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Emtriva

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Emtriva

Emtriva

CLINICAL PHARMACOLOGY

Mechanism of Action

Emtricitabine is an antiviral drug.

Pharmacokinetics

Adults

The pharmacokinetics of emtricitabine were evaluated in healthy subjects and HIV-1- infected subjects. Emtricitabine pharmacokinetics are similar between these populations.

Figure 1 shows the mean steady-state plasma emtricitabine concentration-time profile in 20 HIV-1-infected subjects receiving EMTRIVA capsules.

Figure 1 : Mean (± 95% CI) Steady-State Plasma Emtricitabine Concentrations in HIV- 1-Infected Adults (N=20)

Mean (± 95% CI) Steady-State Plasma Emtricitabine Concentrations - Illustration

Absorption

Emtricitabine is rapidly and extensively absorbed following oral administration with peak plasma concentrations occurring at 1–2 hours post-dose. Following multiple dose oral administration of EMTRIVA capsules to 20 HIV-1-infected subjects, the (mean ± SD) steady-state plasma emtricitabine peak concentration (Cmax) was 1.8 ± 0.7 μg/mL and the area-under the plasma concentration-time curve over a 24-hour dosing interval (AUC) was 10.0 ± 3.1 μg·hr/mL. The mean steady state plasma trough concentration at 24 hours post-dose was 0.09 μg/mL. The mean absolute bioavailability of EMTRIVA capsules was 93% while the mean absolute bioavailability of EMTRIVA oral solution was 75%. The relative bioavailability of EMTRIVA oral solution was approximately 80% of EMTRIVA capsules.

The multiple dose pharmacokinetics of emtricitabine are dose proportional over a dose range of 25–200 mg.

Distribution

In vitro binding of emtricitabine to human plasma proteins was less than 4% and independent of concentration over the range of 0.02–200 μg/mL. At peak plasma concentration, the mean plasma to blood drug concentration ratio was ~1.0 and the mean semen to plasma drug concentration ratio was ~4.0.

Metabolism

In vitro studies indicate that emtricitabine is not an inhibitor of human CYP450 enzymes. Following administration of 14C-emtricitabine, complete recovery of the dose was achieved in urine (~86%) and feces (~14%). Thirteen percent (13%) of the dose was recovered in urine as three putative metabolites. The biotransformation of emtricitabine includes oxidation of the thiol moiety to form the 3'-sulfoxide diastereomers (~9% of dose) and conjugation with glucuronic acid to form 2'-O-glucuronide (~4% of dose). No other metabolites were identifiable.

Elimination

The plasma emtricitabine half-life is approximately 10 hours. The renal clearance of emtricitabine is greater than the estimated creatinine clearance, suggesting elimination by both glomerular filtration and active tubular secretion. There may be competition for elimination with other compounds that are also renally eliminated.

Effects of Food on Oral Absorption

EMTRIVA capsules and oral solution may be taken with or without food. Emtricitabine systemic exposure (AUC) was unaffected while Cmax decreased by 29% when EMTRIVA capsules were administered with food (an approximately 1000 kcal high-fat meal). Emtricitabine systemic exposure (AUC) and Cmax were unaffected when 200 mg EMTRIVA oral solution was administered with either a high-fat or low-fat meal.

Special Populations

Race, Gender

The pharmacokinetics of emtricitabine were similar in adult male and female subjects and no pharmacokinetic differences due to race have been identified.

Pediatric Patients

The pharmacokinetics of emtricitabine at steady state were determined in 77 HIV-1-infected pediatric subjects, and the pharmacokinetic profile was characterized in four age groups (Table 6). The emtricitabine exposure achieved in pediatric subjects receiving a daily dose of 6 mg/kg up to a maximum of 240 mg oral solution or a 200 mg capsule is similar to exposures achieved in adult subjects receiving a once-daily dose of 200 mg.

The pharmacokinetics of emtricitabine were studied in 20 neonates born to HIV-1- positive mothers. Each mother received prenatal and intrapartum combination antiretroviral therapy. Neonates received up to 6 weeks of zidovudine prophylactically after birth. The neonates were administered two short courses of emtricitabine oral solution (each 3 mg/kg once daily x 4 days) during the first 3 months of life. The AUC observed in neonates who received a daily dose of 3 mg/kg of emtricitabine was similar to the AUC observed in pediatric subjects ages 3 months to 17 years who received a daily dose of emtricitabine as a 6 mg/kg oral solution up to 240 mg or as a 200 mg capsule (Table 6).

