Axid

H2 Antagonists

All oral dosage forms: May be administered without regard to meals. Administer with food, water, or milk to minimize gastric irritation. Administer with a full glass of water.
For non-prescription occasional use for symptom prevention: Administer right before eating or up to 60 minutes before consuming food or beverage that may cause heartburn. Administer with a full glass of water.

Oral solution: Administer using a calibrated measuring device to assure accurate dosage.

seizures / Delayed / 0-1.0
exfoliative dermatitis / Delayed / 0-1.0
vasculitis / Delayed / 0-1.0
ventricular tachycardia / Early / 0-1.0
anaphylactoid reactions / Rapid / 0-1.0
bronchospasm / Rapid / 0-1.0
laryngeal edema / Rapid / 0-1.0
serum sickness / Delayed / 0-1.0
atrophic gastritis / Delayed / Incidence not known

chest pain (unspecified) / Early / 2.3-2.3
confusion / Early / 0-1.0
amblyopia / Delayed / 1.0-1.0
impotence (erectile dysfunction) / Delayed / 0-1.0
thrombocytopenia / Delayed / 0-1.0
hyperuricemia / Delayed / 0-1.0
eosinophilia / Delayed / 0-1.0
cholestasis / Delayed / 0-1.0
hepatitis / Delayed / 0-1.0
elevated hepatic enzymes / Delayed / 0-1.0
jaundice / Delayed / 0-1.0
anemia / Delayed / 0.2-0.2
vitamin B12 deficiency / Delayed / Incidence not known
pernicious anemia / Delayed / Incidence not known

headache / Early / 16.6-16.6
rhinitis / Early / 9.8-9.8
dizziness / Early / 4.6-4.6
sinusitis / Delayed / 2.4-2.4
drowsiness / Early / 1.9-1.9
anxiety / Delayed / 1.8-1.8
infection / Delayed / 1.7-1.7
pruritus / Rapid / 1.7-1.7
myalgia / Early / 1.7-1.7
xerostomia / Early / 1.4-1.4
rash / Early / 0-1.0
purpura / Delayed / 0-1.0
gynecomastia / Delayed / 0-1.0
urticaria / Rapid / 0.5-0.5
irritability / Delayed / 5.0
nasal congestion / Early / 5.0
pharyngitis / Delayed / 3.3
cough / Delayed / 5.0
vomiting / Early / 5.0
diarrhea / Early / 5.0
fever / Early / 5.0

Axid

Rx

Oral histamine type 2-receptor antagonist
Used for gastroesophageal reflux disease (GERD), short-term and maintenance treatment of duodenal ulcer, and short-term treatment of active benign gastric ulcer
For GERD, proton pump inhibitors (PPIs) are considered to be more effective than H2-blockers

To prevent heartburn, take 75 mg PO immediately before or up to 60 minutes before consuming food or beverages that are known to cause symptoms. For treatment, take 75 mg PO once or twice daily. Maximum dosage is 150 mg/day PO. Patients should not take for more than 2 weeks without consulting a physician.

150 mg PO twice daily for up to 12 weeks.

150 mg PO twice daily for up to 8 weeks.[53019] Alternatively, 5 mg/kg/dose PO twice daily is recommended by the American Academy of Pediatrics (AAP); however, a maximum dosage is not specified.[55232] While nizatidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.[26115]

5 mg/kg/dose PO twice daily is recommended by the American Academy of Pediatrics (AAP).[55232] Doses of 2.5 to 10 mg/kg/dose PO twice daily have also been reported.[53019] [53036] [55232] In an open-label, multiple-dose, randomized, parallel-group, multicenter study, patients (aged 5 days to 18 years, n = 210) were randomized to receive either of 2 dose levels (2.5 or 5 mg/kg/dose twice daily) for 8 weeks; no clear superiority between doses was observed.[53019] In a separate placebo controlled study, patients (aged 6 months to 8 years, n = 24) with mild to moderate reflux esophagitis received 10 mg/kg/dose PO twice daily for 8 weeks or a matching placebo. Nizatidine therapy was associated with statistically significant improvement in symptoms, reduced esophageal acid exposure, and healed esophagitis.[53036] While nizatidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.[26115]

150 mg PO twice daily for up to 12 weeks.

