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did anybody try artesunate?
it is available as health supplement here in US:
http://www.hepalin.com/hepasunate50.htm
it can be used sublingual and it is plant extracted, it is the most potent antimalaria compound and used for centuries in asia without sides.it has activity on hbv/hbsag, all herpes viruses, hiv and xmvr.CFS patients are using it sublingual
if anybody want to try it, it is very important to have alt/ast and liver function checked closely weekly or every 4 weeks, sublingualis better because it may have liver toxicity if used for long time as most of the drugs.sublingual should have no liver tox
http://www.ncbi.nlm.nih.gov/pubmed/16122816
Abstract
The antiviral effect against hepatitis B virus (HBV) of artemisinin, its derivative artesunate and other compounds highly purified from traditional Chinese medicine remedies, were investigated. HBV production by permanently transfected HepG2 2.2.15 cells was determined by measuring the release of surface protein (HBsAg) and HBV-DNA after drug exposure (0.01-100 microM) for 21 days. The forms of HBV-DNA released were investigated by Southern-blotting. Neutral Red retention test was used to evaluate drug-induced toxicity on host cells. The compounds were classified according to their potential interest as follows: (i) none: they had no effect on viral production (daidzein, daidzin, isonardosinon, nardofuran, nardosinon, tetrahydronardosinon and quercetin); (ii) low: they were able to markedly reduce viral production, but also induced toxicity on host cells (berberine and tannic acid) or they had no toxic effect on host cells but only had a moderate ability to reduce viral production (curcumin, baicalein, baicalin, bufalin, diallyl disulphide, glycyrrhizic acid and puerarin); (iii) high: they induced strong inhibition of viral production at concentrations at which host cell viability was not affected (artemisinin and artesunate). Moreover, artesunate in conjunction with lamivudine had synergic anti-HBV effects, which warrants further evaluation of artemisinin/artesunate as antiviral agents against HBV infection.
http://www.hepalin.com/hepasunate50.htm
it can be used sublingual and it is plant extracted, it is the most potent antimalaria compound and used for centuries in asia without sides.it has activity on hbv/hbsag, all herpes viruses, hiv and xmvr.CFS patients are using it sublingual
if anybody want to try it, it is very important to have alt/ast and liver function checked closely weekly or every 4 weeks, sublingualis better because it may have liver toxicity if used for long time as most of the drugs.sublingual should have no liver tox
http://www.ncbi.nlm.nih.gov/pubmed/16122816
Abstract
The antiviral effect against hepatitis B virus (HBV) of artemisinin, its derivative artesunate and other compounds highly purified from traditional Chinese medicine remedies, were investigated. HBV production by permanently transfected HepG2 2.2.15 cells was determined by measuring the release of surface protein (HBsAg) and HBV-DNA after drug exposure (0.01-100 microM) for 21 days. The forms of HBV-DNA released were investigated by Southern-blotting. Neutral Red retention test was used to evaluate drug-induced toxicity on host cells. The compounds were classified according to their potential interest as follows: (i) none: they had no effect on viral production (daidzein, daidzin, isonardosinon, nardofuran, nardosinon, tetrahydronardosinon and quercetin); (ii) low: they were able to markedly reduce viral production, but also induced toxicity on host cells (berberine and tannic acid) or they had no toxic effect on host cells but only had a moderate ability to reduce viral production (curcumin, baicalein, baicalin, bufalin, diallyl disulphide, glycyrrhizic acid and puerarin); (iii) high: they induced strong inhibition of viral production at concentrations at which host cell viability was not affected (artemisinin and artesunate). Moreover, artesunate in conjunction with lamivudine had synergic anti-HBV effects, which warrants further evaluation of artemisinin/artesunate as antiviral agents against HBV infection.
peginterferon, i know it, i had it, it makes high fever and if not lowered by pracetamol vomiting too
nitazoxanide, i know it, i had it, sides diarrhea common, creatinine increase (rare)
tenofovir, i know it and i take it daily, no sides from my experience
artesunate, i dont know it, check with your doctor or online/on the drug box about its sides.
nitazoxanide, i know it, i had it, sides diarrhea common, creatinine increase (rare)
tenofovir, i know it and i take it daily, no sides from my experience
artesunate, i dont know it, check with your doctor or online/on the drug box about its sides.
