment approaches which are viewed as most promising, including HBsAg gene knockdown.
The fact that HBsAg has emerged as a very important biomarker should aid in garnering support for knockdown approaches, although awareness of them is not great yet. This also showed from the reactions to a talk on the ISIS/GSK antisense candidate that I attended. Although multi-log knockdowns were achieved in certain model systems, I did not see great potency at doses that are clinically relevant. For example, what point is a 3 log HBsAg knockdown when you need 200mg/kg oligos in mice (or don't even show the data)? Granted, Arrowhead Research has also advertised knockdown levels with dosages that will not be used in the clinic, but with 2mg/kg they are close to or even better than something quite potent in humans.
With regard to other new treatment approaches besides HBsAg gene knockdown, there is the HBV entry inhibitor Myrcludex which is receiving more widespread attention, although the downside to that approach is that it has no apparent immune angle and would largely work the way that NUCs do…reduce viral load. Finally, there is the idea of inhibiting the PD-1 pathway as discussed in an earlier blog entry, but I’m quite skeptical about the safety of an antibody/small molecule approach here due to potential toxicity arising from the systemic inhibition of this pathway, including autoimmunity. More interesting would be an RNAi Therapeutics approach that targets thepathway specifically in the liver."
Is gs9620 drug helps to cure HBV from HBeAg negative patients with undetectable viral loads? Thanks.
Combining gs9620 with ifn is a possibility that holds moderate hope towards intensifying interferons effect. Considering 9620s weak results it is unclear to me if Gilead would invest into testing this combo treatment.
Thank you for the link and comments. Although the results are disappointing do you think GS-9620 (4mg dose) can improve PEGASYS HBsAG decreasing effect just because of ISG15 and IP-10 response?
once you read the study results thus far as shown by stephen above it is clear that the key response parameters hbv dna and hbsag did not show a remarkable drug effect at this point in time. the big thing they make about the interferon sensitive genes is to show that at least something important has happened in response to gs9620.
it is still possible, that the desired antiviral effect will appear later, but the results are indeed disappointing.
it is still possible, that the desired antiviral effect will appear later, but the results are indeed disappointing.
Yes, see the following link:
Determinants of Variability in ISG15 Gene Expression in Patients With Chronic Hepatitis B (CHB) Infection During Treatment With Oral TLR-7 Agonist GS-9620
Reported by Jules Levin
EASL 2014 April 9-13 London, UK
Edward J. Gane,1 Stuart C. Gordon,2 Shyamasundaran Kottilil,3 Benedetta Massetto,4 Anuj Gaggar,4 Scott Stem,4 Stefan Pflanz,4 Zhishen Ye,4 G. Mani Subramanian,4 John G. McHutchison,4 Young-Suk Lim,5 Yoon Jun Kim6 1Auckland Clinical Studies, Auckland, New Zealand; 2Henry Ford Health Systems, Detroit, Michigan, USA; 3National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA; 4Gilead Sciences, Inc., Foster City, California, USA; 5Asan Medical Center, Seoul, South Korea; 6Seoul National University Hospital, Seoul, South Korea
http://www.natap.org/2014/EASL/EASL_95.htm
The authors concluded that there should be further evaluation of the safety and efficacy of GS9620. As a layman, I thought the results were disappointing - there was no detection of serum Interferon, and I always think of GS9620 as an oral form of Interferon. So much for my understanding, I hope experts like studyforhope can tell me I am wrong.
Determinants of Variability in ISG15 Gene Expression in Patients With Chronic Hepatitis B (CHB) Infection During Treatment With Oral TLR-7 Agonist GS-9620
Reported by Jules Levin
EASL 2014 April 9-13 London, UK
Edward J. Gane,1 Stuart C. Gordon,2 Shyamasundaran Kottilil,3 Benedetta Massetto,4 Anuj Gaggar,4 Scott Stem,4 Stefan Pflanz,4 Zhishen Ye,4 G. Mani Subramanian,4 John G. McHutchison,4 Young-Suk Lim,5 Yoon Jun Kim6 1Auckland Clinical Studies, Auckland, New Zealand; 2Henry Ford Health Systems, Detroit, Michigan, USA; 3National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA; 4Gilead Sciences, Inc., Foster City, California, USA; 5Asan Medical Center, Seoul, South Korea; 6Seoul National University Hospital, Seoul, South Korea
http://www.natap.org/2014/EASL/EASL_95.htm
The authors concluded that there should be further evaluation of the safety and efficacy of GS9620. As a layman, I thought the results were disappointing - there was no detection of serum Interferon, and I always think of GS9620 as an oral form of Interferon. So much for my understanding, I hope experts like studyforhope can tell me I am wrong.