150 mg PO twice daily for up to 8 weeks.[50745] [53019] Alternatively, 5 mg/kg/dose PO twice daily is recommended by the American Academy of Pediatrics (AAP); however, a maximum dosage is not specified.[55232] While nizatidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.[26115]

5 mg/kg/dose PO twice daily is recommended by the American Academy of Pediatrics (AAP). Doses of 2.5 to 10 mg/kg/dose PO twice daily have also been reported. In an open-label, multiple-dose, randomized, parallel-group, multicenter study, patients (aged 5 days to 18 years, n = 210) were randomized to receive either of 2 dose levels (2.5 or 5 mg/kg/dose twice daily) for 8 weeks; no clear superiority between doses was observed. In a separate placebo controlled study, patients (aged 6 months to 8 years, n = 24) with mild to moderate reflux esophagitis received 10 mg/kg/dose PO twice daily for 8 weeks or a matching placebo. Nizatidine therapy was associated with statistically significant improvement in symptoms, reduced esophageal acid exposure, and healed esophagitis. While nizatidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

2.5 to 5 mg/kg/dose PO twice daily for 8 weeks has been studied for GERD in an open-label, multiple-dose, randomized, parallel-group, multicenter study. Patients (aged 5 days to 18 years, n = 210) were randomized to receive either of 2 dose levels (2.5 or 5 mg/kg/dose twice daily) for 8 weeks; no clear superiority between doses was observed. Neonatal data were not reported separately. While nizatidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

300 mg PO at bedtime, or 150 mg PO every 12 hours, for 8 weeks. In most patients, ulcers heal within 4 weeks.

150 mg PO at bedtime. Treatment beyond 1 year has not been evaluated.

300 mg PO daily, administered once daily at bedtime or as 150 mg every 12 hours, for 8 weeks. Prior to treatment, care should be taken to exclude the possibility of malignant gastric ulceration.

300 mg PO the night prior to or the morning of surgery, before induction of anesthesia. According to guidelines of the American Society of Anesthesiologists, routine preoperative use is NOT recommended in patients who have no apparent increased risk for pulmonary aspiration. However, some guidelines recommend an H2-receptor antagonist (PO or IV) for all women presenting for cesarean delivery.

150—300 mg PO once daily.

†Indicates off-label use

Specific dosage adjustments have not been recommended. Use with caution in patients with hepatorenal syndrome as formal studies have not been done and part of the dose of nizatidine is metabolized in the liver. For patients with normal renal function and uncomplicated hepatic dysfunction, the disposition of nizatidine is similar to that of normal subjects.

Adults:
CrCl more than 50 mL/minute: No dosage adjustment needed.
CrCl 20 to 50 mL/minute: For adults treated for active duodenal ulcer, GERD, or benign gastric ulcer, decrease the dose to 150 mg PO once daily; for adults receiving maintenance therapy, decrease to 150 mg PO every other day.
CrCl less than 20 mL/minute: For adults treated for active duodenal ulcer, GERD, or benign gastric ulcer, decrease the dose to 150 mg PO every other day; for adults receiving maintenance therapy, decrease to 150 mg PO once every 3 days.
 
Pediatric patients 12 years and older:
See adult dosage adjustment recommendations.
 
Intermittent Hemodialysis
See dosage recommendations for CrCl less than 20 mL/minute. Nizatidine is not expected to be efficiently removed from the body by dialysis.

