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Trizivir

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Trizivir

Trizivir

CLINICAL PHARMACOLOGY

Mechanism of Action

TRIZIVIR is an antiviral agent.

Pharmacokinetics

Pharmacokinetics in Adults

TRIZIVIR: In a single-dose, 3-way crossover bioavailability trial of 1 TRIZIVIR Tablet versus 1 ZIAGEN Tablet (300 mg), 1 EPIVIR Tablet (150 mg), plus 1 RETROVIR Tablet (300 mg) administered simultaneously in healthy subjects (n = 24), there was no difference in the extent of absorption, as measured by the area under the plasma concentration-time curve (AUC) and maximal peak concentration (Cmax), of all 3 components. One TRIZIVIR Tablet was bioequivalent to 1 ZIAGEN Tablet (300 mg), 1 EPIVIR Tablet (150 mg), plus 1 RETROVIR Tablet (300 mg) following single-dose administration to fasting healthy subjects (n = 24).

Abacavir: Following oral administration, abacavir is rapidly absorbed and extensively distributed. Binding of abacavir to human plasma proteins is approximately 50%. Binding of abacavir to plasma proteins was independent of concentration. Total blood and plasma drug-related radioactivity concentrations are identical, demonstrating that abacavir readily distributes into erythrocytes. The primary routes of elimination of abacavir are metabolism by alcohol dehydrogenase to form the 5'-carboxylic acid and glucuronyl transferase to form the 5'-glucuronide.

Lamivudine: Following oral administration, lamivudine is rapidly absorbed and extensively distributed. Binding to plasma protein is low. Approximately 70% of an intravenous dose of lamivudine is recovered as unchanged drug in the urine. Metabolism of lamivudine is a minor route of elimination. In humans, the only known metabolite is the trans-sulfoxide metabolite (approximately 5% of an oral dose after 12 hours).

Zidovudine: Following oral administration, zidovudine is rapidly absorbed and extensively distributed. Binding to plasma protein is low. Zidovudine is eliminated primarily by hepatic metabolism. The major metabolite of zidovudine is GZDV. GZDV AUC is about 3-fold greater than the zidovudine AUC. Urinary recovery of zidovudine and GZDV accounts for 14% and 74% of the dose following oral administration, respectively. A second metabolite, 3'-amino-3'-deoxythymidine (AMT), has been identified in plasma. The AMT AUC was one-fifth of the zidovudine AUC.

In humans, abacavir, lamivudine, and zidovudine are not significantly metabolized by cytochrome P450 enzymes.

The pharmacokinetic properties of abacavir, lamivudine, and zidovudine in fasting subjects are summarized in Table 3.

Table 3. Pharmacokinetic Parametersa for Abacavir, Lamivudine, and Zidovudine in Adults

Parameter Abacavir Lamivudine Zidovudine
Oral bioavailability (%) 86 ± 25 n = 6 86 ± 16 n=12 64 ± 10 n=5
Apparent volume of distribution (L/kg) 0.86 ± 0.15 n = 6 1.3 ± 0.4 n = 20 1.6 ±0.6 n = 8
Systemic clearance (L/hr/kg) 0.80 ± 0.24 n = 6 0.33 ± 0.06 n = 20 1.6 ±0.6 n = 6
Renal clearance (L/hr/kg) .007 ± .008 n = 6 0.22 ± 0.06 n = 20 0.34 ± 0.05 n = 9
Elimination half-life (hr) 1.45 ± 0.32 n = 20 5 to 7b 0.5 to 3b
a Data presented as mean ± standard deviation except where noted.
b Approximate range.

Effect of Food on Absorption of TRIZIVIR: Administration with food in a single-dose bioavailability trial resulted in lower Cmax, similar to results observed previously for the reference formulations. The average [90% CI] decrease in abacavir, lamivudine, and zidovudine Cmax was 32% [24% to 38%], 18% [10% to 25%], and 28% [13% to 40%], respectively, when administered with a high-fat meal, compared with administration under fasted conditions. Administration of TRIZIVIR with food did not alter the extent of abacavir, lamivudine, and zidovudine absorption (AUC), as compared with administration under fasted conditions (n = 24) [see DOSAGE AND ADMINISTRATION].

