scispace - formally typeset
D

David R. Langley

Researcher at Bristol-Myers Squibb

Publications -  133
Citations -  5704

David R. Langley is an academic researcher from Bristol-Myers Squibb. The author has contributed to research in topics: Hepatitis C virus & Integrase. The author has an hindex of 39, co-authored 132 publications receiving 5311 citations. Previous affiliations of David R. Langley include University of Texas at Austin & ViiV Healthcare.

Papers
More filters
Journal ArticleDOI

Chemical genetics strategy identifies an HCV NS5A inhibitor with a potent clinical effect

TL;DR: These results provide the first clinical validation of an inhibitor of HCV NS5A, a protein with no known enzymatic function, as an approach to the suppression of virus replication that offers potential as part of a therapeutic regimen based on combinations ofHCV inhibitors.
Patent

Hepatitis C virus inhibitors

TL;DR: The present disclosure relates to compounds, compositions and methods for the treatment of hepatitis C virus (HCV) infection as mentioned in this paper, and also disclosed are pharmaceutical compositions containing such compounds and methods to use these compounds in the treatment.
Journal ArticleDOI

Selective interactions of cationic porphyrins with G-quadruplex structures.

TL;DR: This study provides the first experimental insight into how selectivity might be achieved for different G- quadruplexes by using structural variants within a single group of G-quadruplex-interactive drugs.
Journal ArticleDOI

Biochemical and genetic characterizations of a novel human immunodeficiency virus type 1 inhibitor that blocks gp120-CD4 interactions.

TL;DR: Mapping of resistance substitutions to the HIV-1 envelope, and the lack of compound activity against a CD4-independent viral infection confirm the gp120-CD4 interactions as the target in infected cells and validates gp120 as a viable target for small-molecule inhibitors.
Journal ArticleDOI

Inhibition of Hepatitis B Virus Polymerase by Entecavir

TL;DR: These studies explain the potency, mechanism, and cross-resistance profile of ETV against HBV and account for the successful treatment of naive and LVD- or ADV-experienced chronic HBV patients.