Acalabrutinib: (Moderate) Separate the administration of acalabrutinib capsules and H2-blockers if these agents are used together; administer acalabrutinib capusles 2 hours before the H2-blocker. Acalabrutinib capsule solubility decreases with increasing pH values; therefore, coadministration may result in decreased acalabrutinib exposure and effectiveness.
Albuterol; Budesonide: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant nizatidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Amphetamine; Dextroamphetamine Salts: (Moderate) Use amphetamine; dextroamphetamine and H2-blockers concomitantly with caution. Gastrointestinal alkalinizing agents may increase exposure to amphetamine; dextroamphetamine and exacerbate its actions.
Atazanavir: (Major) Coadministration of H2-blockers with atazanavir reduces serum atazanavir concentrations; however, H2-blockers can be used under specific administration restrictions. Although data are insufficient to recommend atazanavir dosing in children < 40 kg receiving concomitant H2-blockers, the same recommendations regarding timing and maximum doses of concomitant H2-blockers should be followed. In treatment-naive patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 40 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. If a treatment-naive adult or adolescent (>= 40 kg) cannot tolerate ritonavir, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and the atazanavir dose should be increased to 400 mg once daily with food given at least 2 hours before or 10 hours after the H2- blocker. Data are insufficent to recommend atazanavir dosing in children or adolescents < 40 kg not receiving ritonavir boosting. In treatment-naive patients on a cobicistat-boosted regimen, cobicistat and atazanavir may be administered without dosage adjustment if given at the same time or a minimum of 10 hours after dosing of the H2-blocker. The H2-blocker dose should not exceed a dose that is comparable to 40 mg/day of famotidine in treatment-naive patients. In treatment-experienced patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. In treatment-experienced patients >= 40 kg receiving H2-antagonists and tenofovir, atazanavir should be dosed 400 mg with ritonavir 100 mg once daily with food. In antiretroviral-experienced patients on a cobicistat-boosted regimen, the dosage of cobicistat with atazanavir needs to be increased if administered with H2-blockers; the recommended dose is cobicistat 150 mg/day with atazanavir 400 mg/day and 20 mg/day or less of famotidine or other comparably dosed H2-blocker. Significant reductions in atazanavir serum concentrations may lead to therapeutic failure and the development of HIV resistance. Closely monitor patients for antiretroviral therapeutic failure and resistance development during treatment with an H2- blocker.
Atazanavir; Cobicistat: (Major) Coadministration of H2-blockers with atazanavir reduces serum atazanavir concentrations; however, H2-blockers can be used under specific administration restrictions. Although data are insufficient to recommend atazanavir dosing in children < 40 kg receiving concomitant H2-blockers, the same recommendations regarding timing and maximum doses of concomitant H2-blockers should be followed. In treatment-naive patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 40 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. If a treatment-naive adult or adolescent (>= 40 kg) cannot tolerate ritonavir, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and the atazanavir dose should be increased to 400 mg once daily with food given at least 2 hours before or 10 hours after the H2- blocker. Data are insufficent to recommend atazanavir dosing in children or adolescents < 40 kg not receiving ritonavir boosting. In treatment-naive patients on a cobicistat-boosted regimen, cobicistat and atazanavir may be administered without dosage adjustment if given at the same time or a minimum of 10 hours after dosing of the H2-blocker. The H2-blocker dose should not exceed a dose that is comparable to 40 mg/day of famotidine in treatment-naive patients. In treatment-experienced patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. In treatment-experienced patients >= 40 kg receiving H2-antagonists and tenofovir, atazanavir should be dosed 400 mg with ritonavir 100 mg once daily with food. In antiretroviral-experienced patients on a cobicistat-boosted regimen, the dosage of cobicistat with atazanavir needs to be increased if administered with H2-blockers; the recommended dose is cobicistat 150 mg/day with atazanavir 400 mg/day and 20 mg/day or less of famotidine or other comparably dosed H2-blocker. Significant reductions in atazanavir serum concentrations may lead to therapeutic failure and the development of HIV resistance. Closely monitor patients for antiretroviral therapeutic failure and resistance development during treatment with an H2- blocker.
Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with H2-blockers can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid H2-blockers within 1 hour before or after the bisacodyl dosage.
Bismuth Subsalicylate: (Minor) H2-blockers may increase the systemic absorption of bismuth from bismuth-containing compounds like bismuth subsalicylate.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Minor) H2-blockers may increase the systemic absorption of bismuth from bismuth-containing compounds like bismuth subsalicylate.
Bosutinib: (Moderate) Bosutinib displays pH-dependent aqueous solubility; therefore, concomitant use of bosutinib and H2-blockers may result in decreased plasma exposure of bosutinib. Separate the administration of bosutinib and H2-blockers by more than 2 hours.
Budesonide: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant nizatidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Budesonide; Formoterol: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant nizatidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Budesonide; Glycopyrrolate; Formoterol: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant nizatidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Cabotegravir; Rilpivirine: (Moderate) Coadministration with nizatidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of nizatidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Cefpodoxime: (Moderate) H2-blockers should be avoided during treatment with cefpodoxime. Coadministration could result in antibiotic failure. H2-blockers increase gastric pH. Cefpodoxime proxetil requires low gastric pH for dissolution. While the rate of absorption is not affected, coadministration reduces cefpodoxime AUC, peak plasma concentration (by 42%), and extent of absorption (by 32%).
Cefuroxime: (Major) Avoid the concomitant use of H2-blockers and cefuroxime. Drugs that reduce gastric acidity, such as H2-blockers, can interfere with the oral absorption of cefuroxime axetil and may result in reduced antibiotic efficacy.
Cysteamine: (Major) Monitor white blood cell (WBC) cystine concentration closely when administering delayed-release cysteamine (Procysbi) with H2-blockers. Drugs that increase the gastric pH may cause the premature release of cysteamine from delayed-release capsules, leading to an increase in WBC cystine concentration.
Dacomitinib: (Moderate) Administer dacomitinib at least 6 hours before or 10 hours after taking nizatidine due to the risk of decreased plasma concentrations of dacomitinib which may impact efficacy. Although the effect of H2-blockers on dacomitinib pharmacokinetics has not been studied, coadministration with a proton pump inhibitor decreased the dacomitinib Cmax and AUC by 51% and 39%, respectively.
Dasatinib: (Major) Do not administer H2-blockers with dasatinib due to the potential for decreased dasatinib exposure and reduced efficacy. Consider using an antacid if acid suppression therapy is needed. Administer the antacid at least 2 hours prior to or 2 hours after the dose of dasatinib. Concurrent use of an H2-blocker reduced the mean Cmax and AUC of dasatinib by 63% and 61%, respectively.
Delavirdine: (Major) Coadministration of delavirdine with H2-blockers results in decreased absorption of delavirdine. Administration of delavirdine and H2-blockers should be separated by at least 1 hour. Chronic use of H2-blockers with delavirdine is not recommended.
Diphenhydramine; Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Dolutegravir; Rilpivirine: (Moderate) Coadministration with nizatidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of nizatidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Moderate) Coadministration with nizatidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of nizatidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Moderate) Coadministration with nizatidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of nizatidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Erlotinib: (Major) If concomitant use of erlotinib with nizatidine is necessary, erlotinib must be taken 10 hours after the last dose of nizatidine and at least 2 hours before the next dose. Erlotinib displays pH-dependent solubility with decreased solubility at a higher pH; the increased gastric pH resulting from nizatidine therapy may reduce the bioavailability of erlotinib. Increasing the dose of erlotinib without modifying the administration schedule is unlikely to compensate for loss of exposure. Erlotinib exposure was decreased by 33% and the Cmax by 54% when erlotinib was administered 2 hours after a single dose of an H2-antagonist. When administered at least 10 hours after an evening dose of an H2-antagonist and 2 hours before the morning dose, erlotinib exposure was decreased by 15% and Cmax by 17%.
