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Kapidex
Overview
What is Kapidex?
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What are the available doses of Kapidex?
What should I talk to my health care provider before I take Kapidex?
Teratogenic Effects
Pregnancy Category B. There are no adequate and well-controlled
studies with dexlansoprazole in pregnant women. There were no adverse fetal
effects in animal reproduction studies of dexlansoprazole in rabbits. Because
animal reproduction studies are not always predictive of human response, KAPIDEX
should be used during pregnancy only if clearly needed.
A reproduction study conducted in rabbits at oral dexlansoprazole doses up to
30 mg per kg per day (approximately 9-fold the maximum recommended human
dexlansoprazole dose [60 mg] based on body surface area [BSA]) revealed no
evidence of harm to the fetus due to dexlansoprazole. In addition, reproduction
studies performed in pregnant rats with oral lansoprazole at doses up to 150 mg
per kg per day (40 times the recommended human dose based on BSA) and in
pregnant rabbits at oral lansoprazole doses up to 30 mg per kg per day (16 times
the recommended human dose based on BSA) revealed no evidence of impaired
fertility or harm to the fetus due to lansoprazole.
It is not known whether dexlansoprazole is excreted in human
milk. However, lansoprazole and its metabolites are present in rat milk
following the administration of lansoprazole. As many drugs are excreted in
human milk, and because of the potential for tumorigenicity shown for
lansoprazole in rat carcinogenicity studies , a decision should be made whether to discontinue nursing or
to discontinue the drug, taking into account the importance of the drug to the
mother.
Safety and effectiveness of KAPIDEX in pediatric patients (less
than 18 years of age) have not been established.
In clinical studies of KAPIDEX, 11% of patients were aged 65
years and over. No overall differences in safety or effectiveness were observed
between these patients and younger patients, and other reported clinical
experience has not identified significant differences in responses between
geriatric and younger patients, but greater sensitivity of some older
individuals cannot be ruled out .
No dosage adjustment of KAPIDEX is necessary in patients with
renal impairment. The pharmacokinetics of dexlansoprazole in patients with renal
impairment are not expected to be altered since dexlansoprazole is extensively
metabolized in the liver to inactive metabolites, and no parent drug is
recovered in the urine following an oral dose of dexlansoprazole
No dosage adjustment for KAPIDEX is necessary for patients with
mild hepatic impairment (Child-Pugh Class A). KAPIDEX 30 mg should be considered
for patients with moderate hepatic impairment (Child-Pugh Class B). No studies
have been conducted in patients with severe hepatic impairment (Child-Pugh Class
C)
How should I use Kapidex?
KAPIDEX is indicated for healing of all grades of erosive
esophagitis (EE) for up to 8 weeks.
KAPIDEX is indicated to maintain healing of EE for up to 6
months.
KAPIDEX is indicated for the treatment of heartburn associated
with non-erosive gastroesophageal reflux disease (GERD) for 4 weeks.
KAPIDEX is available as capsules in 30 mg and 60 mg strengths for
adult use. Directions for use in each indication are summarized in Table 1.
No adjustment for KAPIDEX is necessary for patients with mild
hepatic impairment (Child-Pugh Class A). Consider a maximum daily dose of 30 mg
for patients with moderate hepatic impairment (Child-Pugh Class B). No studies
have been conducted in patients with severe hepatic impairment (Child-Pugh Class
C)
No dosage adjustment is necessary for elderly patients or for patients with
renal impairment .
KAPIDEX can be taken without regard to food.
KAPIDEX should be swallowed whole.
What interacts with Kapidex?
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What are the warnings of Kapidex?
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What are the precautions of Kapidex?
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What are the side effects of Kapidex?
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What should I look out for while using Kapidex?
KAPIDEX is contraindicated in patients with known
hypersensitivity to any component of the formulation . Hypersensitivity and anaphylaxis have
been reported with KAPIDEX use .
What might happen if I take too much Kapidex?
There have been no reports of significant overdose of KAPIDEX.
Multiple doses of KAPIDEX 120 mg and a single dose of KAPIDEX 300 mg did not
result in death or other severe adverse events. Dexlansoprazole is not expected
to be removed from the circulation by hemodialysis. If an overdose occurs,
treatment should be symptomatic and supportive.
How should I store and handle Kapidex?
