A fusion inhibitor (FP-21399) for the treatment of human immunodeficiency virus infection: A phase I study

Journal of Infectious Diseases

Volumn 182, Issue 2, 2000, Pages 607-610

  Dezube, B J ^a   Dahl, T A ^b   Wong, T K ^b   Chapman, B ^a   Ono, M ^b   Yamaguchi, N ^b   Gillies, S D ^b   Bo Chen, L ^a   Crumpacker, C S ^a  

^a BETH ISRAEL DEACONESS MEDICAL CENTER   (United States)

^b Lexigen Pharmaceuticals   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FP 21399; NAPHTHALENE DERIVATIVE; UNCLASSIFIED DRUG;

ADULT; ARTICLE; CLINICAL ARTICLE; CLINICAL TRIAL; DRUG BLOOD LEVEL; DRUG CLEARANCE; DRUG DISTRIBUTION; DRUG ELIMINATION; DRUG HALF LIFE; DRUG TISSUE LEVEL; DRUG TOLERABILITY; FEMALE; HUMAN; HUMAN CELL; HUMAN IMMUNODEFICIENCY VIRUS INFECTION; INFUSION; LYMPH NODE; LYMPHOCYTE COUNT; MALE; PHASE 1 CLINICAL TRIAL; PRIORITY JOURNAL; SKIN DISCOLORATION; VIRUS ADSORPTION;

ADULT; ANTI-HIV AGENTS; CELL FUSION; CHLOROBENZENES; FEMALE; HIV INFECTIONS; HUMANS; MALE; MIDDLE AGED; NAPHTHALENES;

EID: 0033844736     PISSN: 00221899     EISSN: None     Source Type: Journal    
DOI: 10.1086/315703     Document Type: Article

References (5)

1. Coreceptors: Implications for HIV pathogenesis and therapy
2. The beta-chemokine receptors CCR3 and CCR5 facilitate infection by primary HIV-1 isolates
3. FP-21399 blocks HIV envelope protein-mediated membrane fusion and concentrates in lymph nodes
4. The bis-azo compound FP-21399 inhibits HIV-1 replication by preventing viral entry
5. Potent suppression of HIV-1 replication in humans by T-20, a peptide inhibitor of gp41-mediated virus entry