Special Populations

Renal Impairment: TRIZIVIR: Because lamivudine and zidovudine require dose adjustment in the presence of renal insufficiency, TRIZIVIR is not recommended for use in patients with creatinine clearance < 50 mL/min [see Use In Specific Populations].

Hepatic Impairment: TRIZIVIR: TRIZIVIR is contraindicated for patients with impaired hepatic function because TRIZIVIR is a fixed-dose combination and the dosage of the individual components cannot be adjusted. Abacavir is contraindicated in patients with moderate to severe hepatic impairment and dose reduction is required in patients with mild hepatic impairment.

Pregnancy: See Use In Specific Populations.

Abacavir and Lamivudine: No data are available on the pharmacokinetics of abacavir or lamivudine during pregnancy.

Zidovudine: Zidovudine pharmacokinetics have been studied in a Phase 1 trial of 8 women during the last trimester of pregnancy. As pregnancy progressed, there was no evidence of drug accumulation. The pharmacokinetics of zidovudine were similar to that of nonpregnant adults. Consistent with passive transmission of the drug across the placenta, zidovudine concentrations in neonatal plasma at birth were essentially equal to those in maternal plasma at delivery. Although data are limited, methadone maintenance therapy in 5 pregnant women did not appear to alter zidovudine pharmacokinetics. In a nonpregnant adult population, a potential for interaction has been identified [see Use in Specific Populations].

Nursing Mothers: See Use in Specific Populations.

Abacavir: No data are available on the pharmacokinetics of abacavir in nursing mothers.

Lamivudine: Samples of breast milk obtained from 20 mothers receiving lamivudine monotherapy (300 mg twice daily) or combination therapy (150 mg lamivudine twice daily and 300 mg zidovudine twice daily) had measurable concentrations of lamivudine.

Zidovudine: After administration of a single dose of 200 mg zidovudine to 13 HIV-infected women, the mean concentration of zidovudine was similar in human milk and serum [see Use In Specific Populations].

Pediatric Patients: TRIZIVTR is not intended for use in pediatric patients. TRIZIVIR is not recommended in adolescents who weigh less than 40 kg because it is a fixed-dose tablet that cannot be dose adjusted for this patient population.

Geriatric Patients: The pharmacokinetics of abacavir, lamivudine, and zidovudine have not been studied in subjects over 65 years of age.

Gender: Abacavir: A population pharmacokinetic analysis in HIV-1-infected male (n = 304) and female (n = 67) subjects showed no gender differences in abacavir AUC normalized for lean body weight.

Lamivudine and Zidovudine: A pharmacokinetic trial in healthy male (n = 12) and female (n = 12) subjects showed no gender differences in zidovudine exposure (AUC) or lamivudine (AUC) normalized for body weight. Race:

Abacavir: There are no significant differences between blacks and Caucasians in abacavir pharmacokinetics.

Lamivudine: There are no significant racial differences in lamivudine pharmacokinetics.

Zidovudine: The pharmacokinetics of zidovudine with respect to race have not been determined.

Drug Interactions: The drug interactions described below are based on trials conducted with the individual nucleoside analogues.

Cytochrome P450: In humans, abacavir, lamivudine, and zidovudine are not significantly metabolized by cytochrome P450 enzymes; therefore, it is unlikely that clinically significant drug interactions will occur with drugs metabolized through these pathways.

Glucuronyl Transferase: Due to the common metabolic pathways of abacavir and zidovudine via glucuronyl transferase, 15 HIV-1-infected subjects were enrolled in a crossover trial evaluating single doses of abacavir (600 mg), lamivudine (150 mg), and zidovudine (300 mg) alone or in combination. Analysis showed no clinically relevant changes in the pharmacokinetics of abacavir with the addition of lamivudine or zidovudine or the combination of lamivudine and zidovudine. Lamivudine exposure (AUC decreased 15%) and zidovudine exposure (AUC increased 10%) did not show clinically relevant changes with concurrent abacavir.

