Version July 2025
Serious and sometimes fatal hypersensitivity reactions, with multiple organ involvement, have occurred with abacavir. Patients who carry the HLA-B*5701 allele are at a higher risk of a hypersensitivity reaction to abacavir; although, hypersensitivity reactions have occurred in patients who do not carry the HLA-B*5701 allele.
Abacavir/lamivudine/zidovudine is contraindicated in patients with a prior hypersensitivity reaction to abacavir and in HLA-B*5701-positive patients. All patients should be screened for the HLA-B*5701 allele prior to initiating therapy with abacavir/lamivudine/zidovudine or reinitiation of therapy with abacavir/lamivudine/zidovudine, unless patients have a previously documented HLA-B*5701 allele assessment. Discontinue abacavir/lamivudine/zidovudine immediately if a hypersensitivity reaction is suspected, regardless of HLA-B*5701 status and even when other diagnoses are possible.
Following a hypersensitivity reaction to abacavir, never restart abacavir/lamivudine/zidovudine or any other abacavir-containing product because more severe symptoms, including death, can occur within hours. Similar severe reactions have also occurred rarely following the reintroduction of abacavir-containing products in patient who have no history of abacavir hypersensitivity.
Zidovudine has been associated with hematologic toxicity, including neutropenia and severe anemia, particularly in patients with advanced HIV-1 disease.
Prolonged use of zidovudine has been associated with symptomatic myopathy.
Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues. Discontinue abacavir/lamivudine/zidovudine if clinical or laboratory findings suggestive of lactic acidosis or pronounced hepatotoxicity occur.
Severe acute exacerbations of hepatitis B have been reported in patients who are coinfected with hepatitis B virus (HBV) and HIV-1 and have discontinued lamivudine, which is one component of abacavir/lamivudine/zidovudine. Monitor hepatic function closely with both clinical and laboratory follow-up for at least several months in patients who discontinue abacavir/lamivudine/zidovudine and are coinfected with HIV-1 and HBV. If appropriate, initiation of anti-HBV therapy may be warranted.
Dosage guidance:
Dosage form information: Trizivir tablets (brand and generic) have been discontinued in the United States for >1 year.
HIV-1 infection, treatment: May use alone or in combination with other antiretroviral agents:
Children and Adolescents <40 kg: Not recommended; product is a fixed-dose combination
Children and Adolescents ≥40 kg: Oral: 1 tablet twice daily
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Pediatric patients ≥40 kg:
CrCl ≥50 mL/minute: No dosage adjustment necessary.
CrCl <50 mL/minute: Use not recommended (use individual antiretroviral agents to reduce dosage).
Pediatric patients ≥40 kg:
Mild impairment: Use is not recommended; use individual antiretroviral agents to reduce dosage.
Moderate to severe impairment: Use is contraindicated; safety, efficacy, and pharmacokinetic properties of abacavir have not been established.
(For additional information see "Abacavir, lamivudine, and zidovudine (United States and Canada: Not available): Drug information")
Dosage guidance:
Dosage form information: Trizivir tablets (brand and generic) have been discontinued in the United States for >1 year.
HIV-1 infection, treatment: Oral: One tablet (abacavir 300 mg/lamivudine 150 mg/zidovudine 300 mg) twice daily. Note: Triple nucleoside reverse transcriptase inhibitor regimens are not recommended in HIV treatment guidelines due to suboptimal virologic activity (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
CrCl ≥50 mL/minute: No dosage adjustment necessary.
CrCl <50 mL/minute: Use is not recommended (use dose-adjusted individual components).
Mild impairment (Child-Pugh class A): Use is not recommended (use dose-adjusted individual components).
Moderate to severe hepatic impairment (Child-Pugh Class B or C): Use is contraindicated.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. See individual agents as well as other combination products for additional information. Frequency not always defined.
