Why Dacepton^®

Dacepton should be considered when optimized oral treatment is not sufficiently controlling fluctuations like “on”-off” phenomena any more.

In this case treatments strategy should be revaluated since there is quality of life for PD patients beyond oral medication. Dacepton injections and infusions are the least invasive device-aided therapy option.

Clinical Efficacy

In contrast to Levodopa, the therapeutic efficacy of Apomorphine in PD is executed through direct stimulation of striatal postsynaptic dopamine receptors. It is independent of the presynaptic dopaminergic terminals for storage and release (Hagell, et al., 2001). Although the precise mechanism of action of apomorphine is not known, it is assumed to involve stimulation of the postsynaptic D1 and D2 receptors within the striatum i.e. caudate nucleus and putamen (LeWitt, 2004).

Clinical response correlates well with levels of Apomorphine in the cerebrospinal fluid; the active substance distribution being best described by a two-compartment model. Apomorphine is rapidly and completely absorbed from subcutaneous tissue, correlating with the rapid onset of clinical effects (4-12 minutes), and that the brief duration of clinical action of the active substance (about 1 hour) is explained by its rapid clearance. The metabolism of Apomorphine is by glucuronidation and sulphonation to at least ten per cent of the total; other pathways have not been described (SmPC, in current version).
The variation in absorption of Apomorphine after s.c. injection can differ between individuals; but remains low within individual patients. Hence the lowest effective dose can differ significantly between patients therefore the doses have to be titrated individually (Gancher, et al., 1989).

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