Table 6 : Mean ± SD Pharmacokinetic Parameters by Age Groups for Pediatric Subjects and Neonates Receiving EMTRIVA Capsules or Oral Solution

Age HIV-1- exposed Neonates HIV-1-infected Pediatric Subjects
0-3 mo
(N=20)a
3-24 mo
(N=14)
25 mo-6 yr
(N=19)
7-12yr
(N=17)
13-17 yr
(N=27)
Formulation
  Capsule (n) 0 0 0 10 26
  Oral Solution (n) 20 14 19 7 1
Dose (mg/kg)b 3.1 (2.9-3.4) 6.1 (5.5-6.8) 6.1 (5.6-6.7) 5.6 (3.1-6.6) 4.4 (1.8-7.0)
Cmax (μg/mL) 1.6 ± 0.6 1.9 ± 0.6 1.9 ± 0.7 2.7 ± 0.8 2.7 ± 0.9
AUC (μg•hr/mL) 11.0 ± 4.2 8.7 ± 3.2 9.0 ± 3.0 12.6 ± 3.5 12.6 ± 5.4
T½ (hr) 12.1 ± 3.1 8.9 ± 3.2 11.3 ± 6.4 8.2 ± 3.2 8.9 ± 3.3
a Two pharmacokinetic evaluations were conducted in 20 neonates over the first 3 months of life. Median (range) age of infant on day of pharmacokinetic evaluation was 26 (5–81) days.
b Mean (range)

Geriatric Patients

The pharmacokinetics of emtricitabine have not been fully evaluated in the elderly.

Patients with Impaired Renal Function

The pharmacokinetics of emtricitabine are altered in subjects with renal impairment [See WARNINGS AND PRECAUTIONS]. In adult subjects with creatinine clearance less than 50 mL/min or with end-stage renal disease (ESRD) requiring dialysis, Cmax and AUC of emtricitabine were increased due to a reduction in renal clearance (Table 7). It is recommended that the dosing interval for EMTRIVA be modified in adult patients with creatinine clearance less than 50 mL/min or in adult patients with ESRD who require dialysis [See DOSAGE AND ADMINISTRATION]. The effects of renal impairment on emtricitabine pharmacokinetics in pediatric patients are not known.

Table 7: Mean ± SD Pharmacokinetic Parameters in Adult Subjects with Varying Degrees of Renal Function

Creatinine Clearance (mL/min) > 80
(N=6)
50-80
(N=6)
30-49
(N=6)
< 30
(N=5)
ESRDa < 30
(N=5)
Baseline creatinine clearance (mL/min) 107 ± 21 59.8 ± 6.5 40.9 ± 5.1 22.9 ± 5.3 8.8 ± 1.4
Cmax (μg/mL) 2.2 ± 0.6 3.8 ± 0.9 3.2 ± 0.6 2.8 ± 0.7 2.8 ± 0.5
AUC (μg•hr/mL) 11.8 ± 2.9 19.9 ± 1.2 25.1 ± 5.7 33.7± 2.1 53.2 ± 9.9
CL/F (mL/min) 302 ± 94 168 ± 10 138 ± 28 99 ± 6 64 ± 12
CLr (mL/min) 213 ± 89 121 ± 39 69 ± 32 30 ± 11 NAb
a ESRD subjects requiring dialysis
b NA = Not Applicable

Hemodialysis: Hemodialysis treatment removes approximately 30% of the emtricitabine dose over a 3-hour dialysis period starting within 1.5 hours of emtricitabine dosing (blood flow rate of 400 mL/min and a dialysate flow rate of 600 mL/min). It is not known whether emtricitabine can be removed by peritoneal dialysis.

Patients with Hepatic Impairment

The pharmacokinetics of emtricitabine have not been studied in subjects with hepatic impairment, however, emtricitabine is not metabolized by liver enzymes, so the impact of liver impairment should be limited.