Do you have any news about the results of the finished GS-9620 clinical trial?
http://www.clinicaltrial.gov/ct2/show/NCT01590654?term=gs-9620&rank=2
http://www.clinicaltrial.gov/ct2/show/NCT01590654?term=gs-9620&rank=2
Sorry to ask what sounds like a stupid question but what do you mean "proper"?
But I think in terms of REP9AC' it would only be speculation to say one way or the other if the 8 patients had any bounce back.
But I do agree its a bit disturbing how quiet Replicor are but I'm glad Seattle dude is linked closely with them and he will find out when he speaks with Michel if there was or not. (lets hope for our sake the was no bounce back)
I did speak to a gastro from Bangladesh who is closely linked to the guys involved there & he swears Replicor is the real deal
Studyforhope I know its a bit off topic but I did post a question earlier about vit d 3 whats your opinion please on the ideal amount for HBV people ?
But I think in terms of REP9AC' it would only be speculation to say one way or the other if the 8 patients had any bounce back.
But I do agree its a bit disturbing how quiet Replicor are but I'm glad Seattle dude is linked closely with them and he will find out when he speaks with Michel if there was or not. (lets hope for our sake the was no bounce back)
I did speak to a gastro from Bangladesh who is closely linked to the guys involved there & he swears Replicor is the real deal
Studyforhope I know its a bit off topic but I did post a question earlier about vit d 3 whats your opinion please on the ideal amount for HBV people ?
the surface antigen is in the cuban mix since they hope that the local superantigen effect of the core will stimulate a response against the hbsag as well. it has been shown in much detail in mouse studies by jorg reimann and reinhold schirmbeck that this works very well.
Thank you for the abstract.This is one of the most remarkable achievements with therapeutic vaccines to date. it needs to be used in combo with the NAPs.
multiple doses of arc520 will be a must, as i mentioned, possibly at higher dose levels, side effects permitting. A 90% reduction of hbsag would be way too little to achieve the desired stimulating effect on the adaptive immunity. But it will look good at the meetings and in the press releases. I do sincerely hope they can increase the dose and the frequency of administration.
Why wouldn't they just make a core vaccine as a therapeutic vaccine? Why add the surface Ag? Doesn't everyone infected have enough of that already or am I missing something?
replicor is very silent now regarding the fate of the eight patients. Not a good sign.
the cuban vaccine is a mixed particle vaccine with core particles as the key ingredient. The core particle in itself is a so called superantigen that needs no adjuvant, it is highly immunogenic.
the gs4774 is a string of tcell epitopes engineered to cover all the hbv proteins. The inherent immonogenicity of the carrier particle will need to be proper for presentation and tcell activation in the human patient. One has to wait for the results.
the cuban vaccine is a mixed particle vaccine with core particles as the key ingredient. The core particle in itself is a so called superantigen that needs no adjuvant, it is highly immunogenic.
the gs4774 is a string of tcell epitopes engineered to cover all the hbv proteins. The inherent immonogenicity of the carrier particle will need to be proper for presentation and tcell activation in the human patient. One has to wait for the results.
What about multiple doses? From what I gather they plan to keep it knocked down until they can get Hbsab SRV
I am planing to call the CEO of Replicor back next week and I will ask him about bounce back in the 8 patients. If they are cured I will invest for sure
studyforhope thanks. Yes you are right just checked my emails and conversations with Arrow head this is what they wrote
Yes the blogger is very pro Arrow Head I did notice that.
"The current thinking is that the Phase 2a and 2b (and probably beyond) will be in combination with entecavir or tenofovir. That way the viral load is under control and the variable we are interested in, reduction of s-antigen, can be isolated. Experts in the field believe that current therapies’ inability to reduce s-antigen production has been the limiting factor. The theory is that if you can directly reduce s-antigen, you can prompt the body’s adaptive immune system to come back up and clear the virus. Let me know if you have any additional questions. Thanks"
I must admit Arrow head were super helpful to talk with
studyforhope in terms of Replicor there was no reported bounce back in any of the 8 patients was there?
So in terms of the therapeutic vaccines whats the difference in strategy between GS4774 and the one in Cuba please?
