Pharmacodynamics + Site Affinity(Ki nM) Efficacy(Emax %) Action D1 214–32,000 ? ? D2S 0.5–0.62 102 Full agonist D2L 0.95 75 Partial agonist D3 0.80–1.0 86 Partial agonist D4 56 49 Partial agonist D5 22 ? ? 5-HT1A 1.9–20 93 Partial agonist 5-HT1B 479 102 Full agonist 5-HT1D 8.7 68 Partial agonist 5-HT2A 4.6–6.2 94 Partial agonist 5-HT2B 1.2–9.4 123 Full agonist 5-HT2C 5.8–692 96 Partial agonist 5-HT3 >10,000 – – 5-HT4 3,000 ? ? 5-HT6 1,300 ? ? 5-HT7 2.5 ? Antagonist α1A 288–>10,000 0 Silent antagonist α1B 60–1,000 ? ? α1D 166 ? ? α2A 12–132 0 Silent antagonist α2B 17–72 0 Silent antagonist α2C 22–364 0 Silent antagonist α2D 3.6 ? ? H1 1,380 ? ? M1 >10,000 – – SERT >10,000 – – Notes: All sites are human except α2D-adrenergic, which is rat (no human counterpart). Negligible affinity (>10,000 nM) for various other receptors (β1- and β2-adrenergic, adenosine, GABA, glutamate, glycine, nicotinic acetylcholine, opioid, prostanoid). Sources:<unk>  is a long-acting dopamine D2 receptor agonist. In-vitro rat studies show a direct inhibitory effect of<unk>  on the prolactin secretion in the lactotroph cells of the pituitary gland and<unk>  decreases serum prolactin levels in reserpinized rats. Although<unk>  is commonly described principally as a D2 receptor agonist, it also possesses significant affinity for the dopamine D3, and D4, serotonin 5-HT1A, 5-HT2A, 5-HT2B, and 5-HT2C, and α2-adrenergic receptors, as well as moderate/low affinity for the dopamine D1, serotonin 5-HT7, and α1-adrenergic receptors.<unk>  functions as an partial or full agonist at all of these receptors except for the 5-HT7, α1-adrenergic, and α2-adrenergic receptors, where it acts as an antagonist.<unk>  has been associated with cardiac valvulopathy due to activation of 5-HT2B receptors. Pharmacokinetics Following a single oral dose, resorption of<unk>  from the gastrointestinal (GI) tract is highly variable, typically occurring within 0.5 to 4 hours. Ingestion with food does not alter its absorption rate. Human bioavailability has not been determined since the drug is intended for oral use only. In mice and rats the absolute bioavailability has been determined to be 30 and 63 percent, respectively.<unk>  is rapidly and extensively metabolized in the liver and excreted in bile and to a lesser extent in urine. All metabolites are less active than the parental drug or inactive altogether. The human elimination half-life is estimated to be 63 to 68 hours in patients with Parkinson's disease and 79 to 115 hours in patients with pituitary tumors. Average elimination half-life is 80 hours. The therapeutic effect in treatment of hyperprolactinemia will typically persist for at least 4 weeks after cessation of treatment.
Cabergoline
Metergoline
Tetryzoline
Eluxadoline
Terguride
Allylestrenol
Avacopan
Iopromide