I am taking artesunate 200mg tab twice daily (400mg/day) from last 22 days along with peginterferon for hbv. Yesterday after 2 days of my 8th inj of IFN I had high grade fever and 1episode of vomiting after which fever disappeared. Now this was the first vomit I had during IFN therapy but previously also 2-3 times I felt vomit but subsided.
The question is which drug to blame IFN or artesunate. I am also taking nitazoxanide and tenofovir.
My sgpt and sgot gradually rose to 95iu/ml during IFN therapy till date. Again whom to blame artesunate or IFN?
The question is which drug to blame IFN or artesunate. I am also taking nitazoxanide and tenofovir.
My sgpt and sgot gradually rose to 95iu/ml during IFN therapy till date. Again whom to blame artesunate or IFN?
What should be the dose of artesunate? Currently m taking 200mg tab at night, can it be taken twice a day? M 90kg by weight
you do the injection yourself, you can use the subcutaneous diabetes injections, the needle is about 3mm, anybody can do it.....shall I inject in any part of my body or just arm only? Stef2011
Ok Steff I won't take iron but will take artesunate as it works I ve read, I'll shift to simvastatin from atorvastatin. Was using atorvastatin as it has longer half life while simvastatin has half life of only 2-3hrs. Any ways thanx for ur info, meanwhile other stuffs do work Atleast will make body healthier.
artesunate this didn t work mono
atorvastatin doens t work at all on hbv even in vitro
iron this feeds the virus, do not take iron
amino acid caps, l arginine pure powder may help but just a guess, it may feed cd8 cells
vitamin d3 of course does help baked by few studies
ntz, may work but only one member tried it and did not work
avoid things which clearly dont work or you may suppress peginterferon
atorvastatin doens t work at all on hbv even in vitro
iron this feeds the virus, do not take iron
amino acid caps, l arginine pure powder may help but just a guess, it may feed cd8 cells
vitamin d3 of course does help baked by few studies
ntz, may work but only one member tried it and did not work
avoid things which clearly dont work or you may suppress peginterferon
but keep in mind gcmaf alone doesn t work, it needs vitamind3 high dose and peginterferon and in the end it may only help peginterferon response
we have only one member who tried tdf+goleic gcmaf sublingual+vit d3 but he had hbsag 16iu/ml so it is very difficult to say if it was goleic gcmaf
we have only one member who tried tdf+goleic gcmaf sublingual+vit d3 but he had hbsag 16iu/ml so it is very difficult to say if it was goleic gcmaf
oral colostrum MAF in enteric capsules form, any idea on this stef2011?
i have tried the similar product from gcmaf.eu, totally useless for hbv
Because I have no idea on where to get the injection
you do the injection yourself, you can use the subcutaneous diabetes injections, the needle is about 3mm, anybody can do it
i have tried the similar product from gcmaf.eu, totally useless for hbv
Because I have no idea on where to get the injection
you do the injection yourself, you can use the subcutaneous diabetes injections, the needle is about 3mm, anybody can do it
Complete regimen for battle with hbv-
TNF, ntz, pegifn, phyllanthus, andrographis, vit b complex, vit a,c,d,e, artesunate, zinc, selenium, cobalt, amino acid caps, a statin simvastatin or atorvastatin, liv52hb, iron
Gcmaf is not available in my country so can't do anything for that.
Lets c wat happens. Will keep updating my journey
TNF, ntz, pegifn, phyllanthus, andrographis, vit b complex, vit a,c,d,e, artesunate, zinc, selenium, cobalt, amino acid caps, a statin simvastatin or atorvastatin, liv52hb, iron
Gcmaf is not available in my country so can't do anything for that.