Assessment of Drug Interactions

At concentrations up to 14-fold higher than those observed in vivo, emtricitabine did not inhibit in vitro drug metabolism mediated by any of the following human CYP isoforms: CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4. Emtricitabine did not inhibit the enzyme responsible for glucuronidation (uridine-5'- disphosphoglucuronyl transferase). Based on the results of these in vitro experiments and the known elimination pathways of emtricitabine, the potential for CYP mediated interactions involving emtricitabine with other medicinal products is low.

EMTRIVA has been evaluated in healthy volunteers in combination with tenofovir disoproxil fumarate (DF), zidovudine, indinavir, famciclovir, and stavudine. Tables 8 and 9 summarize the pharmacokinetic effects of coadministered drug on emtricitabine pharmacokinetics and effects of emtricitabine on the pharmacokinetics of coadministered drug.

Table 8 : Drug Interactions: Change in Pharmacokinetic Parameters for Emtricitabine in the Presence of the Coadministered Druga

Coadministered Drug Dose of Coadministered Drug (mg) Emtricitabine Dose (mg) N % Change of Emtricitabine Pharmacokinetic Parameters13 (90% CI)
Cmax AUC Cmin
Tenofovir DF 300 once daily x 7 days 200 once daily x 7 days 17 ↑ 20
(↑ 12 to ↑ 29)
Zidovudine 300 twice daily x 7 days 200 once daily x 7 days 27
Indinavir 800 x 1 200 x 1 12 NA
Famciclovir 500 x 1 200 x 1 12 NA
Stavudine 40 x 1 200 x 1 6 NA
a All interaction trials conducted in healthy volunteers.
b ↑ = Increase; ↓ = Decrease; ⇔ = No Effect; NA = Not Applicable

Table 9 : Drug Interactions: Change in Pharmacokinetic Parameters for Coadministered Drug in the Presence of Emtricitabinea

Coadministered Drug Dose of Coadministered Drug (mg) Emtricitabine Dose (mg) N % Change of Coadministered Drug Pharmacokinetic Parametersb (90% CI)
Cmax AUC Cmin
Tenofovir DF 300 once daily x 7 days 200 once daily x 7 days 17 ⇔  ⇔  ⇔ 
Zidovudine 300 twice daily x 7 days 200 once daily x 7 days 27 ↑ 17
(↑ 0 to ↑ 38)
↑ 13
(↑ 5 to↑ 20)
⇔ 
Indinavir 800 x 1 200 x 1 12 ⇔  ⇔  NA
Famciclovir 500 x 1 200 x 1 12 ⇔  ⇔  NA
Stavudine 40 x 1 200 x 1 6 ⇔  ⇔  NA
a All interaction trials conducted in healthy volunteers.
b ↑ = Increase; ↓ = Decrease; ↔ = No Effect; NA = Not Applicable

Microbiology

Mechanism of Action

Emtricitabine, a synthetic nucleoside analog of cytidine, is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits the activity of the HIV-1 reverse transcriptase by competing with the natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA which results in chain termination. Emtricitabine 5'-triphosphate is a weak inhibitor of mammalian DNA polymerase α, β, ε, and mitochondrial DNA polymerase γ.

Antiviral Activity

The antiviral activity in cell culture of emtricitabine against laboratory and clinical isolates of HIV-1 was assessed in lymphoblastoid cell lines, the MAGI-CCR5 cell line, and peripheral blood mononuclear cells. The 50% effective concentration (EC50) value for emtricitabine was in the range of 0.0013–0.64 μM (0.0003–0.158 μg/mL). In drug combination trials of emtricitabine with nucleoside reverse transcriptase inhibitors (abacavir, lamivudine, stavudine, tenofovir, zalcitabine, zidovudine), non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz, nevirapine), and protease inhibitors (amprenavir, nelfinavir, ritonavir, saquinavir), additive to synergistic effects were observed. Emtricitabine displayed antiviral activity in cell culture against HIV-1 clades A, B, C, D, E, F, and G (EC50 values ranged from 0.007–0.075 μM) and showed strain specific activity against HIV-2 (EC50 values ranged from 0.007–1.5 μM).

