Abstract
The release of protein drugs such as bovine serum albumin (BSA) from poly mers such as macroporous poly(ethylene-co-vinyl acetate) (EVAc) matrices has been shown previously to be much slower than would be predicted from simple considerations of aqueous diffusion. Since drug is released through waterfilled pores, it is necessary to determine the mechanism underlying release retardation. Three mechanisms are considered: (1) concentration-dependent diffusion, (2) random pore topology, and (3) constricted pore geometry. The first two mechanisms are shown to be insufficient, in themselves or together, to account for the order of magnitude of retardation that is observed. The third mechanism, pore constrictions, can account for arbitrarily high retardations. Since the three mechanisms are essentially independent, their contributions to retardation can be considered to be multiplicative.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 153-167 |
| Number of pages | 15 |
| Journal | Journal of Controlled Release |
| Volume | 14 |
| Issue number | 2 |
| DOIs | |
| State | Published - Oct 1990 |
Bibliographical note
Funding Information:This work was funded in part by NIH grant GM 26698 and a predoctoral fellowship to R.A.S. from the Paint Research Institute. The authors thank Richard Guy for critical comments during preparation of the manuscript.
Keywords
- concentration dependent diffusion
- constricted pore geometry
- random pore topology
- retarded diffusion, drug release modeling