Yes the blogger is very pro Arrow Head I did notice that.
"The current thinking is that the Phase 2a and 2b (and probably beyond) will be in combination with entecavir or tenofovir. That way the viral load is under control and the variable we are interested in, reduction of s-antigen, can be isolated. Experts in the field believe that current therapies’ inability to reduce s-antigen production has been the limiting factor. The theory is that if you can directly reduce s-antigen, you can prompt the body’s adaptive immune system to come back up and clear the virus. Let me know if you have any additional questions. Thanks"
I must admit Arrow head were super helpful to talk with
studyforhope in terms of Replicor there was no reported bounce back in any of the 8 patients was there?
So in terms of the therapeutic vaccines whats the difference in strategy between GS4774 and the one in Cuba please?
Phase III study of a therapeutic vaccine candidate (NASVAC)
containing the hepatitis B virus core antigen (HBcAg)
and the HBV surface antigen (HBsAg) for treatment of patients
with chronic hepatitis B
Mamun-Al-Mahtab 1, Mohammed Fazle Akbar 2, Julio Ce´sar
Aguilar 3, Vincent Serra 4, Salimur Rahman 1, Pascale Berthillon 5,
Christian Trepo 5, Josianne Nitcheu 4, Pierre Vandepapelie`re 4,
Gerardo Enrique Guillen Nieto 3
1Department of Hepatology, Bangabandhu Sheikh Mujib Medical University,Dhaka,Bangladesh,
2 Toshiba General Hospital, Tokyo,
Japan,
3 Center for Genetic Engineering and Biotechnology, Havana,
Cuba,
4 Wittycell, Evry, France,
5 INSERM 1052/CRCL, Lyon France
Background and aims: Curative therapies for patients with chronic
Hepatitis B (CHB) include pegylated interferon-alpha (pegIFN-a) and
nucleot(s)ide analogues (NUCs). However, pegIFN-a is effective in
approximately one-third of the treated patients only, while the need for
long term treatment is the main limitation of NUCs. Because immune
responses are impaired in patients suffering from CHB, therapeutic
vaccination has become an important strategy to help viral clearance, by
stimulating patients’ hepatitis B specific immune responses. We have
developed a therapeutic vaccine candidate (NASVAC) which is based
on the use of a combination of recombinant HBsAg and HBcAg. We
conducted a phase III clinical study in Bangladesh to evaluate the
clinical efficacy of repeated intranasal/subcutaneous immunizations of
NASVAC to CHB patients to reduce serum HBV DNA levels and to
induce HBsAg/HBeAg clearance or seroconversion.
Methods: One hundred and sixty subjects (of whom 20 % were
HbeAg positive and 80 % HBeAg negative) naı¨ve to anti-HBV
treatment for at least 6 months were randomly assigned to one of the
two following regimens: either NASVAC (100 mcg antigen per
dose), five intranasal (IN) inoculations every 14 days during the first
cycle followed by 5 IN and 5 subcutaneous (SC) inoculations every
14 days during the second cycle of inoculation for a total duration of
24 weeks or weekly SC injections of pegIFN-a for 48 weeks. Patients
in both groups were evaluated over time at week 12, 24, 48, 72 and 96
after beginning of the treatment for serum HBVDNA (quantitative
PCR), ALT, AST, HBeAg, HBsAg, and for safety.
Results: NASVAC was safe and well tolerated inducing reactions
similar to those caused by pegIFN-a but less frequently and less
severe. Both treatments induced a strong and similar antiviral
response during therapy. After cessation of treatment HBV DNA
levels increased again in both groups, but at very different rates. At
week 72 (24 weeks after the end of pegIFN-a treatment and 48 weeks
after the end of NASVAC treatment), the HBV DNA levels were
significantly lower in the NASVAC group than in the pegIFN-a group
(p = 0.03), with almost 80 % of NASVAC treated patients remaining
under 10’000 c/mL. This delayed rebound in the NASVAC group
suggests a sustained antiviral effect as compared to the pegIFN-a
group. Similarly, while at the end of treatment the percentage of
patients with HBeAg loss was similar in both groups (NASVAC 50 %
at week 24; pegIFN-a 55 % at week 48), at week 96 the percentages
in the NASVAC and pegIFN-a groups were 62 and 33 %
respectively. The level of HBsAg in the pegIFN-a group decreased
following treatment until W48, and then increased back to the baseline
levels at W96. However, while no difference in the level of
HBsAg was found from baseline until W72 in the NASVAC group,
the treatment had a significant influence on lowering the HBsAg at
W96 follow-up (p = 0.0074).
