| Indication |
For the treatment of acid-reflux disorders (GERD), peptic ulcer disease, active benign gastric ulcer, and active duodenal ulcer. |
| Pharmacodynamics |
Nizatidine is a competitive, reversible inhibitor of histamine
at the histamine H2-receptors, particularly those in the gastric
parietal cells. By inhibiting the action of histamine on stomach cells,
nizatidine reduces stomach acid production. Nizatidine had no
demonstrable antiandrogenic action. Full-dose therapy for the problems
treated by nizatidine lasts no longer than 8 weeks. It has been
demonstrated that treatment with a reduced dose of nizatidine is
effective as maintenance therapy following healing of active duodenal
ulcers. |
| Mechanism of action |
Nizatidine competes with histamine for binding at the H2-receptors
on the gastric basolateral membrane of parietal cells. Competitive
inhibition results in reduction of basal and nocturnal gastric acid
secretions. The drug also decreases the gastric acid response to stimuli
such as food, caffeine, insulin, betazole, or pentagastrin. |
| Absorption |
Rapid (bioavailability of nizatidine exceeds 70%) |
| Volume of distribution |
|
| Protein binding |
35% |
| Metabolism |
Hepatic. Less than 7% of an oral dose is metabolized as
N2-monodes-methylnizatidine, an H2-receptor antagonist, which is the
principal metabolite excreted in the urine. Other likely metabolites are
the N2-oxide (less than 5% of the dose) and the S-oxide (less than 6%
of the dose). |
| Route of elimination |
Not Available |
| Half life |
1-2 hours |
| Clearance |
- 40-60 L/h
- 7 – 14 L/h [functionally anephric patients]
|
| Toxicity |
Oral, rat LD50: 301 mg/kg. Symptoms of overdose include
cholinergic-type effects including lacrimation, salivation, emesis,
miosis, and diarrhea. |
