It suggests to me that the structure-function of the pro-drug is not significantly different than the photo-activated form, or the pro-drug form just isn't stable. In other words, any photo-activated structural change is either not activating the action (activity is inherent in both forms) or your pro-drug isn't in a pure un-activated form due to instability or alternative activation of the pro-drug.

Worst case scenario, the photo-activation is only slightly increasing the activity slightly, if at all.

Dear Randolph B Caldwell, thank you very much for your answer! The pro-drug is actually quite stable, as measured by MS and spectroscopy. The structure is close since we have a single dissociating ligand replaced by a water molecule, however, phototoxicity indices (PI) were very high, in vitro. In your experience, if two compounds activate the same apoptotic pathway, is there a chance one might be cancelling the effect of the other?

Thank you very much!

From what I gather:

This is one compound that is activating the same pathway in two different structural forms, and it sounds like the inert form isn't inert at all. In other words, the active site is still active in both conformations (the "stable" photo-activatable form is not stably inert).

It is most improbable that this compound has two different modes of action on the same pathway. More likely is they have the same target and are competing, not canceling, for the same effect. Again, based on limited information, it doesn't sound like the pro-drug needs to be photo-activated, and when it is, is has an additional metric (ROS production?) unrelated to activating the apoptotic pathway.