Conclusions: The data presented here demonstrate that therapeutic
vaccination with NASVAC has a profound antiviral effect that is
more sustained than pegIFN-a after the end of treatment. This delayed
viral rebound is accompanied by a sustained HBeAg loss. These
results do support further developments to evaluate the therapeutic
potential of NASVAC in endemic regions.
containing the hepatitis B virus core antigen (HBcAg)
and the HBV surface antigen (HBsAg) for treatment of patients
with chronic hepatitis B
Mamun-Al-Mahtab 1, Mohammed Fazle Akbar 2, Julio Ce´sar
Aguilar 3, Vincent Serra 4, Salimur Rahman 1, Pascale Berthillon 5,
Christian Trepo 5, Josianne Nitcheu 4, Pierre Vandepapelie`re 4,
Gerardo Enrique Guillen Nieto 3
1Department of Hepatology, Bangabandhu Sheikh Mujib Medical University,Dhaka,Bangladesh,
2 Toshiba General Hospital, Tokyo,
Japan,
3 Center for Genetic Engineering and Biotechnology, Havana,
Cuba,
4 Wittycell, Evry, France,
5 INSERM 1052/CRCL, Lyon France
Background and aims: Curative therapies for patients with chronic
Hepatitis B (CHB) include pegylated interferon-alpha (pegIFN-a) and
nucleot(s)ide analogues (NUCs). However, pegIFN-a is effective in
approximately one-third of the treated patients only, while the need for
long term treatment is the main limitation of NUCs. Because immune
responses are impaired in patients suffering from CHB, therapeutic
vaccination has become an important strategy to help viral clearance, by
stimulating patients’ hepatitis B specific immune responses. We have
developed a therapeutic vaccine candidate (NASVAC) which is based
on the use of a combination of recombinant HBsAg and HBcAg. We
conducted a phase III clinical study in Bangladesh to evaluate the
clinical efficacy of repeated intranasal/subcutaneous immunizations of
NASVAC to CHB patients to reduce serum HBV DNA levels and to
induce HBsAg/HBeAg clearance or seroconversion.
Methods: One hundred and sixty subjects (of whom 20 % were
HbeAg positive and 80 % HBeAg negative) naı¨ve to anti-HBV
treatment for at least 6 months were randomly assigned to one of the
two following regimens: either NASVAC (100 mcg antigen per
dose), five intranasal (IN) inoculations every 14 days during the first
cycle followed by 5 IN and 5 subcutaneous (SC) inoculations every
14 days during the second cycle of inoculation for a total duration of
24 weeks or weekly SC injections of pegIFN-a for 48 weeks. Patients
in both groups were evaluated over time at week 12, 24, 48, 72 and 96
after beginning of the treatment for serum HBVDNA (quantitative
PCR), ALT, AST, HBeAg, HBsAg, and for safety.
Results: NASVAC was safe and well tolerated inducing reactions
similar to those caused by pegIFN-a but less frequently and less
severe. Both treatments induced a strong and similar antiviral
response during therapy. After cessation of treatment HBV DNA
levels increased again in both groups, but at very different rates. At
week 72 (24 weeks after the end of pegIFN-a treatment and 48 weeks
after the end of NASVAC treatment), the HBV DNA levels were
significantly lower in the NASVAC group than in the pegIFN-a group
(p = 0.03), with almost 80 % of NASVAC treated patients remaining
under 10’000 c/mL. This delayed rebound in the NASVAC group
suggests a sustained antiviral effect as compared to the pegIFN-a
group. Similarly, while at the end of treatment the percentage of
patients with HBeAg loss was similar in both groups (NASVAC 50 %
at week 24; pegIFN-a 55 % at week 48), at week 96 the percentages
in the NASVAC and pegIFN-a groups were 62 and 33 %
respectively. The level of HBsAg in the pegIFN-a group decreased
following treatment until W48, and then increased back to the baseline
levels at W96. However, while no difference in the level of
HBsAg was found from baseline until W72 in the NASVAC group,
the treatment had a significant influence on lowering the HBsAg at
W96 follow-up (p = 0.0074).
Conclusions: The data presented here demonstrate that therapeutic
vaccination with NASVAC has a profound antiviral effect that is
more sustained than pegIFN-a after the end of treatment. This delayed
viral rebound is accompanied by a sustained HBeAg loss. These
results do support further developments to evaluate the therapeutic
potential of NASVAC in endemic regions.