Store bottles of 1000 SINGULAIR 5-mg chewable tablets and 8000 SINGULAIR 10-mg film-coated tablets at 25°C (77°F), excursions permitted to 15-30°C (59-86°F) [see USP Controlled Room Temperature]. Protect from moisture and light. Store in original container. When product container is subdivided, repackage into a well-closed, light resistant container. KAPIDEX delayed release capsules, 30 mg, are opaque, blue and gray with TAP and "30" imprinted on the capsule and supplied as:Store at 25°C (77°F); excursions permitted to 15-30°C (59-86°F). [See USP Controlled Room Temperature]KAPIDEX delayed release capsules, 30 mg, are opaque, blue and gray with TAP and "30" imprinted on the capsule and supplied as:Store at 25°C (77°F); excursions permitted to 15-30°C (59-86°F). [See USP Controlled Room Temperature]
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
Dexlansoprazole is a PPI that suppresses gastric acid secretion
by specific inhibition of the (H,K)-ATPase in the gastric parietal cell. By acting specifically
on the proton pump, dexlansoprazole blocks the final step of acid
production.
Antisecretory Activity
The effects of KAPIDEX 60 mg (n = 20) or lansoprazole 30 mg (n = 23) once
daily for five days on 24-hour intragastric pH were assessed in healthy subjects
in a multiple-dose crossover study. The results are summarized in Table 3.
Serum Gastrin Effects
The effect of KAPIDEX on serum gastrin concentrations was evaluated in
approximately 3460 patients in clinical trials up to 8 weeks and in 1023
patients for up to 6 to 12 months. The mean fasting gastrin concentrations
increased from baseline during treatment with KAPIDEX 30 mg and 60 mg doses. In
patients treated for more than 6 months, mean serum gastrin levels increased
during approximately the first 3 months of treatment and were stable for the
remainder of treatment. Mean serum gastrin levels returned to pre-treatment
levels within one month of discontinuation of treatment.
Enterochromaffin-Like Cell (ECL)
Effects
There were no reports of ECL cell hyperplasia in gastric biopsy specimens
obtained from 653 patients treated with KAPIDEX 30 mg, 60 mg or 90 mg for up to
12 months.
During lifetime exposure of rats dosed daily with up to 150 mg per kg per day
of lansoprazole, marked hypergastrinemia was observed followed by ECL cell
proliferation and formation of carcinoid tumors, especially in female rats .
Effect on Cardiac Repolarization
A study was conducted to assess the potential of KAPIDEX to prolong the
QT/QT interval in healthy adult subjects. KAPIDEX doses
of 90 mg or 300 mg did not delay cardiac repolarization compared to placebo. The
positive control (moxifloxacin) produced statistically significantly greater
mean maximum and time-averaged QT/QTintervals compared
to placebo.
The dual delayed release formulation of KAPIDEX results in a
dexlansoprazole plasma concentration-time profile with two distinct peaks; the
first peak occurs 1 to 2 hours after administration, followed by a second peak
within 4 to 5 hours (see ). Dexlansoprazole is
eliminated with a half-life of approximately 1 to 2 hours in healthy subjects
and in patients with symptomatic GERD. No accumulation of dexlansoprazole occurs
after multiple, once daily doses of KAPIDEX 30 mg or 60 mg, although mean
AUC and C values of
dexlansoprazole were slightly higher (less than 10%) on day 5 than on day 1.
Figure 1: Mean Plasma Dexlansoprazole Concentration – Time
Profile Following Oral Administration of 30 or 60 mg KAPIDEXOnce Daily for 5
Days in Healthy Subjects
The pharmacokinetics of dexlansoprazole are highly variable, with percent
coefficient of variation (CV%) values for C, AUC, and
CL/F of greater than 30% (see ).
Absorption
After oral administration of KAPIDEX 30 mg or 60 mg to healthy subjects and
symptomatic GERD patients, mean C and AUC values of
dexlansoprazole increased approximately dose proportionally (see ).
Distribution
Plasma protein binding of dexlansoprazole ranged from 96.1% to 98.8% in
healthy subjects and was independent of concentration from 0.01 to 20 mcg per
mL. The apparent volume of distribution (V/F) after
multiple doses in symptomatic GERD patients was 40.3 L.
Metabolism
Dexlansoprazole is extensively metabolized in the liver by oxidation,
reduction, and subsequent formation of sulfate, glucuronide and glutathione
conjugates to inactive metabolites. Oxidative metabolites are formed by the
cytochrome P450 (CYP) enzyme system including hydroxylation mainly by CYP2C19,
and oxidation to the sulfone by CYP3A4.