Central nervous system: Headache (13%), fatigue (12%), malaise (12%), depression (6%), anxiety (5%)
Dermatologic: Skin rash (5%)
Endocrine & metabolic: Increased amylase (2%), increased serum triglycerides (grade 3-4: 2%), increased gamma-glutamyl transferase, redistribution of body fat
Gastrointestinal: Nausea (19%), nausea and vomiting (10%), diarrhea (7%), pancreatitis
Hematologic & oncologic: Neutropenia (5%)
Hepatic: Increased serum ALT (6%)
Hypersensitivity: Hypersensitivity (1% to 9%; based on abacavir component; higher risk in carriers of the HLA-B*5701 allele)
Immunologic: Immune reconstitution syndrome
Infection: Viral infection (5%)
Miscellaneous: Fever and chills (6%)
Neuromuscular & skeletal: Increased creatine phosphokinase (7%)
Respiratory: ENT infection (5%)
<1%, postmarketing, and/or case reports: Abdominal pain, abnormal breath sounds, allergic sensitization (including anaphylaxis), alopecia, anemia, anorexia, aplastic anemia, arthralgia, cardiomyopathy, decreased appetite, dizziness, dyspepsia, erythema multiforme, exacerbation of hepatitis B (posttreatment), gynecomastia, increased serum bilirubin, increased serum transaminases, insomnia, lactic acidosis, liver steatosis, lymphadenopathy, myalgia, myasthenia, oral mucosa hyperpigmentation, paresthesia, peripheral neuropathy, rhabdomyolysis, seizure, sleep disorder, splenomegaly, Stevens-Johnson syndrome, stomatitis, thrombocytopenia, urticaria, vasculitis, weakness, wheezing
Hypersensitivity to abacavir, lamivudine, zidovudine, or any component of the formulation; patients positive for HLA-B*5701 allele; moderate or severe hepatic impairment.
Canadian labeling: Additional contraindications (not in US labeling): Hepatic impairment (regardless of severity of impairment); ANC <750 cells/mm3; hemoglobin <7.5 g/dL or 4.65 mmol/L
Concerns related to adverse effects:
• Hematologic toxicity: [US Boxed Warning]: Zidovudine has been associated with hematologic toxicities (eg, neutropenia, anemia); use with caution in patients with bone marrow compromise (eg, granulocyte count <1,000 cells/mm3 or hemoglobin <9.5 g/dL). Frequent complete blood counts are recommended in patients with advanced HIV-1 disease. Dosage interruption may be needed if anemia or neutropenia develops.
• Hypersensitivity reactions: [US Boxed Warning]: Serious hypersensitivity reactions (sometimes fatal) have occurred in patients taking abacavir (in Trizivir). Patients who carry the HLA-B*5701 allele are at a higher risk for a hypersensitivity reaction to abacavir, although hypersensitivity reactions have occurred in patients who do not carry the HLA-B*5701 allele. All patients should be screened for the HLA-B*5701 allele prior to initiating therapy with Trizivir or reinitiation of therapy with Trizivir unless patients have had a previously documented HLA-B*5701 allele assessment. Discontinue Trizivir if a hypersensitivity reaction is suspected. Trizivir is contraindicated in patients who have the HLA-B*5701 allele or in patients with a prior hypersensitivity reaction to abacavir. Reintroduction of Trizivir or any other abacavir-containing product can result in life-threatening or fatal hypersensitivity reactions, even in patients who have no history of hypersensitivity to abacavir therapy. Such reactions can occur within hours. Additionally, allele-positive patients (including abacavir treatment naive) should have an allergy to abacavir documented in their medical record. Reactions usually occur within 6 weeks of starting abacavir (median time to onset: 9 days), although these reactions may occur at any time during therapy. These reactions usually include signs or symptoms in 2 or more of the following groups: fever; rash; gastrointestinal (eg, nausea, vomiting, diarrhea, abdominal pain); constitutional (eg, generalized malaise, fatigue, achiness); respiratory (eg, dyspnea, cough, pharyngitis). Other signs and symptoms include lethargy, headache, myalgia, edema, abnormal chest x-ray findings, arthralgia and paresthesia. Anaphylaxis, liver failure, renal failure, hypotension, adult respiratory distress syndrome, respiratory failure, myolysis, and death have occurred in association with hypersensitivity reactions. Physical findings (lymphadenopathy, mucous membrane lesions, and rash [maculopapular, urticarial or variable]) may occur. Erythema multiforme has also been reported. Laboratory abnormalities (eg, elevated liver function tests, elevated creatine phosphokinase, elevated creatinine, and lymphopenia) may occur. Trizivir should be permanently discontinued if hypersensitivity cannot be ruled out, even when other diagnoses are possible. Following a hypersensitivity reaction, Trizivir SHOULD NOT be restarted because more severe symptoms may occur within hours, including LIFE-THREATENING HYPOTENSION AND DEATH. If Trizivir is to be restarted following an interruption in therapy not associated with symptoms of a hypersensitivity reaction, carefully evaluate the patient for previously unsuspected symptoms of hypersensitivity. Do not restart if hypersensitivity is suspected or cannot be ruled out regardless of HLA-B*5701 status. If Trizivir is restarted, continually monitor for symptoms of a hypersensitivity reaction. Make the patient aware that reintroduction should only take place if medical care is readily accessible.
