Completely absorbed from the GI tract. Protein binding: 50%. Undergoes first-pass metabolism. Metabolized in the liver. Primarily excreted in urine. Not removed by hemodialysis. Half-life: PO, 6–8 hr; IV, 5.5 hr.
An anticonvulsant and antineuralgic agent whose exact mechanism is unknown but may be related to enhancement of sodium channel inactivation and modulation of collapsing response mediator protein-2 (CRMP-2). Lacosamide decreases the availability of voltage-gated sodium channels.
Completely absorbed following oral administration (100%), can be taken with food. Peak plasma concentrations reached in 1–5 hr, widely distributed. Protein binding <15%. Undergoes hepatic metabolism (CYP2C19). Half-life: 13 hr. Excreted primarily by the kidneys.
Used in combination with zidovudine for the treatment of HIV infection and to reduce disease progression and death in AIDS; HBV dose form: chronic hepatitis B associated with evidence of hepatitis B viral replication and liver inflammation
Rapidly and completely absorbed from the GI tract. Protein binding: less than 36%. Widely distributed (crosses the blood-brain barrier). Primarily excreted unchanged in urine. Not removed by hemodialysis or peritoneal dialysis. Half-life: 11–15 hr (intracellular), 2–11 hr (serum, adults), 1.7–2 hr (serum, children) (increased in impaired renal function).
|50 ml/min or higher||150 mg twice a day|
|30–49 ml/min||150 mg once a day|
|15–29 ml/min||150 mg first dose, then|
|100 mg once a day||5–14 ml/min|
|150 mg first dose, then||50 mg once a day|
|Less than 5 ml/min||50 mg first dose, then 25 mg once a day|
An anticonvulsant whose exact mechanism is unknown. May block voltage-gated sodium channels, thus stabilizing neuronal membranes and regulating presynaptic transmitter release of excitatory amino acids.
Seizure Control in Patients Receiving Enzyme-Inducing Antiepileptic Drug (EIAEDS), But Not Valproic Acid
Recommended as add-on therapy: 50 mg once a day for 2 wk, followed by 100 mg/day in 2 divided doses for 2 wk. Maintenance: Dosage may be increased by 100 mg/day every wk, up to 300–500 mg/day in 2 divided doses.
Titrate lamotrigine to 200 mg/day, maintaining valproic acid dose. Maintain lamotrigine dose and decrease valproic acid to 500 mg/day, no greater than 500 mg/day/wk, then maintain 500 mg/day for 1 wk. Increase lamotrigine to 300 mg/day and decrease valproic acid to 250 mg/day. Maintain for 1 wk, then discontinue valproic acid and increase lamotrigine by 100 mg/day each wk until maintenance dose of 500 mg/day reached.
Octapeptide somatostatin analog that inhibits insulin-like growth factor-1 (IGF-1) and growth hormone. High affinity for somatostatin type 2 (SSTR2) and 5 (SSTR5) receptors in pituitary gland, pancreas, and growth hormone (GH) secreting neoplasms of pituitary gland. Lesser affinity for somatostatin receptors 1, 3, and 4 (SSTR1, SSTR3 and SSTR4).
Protein binding: 79%–83%. Extensive metabolism in GI tract after biliary excretion. Bioavailability: 69%–83%. Less than 5% of lanreotide excreted in urine; less than 0.5% recovered unchanged in feces, indicative of some biliary excretion. Half-life: 23–36 days.
Short-term treatment for healing and symptomatic relief of active duodenal ulcer and benign gastric ulcer, erosive esophagitis, and gastroesophageal reflux disease (GERD); maintenance of healing of duodenal ulcers; long-term treatment of pathologic hypersecretory syndromes; NSAID-associated gastric ulcers in patients who continue NSAID use; short-term treatment of symptomatic GERD
Rapid and complete absorption (food may decrease absorption) once drug has left stomach. Protein binding: 97%. Distributed primarily to gastric parietal cells and converted to two active metabolites. Extensively metabolized in the liver. Eliminated in bile and urine. Not removed by hemodialysis. Half-life: 1.5 hr (increased in the elderly and in those with hepatic impairment).
A phosphate regulator that dissociates in the acidic environment of the upper GI tract to lanthanum ions, which bind to dietary phosphate released from food during digestion, forming highly insoluble lanthanum phosphate complexes.