hbv dna

RG7834 (RO 7020322) is a highly selective and orally bioavailable inhibitor of HBV, targeting HBsAg, HBeAg, and HBV DNA with IC50s of 2.8 nM, 2.6 nM, and 3.2 nM, respectively, in dHepaRG Cells.

Oleana-2,12-dien-28-oic acid is an HBsAg and HBeAg inhibitor that significantly inhibits HBV deoxyribonucleic acid (HBV-DNA) replication in HepG2.2.15 cells, making it relevant for the study of hepatitis B virus infection.

ccc_R08 is an orally available HBV cccDNA inhibitor that reduces extracellular levels of HBV DNA, HBsAg, and HBeAg in a dose-dependent manner. ccc_R08 is investigational for use in the treatment of HBV infections. ccc_R08 has been shown to be effective in the treatment of hepatitis C virus (HCV).

Osalmid (Oxaphenamide) is a choleretic drug, inhibits ribonucleotide reductase activity by targeting ribonucleotide reductase small subunit M2 (RRM2).

Chlorogenic acid is a natural phenol found in honeysuckle. Chlorogenic acid has a wide range of biological activities including anti-inflammatory, antioxidant, antitumor, antimicrobial, and neuroprotective.

Tenofovir diphosphate TEA (TFV-DP TEA) is the triethylamine salt of TFV-DP, an ATP-competitive DNA polymerase inhibitor that inhibits HIV-1 reverse transcriptase. It has anti-HIV HBV potential through its incorporation into the viral DNA strand to terminate viral DNA synthesis and thus inhibit viral genome replication.

GLP-26 disrupts the encapsidation of pre-genomic RNA, causes nucleocapsid disassembly and reduces cccDNA pools. GLP-26 is a HBV capsid assembly modulators (CAM), inhibits HBV DNA replication in Hep AD38 system (IC50=3 nM), and reduces cccDNA by >90% at 1

Besifovir Dipivoxil (LB80380) maleate is an oral prodrug of LB80317. Besifovir Dipivoxil maleate is effective in hepatitis B virus (HBV) DNA suppression for both treatment-naive and lamivudine-resistant chronic hepatitis B (CHB) patients.

Famciclovir (BRL 42810) is a Herpes Simplex Virus Nucleoside Analog DNA Polymerase Inhibitor. The mechanism of action of famciclovir is as a DNA Polymerase Inhibitor, and DNA Polymerase Inhibitor.

HBV-IN-48, an HBV inhibitor, exhibits potent antiviral activity against HBV in HepDE19 cells, demonstrated by its EC 50 value of 0.005 μM. Additionally, it effectively reduces serum HBV DNA levels in mouse models of HBV infection.

Valtorcitabine is a DNA polymerase inhibitor that may be used in the treatment of HBV infection.

BA-AZT1 acts as an inhibitor of HBV polymerase (HBV polymerase) and sodium taurocholate cotransporting polypeptide (NTCP). It hinders the secretion of viral capsid proteins HBsAg and HBeAg, with IC50 values of 0.65 µM and 13.42 µM, respectively, and inhibits HBV DNA replication with an IC50 of 0.70 µM.

Alamifovir is an antiviral drug specific for HBV. It is a purine nucleotide analog prodrug that is active against wild-type and lamivudine-resistant HBV and acts by inhibiting viral DNA initiation and viral DNA packaging, thereby reducing HBV replication.

AT-130 is a HBV virus inhibitor with improved potency (IC50 = 0.13 μM) and reduced toxicity in the HepAD38 cell line. AT-130 blocks HBV replication at the level of viral RNA packaging.

Bentysrepinine, a novel anti-HBV agent, inhibits DNA-HBV and cccDNA activities for the treatment of hepatitis B virus (HBV)-infected hepatitis.

LB-80317, a DNA polymerase inhibitor, is used potentially for the potential treatment of hepatitis B virus infection.

Valtorcitabine dihydrochloride, a DNA polymerase inhibitor, is used potentially for the treatment of HBV infection.