• Immune reconstitution syndrome: Patients may develop immune reconstitution syndrome resulting in the occurrence of an inflammatory response to an indolent or residual opportunistic infection during initial HIV treatment or activation of autoimmune disorders (eg, Graves disease, polymyositis, Guillain-Barré syndrome) later in therapy; further evaluation and treatment may be required.
• Lactic acidosis/hepatomegaly: [US Boxed Warning]: Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues. Female gender and obesity may increase the risk for development. Suspend treatment in any patient who develops clinical or laboratory findings suggestive of lactic acidosis or hepatotoxicity (transaminase elevation may/may not accompany hepatomegaly and steatosis).
• Lipoatrophy: May cause loss of subcutaneous fat, especially in the face, limbs, and buttocks. Lipoatrophy incidence and severity are related to cumulative exposure and may be only partially reversible; improvement may take months to years after switching to a regimen that does not contain zidovudine. Monitor patients for signs of lipoatrophy and consider switching to a non-zidovudine-containing regimen if lipoatrophy occurs.
• Myopathy: [US Boxed Warning]: Prolonged use of zidovudine has been associated with symptomatic myopathy and myositis.
• Pancreatitis: Pancreatitis has been observed with abacavir, lamivudine and zidovudine; rule out pancreatitis in patients who develop signs/symptoms (eg, nausea/vomiting, abdominal pain, elevated lipase, and amylase) during therapy.
Disease-related concerns:
• Chronic hepatitis B: [US Boxed Warning]: Exacerbation of hepatitis B (including fatalities) has been reported with discontinuation of lamivudine in coinfected HIV/HBV patients; monitor hepatic function (eg, serum ALT) and HBV viral DNA closely for several months after discontinuing Trizivir in coinfected patients.
• Coronary heart disease: Abacavir use has been associated with an increased risk of MI in some cohort studies (Elion 2018; HHS [ARV adult] 2023). Consider using with caution in patients with risks for coronary heart disease and minimizing modifiable risk factors (eg, hypertension, hyperlipidemia, diabetes mellitus, and smoking) prior to use.
• Lamivudine-resistant HBV: Emergence of HBV virus variants associated with resistance to lamivudine have been reported in HIV-1 infected subjects who have received lamivudine-containing antiretroviral regimens in the presence of HBV coinfection.
• Renal impairment: Trizivir, as a fixed-dose combination tablet, should not be used in patients with CrCl <50 mL/minute.
Special populations:
• Pediatric patients <40 kg: Trizivir, as a fixed-dose combination tablet, should not be used in patients <40 kg or those requiring dosage adjustment.
• Therapy-experienced patients: Patients with prolonged prior nucleoside reverse transcriptase inhibitor (NRTI) exposure or presence of HIV-1 isolates containing multiple mutations conferring resistance to NRTIs have limited response to abacavir. The potential for cross resistance between abacavir and other NRTIs should be considered when evaluating new regimens in therapy experienced patients.
