rifampicin

P1, N=36, Completed, Beijing Friendship Hospital ,Capital Medical University; Beijing Friendship Hospital ,Capital Medical University

P2, N=75, Active, not recruiting, Thirty Respiratory Limited | Recruiting --> Active, not recruiting | Trial primary completion date: Apr 2024 --> Apr 2025

P1, N=34, Active, not recruiting, Boehringer Ingelheim | Trial completion date: Aug 2025 --> Feb 2025

This case suggests that in patients with impaired renal function taking edoxaban, co-administration of carboxylesterase-1 inducers such as rifampin and/or OATP1B1 inhibitors such as rifampin or clarithromycin may increase plasma concentrations of M-4 to clinically non-negligible levels.

P1, N=40, Not yet recruiting, Chia Tai Tianqing Pharmaceutical Group Co., Ltd.

P1, N=48, Not yet recruiting, Jemincare

P3, N=120, Not yet recruiting, Huashan Hospital

P4, N=880, Recruiting, VA Office of Research and Development | Trial completion date: Sep 2024 --> Sep 2025 | Trial primary completion date: Sep 2024 --> Sep 2025

Victim drugs brigatinib and lorlatinib were evaluated with the new approach in combination with the perpetrator drugs itraconazole and rifampicin. The model was able to adequately describe the inhibition of CYP3A4 metabolism and the subsequent magnitude of change in exposure. However, it was unable to accurately predict the magnitude of change in exposure of victim drugs in combination with an inducer.

P1, N=56, Not yet recruiting, Jiangsu vcare pharmaceutical technology co., LTD

P1, N=35, Completed, Celgene | Recruiting --> Completed

P2/3, N=3400, Recruiting, Centers for Disease Control and Prevention | Trial completion date: Dec 2028 --> Dec 2029 | Trial primary completion date: Dec 2028 --> Dec 2029

P=N/A, N=280, Not yet recruiting, Albert Einstein College of Medicine

Coadministration with rifampin decreased these same variables by 61.27%, 74.21%, and 75.19%, respectively. These results confirm that olverembatinib is primarily metabolized by CYP3A4 in humans, suggesting that caution should be exercised with concurrent use of olverembatinib and strong CYP3A4 inhibitors or inducers.

P3, N=402, Completed, Wits Health Consortium (Pty) Ltd | Active, not recruiting --> Completed | Trial completion date: Jun 2023 --> Apr 2024 | Trial primary completion date: Jun 2023 --> Apr 2024

This induction was attenuated upon PXR activation in hPXR-LX2 cells by treatment with the destabilization domain-stabilizing chemical Shield-1 and the human PXR ligand rifampicin...Reporter assays with the POSTN promoter showed that PXR inhibited the NF-κB-mediated transcription of POSTN. Consequently, PXR activation in HSCs is expected to inhibit transdifferentiation by downregulating POSTN expression, thereby suppressing EMT of liver cancer cells.

P=N/A, N=300, Not yet recruiting, Assistance Publique - Hôpitaux de Paris

The expression patterns of all HNF4A-AS1 transcripts were further investigated in liver cell growth from human embryonic stem cells to matured hepatocyte-like cells, HepaRG differentiation, and exposure to rifampicin treatment...Significance Statement This study explores the alternative transcripts of HNF4A-AS1, showing how their expression changes in different biological conditions, from various liver diseases to the growth and differentiation of hepatocytes, and drug metabolism. The generated knowledge is essential for understanding the independent roles of different transcripts from the same lncRNA in different liver diseases and drug metabolism situations.

P1, N=40, Not yet recruiting, Hangzhou Zhongmei Huadong Pharmaceutical Co., Ltd.

P3, N=1266, Recruiting, Queen Mary University of London | Not yet recruiting --> Recruiting

P1, N=32, Completed, Abbisko Therapeutics Co, Ltd | Enrolling by invitation --> Completed | Trial completion date: Nov 2023 --> Sep 2023

P2, N=60, Recruiting, Children's Hospital of Philadelphia | N=30 --> 60

Models involving rifampicin combined with midazolam, itraconazole combined with midazolam or digoxin were utilized to showcase the robustness of evaluating DDI effects. PBPK model simulation results showed that the systemic exposure of TQ-B3525 was significantly affected when co-administered with CYP3A4/P-gp inducers and inhibitors. This indicates that the combination with strong inducers and inhibitors should be carefully avoided or adjust the dosage of TQ-B3525 in clinic.

P3, N=100, Not yet recruiting, Taipei Medical University WanFang Hospital

Previous studies have shown that SHR6390 in combination with rifampicin, a potent inducer of CYP3A4, significantly reduces exposure levels. It is recommended to avoid concomitant administration of moderate inducers of CYP3A4 during treatment with SHR6390. http://www.chinadrugtrials.org.cn/index.html, CTR20211571/ https://classic.clinicaltrials.gov, NCT04973020.