Z060228 is an potent anti-HBV inhibitor. The HBV DNA replication was effectively inhibited by Z060228 in the supernatants of the HepG2.2.15 cells. Z060228 exhibited effects on the self-assembly of Cp149. SEC data revealed that Z060228 altered the equilibr

Destruxin B2 is a cyclic hexadepsipeptide mycotoxin that has been found in M. anisopliae and has antiviral, insecticidal, and phytotoxic activities.1,2,3 It inhibits secretion of hepatitis B virus surface antigen (HBsAg) by Hep3B cells expressing hepatitis B virus (HBV) DNA (IC50 = 1.3 μM).1 Destruxin B2 is toxic to Sf9 insect cells in an electric cell-substrate impedance sensing (ECIS) test with a 50% inhibitory concentration (ECIS50) value of 92 μM.4 It is also phytotoxic to B. napus leaves.3 |1. Yeh, S.F., Pan, W., Ong, G.-T., et al. Study of structure-activity correlation in destruxins, a class of cyclodepsipeptides possessing suppressive effect on the generation of hepatitis B virus surface antigen in human hepatoma cells. Biochem. Biophys. Res. Commun. 229(1), 65-72 (1996).|2. Male, K.B., Tzeng, Y.-M., Montes, J., et al. Probing inhibitory effects of destruxins from Metarhizium anisopliae using insect cell based impedance spectroscopy: Inhibition vs chemical structure. Analyst 134(7), 1447-1452 (2009).|3. Buchwaldt, L., and Green, H. Phytotoxicity of destruxin B and its possible role in the pathogenesis of Alternaria brassicae. Plant Pathol. 41(1), 55-63 (1992).

AZT triphosphate TFA (3'-Azido-3'-deoxythymidine-5'-triphosphate TFA) is a active triphosphate metabolite of Zidovudine (AZT). AZT triphosphate TFA exhibits antiretroviral activity and inhibits replication of HIV. AZT triphosphate TFA also inhibits the DNA polymerase of HBV. AZT triphosphate TFA activates the mitochondria-mediated apoptosis pathway[1][2][3]. Treatment with 100 μM Zidovudine (AZT) for 48h disrupts the mitochondrial tubular network via accumulation of AZT triphosphate (AZT-TP) in H9c2 cells. AZT triphosphate accumulation causes downregulation of Opa1 and upregulation of Drp1. AZT triphosphate causes mitochondrial dysfunction, increases the production of cytotoxic reactive oxygen species (ROS), and impairs the balance of the mitochondrial quality control system in H9c2 cell model established from rat embryonic myoblasts[1]. [1]. Ryosuke Nomura, et al. Azidothymidine-triphosphate Impairs Mitochondrial Dynamics by Disrupting the Quality Control System. Redox Biol. 2017 Oct;13:407-417. [2]. Takeya Sato, et al. Engineered Human tmpk/AZT as a Novel Enzyme/Prodrug Axis for Suicide Gene Therapy. Mol Ther. 2007 May;15(5):962-70. [3]. K Y Hostetler, et al. Enhanced Oral Absorption and Antiviral Activity of 1-O-octadecyl-sn-glycero-3-phospho-acyclovir and Related Compounds in Hepatitis B Virus Infection, in Vitro. Biochem Pharmacol. 1997 Jun 15;53(12):1815-22.

HBV-IN-4, a derivative of phthalazinone, functions as a potent, orally active inhibitor of HBV DNA replication, exhibiting an IC50 value of 14 nM. It effectively induces the formation of genome-free capsids, demonstrating significant anti-HBV potency[1].

Tenofovir diphosphate is an inhibitor of HIV reverse transcriptase (Kis = 0.022 and 1.55 μM for RNA and DNA, respectively) and hepatitis B virus (HBV) polymerase (Ki = 0.18 μM). It is selective for these enzymes over DNA polymerase α and β, as well as mitochondrial DNA polymerase γ (Kis = 5.2, 81.7, and 59.5 μM, respectively). Tenofovir diphosphate is formed intracellularly through phosphorylation of the prodrugs tenofovir and tenofovir disoproxil by nucleotide kinases. Increased levels of tenofovir diphosphate in isolated peripheral blood mononuclear cells (PBMCs) correlate with a decrease in the risk of simian HIV (SHIV) acquisition in a macaque model of rectal SHIV transmission.

HBV-IN-21 (Compound II-8b) is a potent inhibitor of HBV DNA replication with an IC50 of 2.2 μM and demonstrates favorable binding affinity (K D = 60.0 μM) for the HBV 4 capsid protein, enabling effective interaction [1].

HBV-IN-16 is a quinoline derivative, which has an effective inhibitory effect on covalent closed circular DNA (cccDNA). CccDNA is the template for viral RNA transcription and subsequent viral DNA generation. HBV-IN-16 has potential in the research of HBV infection.