51 results about "Entry inhibitor" patented technology

Compounds, compositions, and methods of treatment and prevention of HIV infection are disclosed. The compounds are pyrrolo[2,3-b]pyridines and pyrrolo[2,3-b]pyrimidine JAK inhibitors. Combinations of these JAK inhibitors and additional antiretroviral compounds, such as NRTI, NNRTI, integrase inhibitors, entry inhibitors, protease inhibitors, and the like, are also disclosed. In one embodiment, the combinations include a combination of adenine, cytosine, thymidine, and guanine nucleoside antiviral agents, optionally in further combination with at least one additional antiviral agent that works via a different mechanism than a nucleoside analog. This combination has the potential to eliminate the presence of HIV in an infected patient.

The invention provides a peptide triazole conjugate and derivatives thereof, and methods of its use. Further provided are an antibody to the peptide triazole conjugate, and a method of identifying an HIV-I entry inhibitor candidate.

The invention relates peptide entry inhibitors and methods of determining such inhibitors that are bindable to regions of viruses having class II E proteins, such as the dengue virus E protein, as candidates for in vivo anti-viral compounds.

The present invention features interferon-free therapies for the treatment of HCV. The therapies comprise administering 2R,6S,13aS,14aR,16aS,Z)-N-(cyclopropylsulfonyl)-6-(5-methylpyrazine-2-carboxamido)-5,16-dioxo-2-(phenanthridin-6-yloxy)-1,2,3,5,6,7,8,9,10,11,13a,14,14a,15,16,16a-exadecahydrocyclopropa[e]pyrrolo[1,2-a][1,4]diazacyclopentadecine-14a-carboxamide (Compound I), or a pharmaceutically acceptable salt thereof, and another anti-HCV agent. Preferably, the therapies are both interferon- and ribavirin-free. The other anti-HCV agent can be a HCV polymerase inhibitor, an HCV NS5A inhibitor, an HCV entry inhibitor, a cyclophilin inhibitor, or an internal ribosome entry site inhibitor. Preferably, the other anti-HCV agent is an HCV polymerase inhibitor. Also preferably, the other anti-HCV agent is an HCV NS5A inhibitor. Also preferably, the other anti-HCV agent is administered concurrently with Compound I or a pharmaceutically acceptable salt thereof. In another example, the other anti-HCV agent is administered sequentially with Compound I or a pharmaceutically acceptable salt thereof. In still another embodiment, Compound I (or a pharmaceutically acceptable salt thereof) is co-administered with two or more other anti-HCV agents. For instance, Compound I (or a pharmaceutically acceptable salt thereof) can be co-administered with an HCV polymerase inhibitor and an HCV NS5A inhibitor. For another instance, Compound I (or a pharmaceutically acceptable salt thereof) can be co-administered with two different HCV polymerase inhibitors (e.g., one is a nucleoside polymerase inhibitor and the other is a non-nucleoside polymerase inhibitor; or both are nucleoside polymerase inhibitors; or both are non-nucleoside polymerase inhibitor). In yet another example, Compound I (or a pharmaceutically acceptable salt thereof) is co-administered with another HCV protease inhibitor and an HCV polymerase inhibitor. In still another example, Compound I (or a pharmaceutically acceptable salt thereof) is administered with two different HCV NS5A inhibitors.

Methods for treating HIV positive patients, and purging and eradicating latent HIV virus from a patient's system, are disclosed. The bulk of viral load is eradicated using conventional antiretroviral (ARV) therapy. Compounds that encourage viral production in the latent cells are then administered, preferably without activating those cells, while maintaining the ARV therapy. The administration of compounds that encourage viral production in latent cells is cycled, and after around 7-10 cycles, the methods can virtually eliminate latent HIV in the patient. Ideally, the ARV regimen includes at least one integrase inhibitor, at least one entry inhibitor, such as a CCR5 antagonist, and at least one, and preferably two, reverse transcriptase inhibitors. The compounds that encourage viral production in latent cells ideally include a combination of prostratin or a prostratin analog and an HDAC inhibitor, such as butyrate, valproate, or SAHA.

The invention provides a peptide triazole conjugate and derivatives thereof, and methods of its use. The invention also provides an antibody to the peptide triazole conjugate. The invention further provides a method of identifying an HIV-1 entry inhibitor candidate.

The present invention relates generally to the use of recombinant adeno-associated viruses (rAAV) for gene delivery and more specifically to the use of rAAV to deliver genes encoding human immunodeficiency virus entry inhibitors to target cells in mammals.

The invention discloses low molecular weight carboxyl-reduced derivatives of fucosylated glycosaminoglycans (LCRG). The extent of carboxyl reduction is not less than 20%. Weight-average molecular weight of the LCRG is about 3000-20000Da, and monosaccharides comprise acetyl galactosamine (GalNAc), glucose (Glc) or glucuronic acid (GlcUA) and fucose (Fuc) or sulfates of fucose (shown as -OSO3-). The mole ratio of GalNAc, Glc (containing GlcUA), Fuc and -OSO3- is about 1: (1+-0.3): (1+-0.3): (3.0+-1.0). The LCRG is a potent human immunodeficiency virus (HIV) Type 1 entry inhibitor which acts on conserved regions and has the advantages of high activity against HIV Type 1, high therapeutic index and no-drug-resistance, and the LCRG can be used for preventing or curing HIV. The invention further provides a preparation method of the LCRG. The carboxyl-reduced derivatives of fucosylated glycosaminoglycans and medicinal compositions of the carboxyl-reduced derivatives can be prepared into injection agents, lyophilized powder or suppository and the like.

The invention discloses a fast-growing eucalyptus leaf extract, which is obtained by ultrasonically extracting the fast-growing eucalyptus leaves with a methanol aqueous solution with a volume concentration of 90%, and then separating them by a preparative high-efficiency liquid phase. The inventors used the in vitro cell TZM-bl-HIV-IIIB infection system to conduct research on anti-HIV-1 activity, and found that the cytotoxicity of Su Liuhao is very low, but it has obvious inhibitory effect on the replication of HIV-1. Using the TOA (Time of Addition) method to study the inhibitory mechanism of Su Liuhao on the HIV virus, it was found that the mode of action of Su Liuhao in inhibiting the virus is very similar to that of the clinical drug Enfuvirtide, and it may be a virus entry inhibitor. So far, there are few in vivo and in vitro research reports on the components of fast-growing eucalyptus leaves inhibiting HIV-1 replication. The present invention firstly proposes and confirms that the fast-growing eucalyptus leaves extract has good anti-HIV-1 activity, which provides a new method for the development of clinical AIDS drugs. choose.

The present invention relates to cyclic NTCP targeting peptides which are preS-derived peptides of hepatitis B virus (HBV). The present invention further relates to pharmaceutical compositions comprising at least one cyclic peptide. The present invention further relates to medical uses of said cyclic peptides and the pharmaceutical compositions, such as in the diagnosis, prevention and / or treatment of a liver disease or condition, and / or in the inhibition of HBV and / or HDV infection. The present invention further relates to methods of diagnosis, prevention and / or treatment of a liver disease or condition and / or the inhibition of HBV and / or HDV infection.