The in vivo activity of emtricitabine was evaluated in two clinical trials in which 101 subjects were administered 25–400 mg a day of EMTRIVA as monotherapy for 10– 14 days. A dose-related antiviral effect was observed, with a median decrease from baseline in plasma HIV-1 RNA of 1.3 log10 at a dose of 25 mg once daily and 1.7 log10 to 1.9 log10 at a dose of 200 mg once daily or twice daily.

Resistance

Emtricitabine-resistant isolates of HIV-1 have been selected in cell culture and in vivo. Genotypic analysis of these isolates showed that the reduced susceptibility to emtricitabine was associated with a substitution in the HIV-1 reverse transcriptase gene at codon 184 which resulted in an amino acid substitution of methionine by valine or isoleucine (M184V/I).

Emtricitabine-resistant isolates of HIV-1 have been recovered from some subjects treated with emtricitabine alone or in combination with other antiretroviral agents. In a clinical trial of treatment-naive subjects treated with EMTRIVA, didanosine, and efavirenz [See Clinical Studies], viral isolates from 37.5% of subjects with virologic failure showed reduced susceptibility to emtricitabine. Genotypic analysis of these isolates showed that the resistance was due to M184V/I substitutions in the HIV-1 reverse transcriptase gene.

In a clinical trial of treatment-naive subjects treated with either EMTRIVA, VIREAD, and efavirenz or zidovudine/lamivudine and efavirenz [See Clinical Studies], resistance analysis was performed on HIV-1 isolates from all confirmed virologic failure subjects with greater than 400 copies/mL of HIV-1 RNA at Week 144 or early discontinuation. Development of efavirenz resistance-associated substitutions occurred most frequently and was similar between the treatment arms. The M184V amino acid substitution, associated with resistance to EMTRIVA and lamivudine, was observed in 2/19 analyzed subject isolates in the EMTRIVA + VIREAD group and in 10/29 analyzed subject isolates in the lamivudine/zidovudine group. Through 144 weeks of Study 934, no subjects have developed a detectable K65R substitution in their HIV-1 as analyzed through standard genotypic analysis.

Cross Resistance

Cross-resistance among certain nucleoside analog reverse transcriptase inhibitors has been recognized. Emtricitabine-resistant isolates (M184V/I) were cross-resistant to lamivudine and zalcitabine but retained sensitivity in cell culture to didanosine, stavudine, tenofovir, zidovudine, and NNRTIs (delavirdine, efavirenz, and nevirapine). HIV-1 isolates containing the K65R substitution, selected in vivo by abacavir, didanosine, tenofovir, and zalcitabine, demonstrated reduced susceptibility to inhibition by emtricitabine. Viruses harboring substitutions conferring reduced susceptibility to stavudine and zidovudine (M41L, D67N, K70R, L210W, T215Y/F, K219Q/E) or didanosine (L74V) remained sensitive to emtricitabine. HIV-1 containing the K103N substitution associated with resistance to NNRTIs was susceptible to emtricitabine.

Clinical Studies

Treatment-Naive Adult Patients

Study 934

Data through 144 weeks are reported for Study 934, a randomized, open-label, activecontrolled multicenter clinical trial comparing EMTRIVA + tenofovir disoproxil fumarate (tenofovir DF) administered in combination with efavirenz versus zidovudine/lamivudine fixed-dose combination administered in combination with efavirenz in 511 antiretroviralnaive subjects. From Weeks 96 to 144 of the trial, subjects received EMTRIVA/tenofovir DF fixed-dose combination with efavirenz in place of EMTRIVA + tenofovir DF with efavirenz. Subjects had a mean age of 38 years (range 18–80), 86% were male, 59% were Caucasian and 23% were Black. The mean baseline CD4+ cell count was 245 cells/mm³ (range 2–1191) and median baseline plasma HIV-1 RNA was 5.01 log10 copies/mL (range 3.56–6.54). Subjects were stratified by baseline CD4+ cell count ( < or ≥ 200 cells/mm³); 41% had CD4+ cell counts < 200 cells/mm³ and 51% of subjects had baseline viral loads > 100,000 copies/mL. Treatment outcomes through 48 and 144 weeks for those subjects who did not have efavirenz resistance at baseline are presented in Table 10.

