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Phosphodiesterase 4 (PDE4) inhibitors such as rolipram and piclamilast have demonstrated a number of potential therapeutic effects in preclinical studies and even the odd clinical study, but their development has been significantly hampered by their prominent gastrointestinal side effects including nausea and emesis (vomiting).1 α2 adrenoceptor agonists (for example, clonidine) have been found to, in ferrets, attenuate PDE4 inhibitor-induced emesis.2 For this reason I can't help but to ask why α2 adrenoceptor agonists haven't been tried in clinical tries as a means of attenuating these problematic emetic effects that are characteristic of PDE4 inhibitors.

Reference List:

  1. Spina D. PDE4 inhibitors: current status. Br J Pharmacol [Internet]. 2008 Oct [cited 2013 Nov 25];155(3):308–15. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567892/
  2. Robichaud A, Savoie C, Stamatiou PB, Tattersall FD, Chan CC. PDE4 inhibitors induce emesis in ferrets via a noradrenergic pathway. Neuropharmacology [Internet]. 2001 [cited 2013 Nov 25];40(2):262–9. Available from: http://www.sciencedirect.com/science/article/pii/S0028390800001428
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Clonidine has a side effect profile that would make it delicate to use: potential for hypertensive spikes, profound hypotension, delirium... –  Raoul Sep 5 at 2:34

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