UGT1A9 (UDP Glucuronosyltransferase Family 1 Member A9)

P2, N=30, Recruiting, M.D. Anderson Cancer Center | Active, not recruiting --> Recruiting | N=20 --> 30

P2, N=20, Recruiting, M.D. Anderson Cancer Center | Active, not recruiting --> Recruiting

P2, N=2, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting | N=20 --> 2

The results of in vitro-in vivo extrapolation (IVIVE) indicated that coadministration of pexidartinib at a clinically approved dose (400 mg twice daily) with the drugs primarily cleared by UGT1A1, UGT1A6, UGT1A7, UGT1A9, and UGT2B15 would result in a higher risk of DDI. In summary, our results provide useful information for the mechanism underlying pexidartinib-induced hepatotoxicity and clinical safe medication of pexidartinib.

CYP3A4 is a major contributor in the metabolism of 6 drugs, followed by CYP3A (3), CYP1A2 (2), CYP3A4/5 (2), and one each by CYP2C9, UGT1A9, CYP2C8, aldehyde oxidase, and other non-CYP enzymes. The present medicinal chemistry perspective is thus expected to be a valuable read for the medicinal and allied sciences community.

P2, N=20, Active, not recruiting, M.D. Anderson Cancer Center | N=30 --> 20 | Recruiting --> Active, not recruiting

The use of cannabidiol is strongly discouraged. Pharmacists, through their participation in multidisciplinary interviews for the initiation of oral anti-cancer therapies, contribute their expertise in the detection and analysis of potentially clinically significant interactions.

Herein, we report for the first time on the pharmacokinetics, tissue distribution, and metabolism of six constituents in DBD during myelosuppression treatment. The in vivo disposition mechanisms were explained through analyses of intestinal integrity, protein expression and microbial abundance. This work provides valuable data and new insights for identifying the efficacy-related substance basis of DBD against GEM-induced myelosuppression.

Crepidatin was primarily metabolized by CYP3A4, 2C8, 2C19, UGT1A1, UGT1A8, and UGT1A9. This study describes the first integrated HPLC-MS/MS and HPLC-Q-Orbitrap-HRMS method for its in vitro metabolic profiling, and the results facilitate prediction of in vivo pharmacokinetics.

Model interpretability was further achieved using Shapley Additive Explanations (SHAP), which identified key molecular descriptors influencing pharmacokinetic and toxicity predictions. Ligand-2 demonstrated comparable or improved pharmacokinetics versus doxorubicin, supporting its potential as a safer anthracycline analog.

A distinct molecular landscape of non-driver genes was observed in MPNs from Pakistan and most of the genes detected belonged to drug metabolizing pathways.

P1, N=0, Withdrawn, National Institute of Allergy and Infectious Diseases (NIAID) | N=42 --> 0 | Not yet recruiting --> Withdrawn