TABLE 1

Summary of potential DDI mechanisms

Enzyme or TransporterHCV DAA
SMPSOFDCV + SOFLDV/SOFOBV/PTV/r ± DSVEBR/GZRSOF/VELSOF/VEL/VOXGLE/PIB
DCVLDVOBVPTVRTVDSVEBRGZRVELVOXGLEPIB
BCRPSUB, INHSUBINHSUB, INHaSUBSUB, INHINHSUB, INHINHaINHaSUB, INHaSUB, INHaSUB, INHSUB, INH
OATP1B1/1B3SUB, INHINHSUB, INHSUBSUB, INHaSUB, INHaSUB, INHINH
OATP2B1SUBINHINHINHa
P-gpSUB, INHSUBSUB, INHSUB, INHaSUBSUBSUB, INHSUBSUB, INHSUBSUB, INHaSUB, INHaSUB, INHSUB, INH
CYP1A2INH (weak)cSUBINHINH
CYP2B6SUB
CYP2C8SUBSUBSUB
CYP3A4SUB, INH (weak)aSUB, INDbSUBSUBSUB, INHSUBSUB, INH (weak)SUBSUBSUB,d INHINH
UGT1A1INHINHINHINHINH
  • DCV, daclatasvir; DSV, dasabuvir; EBR, elbasvir; GLE, glecaprevir; GZR, grazoprevir; IND, inducer; INH, inhibitor; LDV, ledipasvir; OBV, ombitasvir; PIB, pibrentasvir; PTV, paritaprevir; RTV or/r, ritonavir; SMP, simeprevir; SOF, sofosbuvir; SUB, substrate; VEL, velpatasvir; VOX, voxilaprevir.

  • a Limited primarily to the process of absorption/intestine (Epclusa, 2017; Harvoni, 2017; Zepatier, 2018).

  • b Very weak inducer in vivo with no dose adjustment of substrates needed (Daklinza, 2018).

  • c CYP1A2 substrates may require monitoring (Viekirax, 2018).