Adult: Treatment-experienced patients w/ CCR5-tropic infection: In combination w/ other antiretrovirals that are not potent CYP3A inhibitors or inducers (e.g. ritonavir-boosted tipranavir, nevirapine, enfuvirtide, raltegravir, NRTIs): 300 mg bid.
Hypersensitivity. Lactation. Concomitant use w/ potent CYP3A enzyme inhibitors and inducers in patients w/ severe (CrCl <30 mL/min) renal impairment or ESRD.
Patient w/ severe CV disease, history of postural hypotension. Hepatic (e.g. chronic active hepatitis B or C) and renal impairment. Pregnancy. Patients taking potent CYP3A enzyme inhibitors (w/ or w/o potent inducers) or potent CYP3A enzyme inducers (w/o potent inhibitors). Not indicated for use in patients w/ CXCR4- or dual/mixed tropic HIV-1 infection.
This drug may cause dizziness, if affected, do not drive or operate machinery.
Perform coreceptor tropism testing prior to initiation. Monitor transaminases and bilirubin prior to initiation and periodically during treatment; viral load, CD4 count. Monitor for signs and symptoms of infection, rash, severe skin reactions, hepatitis, and postural hypotension.
Symptoms: Postural hypotension. Management: Supportive treatment including keeping the patient in supine position. Assess vital signs, BP, and ECG. Employ gastric lavage/activated charcoal, or induce emesis to remove unabsorbed drug.
Increased plasma concentration w/ CYP3A enzyme inhibitors (e.g. protease inhibitors except ritonavir-boosted tipranavir, delavirdine, ketoconazole, itraconazole, voriconazole, clarithromycin, telithromycin, nefazodone, boceprevir). Decreased plasma concentration w/ CYP3A enzyme inducers (e.g. efavirenz, etravirine, rifampicin, carbamazepine, phenobarbital, phenytoin). Increased risk of CV events w/ medications that lower BP. Potentially Fatal: Increased risk of postural hypotension which may trigger CV events in patients w/ severe renal impairment or ESRD who are taking CYP3A inhibitors and inducers.
Development of resistance and decreased plasma concentration w/ St. John’s wort.
Description: Maraviroc, a synthetic HIV-1 entry inhibitor, selectively and reversibly antagonises CC chemokine receptor-5 (CCR5) coreceptors found on human CD4+ cells. This prevents interaction of HIV-1 glycoprotein 120 (gp120) and CCR5 necessary for CCR5-tropic HIV-1 to enter cells. Pharmacokinetics: Absorption: Absorbed after oral doses. Bioavailability: 23-33%. Time to peak plasma concentration: 0.5-4 hr. Distribution: Crosses the placenta. Volume of distribution: Approx 194 L. Plasma protein binding: Approx 76%, w/ moderate affinity for albumin and α1-acid glycoprotein. Metabolism: Metabolised in the liver by CYP3A4/5 enzymes to inactive metabolites. Excretion: Via urine (approx 20%, 8% as unchanged drug) and faeces (76%, 25 % as unchanged drug). Terminal elimination half-life: 14-18 hr.
J05AX09 - maraviroc ; Belongs to the class of other antivirals. Used as a direct acting antiviral in the systemic treatment of viral infections.
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