Table 10 : Outcomes of Randomized Treatment at Week 48 and 144 (Study 934)

Outcomes Week 48 Week 144
EMTRIVA +TDF +EFV
(N=244)
AZT/3TC +EFV
(N=243)
EMTRIVA + TDF +EFV
(N=227)a
AZT/3TC +EFV
(N=229)a
Responderb 84% 73% 71% 58%
Virologic failurec 2% 4% 3% 6%
  Rebound 1% 3% 2% 5%
  Never suppressed 0% 0% 0% 0%
  Change in antiretroviral regimen 1% 1% 1% 1%
Death <1% 1% 1% 1%
Discontinued due to adverse event 4% 9% 5% 12%
Discontinued for other reasonsd 10% 14% 20% 22%
a Subjects who were responders at Week 48 or Week 96 (HIV-1 RNA < 400 copies/mL) but did not consent to continue in the trial after Week 48 or Week 96 were excluded from analysis.
b Subjects achieved and maintained confirmed HIV-1 RNA < 400 copies/mL through Weeks 48 and 144.
c Includes confirmed viral rebound and failure to achieve confirmed < 400 copies/mL through Weeks 48 and 144.
d Includes lost to follow-up, subject withdrawal, noncompliance, protocol violation and other reasons.

Through Week 48, 84% and 73% of subjects in the EMTRIVA + tenofovir DF group and the zidovudine/lamivudine group, respectively, achieved and maintained HIV-1 RNA < 400 copies/mL (71% and 58% through Week 144). The difference in the proportion of subjects who achieved and maintained HIV-1 RNA < 400 copies/mL through 48 weeks largely results from the higher number of discontinuations due to adverse events and other reasons in the zidovudine/lamivudine group in this open-label trial. In addition, 80% and 70% of subjects in the EMTRIVA + tenofovir DF group and the zidovudine/lamivudine group, respectively, achieved and maintained HIV-1 RNA < 50 copies/mL through Week 48 (64% and 56% through Week 144). The mean increase from baseline in CD4+ cell count was 190 cells/mm³ in the EMTRIVA + tenofovir DF group and 158 cells/mm³ in the zidovudine/lamivudine group at Week 48 (312 and 271 cells/mm³ at Week 144).

Through 48 weeks, 7 subjects in the EMTRIVA + tenofovir DF group and 5 subjects in the zidovudine/lamivudine group experienced a new CDC Class C event (10 and 6 subjects through 144 weeks).

Study 301A

Study 301A was a 48 week double-blind, active-controlled multicenter clinical trial comparing EMTRIVA (200 mg once daily) administered in combination with didanosine and efavirenz versus stavudine, didanosine and efavirenz in 571 antiretroviral na´ve adult subjects. Subjects had a mean age of 36 years (range 18–69), 85% were male, 52% Caucasian, 16% African-American and 26% Hispanic. Subjects had a mean baseline CD4+ cell count of 318 cells/mm³ (range 5–1317) and a median baseline plasma HIV-1 RNA of 4.9 log10 copies/mL (range 2.6–7.0). Thirty-eight percent of subjects had baseline viral loads > 100,000 copies/mL and 31% had CD4+ cell counts < 200 cells/mL. Treatment outcomes are presented in Table 11 below.

Table 11 : Outcomes of Randomized Treatment at Week 48 (Study 301A)

Outcomes EMTRIVA + Didanosine + Efavirenz (N=286) Stavudine + Didanosine + Efavirenz (N=285)
Respondera 81% (78%) 68% (59%)
Virologic Failureb 3% 11%
Death 0% < 1%
Discontinuation Due to Adverse Event 7% 13%
Discontinuation for Other Reasonsc 9% 8%
a Subjects achieved and maintained confirmed HIV RNA < 400 copies/mL ( < 50 copies/mL) through Week 48.
b Includes subjects who failed to achieve virologic suppression or rebounded after achieving virologic suppression.
c Includes lost to follow-up, subject withdrawal, non-compliance, protocol violation and other reasons.

The mean increase from baseline in CD4+ cell count was 168 cells/mm³ for the EMTRIVA arm and 134 cells/mm³ for the stavudine arm.

Through 48 weeks in the EMTRIVA group, 5 subjects (1.7%) experienced a new CDC Class C event, compared to 7 subjects (2.5%) in the stavudine group.

