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DOI: 10.1023/B:PHAM.0000003377.39548.f6Pages: 1794-1803

Structural Determinants of P-Glycoprotein-Mediated Transport of Glucocorticoids

1. The University of Tennessee, Department of Pharmaceutical Sciences

2. The Ohio State University, Biophysics Program

3. University of Maryland, Department of Pharmaceutical Sciences

4. St. Jude Children's Research Hospital, Department of Pharmaceutical Sciences

5. The University of Tennessee, Department of Pharmaceutical Sciences

Correspondence to:
James T. Dalton
Email: dalton.1@osu.edu

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Abstract

Purpose. The aim of this study was to determine requisite structural features for P-glycoprotein-mediated transport of a series of structurally related glucocorticoids (GCs).

Methods. Transport experiments were conducted in wild-type and stably transfected MDR1 LLC-PK cell line. Transport efficiency (Teff = Peff, B→A / Peff, A→B) in both cell lines was compared as a measure of passive diffusion and P-glycoprotein-mediated transepithelial transport for each steroid. Three-dimensional structure-activity relationships were built to determine how specific structural features within the steroids affect their P-gp-mediated efflux.

Results. Mean (± SD) Teff in LLC-PK cells was 1.1 ± 0.17, indicating that differences in structure and partition coefficient did not affect drug flux in the absence of P-glycoprotein. Teff in L-MDR1 cells ranged from 3.6 to 26.6, demonstrating the importance of glucocorticoid structure to P-glycoprotein transport. The rank order of Teff in MDR1 cells was: methylprednisolone> prednisolone > betamethasone > dexamethasone/prednisone > cortisol. There was no correlation between individual Teff values and partition coefficient. 3D-QSAR models were built using CoMFA and CoMSIA with a q2 (r2) of 0.48 (0.99) and 0.41 (0.95), respectively.

Conclusions. Nonpolar bulky substituents around the C-6α position, as well as a hydrogen-bond donor at position C-11, enhance P-glycoprotein affinity and cellular efflux, whereas bulky substituents at C-16 diminish transporter affinity.

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