Lamivudine and Zidovudine: No clinically significant alterations in lamivudine or zidovudine pharmacokinetics were observed in 12 asymptomatic HIV-l-infected adult subjects given a single dose of zidovudine (200 mg) in combination with multiple doses of lamivudine (300mgql2hr).

Methadone: In a trial of 11 HIV-1-infected subjects receiving methadone-maintenance therapy (40 mg and 90 mg daily), with 600 mg of ZIAGEN twice daily (twice the currently recommended dose), oral methadone clearance increased 22% (90% CI: 6% to 42%) [see DRUG INTERACTIONS].

Ribavirin: In vitro data indicate ribavirin reduces phosphorylation of lamivudine, stavudine, and zidovudine. However, no pharmacokinetic (e.g., plasma concentrations or intracellular triphosphorylated active metabolite concentrations) or pharmacodynamic (e.g., loss of HIV-1/HCV virologic suppression) interaction was observed when ribavirin and lamivudine (n = 18), stavudine (n = 10), or zidovudine (n = 6) were coadministered as part of a multi-drug regimen to HIV-1/HCV co-infected subjects [see WARNINGS AND PRECAUTIONS].

The effects of other coadministered drugs on abacavir, lamivudine, or zidovudine are provided in Table 4.

Table 4. Effect of Coadministered Drugs on Abacavir, Lamivudine, and Zidovudine AUCa Note: ROUTINE DOSE MODIFICATION OF ABACAVIR, LAMIVUDINE, AND ZIDOVUDINE IS NOT WARRANTED WITH COADMINISTRATION OF THE FOLLOWING DRUGS.

Drugs That May Alter Lamivudine Blood Concentrations
Coadministered Drug and Dose Lamivudine Dose n Lamivudine Concentrations Concentration of Coadministered Drug
AUC Variability
Nelfinavir
750 mg q 8 hr x 7 to 10 days
single 150 mg 11 ↑10% 95% CI:
1% to 20%
Trimethoprim 160 mg/
Sulfamethoxazole 800 mg daily x 5 days
single 300 mg 14 ↑43% 90% CI:
32% to 55%
Drugs That May Alter Zidovudine Blood Concentrations
Coadministered Drug and Dose Zidovudine Dose n Zidovudine Concentrations Concentration of Coadministered Drug
AUC Variability
Atovaquone
750 mg q 12 hr with food
200 mg q 8 hr 14 ↑31% Range:
23% to 78%b
Clarithromycin
500 mg twice daily
100 mgq 4 hr x 7 days 4 ↓ 12% Range:
↓34% to ↑l4%
Not Reported
Fluconazole
400 mg daily
200 mg q 8 hr 12 ↑74% 95% CI:
54% to 98%
Not Reported
Methadone
30 to 90 mg daily
200 mg q 4 hr 9 ↑43% Range:
16% to 64%b
Nelfinavir
750 mg q 8 hr x 7 to 10 days
single 200 mg 11 ↓35% Range:
28% to 41%
Probenecid
500 mg q 6 hr x 2 days
2 mg/kg q 8 hr x 3 days 3 ↑l06% Range:
100% to 170%b
Not Assessed
Rifampin
600 mg daily x 14 days
200 mg q 8 hr x 14 days 8 ↓47% 90% CI:
41% to 53%
Not Assessed
Ritonavir
300 mg q 6 hr x 4 days
200 mg q 8 hr x 4 days 9 ↓25% 95% CI:
15% to 34%
Valproic acid
250 mg or 500 mg q 8 hr x 4 days
100 mg q 8 hr x 4 days 6 ↑80% Range:
64% to 130%b
Not Assessed
Drugs That May Alter Abacavir Blood Concentrations
Coadministered Drug and Dose Abacavir Dose n Abacavir Concentrations Concentration of Coadministered Drug
AUC Variability
Ethanol
0.7 g/kg
single 600 mg 24 ↑41% 90% CI:
35% to 48%
↑ = Increase; ↓ = Decrease; ↔ = no significant change; AUC = area under the concentration versus time curve; CI = confidence interval.
a See DRUG INTERACTIONS for additional information on drug interactions.
b Estimated range of percent difference.

