No. entecavir 是从抑制艾滋病研发的,它可以抑制艾滋病毒。只是它的药效有多好的问题?
Entecavir, a drug approved by the Food and Drug Administration for the treatment of chronic hepatitis B virus (HBV) infection, is not believed to inhibit replication of human immunodeficiency virus type 1 (HIV-1) at clinically relevant doses. We observed that entecavir led to a consistent 1-log10 decrease in HIV-1 RNA in three persons with HIV-1 and HBV coinfection, and we obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replication 作者: lifflefield 时间: 2012-3-25 17:55
No. entecavir 是从抑制艾滋病研发的,它可以抑制艾滋病毒。只是它的药效有多好的问题?
Entecavir, a drug approved by the Food and Drug Administration for the treatment of chronic hepatitis B virus (HBV) infection, is not believed to inhibit replication of human immunodeficiency virus type 1 (HIV-1) at clinically relevant doses. We observed that entecavir led to a consistent 1-log10 decrease in HIV-1 RNA in three persons with HIV-1 and HBV coinfection, and we obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replication.
I know the paper you that you are quoting from. I find it difficult to understand how it can be "potent" yet only "partial" inhibitor of HIV replaction.
The following is from Wikipedia:
USES Entecavir is used to treat chronic hepatitis B. It also helps prevent the hepatitis B virus from multiplying and infecting new liver cells. Entecavir is also indicated for the treatment of chronic hepatitis B in adults with HIV/AIDS infection. However, entecavir is not active against HIV.
History
1992: SQ-34676 at Squibb as part of anti-herpes virus program[3]
1997: BMS 200475 developed at BMS pharmaceutical research institute as antiviral nucleoside analogue à Activity demonstrated against HBV, HSV-1, HCMV, VZV in cell lines & no or little activity against HIV or influenza[4]
Superior activity observed against HBV pushed research towards BMS 200475, its base analogues and its enantiomer against HBV in HepG2.2.15 cell line[4]
Comparison to other NAs, proven more selective potent inhibitor of HBV by virtue of being Guanine NA[5]
1998: Inhibition of hepadnaviral polymerases was demonstrated in vitro in comparison to a number of NAs-TP[6]
Metabolic studies showed more efficient phosphorylation to triphosphate active form[7]
3 year treatment of woodchuck model of CHB à sustained antiviral efficacy and prolonged life spans without detectable emergence of resistance[8]
Efficacy # LVD resistant HBV replication in vitro[9]
Superior activity compared to LVD invivo for both HBeAg + & HBeAg- patients[10][11]