Lets c wat happens. Will keep updating my journey
The requested the inquiry for the one from Japan and they are saying they have oral colostrum MAF in enteric capsules form, any idea on this stef2011? Because I have no idea on where to get the injection in here better to have the capsule and have it.
gcmaf is available from:
gcmaf.se (the one i used goleic injections) and it is available
saisei mirai japan (they have a european distributor too)
other gcmaf produced for compassionate studies in belgium
approved in netherlands since many years but dont know if potency is good there
gcmaf.se (the one i used goleic injections) and it is available
saisei mirai japan (they have a european distributor too)
other gcmaf produced for compassionate studies in belgium
approved in netherlands since many years but dont know if potency is good there
But stef2011 gcmaf they don't have the one you always recommend i mean the probiotic currently they just got the Oleic gcmaf only, will this helps to the Hbver's stiff coz i just wanna try it to regress my fibrosisi?
another member tried it mono and did work.i also tried ntz and didn t work
i suggest you try gcmaf and high dose vit d3 instead which we sure know works to boost peg
i suggest you try gcmaf and high dose vit d3 instead which we sure know works to boost peg
I will start taking artesunate 200mg od from today 18th june15,, I have taken 5 doses of peginterferon 2b and taking nitazoxanide tenofovir and phyllanthus from 3months.
http://www.biomedexperts.com/Abstract.bme/11976732/Antiviral_activity_of_artesunate_towards_wild-type_recombinant_and_ganciclovir-resistant_human_cytomegaloviruses
Antiviral therapy of primary and recurrent infections with human cytomegalovirus is reserved for severe manifestations and faces several limitations. Presently candidates for novel drugs with lower adverse side effects and a minimized frequency of resistance formation are under investigation. Here we demonstrate that artesunate, an antimalaria drug with highly valuable pharmacological properties, possesses antiviral activity. A concentration-dependent inhibition of the replication of human cytomegaloviruses with wild-type phenotype was demonstrated in several cell lines. Inhibition was quantified using recombinant green fluorescent protein expressing virus variants. The IC50 values were in the same range for ganciclovir-sensitive and ganciclovir-resistant human cytomegalovirus, as calculated with 5.8+/-0.4 microM and 6.9+/-0.2 microM, respectively. This indicated a strong antiviral potential and a lack of cross-resistance. The optimal antiviral concentrations of artesunate were separable from those inducing cytotoxicity. In addition, the replication of viruses from three genera was seen to be artesunate-sensitive to varying degrees. This suggests a mechanism linked to cellular activation pathways. Both the protein levels and the DNA binding activity of the two virus-induced cellular transcription factors Sp1 and NF-kappaB were found to be markedly reduced in the presence of artesunate. We also analyzed the cellular signaling kinase phosphoinositide 3-kinase, required for the activation of factors such as Sp1 and NF-kappaB in infected fibroblasts. The phosphorylation of two downstream effectors of phosphoinositide 3-kinase, Akt and p70S6K, was markedly inhibited in the presence of artesunate. Thus, artesunate possesses attractive antiviral characteristics which are suggestively based on the interference with essential steps in the host cell kinase cascades.
Antiviral therapy of primary and recurrent infections with human cytomegalovirus is reserved for severe manifestations and faces several limitations. Presently candidates for novel drugs with lower adverse side effects and a minimized frequency of resistance formation are under investigation. Here we demonstrate that artesunate, an antimalaria drug with highly valuable pharmacological properties, possesses antiviral activity. A concentration-dependent inhibition of the replication of human cytomegaloviruses with wild-type phenotype was demonstrated in several cell lines. Inhibition was quantified using recombinant green fluorescent protein expressing virus variants. The IC50 values were in the same range for ganciclovir-sensitive and ganciclovir-resistant human cytomegalovirus, as calculated with 5.8+/-0.4 microM and 6.9+/-0.2 microM, respectively. This indicated a strong antiviral potential and a lack of cross-resistance. The optimal antiviral concentrations of artesunate were separable from those inducing cytotoxicity. In addition, the replication of viruses from three genera was seen to be artesunate-sensitive to varying degrees. This suggests a mechanism linked to cellular activation pathways. Both the protein levels and the DNA binding activity of the two virus-induced cellular transcription factors Sp1 and NF-kappaB were found to be markedly reduced in the presence of artesunate. We also analyzed the cellular signaling kinase phosphoinositide 3-kinase, required for the activation of factors such as Sp1 and NF-kappaB in infected fibroblasts. The phosphorylation of two downstream effectors of phosphoinositide 3-kinase, Akt and p70S6K, was markedly inhibited in the presence of artesunate. Thus, artesunate possesses attractive antiviral characteristics which are suggestively based on the interference with essential steps in the host cell kinase cascades.
