In particular, drugs sharing side effects tend to bind to common protein targets [ 8] and mouse models of functionally related genes often show similar phenotypes [ 9].
For instance, this has been demonstrated in protein protein interactions [1], disease underlying protein networks [2], protein binding pocket analysis [3], shared side-effects networks for drug target identification [4], protein ligand phylogenetic analysis [5], cross-binding ligand networks [6], and even in network pharmacology [7].
As might be expected from their common mechanisms of action, many of the anti-inflammatory analgesic drugs share similar side effects.
As elaborated previously, interactive drugs always share similar side effects.
Both cohorts stressed that they did not share such side effects in isolation, but together with reassurances of their management.
Similarly, based on the argument in Section 2.2 and some previous studies [ 13, 16], interactive drugs are more likely to share similar side effects than noninteractive ones.
Consequently, a drug targeting one of these two proteins might also bind to the other, which might explain why these two proteins share some side effects and are found in the same component.
This indicates that drugs-targeting sodium channels or neurotransmitter transporters share some side effects, indeed, drugs such as Venlafaxine or Bupropion that target neurotransmitter transporters gained high score in CC1, together with drugs such as Flecainide or Lamotrigine that target sodium channels.
Shared targets between side effects have a different color, and drug target links follow the same color code.
I tell myself that this arises from the august wisdom of my clinical experience, from having witnessed my fair share of side effects and adverse outcomes due to medical meddling.
Like all antidepressants Effexor had its share of side effects, including nausea and insomnia.