The major clinical toxicity of lamivudine in pediatric patients is pancreatitis; discontinue therapy if clinical signs, symptoms, or laboratory abnormalities suggestive of pancreatitis occur. Abacavir may cause mild hyperglycemia; more common in pediatric patients.
Trizivir tablets (brand and generic) have been discontinued in the United States for >1 year.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Trizivir: Abacavir sulfate 300 mg, lamivudine 150 mg, and zidovudine 300 mg [DSC] [contains fd&c blue #2 (indigotine,indigo carmine)]
Generic: Abacavir sulfate 300 mg, lamivudine 150 mg, and zidovudine 300 mg [DSC]
Yes
Tablets (Trizivir Oral)
300-150-300 mg (per each): $32.19
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Generic: Abacavir sulfate 300 mg, lamivudine 150 mg, and zidovudine 300 mg [DSC]
The development of the abacavir hypersensitivity reaction has been associated with certain HLA genotypes (eg, HLA-B*5701, HLA-DR7, HLA-DQ3) which may help predict which patients are at risk for developing the abacavir hypersensitivity reaction (Hetherington 2002; Lucas 2007; Mallal 2002). Patients who test positive for the HLA-B*5701 allele should have an abacavir allergy recorded in their medical record and should not receive abacavir. All patients who receive abacavir (and their caregivers) should be educated about the risk of abacavir hypersensitivity reactions (including patients who test negative for the HLA-B*5701 allele, as the risk for the reaction is not completely eliminated). Approximately 4% of patients who test negative for the HLA-B*5701 allele will experience a clinically suspected abacavir hypersensitivity reaction compared to 61% of those who test positive for the HLA-B*5701 allele.
The prevalence of HLA-B*5701 in the United States has been estimated to be 8% in Caucasians, 2.5% in African-Americans, 2% in Hispanics, 1% in Asians; in the sub-Saharan Africa it is <1%. Pretherapy identification of HLA-B*5701-positive patients and subsequent avoidance of abacavir therapy in these patients has been shown to significantly reduce the occurrence of abacavir-associated hypersensitivity reactions. A skin patch test is in development for clinical screening purposes; however, only PCR-mediated genotyping methods are currently in clinical practice use for documentation of this susceptibility marker. A familial predisposition to the abacavir hypersensitivity reaction has been reported; use abacavir with great caution in children of parents who experience a hypersensitivity reaction to abacavir (Peyriére 2001).
Reverse transcriptase mutations of K65R, L74V, Y115F, and M184V have been associated with abacavir resistance; at least 2 to 3 mutations are needed to decrease HIV susceptibility by 10-fold. The presence of a multiple number of these abacavir resistance-associated mutations may confer cross-resistance for other nucleoside or nucleotide reverse transcriptase inhibitors (eg, didanosine, emtricitabine, lamivudine, zalcitabine, or tenofovir). A progressive decrease in abacavir susceptibility is associated with an increasing number of thymidine analogue mutations (TAMs; M41L, D67N, K70R, L210W, T215Y/F, K219E/R/H/Q/N).
Oral: May be administered without regard to meals.
Administer without regard to food.
Abacavir and zidovudine are hazardous agents (NIOSH 2024 [table 2]).
Use appropriate precautions for receiving, handling, storage, preparation, dispensing, transporting, administration, and disposal. Follow NIOSH and USP 800 recommendations and institution-specific policies/procedures for appropriate containment strategy (NIOSH 2023; NIOSH 2024; USP-NF 2020).
Note: Facilities may perform risk assessment of some hazardous drugs to determine if appropriate for alternative handling and containment strategies (USP-NF 2020). Refer to institution-specific handling policies/procedures.
Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F).
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/021205s038lbl.pdf#page=34, must be dispensed with this medication. A Warning Card (summarizing symptoms of hypersensitivity), which is available with the product information, must also be dispensed with this medication for each new outpatient prescription and refill.
Treatment of HIV-1 infection, either alone or in combination with other antiretroviral agents (FDA approved in pediatric patients ≥40 kg and adults); Note: HIV regimens consisting of three antiretroviral agents are strongly recommended; Note: Data on the use of this triple NRTI combination regimen in patients with baseline viral loads >100,000 copies/mL is limited.
