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Fosamprenavir/
Ritonavir Once Daily in Treatment-naive HIV Patients Shows No PI
Resistance at 48 Weeks
Fosamprenavir (GW433908; Lexiva)
is a potent and durable HIV protease inhibitor (PI), the prodrug
of amprenavir, with a favorable safety profile as demonstrated by
two Phase III clinical trials in antiretroviral-naive patients.
Co-administration of fosamprenavir with low dose ritonavir
(Norvir) boosts exposure of amprenavir (APV), which facilitates
flexible dosing, including once daily (q.d.) dosing, and requires
no food or fluid restrictions.
The
purpose of the current study (The SOLO Study) was to investigate
the emergence of resistance to fosamprenavir, a protease inhibitor
(PI) with demonstrated antiviral efficacy, safety and tolerability,
when administered once daily (q.d.) with low dose ritonavir (fosamprenavir/r).
Preliminary
results of the SOLO Study were reported by HIV and Hepatitis.com
in 2002. Final results are published in the March 5, 2004 issue
of AIDS. Following is a brief summary of that review:
SOLO
was a 48-week Phase III open-label study in which antiretroviral
therapy-naive patients (n = 649) were treated with fosamprenavir/r,
(1400 mg/200 mg, q.d.) or nelfinavir (Viracept) [1250 mg, twice
daily (b.i.d.)] with two nucleoside reverse transcriptase inhibitors
(NRTI), abacavir (Ziagen) 300 mg, b.i.d. and lamivudine (Epivir)
150 mg, b.i.d.
Viral
genotype and phenotype were analyzed at baseline and on treatment
up to 48 weeks and beyond.
Results
Emergence
of genotypic resistance was significantly different between the
fosamprenavir/r q.d. and the nelfinavir b.i.d. treatment arms for
both PIs (0 versus 50%; P < 0.001) and the NRTI (13%
versus 69%; P < 0.001) received.
In
the nelfinavir arm the key protease mutations D30N and/or L90M were
frequently observed. The absence of protease resistance mutations
and reduced incidence of NRTI resistance mutations in the fosamprenavir/r
q.d. arm was confirmed by phenotyping, which showed a lack of PI
cross-resistance.
The
absence of resistance to fosamprenavir or cross-resistance to other
PIs, and reduced NRTI resistance, following a fosamprenavir/r q.d.
regimen supports the use of this boosted PI early in therapy.
Discussion
Analysis of the virological failure samples from patients in
SOLO have revealed significantly lower incidence of the emergence
of resistance to both the PI and NRTI components of the regimen
in the fosamprenavir/r q.d. arm compared with the NFV b.i.d. arm. No PI cross-resistance
was observed except in patient 1, where archival resistance mutations
contributed to phenotypic resistance to the six PIs tested.
Evaluation of the viral load profiles in the NFV b.i.d. and
fosamprenavir/r q.d. arms revealed differences associated with the slopes
of virological failure, and acquisition of mutations.
This suggested that rapid rebounds which possibly result from
stopping therapy are more frequently associated with few or no mutations,
whereas gradual rebound or ongoing replication, possibly due to
prolonged suboptimal drug exposure, are associated with acquisition
of mutations.
The high drug exposure of the fosamprenavir/r regimen would be consistent
with the greater genetic barrier producing a delay in the emergence
of resistance to both PIs and NRTI.
Questionnaire adherence data showed that the fosamprenavir/r q.d. regimen had higher overall adherence than the NFV b.i.d.
regimen, but that the fosamprenavir/r q.d. virological failures
were more frequently associated with poor adherence than the NFV
b.i.d. virological failures, suggesting a lower barrier to resistance
of the NFV arm.
In conclusion, the authors write, “The absence of emergent
protease resistance to fosamprenavir or cross-resistance to other PI and
reduced NRTI resistance during treatment with a fosamprenavir/r
q.d. regimen supports the use of this boosted PI early in the treatment
continuum.”
Note: The HIV protease inhibitor fosamprenavir (Lexiva) was
approved by the FDA for the treatment of HIV infection in October
2003.
03/26/04
Reference
S MacManus and others. GW433908/ritonavir once daily in antiretroviral
therapy-naive HIV-infected patients: absence of protease resistance
at 48 weeks. AIDS 18(4): 651-655. March 5, 2004.
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