Microbiology

Mechanism of Action

Abacavir: Abacavir is a carbocyclic synthetic nucleoside analogue. Abacavir is converted by cellular enzymes to the active metabolite, carbovir triphosphate (CBV-TP), an analogue of deoxyguanosine-5'-triphosphate (dGTP). CBV-TP inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA. The lack of a 3'-OH group in the incorporated nucleotide analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated. CBV-TP is a weak inhibitor of cellular DNA polymerases α, β, and γ.

Lamivudine: Lamivudine is a synthetic nucleoside analogue. Intracellularly, lamivudine is phosphorylated to its active 5'-triphosphate metabolite, lamivudine triphosphate (3TC-TP). The principal mode of action of 3TC-TP is inhibition of RT via DNA chain termination after incorporation of the nucleotide analogue. 3TC-TP is a weak inhibitor of cellular DNA polymerases α, β, and γ.

Zidovudine: Zidovudine is a synthetic nucleoside analogue. Intracellularly, zidovudine is phosphorylated to its active 5'-triphosphate metabolite, zidovudine triphosphate (ZDV-TP). The principal mode of action of ZDV-TP is inhibition of RT via DNA chain termination after incorporation of the nucleotide analogue. ZDV-TP is a weak inhibitor of the cellular DNA polymerases α and γ and has been reported to be incorporated into the DNA of cells in culture.

Antiviral Activity

Abacavir: The antiviral activity of abacavir against HIV-1 was evaluated against a T-cell tropic laboratory strain HlV-1IIIB in lymphoblastic cell lines, a monocyte/macrophage tropic laboratory strain HIV-1BaL in primary monocytes/macrophages, and clinical isolates in peripheral blood mononuclear cells. The concentration of drug necessary to effect viral replication by 50 percent (EC50) ranged from 3.7 to 5.8 µM (1 µM = 0.28 mcg/mL) and 0.07 to 1.0 µM against HlV-1IIIB and HIV-1BaL, respectively, and was 0.26 ± 0.18 µM against 8 clinical isolates. The EC50 values of abacavir against different HIV-1 clades (A-G) ranged from 0.0015 to 1.05 µM, and against HIV-2 isolates, from 0.024 to 0.49 µM. Abacavir had synergistic activity in cell culture in combination with the NRTI zidovudine, the non-nucleoside reverse transcriptase inhibitor (NNRTI) nevirapine, and the protease inhibitor (PI) amprenavir; and additive activity in combination with the NRTIs didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine. Ribavirin (50 µM) had no effect on the anti-HIV-1 activity of abacavir in cell culture.

Lamivudine: The antiviral activity of lamivudine against HIV-1 was assessed in a number of cell lines (including monocytes and fresh human peripheral blood lymphocytes) using standard susceptibility assays. EC50 values (50% effective concentrations) were in the range of 0.003 to 15 µM (1 µM = 0.23 mcg/mL). HIV-1 from therapy-naive subjects with no amino acid substitutions associated with resistance gave median EC50 values of 0.429 µM (range: 0.200 to 2.007 µM) from Virco (n = 92 baseline sa mples from COLA40263) and 2.35 µM (1.37 to 3.68 µM) from Monogram Biosciences (n = 135 baseline samples from ESS30009). The EC50 values of lamivudine against different HIV-1 clades (A-G) ranged from 0.001 to 0.120 µM, and against HIV-2 isolates from 0.003 to 0.120 µM in peripheral blood mononuclear cells. Ribavirin (50 µM) decreased the anti-HIV-1 activity of lamivudine by 3.5-fold in MT-4 cells.