P=N/A, N=100, Recruiting, Region Skane | Trial completion date: Dec 2024 --> Dec 2026 | Trial primary completion date: Jun 2024 --> Dec 2026

P2/3, N=1800, Not yet recruiting, McGill University Health Centre/Research Institute of the McGill University Health Centre

P2/3, N=26, Completed, University of Liverpool | Active, not recruiting --> Completed

P3, N=150, Not yet recruiting, Johns Hopkins University

P1, N=36, Not yet recruiting, Betta Pharmaceuticals Co., Ltd.

P3, N=100, Recruiting, Rush University Medical Center

Despite being on conventional immunosuppressive regimens (tacrolimus and mycophenolate mofetil with initial corticosteroids tapered), this patient still developed two severe rejection episodes, one of which necessitated retransplantation (DCD). Both episodes were preceded by alterations in tacrolimus trough levels, either intentionally, when tacrolimus was reduced within a nephroprotective regimen, or unintentionally, when rifampicin, a CYP3A4 inducer, significantly lowered the trough levels...Furthermore, the patient experienced an everolimus-linked drug-induced thrombotic microangiopathy, underwent multiple ERCPs for an anastomotic stricture and only one and a half year after the first liver transplantation she already suffers from long-term immunosuppressive-related side effects such as impaired glucose tolerance, hypertension and a potential cardiomyopathy. At present, she is still alive and experienced no recurrence of her primary tumor. Her case underscores the significant challenges in post-liver transplantation care.

P4, N=45, Recruiting, Beijing Chest Hospital

P1, N=32, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting

P3, N=1266, Not yet recruiting, Queen Mary University of London | Initiation date: Mar 2024 --> Jul 2024 | Trial primary completion date: Mar 2026 --> Jul 2026

We report a case of successful treatment involving the concomitant administration of osimertinib and antituberculosis drugs in an older patient, an 89-year-old female, diagnosed with epidermal growth factor receptor (EGFR)-mutant lung cancer and pulmonary tuberculosis. Accumulating evidence is warranted to develop an optimal treatment strategy for patients with lung cancer and tuberculosis.

P1, N=66, Completed, Jacobio Pharmaceuticals Co., Ltd. | Recruiting --> Completed | Trial completion date: Jul 2024 --> Feb 2024 | Trial primary completion date: Jun 2024 --> Feb 2024

P3, N=690, Not yet recruiting, University of California, San Francisco

The purpose of this study was to develop and validate a physiologically based pharmacokinetic (PBPK) model combined with an EGFR occupancy (EO) model for osimertinib (OSI) to predict plasma trough concentration (Ctrough) and the intracranial time-course of EGFR (T790M and L858R mutants) engagement in patient populations. When used concomitantly with CYP enzyme perpetrators, the PBPK-EO model suggested appropriate dosing regimens of 80 mg OD with fluvoxamine (FLUV) itraconazole (ITR) or fluvoxamine (FLUC) for co-administration and an increase to 160 mg OD with rifampicin (RIF) or efavirenz (EFA). In conclusion, the PBPK-EO model has been shown to be capable of simulating the pharmacokinetic concentration-time profiles and the time-course of EGFR engagement for OSI, as well as determining the optimum dosing in various clinical situations.

In C3A cells (endogenous CYPs being substantial), TBOEP exposing for 72 h (2-cell cycle) at low micromolar levels induced micronucleus, which was abolished by 1-aminobenzotriazole (inhibitor of CYPs); in HepG2 cells (CYPs being insufficient) TBOEP did not induce micronucleus, whose effect was however potentiated by pretreating the cells with PCB126 (CYP1A1 inducer) or rifampicin (CYP3A4 inducer)...In C3A cells, TBOEP selectively induced centromere protein B-free micronucleus (visualized by immunofluorescence) and PIG-A gene mutations, and elevated γ-H2AX rather than p-H3 (by Western blot), indicating double-strand DNA breaks. Therefore, this study suggests that TBOEP may induce DNA/chromosome breaks and gene mutations in human cells, which requires metabolic activation by CYPs, primarily CYP1A1 and 3A4.

For example, the combination of cannabis-derived compounds and the antifungal drug ketoconazole, a CYP3A4 inhibitor, increases the plasma concentration of Δ-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). In contrast, rifampicin, a CYP3A4 inducer, stands out for reducing plasma THC levels by approximately 20-40% and 50% to 60% for CBD...Although further studies are still pending, there is currently clinical evidence supporting drug interactions with cannabinoids, requiring doctors to evaluate the risk of drug combinations with cannabinoids and vice versa. The tables provided here were designed to facilitate the identification of biorelevant interactions that may compromise therapeutic efficacy and toxicity.

His HCL was put into remission with a single course of cladribine and rituximab chemotherapy; however, his M kansasii infection persisted for 6 months despite aggressive antimicrobial and surgical therapy. It was finally controlled using high-dose rifampin in combination with azithromycin and ethambutol...Notable possibilities include HCL cells acting as sanctuary sites for M kansasii to evade the immune system, and subclinical M kansasii infections causing NLRP3 inflammasome overactivation to trigger the oncogenic transformation to HCL. More research into the pathophysiologic link between HCL and M kansasii infections would allow for more effective prevention, diagnosis, and treatment of these severe atypical infections which are the major cause of morbidity in the cladribine era of HCL treatment.