Source: FDA, National Drug Code (US) Revision Year: 2026
None.
Concomitant use of HOVILPRI with certain acid-reducing agents may reduce pritelivir exposure, potentially resulting in reduced therapeutic effect and development of resistance. Avoid concomitant use with certain proton pump inhibitors, and stagger concomitant use with H2-receptor antagonists and antacids [see Dosage and Administration (2.2), Drug Interactions (7.2), Clinical Pharmacology (12.3)].
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
The safety of HOVILPRI was evaluated in 206 adults treated with HOVILPRI and an additional 100 healthy adult participants exposed to HOVILPRI in clinical trials.
Immunocompromised Adults with Mucocutaneous HSV Infection that is Refractory (with or without Documented Resistance) to Treatment with Acyclovir, Valacyclovir, or Famciclovir:
The safety of HOVILPRI was evaluated in a Phase 3, randomized, open-label, comparator-controlled trial, PRIOH-1 (Part C), in immunocompromised participants with mucocutaneous (mucosal and/or cutaneous lesions) HSV infection that was refractory (with or without documented resistance) to treatment with acyclovir, valacyclovir, or famciclovir [see Clinical Studies (14)]. Participants received HOVILPRI (400 mg loading dose on Day 1 followed by 100 mg once daily) or Investigator's Choice treatment (IV foscarnet, IV/topical cidofovir, or 5% topical imiquimod) for up to 28 days until all lesions healed, extended up to 42 days if lesions were improving. A total of 101 participants were randomized 1:1 and treated with either HOVILPRI or the Investigator's Choice. Across the 51 participants treated with HOVILPRI, the mean duration of treatment was 27.1 days (range 6–43).
The adverse reaction (all grades) occurring in more than 5% of participants receiving HOVILPRI was headache, which occurred in 6% and 4% of the HOVILPRI and Investigator's choice participants, respectively.
Adverse reactions were reported in 22% of HOVILPRI-treated participants, compared with 54% of participants in the Investigator's Choice treatment arm. Discontinuations due to adverse drug reactions occurred in 2% and 20% of participants, respectively.
Hepatic laboratory abnormalities were observed in both treatment groups in PRIOH-1, Part C. ALT elevations ≥2.5 × upper limit of normal (ULN) were reported in 4/51 (8%) participants receiving HOVILPRI and 1/50 (2%) receiving Investigator's Choice, while AST elevations ≥2.5 × ULN were reported in 3/51 (6%) and 2/50 (4%) participants, respectively. One participant discontinued HOVILPRI due to elevated liver enzymes.
The safety of HOVILPRI was also evaluated in a non-randomized, open-label, multicenter, single-arm Phase 3 trial, PRIOH-1 (Parts D and F) in immunocompromised adults with acyclovir/foscarnet (ACV/FOS) refractory HSV infection or who were FOS intolerant (N=35). The safety and tolerability profile observed in these populations was consistent with that observed in Part C, with no new or unexpected adverse drug reactions identified.
Pritelivir is a breast cancer resistance protein (BCRP) inhibitor. Co-administration of HOVILPRI with a BCRP substrate may increase the plasma concentrations of the BCRP substrate [see Clinical Pharmacology (12.3)], which may increase the risk of adverse reactions. Refer to the prescribing information for co-administered drugs for additional information.
Elevation of gastric pH may decrease the systemic bioavailability of HOVILPRI [see Clinical Pharmacology (12.3)], which may reduce its effectiveness or cause drug resistance to HOVILPRI [see Dosage and Administration (2.2), Warnings and Precautions (5.1)].
Table 1. Clinically Significant Drug Interactions:
| Proton Pump Inhibitors/ H2-Receptor Antagonists/Antacids | ||
| Prevention or Management | Proton Pump Inhibitors: | Avoid concomitant use of esomeprazole or rabeprazole with HOVILPRI. Avoid concomitant use of omeprazole or lansoprazole at daily doses above 20 mg with HOVILPRI. Avoid concomitant use of pantoprazole at daily doses above 40 mg with HOVILPRI [see Dosage and Administration (2.2)]. Concomitant use of omeprazole, lansoprazole, or pantoprazole below the doses listed above is acceptable, as these lower doses do not reduce pritelivir exposure to a clinically relevant extent. |
| H2-Receptor Antagonists: | Take HOVILPRI at least 2 hours before or 12 hours after H2- receptor antagonist intake [see Dosage and Administration (2.2)]. | |
| Antacids: | Take HOVILPRI at least 2 hours before or 2 hours after antacid intake [see Dosage and Administration (2.2)]. | |
There are no available data on HOVILPRI use in pregnant women to inform a drug-associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. In animal reproduction studies, no adverse developmental effects were observed when pritelivir was administered to rats and rabbits at exposures (AUC) approximately 16- (rats) and 2- (rabbits) times the systemic pritelivir exposure in humans at the therapeutic dose of 100 mg (see Data).
