Review of Clinically Relevant Drug Interactions with Next Generation Hepatitis C Direct-acting Antiviral Agents

Hong, Jenny; Wright, Robert C.; Partovi, Nilufar; Yoshida, Eric M.; Hussaini, Trana

doi:10.14218/jcth.2020.00034

Cited by 12 publications

(10 citation statements)

References 42 publications

(85 reference statements)

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“…Indeed, DAA drugs can inhibit CYP3A4 (glecaprevir, grazoprevir) and/or P-gp (voxilaprevir, ledipasvir, velpatasvir) and interact with anticancer TKIs that are mostly CYP3A4 and/or P-gp substrates (gefitinib, afatinib, erlotinib, crizotinib, ceritinib, lorlatinib, brigatinib, capmatinib etc.). 14,15 Clinicians should be aware of the major consequences of DDIs and the importance of plasma drug monitoring in cancer patients receiving treatment for HCV.…”

Section: Discussionmentioning

confidence: 99%

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: A case report

Monribot

Huillard

Khoudour

et al. 2023

Brit J Clinical Pharma

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This case report describes a pharmacokinetic drug–drug interaction between crizotinib, a tyrosine kinase inhibitor, and sofosbuvir/velpatasvir, a direct‐acting antiviral drug, leading to cardiac toxicity. A 75‐year‐old man, with no cardiovascular history but a diagnosis of metastatic nonsmall cell lung cancer with mesenchymal–epithelial transition exon‐14 deletion and hepatitis C virus infection genotype 1A, received both crizotinib and sofosbuvir/velpatasvir. Crizotinib was well tolerated, but 1 week after sofosbuvir/velpatasvir initiation, the patient experienced bilateral lower‐limb oedema and class III New York Heart Association dyspnoea. We assumed that increased exposure to crizotinib could account for this cardiac toxicity. Drug causality was probable according to the Naranjo scale. We hypothesized a reciprocal interaction between crizotinib and velpatasvir, mediated by both cytochrome 3A4 (CYP3A4) and P‐glycoprotein (P‐gp). Clinicians should be aware of the risk of drug–drug interactions between direct‐acting antiviral agents that inhibit CYP3A4 (glecaprevir) and/or P‐gp (voxilaprevir, velpatasvir) and anticancer tyrosine kinase inhibitors that are mostly CYP3A4 and/or P‐gp substrates (gefitinib, afatinib, erlotinib, crizotinib, ceritinib, lorlatinib, brigatinib, capmatinib etc.).

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Section: Discussionmentioning

confidence: 99%

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: A case report

Monribot

Huillard

Khoudour

et al. 2023

Brit J Clinical Pharma

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show abstract

“…However, relying exclusively on RHD123 as an ABCB1 probe may prevent the detection of ABCB1 inhibitors that bind to other transporter-competent sites [20][21][22]. Digoxin, the probe used in this study, is frequently prescribed by clinicians despite its narrow therapeutic index and high frequency of DDI, including with antiviral drugs [11,15,42,46]. Importantly, it is considered to be a sensitive substrate for testing ABCB1 transport and the inhibition of ABCB1-mediated efflux in cell lines [39,47] because it undergoes minimal metabolism and exhibits low inhibitory potency towards clinically relevant intestinal transporters other than ABCB1 [38,48].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Potency of Anti-HIV and Anti-HCV Drugs to Inhibit P-Glycoprotein Mediated Efflux of Digoxin in Caco-2 Cell Line and Human Precision-Cut Intestinal Slices

et al. 2022

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The inhibition of P-glycoprotein (ABCB1) could lead to increased drug plasma concentrations and hence increase drug toxicity. The evaluation of a drug’s ability to inhibit ABCB1 is complicated by the presence of several transport-competent sites within the ABCB1 binding pocket, making it difficult to select appropriate substrates. Here, we investigate the capacity of antiretrovirals and direct-acting antivirals to inhibit the ABCB1-mediated intestinal efflux of [3H]-digoxin and compare it with our previous rhodamine123 study. At concentrations of up to 100 µM, asunaprevir, atazanavir, daclatasvir, darunavir, elbasvir, etravirine, grazoprevir, ledipasvir, lopinavir, rilpivirine, ritonavir, saquinavir, and velpatasvir inhibited [3H]-digoxin transport in Caco-2 cells and/or in precision-cut intestinal slices prepared from the human jejunum (hPCIS). However, abacavir, dolutegravir, maraviroc, sofosbuvir, tenofovir disoproxil fumarate, and zidovudine had no inhibitory effect. We thus found that most of the tested antivirals have a high potential to cause drug–drug interactions on intestinal ABCB1. Comparing the Caco-2 and hPCIS experimental models, we conclude that the Caco-2 transport assay is more sensitive, but the results obtained using hPCIS agree better with reported in vivo observations. More inhibitors were identified when using digoxin as the ABCB1 probe substrate than when using rhodamine123. However, both approaches had limitations, indicating that inhibitory potency should be tested with at least these two ABCB1 probes.

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“…Indeed, DAA drugs can inhibit CYP3A4 agents (glecaprevir, grazoprevir) and/or P-gp agents (voxilaprevir, ledipasvir) and interact with anticancer TKIs that are mostly CYP3A4 and/or P-gp substrates (gefitinib, afatinib, erlotinib, crizotinib, ceritinib, lorlatinib, brigatinib, capmatinib etc.) (14,15). Clinicians should be aware of the major consequences of DDIs and the importance of plasma drug monitoring in cancer patients receiving treatment for HCV.…”

Section: Discussionmentioning

confidence: 99%

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: a case report

Monribot

Huillard

Khoudour

et al. 2022

Preprint

View full text Add to dashboard Cite

This case report describes of a pharmacokinetic drug–drug interaction between crizotinib, a tyrosine kinase inhibitor, and sofosbuvir/velpatasvir, a direct-acting antiviral drug, leading to cardiac toxicity. A 75-year-old man, with no cardiovascular history but a diagnosis of metastatic non-small cell lung cancer with MET exon-14 deletion and hepatitis C virus infection genotype 1A, received both crizotinib and sofosbuvir/velpatasvir. Crizotinib was well tolerated, but 1 week after sofosbuvir/velpatasvir initiation, the patient experienced bilateral lower-limb edema and class III NYHA dyspnea. We assumed that increased exposure to crizotinib could account for this cardiac toxicity. Drug causality was probable according to the Naranjo scale. We hypothesized a reciprocal interaction between crizotinib and velpatasvir, mediated by both cytochrome 3A4 (CYP3A4) and P-glycoprotein (P-gp). Clinicians should be aware of the risk of drug–drug interactions between direct-acting antiviral agents that inhibit CYP3A4 (glecaprevir) and/or P-gp (voxilaprevir) and anticancer tyrosine kinase inhibitors that are mostly CYP3A4 and/or P-gp substrates (gefitinib, afatinib, erlotinib, crizotinib, ceritinib, lorlatinib, brigatinib, capmatinib etc.).

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Review of Clinically Relevant Drug Interactions with Next Generation Hepatitis C Direct-acting Antiviral Agents

Cited by 12 publications

References 42 publications

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: A case report

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: A case report

Evaluation of the Potency of Anti-HIV and Anti-HCV Drugs to Inhibit P-Glycoprotein Mediated Efflux of Digoxin in Caco-2 Cell Line and Human Precision-Cut Intestinal Slices

Cardiac toxicity associated with pharmacokinetic drug–drug interaction between crizotinib and sofosbuvir/velpatasvir: a case report

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