Author's reply
- L B Cantor, Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN 46202, USA; lcantor{at}iupui.edu
- Accepted 4 January 2008
We thank Dr Camras for his interest in our report on levels of bimatoprost and its free acid in the aqueous humour of cataract patients after a single topical dose of bimatoprost1 and welcome the opportunity to respond to his comments. We are in agreement with Dr Camras that the results of our study1 and those of his previously reported study2 are similar, showing low nanomolar concentrations of 17-phenyl PGF2α (bimatoprost acid) in the aqueous humour. There is no question that bimatoprost acid is a metabolite of bimatoprost. The issue is whether bimatoprost acid levels account for the intraocular pressure (IOP)-lowering activity of bimatoprost. The evidence suggests that they are insufficient to do so. As Dr Camras stated in his correspondence: “bimatoprost yields peak free acid concentrations in the aqueous three to six times lower than latanoprost acid.” It is accepted that the biological effects of latanoprost are exerted by latanoprost acid: the relatively high concentration of latanoprost acid achieved after latanoprost dosing1–3 is sufficient to activate a substantial proportion of the prostaglandin FP receptors present in the target tissues and account for the IOP-lowering effect of latanoprost. It is difficult to understand, however, how the much lower levels of bimatoprost acid achieved could be believed to account for the IOP-lowering effect …