Refer to individual components.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program
5-Aminosalicylic Acid Derivatives: May increase myelosuppressive effects of Myelosuppressive Agents. Risk C: Monitor
Acemetacin: May increase adverse/toxic effects of Zidovudine. Specifically, the risk for hematologic toxicity may be increased. Risk C: Monitor
Amodiaquine: Zidovudine may increase neutropenic effects of Amodiaquine. Management: Avoid coadministration of zidovudine-containing antiretroviral therapy with amodiaquine when possible. If combined, monitor closely for neutropenia. Risk D: Consider Therapy Modification
Antithyroid Agents: Myelosuppressive Agents may increase neutropenic effects of Antithyroid Agents. Risk C: Monitor
Arimoclomol: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Atidarsagene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Atidarsagene Autotemcel. Risk X: Avoid
BCG (Intravesical): Myelosuppressive Agents may decrease therapeutic effects of BCG (Intravesical). Myelosuppressive Agents may increase adverse/toxic effects of BCG (Intravesical). Risk X: Avoid
Betibeglogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Betibeglogene Autotemcel. Risk X: Avoid
Cabozantinib: MRP2 Inhibitors may increase serum concentration of Cabozantinib. Risk C: Monitor
Chloramphenicol (Ophthalmic): May increase adverse/toxic effects of Myelosuppressive Agents. Risk C: Monitor
Chloramphenicol (Systemic): Myelosuppressive Agents may increase myelosuppressive effects of Chloramphenicol (Systemic). Risk X: Avoid
Cladribine: Agents that Undergo Intracellular Phosphorylation may decrease therapeutic effects of Cladribine. Risk X: Avoid
Clarithromycin: May increase myelosuppressive effects of Zidovudine. Clarithromycin may decrease serum concentration of Zidovudine. Management: Monitor response to zidovudine closely when used with clarithromycin, and consider staggering zidovudine and clarithromycin doses when possible in order to minimize the potential for interaction. Risk D: Consider Therapy Modification
CloZAPine: Myelosuppressive Agents may increase adverse/toxic effects of CloZAPine. Specifically, the risk for neutropenia may be increased. Risk C: Monitor
Deferiprone: Myelosuppressive Agents may increase neutropenic effects of Deferiprone. Management: Avoid the concomitant use of deferiprone and myelosuppressive agents whenever possible. If this combination cannot be avoided, monitor the absolute neutrophil count more closely. Risk D: Consider Therapy Modification
Dexketoprofen: May increase adverse/toxic effects of Zidovudine. Risk C: Monitor
DOXOrubicin (Conventional): May decrease therapeutic effects of Zidovudine. DOXOrubicin (Conventional) may increase adverse/toxic effects of Zidovudine. Management: Avoid concomitant use of doxorubicin and zidovudine due to the possibility of reduced zidovudine efficacy and increased myelosuppressive effects. Risk D: Consider Therapy Modification
DOXOrubicin (Liposomal): May decrease therapeutic effects of Zidovudine. DOXOrubicin (Liposomal) may increase adverse/toxic effects of Zidovudine. Management: Avoid concomitant use of doxorubicin and zidovudine. Reduced efficacy of zidovudine is possible based on in vitro data. Also, increased myelosuppressive effects are possible with combined administration. Risk D: Consider Therapy Modification
Elivaldogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Elivaldogene Autotemcel. Management: Avoid use of antiretroviral medications for at least one month, or for the amount of time required for elimination of the retroviral medication, prior to stem cell mobilization and until the all apheresis cycles are finished Risk X: Avoid
Fedratinib: May increase serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Fedratinib: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Fexinidazole: Myelosuppressive Agents may increase myelosuppressive effects of Fexinidazole. Risk X: Avoid
Foslevodopa: May increase serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Ganciclovir-Valganciclovir: May increase adverse/toxic effects of Zidovudine. Specifically, hematologic toxicity may be enhanced. Risk C: Monitor
Gilteritinib: May increase serum concentration of OCT1 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Givinostat: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Interferons: May increase adverse/toxic effects of Zidovudine. Interferons may decrease metabolism of Zidovudine. Risk C: Monitor
Levomethadone: May decrease therapeutic effects of Abacavir. Abacavir may decrease serum concentration of Levomethadone. Risk C: Monitor
Levomethadone: May increase serum concentration of Zidovudine. Risk C: Monitor
Linezolid: May increase myelosuppressive effects of Myelosuppressive Agents. Risk C: Monitor
Lopinavir: May decrease serum concentration of Zidovudine. Risk C: Monitor