Treatment-Experienced Adult Patients

Study 303

Study 303 was a 48 week, open-label, active-controlled multicenter clinical trial comparing EMTRIVA (200 mg once daily) to lamivudine, in combination with stavudine or zidovudine and a protease inhibitor or NNRTI in 440 adult subjects who were on a lamivudine-containing triple-antiretroviral drug regimen for at least 12 weeks prior to trial entry and had HIV-1 RNA ≤ 400 copies/mL.

Subjects were randomized 1:2 to continue therapy with lamivudine (150 mg twice daily) or to switch to EMTRIVA (200 mg once daily). All subjects were maintained on their stable background regimen. Subjects had a mean age of 42 years (range 22–80), 86% were male, 64% Caucasian, 21% African-American and 13% Hispanic. Subjects had a mean baseline CD4+ cell count of 527 cells/mm³ (range 37–1909), and a median baseline plasma HIV-1 RNA of 1.7 log10 copies/mL (range 1.7–4.0).

The median duration of prior antiretroviral therapy was 27.6 months. Treatment outcomes are presented in Table 12 below.

Table 12 : Outcomes of Randomized Treatment at Week 48 (Study 303)

Outcomes EMTRIVA + ZDV/d4T + NNRTI/PI
(N=294)
Lamivudine + ZDV/d4T + NNRTI/PI
(N=146)
Respondera 77% (67%) 82% (72%)
Virologic Failureb 7% 8%
Death 0% < 1%
Discontinuation Due to Adverse Event 4% 0%
Discontinuation for Other Reasonsc 12% 10%
a Subjects achieved and maintained confirmed HIV RNA < 400 copies/mL ( < 50 copies/mL) through Week 48.
b Includes subjects who failed to achieve virologic suppression or rebounded after achieving virologic suppression.
c Includes lost to follow-up, subject withdrawal, non-compliance, protocol violation and other reasons.

The mean increase from baseline in CD4+ cell count was 29 cells/mm³ for the EMTRIVA arm and 61 cells/mm³ for the lamivudine arm.

Through 48 weeks, in the EMTRIVA group 2 subjects (0.7%) experienced a new CDC Class C event, compared to 2 subjects (1.4%) in the lamivudine group.

Pediatric Patients

In three open-label, non-randomized clinical trials, emtricitabine was administered to 169 HIV-1 infected treatment-naive and experienced (defined as virologically suppressed on a lamivudine containing regimen for which emtricitabine was substituted for lamivudine) subjects between 3 months and 21 years of age. Subjects received once-daily EMTRIVA oral solution (6 mg/kg to a maximum of 240 mg/day) or EMTRIVA capsules (a single 200 mg capsule once daily) in combination with at least two other antiretroviral agents.

Subjects had a mean age of 7.9 years (range 0.3–21), 49% were male, 15% Caucasian, 61% Black and 24% Hispanic. Subjects had a median baseline HIV-1 RNA of 4.6 log10 copies/mL (range 1.7–6.4) and a mean baseline CD4+ cell count of 745 cells/mm³ (range 2–2650). Through 48 weeks of therapy, the overall proportion of subjects who achieved and sustained an HIV-1 RNA < 400 copies/mL was 86%, and < 50 copies/mL was 73%. The mean increase from baseline in CD4+ cell count was 232 cells/mm³ (- 945, +1512). The adverse reaction profile observed during these clinical trials was similar to that of adult subjects, with the exception of the occurrence of anemia and higher frequency of hyperpigmentation in children [See ADVERSE REACTIONS].

The pharmacokinetics of emtricitabine were studied in 20 neonates born to HIV-1- positive mothers. Each mother received prenatal and intrapartum combination antiretroviral therapy. Neonates received up to 6 weeks of zidovudine prophylactically after birth. The neonates were administered two short courses of emtricitabine oral solution (each 3 mg/kg once daily x 4 days) during the first 3 months of life. Emtricitabine exposures in neonates were similar to the exposures achieved in subjects ages 3 months to 17 years [See CLINICAL PHARMACOLOGY]. During the two short dosing periods on emtricitabine there were no safety issues identified in the treated neonates. All neonates were HIV-1 negative at the end of the trial; the efficacy of emtricitabine in preventing or treating HIV-1 could not be determined.

Last reviewed on RxList: 4/22/2013
This monograph has been modified to include the generic and brand name in many instances.

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