Zidovudine: The antiviral activity of zidovudine against HIV-1 was assessed in a number of cell lines (including monocytes and fresh human peripheral blood lymphocytes). The EC50 and EC90 values for zidovudine were 0.01 to 0.49 µM (1 µM = 0.27 mcg/mL) and 0.1 to 9 µM, respectively. HIV-1 from therapy-naive subjects with no amino acid substitutions associated with resistance gave median EC50 values of 0.011 µM (range: 0.005 to 0.110 µM) from Virco (n = 92 baseline samples from COLA40263) and 0.0017 µM (0.006 to 0.0340 µM) from Monogram Biosciences (n = 135 baseline samples from ESS30009). The EC50 values of zidovudine against different HIV-1 clades (A-G) ranged from 0.00018 to 0.02 µM, and against HIV-2 isolates from 0.00049 to 0.004 µM. In cell culture drug combination studies, zidovudine demonstrates synergistic activity with the NRTIs abacavir, didanosine, lamivudine, and zalcitabine; the NNRTIs delavirdine and nevirapine; and the Pis indinavir, nelfinavir, ritonavir, and saquinavir; and additive activity with interferon alfa. Ribavirin has been found to inhibit the phosphorylation of zidovudine in cell culture.

Resistance

HIV-1 isolates with reduced sensitivity to abacavir, lamivudine, or zidovudine have been selected in cell culture and were also obtained from subjects treated with abacavir, lamivudine, and zidovudine, or the combination of lamivudine and zidovudine.

Abacavir: Genotypic analysis of isolates selected in cell culture and recovered from abacavir-treated subjects demonstrated that amino acid substitutions K65R, L74V, Yl 15F, and M184V/I in HIV-1 RT contributed to abacavir resistance. In a trial of subjects receiving abacavir once or twice daily in combination with lamivudine and efavirenz once daily, 39% (7/18) of the isolates from subjects who experienced virologic failure in the abacavir once-daily arm had a > 2.5-fold decrease in abacavir susceptibility with a median-fold decrease of 1.3 (range: 0.5 to 11) compared with 29% (5/17) of the failure isolates in the twice-daily arm with a median-fold decrease of 0.92 (range: 0.7 to 13).

Lamivudine: Genotypic analysis of isolates selected in cell culture and recovered from lamivudine-treated subjects showed that the resistance was due to a specific amino acid substitution in the HIV-1 RT at codon 184 changing the methionine to either valine or isoleucine (M184V/I).

Zidovudine: Genotypic analyses of the isolates selected in cell culture and recovered from zidovudine-treated subjects showed mutations in the HIV-1 RT gene resulting in 6 amino acid substitutions (M41L, D67N, K70R, L210W, T215Y or F, and K219Q) that confer zidovudine resistance. In general, higher levels of resistance were associated with greater number of mutations. In some subjects harboring zidovudine-resistant virus at baseline, phenotypic sensitivity to zidovudine was restored by 12 weeks of treatment with lamivudine and zidovudine. Combination therapy with lamivudine plus zidovudine delayed the emergence of substitutions conferring resistance to zidovudine.

Cross-Resistance

Cross-resistance has been observed among NRTIs.

Abacavir: Isolates containing abacavir resistance-associated amino acid substitutions, namely, K65R, L74V, Yl 15F, and Ml 84V, exhibited cross-resistance to didanosine, emtricitabine, lamivudine, tenofovir, and zalcitabine in cell culture and in subjects. The K65R substitution can confer resistance to abacavir, didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine; the L74V substitution can confer resistance to abacavir, didanosine, and zalcitabine; and the Ml 84V substitution can confer resistance to abacavir, didanosine, emtricitabine, lamivudine, and zalcitabine. An increasing number of thymidine analogue mutations (TAMs: M41L, D67N, K70R, L210W, T215Y/F, K219E/R/H/Q/N) is associated with a progressive reduction in abacavir susceptibility.

Lamivudine: Cross-resistance to abacavir, didanosine, tenofovir, and zalcitabine has been observed in some subjects harboring lamivudine-resistant HIV-1 isolates. In some subjects treated with zidovudine plus didanosine or zalcitabine, isolates resistant to multiple drugs, including lamivudine, have emerged (see under Zidovudine below). Cross-resistance between lamivudine and zidovudine has not been reported.