Lovotibeglogene Autotemcel: Antiretroviral Agents may decrease therapeutic effects of Lovotibeglogene Autotemcel. Risk X: Avoid
Methadone: May decrease therapeutic effects of Abacavir. Abacavir may decrease serum concentration of Methadone. Risk C: Monitor
Methadone: May increase serum concentration of Zidovudine. Risk C: Monitor
Nelfinavir: May decrease serum concentration of Zidovudine. Risk C: Monitor
Nirmatrelvir and Ritonavir: May decrease serum concentration of Zidovudine. Risk C: Monitor
Olaparib: Myelosuppressive Agents may increase myelosuppressive effects of Olaparib. Risk C: Monitor
Orlistat: May decrease serum concentration of Antiretroviral Agents. Risk C: Monitor
Probenecid: May increase serum concentration of Zidovudine. Risk C: Monitor
Promazine: May increase myelosuppressive effects of Myelosuppressive Agents. Risk C: Monitor
Raltegravir: May increase myopathic (rhabdomyolysis) effects of Zidovudine. Risk C: Monitor
Ribavirin (Oral Inhalation): Zidovudine may increase adverse/toxic effects of Ribavirin (Oral Inhalation). Specifically, the risk/severity of anemia may be increased. Management: Due to significantly increased risk of anemia, consider even closer monitoring for anemia than routinely recommended. Alternative therapies should be considered when clinically possible, particularly for patients with other risk factors. Risk D: Consider Therapy Modification
Ribavirin (Systemic): Zidovudine may increase adverse/toxic effects of Ribavirin (Systemic). Specifically, the risk/severity of anemia may be increased. Management: Due to significantly increased risk of anemia, consider even closer monitoring for anemia than routinely recommended for ribavirin. Alternative therapies should be considered when clinically possible, particularly for patients with other risk factors. Risk D: Consider Therapy Modification
RifAMPin: May decrease serum concentration of Zidovudine. Risk C: Monitor
Riociguat: Abacavir may increase serum concentration of Riociguat. Risk C: Monitor
Risdiplam: May increase serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of risdiplam with MATE substrates if possible. If the combination cannot be avoided, monitor closely for adverse effects. Consider a reduced dose of the MATE substrate according to that substrate's labeling if appropriate. Risk D: Consider Therapy Modification
Ritonavir: May decrease serum concentration of Zidovudine. Risk C: Monitor
Ropeginterferon Alfa-2b: Myelosuppressive Agents may increase myelosuppressive effects of Ropeginterferon Alfa-2b. Management: Avoid coadministration of ropeginterferon alfa-2b and other myelosuppressive agents. If this combination cannot be avoided, monitor patients for excessive myelosuppressive effects. Risk D: Consider Therapy Modification
Sorbitol: May decrease serum concentration of LamiVUDine. Management: When possible, avoid chronic coadministration of sorbitol-containing solutions with lamivudine, but if this combination cannot be avoided, monitor patients more closely for possible therapeutic failure associated with decreased lamivudine exposure. Risk D: Consider Therapy Modification
Stavudine: Zidovudine may decrease therapeutic effects of Stavudine. Risk X: Avoid
Tafenoquine: May increase serum concentration of MATE1/2-K Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of MATE substrates with tafenoquine, and if the combination cannot be avoided, monitor closely for evidence of toxicity of the MATE substrate and consider a reduced dose of the MATE substrate according to that substrate's labeling. Risk D: Consider Therapy Modification
Tafenoquine: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of OCT2 substrates with tafenoquine, and if the combination cannot be avoided, monitor closely for evidence of toxicity of the OCT2 substrate and consider a reduced dose of the OCT2 substrate according to that substrate's labeling. Risk D: Consider Therapy Modification
Tenoxicam: May increase adverse/toxic effects of Zidovudine. Risk C: Monitor
Tipranavir: May decrease serum concentration of Zidovudine. Risk C: Monitor
Trimethoprim: May increase serum concentration of LamiVUDine. Risk C: Monitor
Trimethoprim: Zidovudine may increase neutropenic effects of Trimethoprim. Trimethoprim may increase serum concentration of Zidovudine. Risk C: Monitor
Valproic Acid and Derivatives: May increase serum concentration of Zidovudine. Risk C: Monitor
Vimseltinib: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and OCT2 substrates when possible. If combined, monitor for increased effects and toxicities of the OCT2 substrate and consider dose adjustments. Risk D: Consider Therapy Modification
This fixed-dose combination of abacavir, lamivudine, and zidovudine is not a preferred or alternative regimen in patients who are not yet pregnant but are trying to conceive (HHS [perinatal] 2024).
