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Recommendations for Use of Antiretroviral Drugs in Pregnant HIV-1-Infected Women for Maternal Health and Interventions to Reduce Perinatal HIV Transmission in the United States

Nucleoside and Nucleotide Analogue Reverse Transcriptase Inhibitors

Abacavir (Ziagen, ABC)

(Last updated: August 6, 2015; last reviewed: August 6, 2015)

Abacavir is classified as Food and Drug Administration Pregnancy Category C.

Animal Studies

Abacavir is mutagenic and clastogenic in some in vitro and in vivo assays. In long-term carcinogenicity studies in mice and rats, malignant tumors of the preputial gland of males and the clitoral gland of females were observed in both species, and malignant hepatic tumors and nonmalignant hepatic and thyroid tumors were observed in female rats. The tumors were seen in rodents at doses that were 6 to 32 times that of human therapeutic exposure.

No effect of abacavir on reproduction or fertility in male and female rodents has been seen at doses of up to 500 mg/kg/day (about 8 times that of human therapeutic exposure based on body surface area).

Teratogenicity/Developmental Toxicity
Abacavir is associated with developmental toxicity (decreased fetal body weight and reduced crown-rump length) and increased incidence of fetal anasarca and skeletal malformations in rats treated with abacavir during organogenesis at doses of 1000 mg/kg (about 35 times that of human therapeutic exposure based on area under the curve [AUC]). Toxicity to the developing embryo and fetus (increased resorptions and decreased fetal body weight) occurred with administration of 500 mg/kg/day of abacavir to pregnant rodents. The offspring of female rats were treated with 500 mg/kg of abacavir, beginning at embryo implantation and ending at weaning. In these animals, an increased incidence of stillbirth and lower body weight was seen throughout life. However, in the rabbit, no evidence of drug-related developmental toxicity was observed and no increase in fetal malformations was observed at doses up to 700 mg/kg (about 8.5 times that of human therapeutic exposure).

Placental and Breast Milk Passage
Abacavir crosses the placenta and is excreted into the breast milk of lactating rats.1

Human Studies in Pregnancy

A Phase I study of abacavir in pregnant women indicates that the AUC drug concentration during pregnancy was similar to that at 6 to 12 weeks postpartum and in non-pregnant individuals.2 Thus, no dose adjustment for abacavir is needed during pregnancy.

Placental and Breast Milk Passage
In the Mma Bana study,1 at 1 month postpartum, the median breast milk-to-plasma ratio for abacavir was 0.85 in the 15 women tested, and the drug was detected in the plasma of 1 of 9 breastfeeding infants whose mothers were receiving abacavir.

In the Antiretroviral Pregnancy Registry, sufficient numbers of first-trimester exposures to abacavir in humans have been monitored to be able to detect at least a 2-fold increase in risk of overall birth defects. No such increase in birth defects has been observed with abacavir. Among cases of first-trimester abacavir exposure reported to the Antiretroviral Pregnancy Registry, the prevalence of birth defects was 3.0% (27 of 905 births; 95% CI, 2.0% to 4.3%) compared with 2.7% in the U.S. population, based on Centers for Disease Control and Prevention surveillance.3 There was no association of birth defects with first trimester exposure to abacavir in the SMARTT study (aOR 0.94 [0.53–1.65])4 or in the French Perinatal Study (aOR 1.01, [0.73–1.41]).5

Serious hypersensitivity reactions have been associated with abacavir therapy in non-pregnant adults, but these reactions have rarely been fatal; symptoms include fever, skin rash, fatigue, and gastrointestinal symptoms such as nausea, vomiting, diarrhea, or abdominal pain. Abacavir should not be restarted following a hypersensitivity reaction because more severe symptoms will occur within hours and may include life-threatening hypotension and death. Patients who test positive for HLA-B*5701 are at highest risk; HLA screening should be done before initiation of abacavir.

Excerpt from Table 7a
Generic Name
Trade Name
Formulation  Dosing Recommendations Use in Pregnancy



ABC (Ziagen)
  • 300 mg
  • 20 mg/mL
  • ABC 600 mg plus 3TC 300 mg tablet
  • ABC 300 mg plus 3TC 150 mg plus ZDV 300 mg tablet 
  • Dolutegravir 50 mg plus ABC 600 mg plus 3TC 300 mg
Standard Adult Doses
ABC (Ziagen): 
  • 300 mg twice daily or 600 mg once daily, without regard to food
  • 1 tablet once daily without regard to food
  • 1 tablet twice daily without regard to food
PK in Pregnancy:
  • PK not significantly altered in pregnancy.
Dosing in Pregnancy:
  • No change in dose indicated.
High placental transfer to fetus.b 

No evidence of human teratogenicity (can rule out 2-fold increase in overall birth defects). 

Hypersensitivity reactions occur in approximately 5% to 8% of non-pregnant individuals; a much smaller percentage are fatal and are usually associated with re-challenge. Rate in pregnancy is unknown. Testing for HLA-B*5701 identifies patients at risk of reactions and should be done and documented as negative before starting ABC. Patients should be educated regarding symptoms of hypersensitivity reaction.
a Individual antiretroviral drug dosages may need to be adjusted in renal or hepatic insufficiency (for details, see Adult Guidelines, Appendix B, Table 7).
b Placental transfer categories—Mean or median cord blood/maternal delivery plasma drug ratio:
   High: >0.6
   Moderate: 0.3–0.6
   Low: <0.3

Key to Abbreviations: 3TC = lamivudine; ABC = abacavir; DTG = dolutegravir; PK = pharmacokinetic; ZDV = zidovudine 



  1. Shapiro RL, Rossi S, Ogwu A, et al. Therapeutic levels of lopinavir in late pregnancy and abacavir passage into breast milk in the Mma Bana Study, Botswana. Antivir Ther. 2013;18(4):585-590. Available at
  2. Best BM, Mirochnick M, Capparelli EV, et al. Impact of pregnancy on abacavir pharmacokinetics. AIDS. 2006;20(4):553-560. Available at
  3. Antiretroviral Pregnancy Registry Steering Committee. Antiretroviral Pregnancy Registry international interim report for 1 Jan 1989–31 July 2014. Wilmington, NC: Registry Coordinating Center. 2014. Available at
  4. Williams PL, Crain MJ, Yildirim C, et al. Congenital anomalies and in utero antiretroviral exposure in human immunodeficiency virus-exposed uninfected infants. JAMA Pediatr. 2015;169(1):48-55. Available at
  5. Sibiude J, Le Chenadec J, Bonnet D, et al. In utero exposure to zidovudine and heart anomalies in the ANRS French Perinatal Cohort and the Nested PRIMEVA Randomized Trial. Clin Infect Dis. 2015. Available at

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