CYP2C19 is a polymorphic liver enzyme which exhibits three phenotypes in the
metabolism of CYP2C19 substrates; extensive metabolizers (*1/*1), intermediate
metabolizers (*1/mutant) and poor metabolizers (mutant/mutant). Dexlansoprazole
is the major circulating component in plasma regardless of CYP2C19 metabolizer
status. In CYP2C19 intermediate and extensive metabolizers, the major plasma
metabolites are 5-hydroxy dexlansoprazole and its glucuronide conjugate, while
in CYP2C19 poor metabolizers dexlansoprazole sulfone is the major plasma
metabolite.
Elimination
Following the administration of KAPIDEX, no unchanged dexlansoprazole is
excreted in urine. Following the administration of [C]dexlansoprazole to 6 healthy male subjects, approximately
50.7% (standard deviation (SD): 9.0%) of the administered radioactivity was
excreted in urine and 47.6% (SD: 7.3%) in the feces. Apparent clearance (CL/F)
in healthy subjects was 11.4 to 11.6 L/h, respectively, after 5-days of 30 or 60
mg once daily administration.
Effect of CYP2C19 Polymorphism on Systemic
Exposure of Dexlansoprazole
Systemic exposure of dexlansoprazole is generally higher in intermediate and
poor metabolizers. In male Japanese subjects who received a single dose of
KAPIDEX 30 mg or 60 mg (N=2 to 6 subjects/group), mean dexlansoprazole C and AUC values were up to 2 times higher in intermediate
compared to extensive metabolizers; in poor metabolizers, mean C was up to 4 times higher and mean AUC was up to 12 times
higher compared to extensive metabolizers. Though such study was not conducted
in Caucasians and African Americans, it is expected dexlansoprazole exposure in
these races will be affected by CYP2C19 phenotypes as well.
In food-effect studies in healthy subjects receiving KAPIDEX
under various fed conditions compared to fasting, increases in C ranged from 12% to 55%, increases in AUC ranged from 9% to
37%, and t varied (ranging from a decrease of 0.7
hours to an increase of 3 hours). No significant differences in mean
intragastric pH were observed between fasted and various fed conditions.
However, the percentage of time intragastric pH exceeded 4 over the 24-hour
dosing interval decreased slightly when KAPIDEX was administered after a meal
(57%) relative to fasting (64%), primarily due to a decreased response in
intragastric pH during the first 4 hours after dosing. Because of this, while
KAPIDEX can be taken without regard to food, some patients may benefit from
administering the dose prior to a meal if post-meal symptoms do not resolve
under post-fed conditions.
Pediatric Use
The pharmacokinetics of dexlansoprazole in patients under the age of 18 years
have not been studied.
Geriatric Use
The terminal elimination half-life of dexlansoprazole is significantly
increased in geriatric subjects compared to younger subjects (2.23 and 1.5
hours, respectively); this difference is not clinically relevant.
Dexlansoprazole exhibited higher systemic exposure (AUC) in geriatric subjects
(34.5% higher) than younger subjects. No dosage adjustment is needed in
geriatric patients
Renal Impairment
Dexlansoprazole is extensively metabolized in the liver to inactive
metabolites, and no parent drug is recovered in the urine following an oral dose
of dexlansoprazole. Therefore, the pharmacokinetics of dexlansoprazole are not
expected to be altered in patients with renal impairment, and no studies were
conducted in subjects with renal impairment . In addition, the
pharmacokinetics of lansoprazole were studied in patients with mild, moderate or
severe renal impairment; results demonstrated no need for a dose adjustment for
this patient population
Hepatic Impairment
In a study of 12 patients with moderately impaired hepatic function who
received a single oral dose of KAPIDEX 60 mg, plasma exposure (AUC) of bound and
unbound dexlansoprazole in the hepatic impairment group was approximately 2
times greater compared to subjects with normal hepatic function. This difference
in exposure was not due to a difference in protein binding between the two liver
function groups. No adjustment for KAPIDEX is necessary for patients with mild
hepatic impairment (Child-Pugh Class A). KAPIDEX 30 mg should be considered for
patients with moderate hepatic impairment (Child-Pugh Class B). No studies have
been conducted in patients with severe hepatic impairment (Child-Pugh Class C)
Gender
In a study of 12 male and 12 female healthy subjects who received a single
oral dose of KAPIDEX 60 mg, females had higher systemic exposure (AUC) (42.8%
higher) than males. No dosage adjustment is necessary in patients based on
gender.