http://cid.oxfordjournals.org/content/47/6/804.long
Activity Against Hepatitis B Virus (HBV)
the family Hepadnaviridae includes a group of highly species-specific viruses that all have a virus-encoded DNA polymerase with reverse-transcriptase activity [73–75]. One member of this family, human HBV, is characterized by a high level of hepatotropism. This virus belongs to the genus Orthohepadnavirus and is not cytopathic itself, although it may cause acute fulminant hepatitis [76] or chronic liver disease, which may progress to cirrhosis and, eventually, hepatocellular carcinoma [77]. In spite of the availability of an effective and safe vaccine against HBV, infection by this virus has remained a major worldwide health problem [78, 79]. Although several pharmacological strategies are currently being implemented to treat HBV-infected patients (i.e., the use of IFN and a nucleoside derivative, lamivudine), no effective antiviral therapy against HBV infection has yet been fully developed.
In a recent investigation [80], a panel of natural products derived from medicinal herbs used in traditional Chinese medicine has been assayed for anti-HBV activity. Among these products, artesunate displayed anti-HBV activity. HBV DNA release was inhibited at an IC(50) of 0.5 µM. Host cell viability was reduced at a concentration 40-times greater (20 µM). Moreover, the treatment potential is enhanced by synergistic effects with lamivudine and by the absence of drug-induced toxicity in host cells. This is important in clinical practice because of frequent cases of infection by lamivudine-resistant HBV strains.
The concentration at which artesunate was active against HBV (>10 µM) was similar to that previously reported for its activity against HCMV [59]. Interestingly, these levels are close to the drug concentrations achieved in the plasma of patients in whom this drug is used for anti-malarial treatment (∼7 µM) [81]. This result was similar to that reported elsewhere [82] for artesunate use in HepG2 2.2.15 cells.
Activity Against Hepatitis C Virus (HCV) and Related Viruses
The family Flaviviridae includes 3 genera: Pestivirus (e.g., bovine viral diarrhea virus), Flavivirus (e.g., Japanese encephalitis virus), and Hepacivirus (e.g., HCV). Pathogens of the family Flaviviridae constitute a major cause of disease worldwide. Infection with HCV frequently causes chronic hepatitis, which may progress to cirrhosis and hepatocellular carcinoma [83]. The problem is aggravated by the absence of an efficient vaccine against HCV and because the standard treatment (pegylated IFN-α and the purine nucleoside analogue ribavirin [1β-D-ribofuranosyl-1,2,4-triazole-3-carboxamide]), in addition to having adverse effects, is not effective in approximately one-half of infected patients [83]. Therefore, the search for more effective therapies is crucial. Because all members of the Flaviviridae share similarities in virion structure, genome organization, and replication machinery, some viruses, in particular bovine viral diarrhea virus, have been used as in vitro models [84].
The pharmacological interest in artemisinin and its derivatives for the treatment of infections by these viruses is increased by the severe limitations of currently available antiviral therapy. Because the mechanisms of action of IFN-α [85, 86] and ribavirin [86, 87] against Flaviviridae viruses are probably different than the mechanisms of artemisinin [88], it was possible that a combination of these drugs would demonstrate additive effects; indeed, additive effects were observed by Romero et al. [89]. IFN binds to cell surface receptors and stimulates signal pathways that lead to the activation of cellular enzymes that repress viral replication [85], whereas ribavirin, in addition to its immunomodulatory properties, has direct antiviral activities that can be ascribed to several possible mechanisms. These mechanisms include the inhibition of the HCV RNA–dependent RNA polymerase NS5B and ribavirin's activity as an RNA mutagen, which enables it to impair viral replication [90]. Paeshuyse et al. [91] reported that the antimalarial drug artemisinin inhibited HCV replicon replication in a dose-dependent manner in 2 HCV subgenomic replicon constructs at concentrations that did not affect Huh 5–2 host cells. Hemin, an iron donor, inhibits HCV replicon replication by inhibiting the viral polymerase [92]. The combination treatment of artemisinin and hemin had a pronounced synergistic antiviral activity without affecting host cells.