Do you have an abstract of the NASVAC results presented at the Brisbane meeting.
The results of the phase 2 clinical trial of the Cuban NASVAC therapeutic vaccine were presented at the APASL meeting in Brisbane in March this year.
The viral load decline and rebounce, HBeAg seroconversion rates were similar to PEGIFN. Intriguingly, there was no serum HBsAg decline except at w96 of follow up. The vaccine is now called ABX203, a startup French pharma, abivax, is planning to conduct further clinical trials.
The viral load decline and rebounce, HBeAg seroconversion rates were similar to PEGIFN. Intriguingly, there was no serum HBsAg decline except at w96 of follow up. The vaccine is now called ABX203, a startup French pharma, abivax, is planning to conduct further clinical trials.
The blogger seems to seed high expectations in arrowheads irna possibly to enhance its stock price that is driven by such expectations. This is a very smart approach indeed...
IRNA is not an antibody enhancing therapy as you write. It knocks down HBV viral messenger RNA to limit the production of the respective proteins.
IRNA is not an antibody enhancing therapy as you write. It knocks down HBV viral messenger RNA to limit the production of the respective proteins.
A T cell vaccine like the one Gilead tests ..gs4774..in collaboration with globe immune has chances if it is used at a stage of internal or external induced hbsag suppression as adjuvant therapy.
If all the HBV TCell epitopes build into this immunogenic are relevant is doubtful, but a single one of them only needs to be truly effective.
Just as theoretical considerations would predict, the Cuban core vaccine seems to be the first therapeutic vaccine to have a noticeable effect, in the order of magnitude of ifn treatment. This was shown in the study on Bangladeshi patients presented at the last AASLD, strangely by the same local group that tested replicors drug in Bangladesh.
If all the HBV TCell epitopes build into this immunogenic are relevant is doubtful, but a single one of them only needs to be truly effective.
Just as theoretical considerations would predict, the Cuban core vaccine seems to be the first therapeutic vaccine to have a noticeable effect, in the order of magnitude of ifn treatment. This was shown in the study on Bangladeshi patients presented at the last AASLD, strangely by the same local group that tested replicors drug in Bangladesh.
Unless multiple higher doses can be given and tolerated, the arrowhead hbsag suppression will not be sufficient to achieve a lasting effect.
The suppression of hbsag by replicor is much much more efficient. But even then we see that the effect does not last permanently after the end of therapy. Concomitant ifn therapy intensifies and extends the duration of the NAP hbsag suppression after the intervention end, but it seems to just take longer until the cccDNA slowly comes back. Effective therapeutic vaccination mainly targeting core epitopes has the best chance to stabilize the svr.
Myrcludex has a dose limiting toxicity that does not allow fully effective blocking of the NTCP, the workhorse of bile acid detoxification from the portal blood to the systemic circulation.
The suppression of hbsag by replicor is much much more efficient. But even then we see that the effect does not last permanently after the end of therapy. Concomitant ifn therapy intensifies and extends the duration of the NAP hbsag suppression after the intervention end, but it seems to just take longer until the cccDNA slowly comes back. Effective therapeutic vaccination mainly targeting core epitopes has the best chance to stabilize the svr.
Myrcludex has a dose limiting toxicity that does not allow fully effective blocking of the NTCP, the workhorse of bile acid detoxification from the portal blood to the systemic circulation.
Maybe the first available next gen drug will be a non-interferon immune enhancer of Gilead, namely GS4774.
Do you think after a 2-3 years NUCs therapy (TDF or ETV), adding GS4774 is a good option instead of adding PEGASYS?
Do you think after a 2-3 years NUCs therapy (TDF or ETV), adding GS4774 is a good option instead of adding PEGASYS?
I read this before. I find the blogger has an interesting view & is clearing trying to keep informed.
studyforhope. Would it be fair to say in your opinion a better strategy is VL knockdown with Nucs etc then followed by immune modulator then anti body production via RNAI silencer? for a lasting immune controlled response?
studyforhope. Would it be fair to say in your opinion a better strategy is VL knockdown with Nucs etc then followed by immune modulator then anti body production via RNAI silencer? for a lasting immune controlled response?
What is your take on the most promising of these therapies? Do you like the approach of ARC-520? Or do you think Myrc or Replicor are more promising ?
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