Warfarin
In a study of 20 healthy subjects, co-administration of KAPIDEX 90 mg once
daily for 11 days with a single 25 mg oral dose of warfarin on day 6 did not
result in any significant differences in the pharmacokinetics of warfarin or INR
compared to administration of warfarin with placebo. However, there have been
reports of increased INR and prothrombin time in patients receiving PPIs and
warfarin concomitantly .
Cytochrome P 450 Interactions
Dexlansoprazole is metabolized, in part, by CYP2C19 and CYP3A4 .
In vitro studies have shown that KAPIDEX is not likely to inhibit CYP
isoforms 1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 or 3A4. As such, no
clinically relevant interactions with drugs metabolized by these CYP enzymes
would be expected. Furthermore, clinical drug-drug interaction studies in mainly
CYP2C19 extensive and intermediate metabolizers have shown that KAPIDEX does not
affect the pharmacokinetics of diazepam, phenytoin, or theophylline. The
subjects' CYP1A2 genotypes in the drug-drug interaction study with theophylline
were not determined.
Non-Clinical Toxicology
KAPIDEX is contraindicated in patients with known hypersensitivity to any component of the formulation . Hypersensitivity and anaphylaxis have been reported with KAPIDEX use .Increased nephrotoxicity has been reported following concomitant administration of cephalosporins and aminoglycoside antibiotics.
Symptomatic response with KAPIDEX does not preclude the presence of gastric malignancy.
The safety of KAPIDEX was evaluated in 4548 patients in controlled and uncontrolled clinical studies, including 863 patients treated for at least 6 months and 203 patients treated for one year. Patients ranged in age from 18 to 90 years (median age 48 years), with 54% female, 85% Caucasian, 8% Black, 4% Asian, and 3% other races. Six randomized controlled clinical trials were conducted for the treatment of EE, maintenance of healed EE, and symptomatic GERD, which included 896 patients on placebo, 455 patients on KAPIDEX 30 mg, 2218 patients on KAPIDEX 60 mg, and 1363 patients on lansoprazole 30 mg once daily.
As clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Most Commonly Reported Adverse Reactions
The most common adverse reactions (≥2%) that occurred at a higher incidence for KAPIDEX than placebo in the controlled studies are presented in Table 2.
Adverse Reactions Resulting in Discontinuation
In controlled clinical studies, the most common adverse reaction leading to discontinuation from KAPIDEX therapy was diarrhea (0.7%).
Other Adverse Reactions
Other adverse reactions that were reported in controlled studies at an incidence of less than 2% are listed below by body system:
Blood and Lymphatic System Disorders:
Cardiac Disorders:
Ear and Labyrinth Disorders:
Endocrine Disorders:
Eye Disorders:
Gastrointestinal Disorders:
General Disorders and Administration Site Conditions:
Hepatobiliary Disorders:
Immune System Disorders:
Infections and Infestations:
Injury, Poisoning and Procedural Complications:
Laboratory Investigations:
Metabolism and Nutrition Disorders:
Musculoskeletal and Connective Tissue Disorders:
Nervous System Disorders:
Psychiatric Disorders:
Renal and Urinary Disorders:
Reproductive System and Breast Disorders:
Respiratory, Thoracic and Mediastinal Disorders:
Skin and Subcutaneous Tissue Disorders:
Vascular Disorders:
Additional adverse reactions that were reported in a long-term uncontrolled study and were considered related to KAPIDEX by the treating physician included: anaphylaxis, auditory hallucination, B-cell lymphoma, central obesity, cholecystitis acute, decreased hemoglobin, dehydration, diabetes mellitus, dysphonia, epistaxis, folliculitis, gastrointestinal pain, gout, herpes zoster, hyperglycemia, hyperlipidemia, hypothyroidism, increased neutrophils, MCHC decrease, neutropenia, oral soft tissue disorder, rectal tenesmus, restless legs syndrome, somnolence, thrombocythemia, tonsillitis.
Other adverse reactions not observed with KAPIDEX, but occurring with the racemate lansoprazole can be found in the lansoprazole package insert, ADVERSE REACTIONS section.
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
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