Activity Against Hepatitis B Virus (HBV)
the family Hepadnaviridae includes a group of highly species-specific viruses that all have a virus-encoded DNA polymerase with reverse-transcriptase activity [73–75]. One member of this family, human HBV, is characterized by a high level of hepatotropism. This virus belongs to the genus Orthohepadnavirus and is not cytopathic itself, although it may cause acute fulminant hepatitis [76] or chronic liver disease, which may progress to cirrhosis and, eventually, hepatocellular carcinoma [77]. In spite of the availability of an effective and safe vaccine against HBV, infection by this virus has remained a major worldwide health problem [78, 79]. Although several pharmacological strategies are currently being implemented to treat HBV-infected patients (i.e., the use of IFN and a nucleoside derivative, lamivudine), no effective antiviral therapy against HBV infection has yet been fully developed.
In a recent investigation [80], a panel of natural products derived from medicinal herbs used in traditional Chinese medicine has been assayed for anti-HBV activity. Among these products, artesunate displayed anti-HBV activity. HBV DNA release was inhibited at an IC(50) of 0.5 µM. Host cell viability was reduced at a concentration 40-times greater (20 µM). Moreover, the treatment potential is enhanced by synergistic effects with lamivudine and by the absence of drug-induced toxicity in host cells. This is important in clinical practice because of frequent cases of infection by lamivudine-resistant HBV strains.
The concentration at which artesunate was active against HBV (>10 µM) was similar to that previously reported for its activity against HCMV [59]. Interestingly, these levels are close to the drug concentrations achieved in the plasma of patients in whom this drug is used for anti-malarial treatment (∼7 µM) [81]. This result was similar to that reported elsewhere [82] for artesunate use in HepG2 2.2.15 cells.
Activity Against Hepatitis C Virus (HCV) and Related Viruses
The family Flaviviridae includes 3 genera: Pestivirus (e.g., bovine viral diarrhea virus), Flavivirus (e.g., Japanese encephalitis virus), and Hepacivirus (e.g., HCV). Pathogens of the family Flaviviridae constitute a major cause of disease worldwide. Infection with HCV frequently causes chronic hepatitis, which may progress to cirrhosis and hepatocellular carcinoma [83]. The problem is aggravated by the absence of an efficient vaccine against HCV and because the standard treatment (pegylated IFN-α and the purine nucleoside analogue ribavirin [1β-D-ribofuranosyl-1,2,4-triazole-3-carboxamide]), in addition to having adverse effects, is not effective in approximately one-half of infected patients [83]. Therefore, the search for more effective therapies is crucial. Because all members of the Flaviviridae share similarities in virion structure, genome organization, and replication machinery, some viruses, in particular bovine viral diarrhea virus, have been used as in vitro models [84].
The pharmacological interest in artemisinin and its derivatives for the treatment of infections by these viruses is increased by the severe limitations of currently available antiviral therapy. Because the mechanisms of action of IFN-α [85, 86] and ribavirin [86, 87] against Flaviviridae viruses are probably different than the mechanisms of artemisinin [88], it was possible that a combination of these drugs would demonstrate additive effects; indeed, additive effects were observed by Romero et al. [89]. IFN binds to cell surface receptors and stimulates signal pathways that lead to the activation of cellular enzymes that repress viral replication [85], whereas ribavirin, in addition to its immunomodulatory properties, has direct antiviral activities that can be ascribed to several possible mechanisms. These mechanisms include the inhibition of the HCV RNA–dependent RNA polymerase NS5B and ribavirin's activity as an RNA mutagen, which enables it to impair viral replication [90]. Paeshuyse et al. [91] reported that the antimalarial drug artemisinin inhibited HCV replicon replication in a dose-dependent manner in 2 HCV subgenomic replicon constructs at concentrations that did not affect Huh 5–2 host cells. Hemin, an iron donor, inhibits HCV replicon replication by inhibiting the viral polymerase [92]. The combination treatment of artemisinin and hemin had a pronounced synergistic antiviral activity without affecting host cells.
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