Zidovudine: In a trial of 167 HIV-infected subjects, isolates (n = 2) with multi-drug resistance to didanosine, lamivudine, stavudine, zalcitabine, and zidovudine were recovered from subjects treated for ≥ 1 year with zidovudine plus didanosine or zidovudine plus zalcitabine. The pattern of resistance-associated amino acid substitutions with such combination therapies was different (A62V, V75I, F77L, Fl 16Y, Q151M) from the pattern with zidovudine monotherapy, with the Q151M substitution being most commonly associated with multi-drug resistance. The substitution at codon 151 in combination with substitutions at 62, 75, 77, and 116 results in a virus with reduced susceptibility to didanosine, lamivudine, stavudine, zalcitabine, and zidovudine. TAMs are selected by zidovudine and confer cross-resistance to abacavir, didanosine, stavudine, tenofovir, and zalcitabine.

Animal Toxicology and/or Pharmacology

Myocardial degeneration was found in mice and rats following administration of abacavir for 2 years. The systemic exposures were equivalent to 7 to 24 times the expected systemic exposure in humans. The clinical relevance of this finding has not been determined.

Clinical Studies

The following trial was conducted with the individual components of TRIZIVIR [see CLINICAL PHARMACOLOGY].

CNA3005 was a multicenter, double-blind, controlled trial in which 562 HIV-l-infected, therapy-naive adults were randomized to receive either ZIAGEN (300 mg twice daily) plus COMBIVIR (lamivudine 150 mg/zidovudine 300 mg twice daily), or indinavir (800 mg 3 times a day) plus COMBIVIR twice daily. The trial was stratified at randomization by pre-entry plasma HIV-1 RNA 10,000 to 100,000 copies/mL and plasma HIV-1 RNA > 100,000 copies/mL. Trial participants were male (87%), Caucasian (73%), black (15%), and Hispanic (9%). At baseline the median age was 36 years,; the median pretreatment CD4+ cell count was 360 cells/mm3, and median plasma HIV-1 RNA was 4.8 log10 copies/mL. Proportions of subjects with plasma HIV-1 RNA < 400 copies/mL (using Roche AMPLICOR HIV-1 MONITOR® Test) through 48 weeks of treatment are summarized in Table 5.

Table 5. Outcomes of Randomized Treatment Through Week 48 (CNA3005)

Outcome ZIAGEN plus
Lamivudine/ Zidovudine
(n = 262)
Indinavir plus
Lamivudine/ Zidovudine
(n = 265)
Respondera 49% 50%
Virologic failureb 31% 28%
Discontinued due to adverse reactions 10% 12%
Discontinued due to other reasonsc 11% 10%
a Subjects achieved and maintained confirmed HIV-1 RNA < 400 copies/mL.
b Includes viral rebound and failure to achieve confirmed < 400 copies/mL by Week 48.
c Includes consent withdrawn, lost to follow-up, protocol violations, those with missing data, clinical progression, and other.

Treatment response by plasma HIV-1 RNA strata is shown in Table 6.

Table 6. Proportions of Responders Through Week 48 By Screening Plasma HIV-1 RNA Levels (CNA3005)

Screening
HIV-1 RNA (copies/mL)
ZIAGEN plus
Lamivudine/Zidovudine
(n = 262)
Indinavir plus
Lamivudine/Zidovudine
(n = 265)
< 400 copies/mL n < 400 copies/mL n
≥ 1 0,000 - ≤ 1 00,000 50% 166 48% 165
> 1 00,000 48% 96 52% 100

In subjects with baseline viral load > 100,000 copies/mL, percentages of subjects with HIV-1 RNA levels < 50 copies/mL were 31% in the group receiving abacavir vs. 45% in the group receiving indinavir.

Through Week 48, an overall mean increase in CD4+ cell count of about 150 cells/mm3 was observed in both treatment arms. Through Week 48, 9 subjects (3.4%) in the group receiving abacavir sulfate (6 CDC classification C events and 3 deaths) and 3 subjects (1.5%) in the group receiving indinavir (2 CDC classification C events and 1 death) experienced clinical disease progression.

REFERENCES

1. Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) Study Group. Lancet. 2008;371 (9622): 1417-1426.

Last reviewed on RxList: 6/7/2012
This monograph has been modified to include the generic and brand name in many instances.

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