Fosamprenavir: (Moderate) Monitor for decreased fosamprenavir efficacy if coadministered with H2-blockers. Concurrent use may decrease the plasma concentrations of fosamprenavir leading to a reduction of antiretroviral efficacy and the potential development of viral resistance.
Gefitinib: (Major) Avoid coadministration of nizatidine with gefitinib if possible due to decreased exposure to gefitinib, which may lead to reduced efficacy. If concomitant use is unavoidable, take gefitinib 6 hours after the last dose or 6 hours before the next dose of nizatidine. Gefitinib exposure is affected by gastric pH. Coadministration with high doses of an H2-blocker to maintain gastric pH above 5 decreased gefitinib exposure by 47%.
Infigratinib: (Moderate) Separate the administration of infigratinib and H2-receptor antagonists if concomitant use is necessary. Coadministration may decrease infigratinib exposure resulting in decreased efficacy. Administer infigratinib two hours before or ten hours after an H2-receptor antagonist.
Iron: (Minor) The bioavailability of oral iron salts is influenced by gastric pH, and the concomitant administration of H2-blockers can decrease iron absorption. The non-heme ferric form of iron needs an acidic intragastric pH to be reduced to ferrous and to be absorbed. Iron salts and polysaccharide-iron complex provide non-heme iron. H2-blockers have long-lasting effects on the secretion of gastric acid and thus, increase the pH of the stomach. The increase in intragastric pH can interfere with the absorption of iron salts.
Itraconazole: (Moderate) When administering H2-blockers with the 100 mg itraconazole capsule and 200 mg itraconazole tablet formulations, systemic exposure to itraconazole is decreased. Conversely, exposure to itraconazole is increased when H2-blockers are administered with the 65 mg itraconazole capsule. Administer H2-blockers at least 2 hours before or 2 hours after the 100 mg capsule or 200 mg tablet. Monitor for increased itraconazole-related adverse effects if H2-blockers are administered with itraconazole 65 mg capsules.
Ketoconazole: (Major) Avoid use of H2-blockers with ketoconazole. Medications that increase gastric pH may impair ketoconazole absorption.
Ledipasvir; Sofosbuvir: (Major) Solubility of ledipasvir decreases as gastric pH increases; thus, coadministration of ledipasvir; sofosbuvir with H2-blockers may result in lower ledipasvir plasma concentrations. Ledipasvir; sofosbuvir can be administered with H2-blockers if given simultaneously or separated by 12 hours. The H2-blocker dose should not exceed a dose that is comparable to famotidine 40 mg twice daily.
Levoketoconazole: (Major) Avoid use of H2-blockers with ketoconazole. Medications that increase gastric pH may impair ketoconazole absorption.
Mefloquine: (Moderate) H2-blockers may increase plasma concentrations of mefloquine. Patients on chronic mefloquine therapy might be at increased risk of adverse reactions, especially patients with a neurological or psychiatric history. In a small study involving 6 healthy subjects and 6 peptic ulcer patients, cimetidine increased the Cmax and AUC of mefloquine. In the study, the pharmacokinetics of mefloquine were determined after receiving a single oral mefloquine 500 mg dose alone and after 3-days of cimetidine 400 mg PO twice daily. In both healthy subjects and peptic ulcer patients, Cmax was increased 42.4% and 20.5%, respectively. The AUC was increased by 37.5% in both groups. Elimination half-life, total clearance, and volume of distribution were not significantly affected. An increase in adverse reactions was not noted.
Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Naproxen; Esomeprazole: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Naproxen; Pseudoephedrine: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Neratinib: (Major) Take neratinib at least 2 hours before the next dose of an H2-blocker or 10 hours after the last dose of an H2-blocker due to decreased absorption and systemic exposure of neratinib; the solubility of neratinib decreases with increasing pH of the GI tract. The Cmax and AUC of neratinib were reduced by 57% and 48%, respectively, when administered 2 hours after a daily dose of ranitidine 300 mg. The Cmax and AUC of neratinib were reduced by 44% and 32%, respectively, when administered 2 hours before ranitidine 150 mg twice daily (given approximately 12 hours apart).
Nilotinib: (Moderate) If concomitant use of these agents is necessary, administer the H2-blocker approximately 10 hours before and approximately 2 hours after the nilotinib dose. Nilotinib displays pH-dependent solubility with decreased solubility at a higher pH. The concomitant use of nilotinib and H2-blockers that elevate the gastric pH may reduce the bioavailability of nilotinib. In a study in healthy subjects, there was no significant change in nilotinib pharmacokinetics when a single 400-mg nilotinib dose was given 10 hours after and 2 hours prior to famotidine.