Refer to individual monographs for additional information.
This fixed-dose combination regimen of abacavir, lamivudine, and zidovudine should not be used during pregnancy. Patients who become pregnant while taking this combination should be changed to a recommended regimen (HHS [perinatal] 2024).
Refer to individual monographs for additional information.
HLA-B*5701 genotype status prior to initiating therapy or resuming therapy in patients of unknown HLA-B*5701 status (including patients previously tolerating therapy); signs and symptoms of abacavir hypersensitivity reaction (in all patients, but especially in those untested for the HLA-B*5701 allele)
Note: The absolute CD4 cell count is currently recommended to monitor immune status in children of all ages; CD4 percentage can be used as an alternative in children <5 years of age. This recommendation is based on the use of absolute CD4 cell counts in the current pediatric HIV infection stage classification and as thresholds for urgency of initiation of antiretroviral treatment (HHS [pediatric] 2017).
Prior to initiation of therapy: Genotypic resistance testing, CD4 and viral load (every 3 to 4 months), CBC with differential, LFTs, BUN, creatinine, electrolytes, glucose, urinalysis (every 6 to 12 months), hepatitis B screening (if previously demonstrated no immunity to hepatitis B), and assessment of readiness for adherence with medication regimen. At initiation and with any change in treatment regimen: CBC with differential, electrolytes, calcium, phosphate, glucose, LFTs, bilirubin, urinalysis (at initiation), BUN, creatinine, albumin, total protein, lipid panel (at initiation), CD4, and viral load. After 1 to 2 weeks of therapy: Signs of medication toxicity and adherence. After 2 to 4 weeks of therapy: CBC with differential, viral load, signs of medication toxicity and adherence; then every 3 to 4 months: CBC with differential, electrolytes, glucose, LFTs, bilirubin, BUN, creatinine, CD4, viral load, signs of medication toxicity, and adherence. Lipid panel and urinalysis every 6 to 12 months. CD4 monitoring frequency may be decreased to every 6 to 12 months in children who are adherent to therapy if the value is well above the threshold for opportunistic infections, viral suppression is sustained, and the clinical status is stable for more than 2 to 3 years. In patients with known or suspected complex drug resistance patterns, phenotypic resistance testing (usually in addition to genotypic resistance testing) should be performed (HHS [pediatric] 2017). Monitor for growth and development, signs of HIV-specific physical conditions, HIV disease progression, opportunistic infections, hepatotoxicity, anemia, pancreatitis, or lactic acidosis; serum creatine kinase
The combination of abacavir, lamivudine, and zidovudine is believed to act synergistically to inhibit reverse transcriptase via DNA chain termination after incorporation of the nucleoside analogue as well as to delay the emergence of mutations conferring resistance.
Bioavailability studies of Trizivir® show no difference in AUC or Cmax when compared to abacavir, lamivudine, and zidovudine given together as individual agents. See individual agents.