The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.
Pritelivir was administered orally to pregnant rats at 30, 200 and 1,000 mg/kg/day from gestation days 6 to 17 and to pregnant rabbits at 5, 20, 40, 60 and 80 mg/kg/day from gestation days 6 to 20. In both species, developmental toxicities were only observed at maternally toxic doses, ≥200 mg/kg/day in the rat, and ≥40 mg/kg/day in the rabbit, resulting in low birth weights in both species, skeletal variations in the rat and fetal loss in rabbits at doses ≥60 mg/kg/day. No adverse maternal or embryofetal effects were observed in rats at the low dose (30 mg/kg/day) and rabbits at 20 mg/kg/day resulting in systemic pritelivir exposures (AUC) approximately 5-times for rat, and equal to the human exposure at the therapeutic dose of 100 mg, for rabbits.
In the prenatal and postnatal development study, pritelivir was orally administered to pregnant rats at 25, 75 and 150 mg/kg/day from gestation day 6 to postpartum/lactation day 20. Maternal toxicity occurred at 75 and 150 mg/kg/day resulting in fetal loss, lower birth weights and a delay in sexual maturation but with no influence on physical, functional, or reproductive development. No adverse effects were observed in the offspring at 25 mg/kg/day resulting in maternal systemic pritelivir exposures (AUC) approximately 5-times the human exposure at the therapeutic dose of 100 mg.
There are no data on the presence of pritelivir or its metabolites in human milk, the effects on the breastfed infant, or the effects on milk production. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for HOVILPRI and any potential adverse effects on the breastfed infant from HOVILPRI or from the underlying maternal condition.
Infertility
There are no data on the effect of pritelivir on human fertility. A fertility study of pritelivir in rats (50, 150 and 500 mg/kg/day) showed adverse effects on male fertility at 500 mg/kg/day. Male rats dosed at 500 mg/kg/day exhibited direct effects on epididymal sperm counts, sperm motility and morphology and a minor increase in severity in lumen detritus in the epididymis. At 150 mg/kg/day, male rats exhibited slight reduction of epididymal sperm counts as well as minor changes in sperm morphology. The effects were confirmed to be reversible after 6 weeks of discontinuing pritelivir with no lasting adverse effects on male reproduction. Malemediated effects on early embryonic development occurred at 150 and 500 mg/kg/day (i.e., increase in fetal loss in treated and untreated females). No effects on fertility or the offspring occurred at 50 mg/kg/day approximately 6-times the human exposure (AUC) at the therapeutic dose of 100 mg. Sexually mature male monkeys dosed at 1,000 mg/kg/day for 39 weeks had no findings in the reproductive organs or semen [see Nonclinical Toxicology (13.1)].
The safety and efficacy of HOVILPRI have not been established in pediatric patients 18 years of age and younger.
Of the 51 immunocompromised participants treated with HOVILPRI in the Phase 3 PRIOH-1 Part C trial, 20% (10/51) were 65 years and older and 4% (2/51) were 75 years of age and older (range 19-84 years) [see Clinical Studies (14)]. No overall differences in safety or effectiveness were observed between patients 65 years of age and older and younger adult patients.
No dose adjustment is recommended for patients with mild, moderate, or severe renal impairment. The pharmacokinetics and safety of pritelivir in patients requiring hemodialysis have not been evaluated [see Clinical Pharmacology (12.3)].
No dose adjustment is recommended for patients with mild (Child-Pugh Class A) or moderate (Child-Pugh Class B) hepatic impairment. The pharmacokinetics and safety of pritelivir in patients with severe hepatic impairment (Child-Pugh Class C) have not been evaluated [see Clinical Pharmacology (12.3)].
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