Octreotide: (Moderate) Coadministration of oral octreotide with H2-blockers may require increased doses of octreotide. Coadministration of oral octreotide with drugs that alter the pH of the upper GI tract, including H2-blockers, may alter the absorption of octreotide and lead to a reduction in bioavailability.
Pazopanib: (Major) Avoid coadministration of pazopanib with H2-blockers due to decreased absorption of pazopanib, which may decrease efficacy. If concomitant administration with a gastric acid-reducing agent is unavoidable, consider the use of a short-acting antacid in place of an H2-blocker; separate administration of the short-acting antacid and pazopanib by several hours to avoid a reduction in pazopanib exposure. Concomitant use of pazopanib with a proton pump inhibitor decreased pazopanib exposure (AUC and Cmax) by approximately 40%.
Pexidartinib: (Moderate) Administer pexidartinib 2 hours before or 10 hours after H2-blockers as concurrent administration may reduce pexidartinib exposure. Although the effects of H2-blockers on pexidartinib pharmacokinetics have not been studied, other acid-reducing agents have been shown to decrease pexidartinib exposure by 50%.
Polyethylene Glycol; Electrolytes; Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with H2-blockers can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid H2-blockers within 1 hour before or after the bisacodyl dosage.
Rilpivirine: (Moderate) Coadministration with nizatidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of nizatidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Risedronate: (Major) Use of H2-blockers with delayed-release risedronate tablets (Atelvia) is not recommended. Co-administration of drugs that raise stomach pH increases risedronate bioavailability due to faster release of the drug from the enteric coated tablet. This interaction does not apply to risedronate immediate-release tablets.
Secretin: (Major) Discontinue use of H2-blockers at least 2 days before administering secretin. Patients who are receiving H2-blockers at the time of stimulation testing may be hyperresponsive to secretin stimulation, falsely suggesting gastrinoma.
Selpercatinib: (Major) Avoid coadministration of selpercatinib with nizatidine due to the risk of decreased selpercatinib exposure which may reduce its efficacy. If concomitant use is unavoidable, take selpercatinib 2 hours before or 10 hours after administration of nizatidine. Coadministration with acid-reducing agents decreases selpercatinib plasma concentrations; however, no clinically significant differences in the pharmacokinetics of selpercatinib were observed when given under fasting conditions with multiple daily doses of another H2-receptor antagonist given 10 hours prior to and 2 hours after the selpercatinib dose.
Sofosbuvir; Velpatasvir: (Major) H2-blockers may be administered simultaneously with or 12 hours apart from velpatasvir. H2-blocker doses should not exceed doses comparable to famotidine 40 mg twice daily. Velpatasvir solubility decreases as pH increases; therefore, drugs that increase gastric pH are expected to decrease the concentrations of velpatasvir, potentially resulting in loss of antiviral efficacy.
Sofosbuvir; Velpatasvir; Voxilaprevir: (Major) H2-blockers may be administered simultaneously with or 12 hours apart from velpatasvir. H2-blocker doses should not exceed doses comparable to famotidine 40 mg twice daily. Velpatasvir solubility decreases as pH increases; therefore, drugs that increase gastric pH are expected to decrease the concentrations of velpatasvir, potentially resulting in loss of antiviral efficacy.
Sonidegib: (Moderate) Based on population PK analysis, the concomitant administration of a histamine-2-receptor antagonist such as nizatidine decreases the geometric mean sonidegib steady-state AUC (0-24 hours) value by 34%.
Sotorasib: (Major) Avoid coadministration of sotorasib and gastric acid-reducing agents, such as H2-receptor antagonists. Coadministration may decrease sotorasib exposure resulting in decreased efficacy. If necessary, sotorasib may be administered 4 hours before or 10 hours after a locally acting antacid. Coadministration with an H2-receptor antagonist decreased sotorasib exposure by 38% under fed conditions.
Sparsentan: (Major) Avoid concurrent use of sparsentan and H2 receptor antagonists due to the risk for decreased sparsentan exposure which may reduce its efficacy. Medications that affect gastric pH may reduce sparsentan absorption.
Sumatriptan; Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Thalidomide: (Moderate) Thalidomide and other agents that slow cardiac conduction such as H2-blockers should be used cautiously due to the potential for additive bradycardia.

Axid/Nizatidine Oral Cap: 150mg, 300mg

300 mg/day PO.

300 mg/day PO.

300 mg/day PO.

12 years and older: 300 mg/day PO.
1 to 11 years: 10 to 20 mg/kg/day PO has been studied.

6 months and older: 10 to 20 mg/kg/day PO has been studied.
1 to 5 months: 10 mg/kg/day PO has been studied.

10 mg/kg/day PO has been studied.

Mechanism of Action: Nizatidine competitively inhibits the binding of histamine to the H2-receptors on the gastric basolateral membrane of parietal cells, reducing basal and nocturnal gastric acid secretions. The drug also decreases the gastric acid response to stimuli such as food, caffeine, insulin, betazole, or pentagastrin. Nizatidine reduces the total volume of gastric juice, thus indirectly decreasing pepsin secretion. The drug does not appear to alter gastric motility, gastric emptying, esophageal pressures, biliary secretions, or pancreatic secretions. Nizatidine may aid in gastromucosal healing, and it may protect the mucosa from the irritant effects caused by aspirin and nonsteroidal antiinflammatory agents. H2-blockers, as single agents, do not erradicate H. pylori infection.

Nizatidine is administered orally.
 
The drug is roughly 35% protein-bound. Approximately 7% of an oral dose is metabolized in the liver to N2-monodesmethylnizatidine, which has H2-antagonist activity. Approximately 60% of unchanged drug and its metabolites are excreted in the urine and approximately 6% in the feces. Nizatidine is eliminated by both glomerular filtration and active tubular secretion. The elimination half-life is 1 to 2 hours.

The bioavailability of nizatidine is about 95% in patients with normal renal function. The presence of food in the GI tract appears to increase the absorption of nizatidine. The drug distribution is unknown.

There are no adequate and well-controlled studies of nizatidine use during pregnancy; however, animal reproduction studies do not suggest a risk for fetal harm and epidemiologic data are available. Reproduction studies in pregnant rats at nizatidine oral doses up to 1,500 mg/kg/day (40.5 times the recommended human dose based on body surface area) and in pregnant rabbits at doses up to 275 mg/kg/day (14.6 times the recommended human dose based on body surface area) have revealed no evidence of impaired fertility or harm to the fetus. Epidemiological evidence based on the use of H2-blockers during pregnancy does not suggest an increase in fetal malformations compared to the normal population, even with first trimester use. In another study of human data, exposure to H2-blockers was not associated with an increased risk for congenital malformations (adjusted OR 1.03, 95% CI: 0.80, 1.32); also, no such association was found when therapeutic pregnancy terminations were included in the analysis (adjusted OR 1.17, 95% CI: 0.93, 1.46). Exposure to H2-blockers was not associated with perinatal mortality, premature delivery, low birth weight, or low Apgar scores. Guidelines recommend a trial of lifestyle modifications as first-line therapy for heartburn and gastroesophageal reflux disease (GERD) during pregnancy, followed by antacids if lifestyle adjustments are ineffective. For ongoing symptoms, an H2-blocker can be used. Other medications should be reserved for pregnant patients who fail H2-blocker therapy. Due to the relatively smaller amount of data available with nizatidine as compared with other H2-blockers, some experts recommend consideration of an H2-blocker with more data if needed during pregnancy, such as famotidine. Self-medication with H2-blockers (OTC formulations) during pregnancy is not recommended. Pregnant patients should see their health care professional for a proper diagnosis and for treatment recommendations. H2-blockers have been used in limited circumstances at term to prevent acid aspiration during labor; some guidelines recommend an H2-blocker (PO or IV) for all women presenting for cesarean delivery.

Studies conducted in lactating women have shown that 0.1% of the administered oral dose of nizatidine is secreted in human milk in proportion to plasma concentrations. Because of the growth depression in pups reared by lactating rats treated with nizatidine in animal studies, the prescribing label recommends that a decision be made whether to discontinue breast-feeding or discontinue the drug, taking into account the importance of the drug to the lactating individual.  According to guidelines, if heartburn/gastroesophageal reflux (GERD) symptoms persist after delivery, antacids and sucralfate are safe to use during lactation because they are not concentrated in breast milk. H2-blockers are excreted in breast milk, but cimetidine and famotidine are considered safe for use during lactation and may be used if symptoms persist despite antacid use.