What Is The Chemical Makeup Of Dexilant
Pharmacology refers to the chemical makeup and behavior of DEXILANT (dexlansoprazole capsule, delayed release).
Description
The active ingredient in DEXILANT (dexlansoprazole) delayed-release capsules, a proton pump inhibitor, is (+)-2-[(R)-{[3-methyl-4-(2,two,ii-trifluoroethoxy)pyridin-2-yl] methyl} sulfinyl]-1H-benzimidazole, a compound that inhibits gastric acid secretion. Dexlansoprazole is the R-enantiomer of lansoprazole (a racemic mixture of the R- and S-enantiomers). Its empirical formula is: C16H14F3NthreeO2South, with a molecular weight of 369.36. Dexlansoprazole has the following chemic construction:
Dexlansoprazole is a white to nearly white crystalline powder which melts with decomposition at 140°C. Dexlansoprazole is freely soluble in dimethylformamide, methanol, dichloromethane, ethanol, and ethyl acetate; and soluble in acetonitrile; slightly soluble in ether; and very slightly soluble in water; and practically insoluble in hexane.
Dexlansoprazole is stable when exposed to light. Dexlansoprazole is more than stable in neutral and alkaline conditions than acidic weather condition.
Dexlansoprazole is supplied for oral assistants as a dual delayed-release conception in capsules. The capsules comprise dexlansoprazole in a mixture of ii types of enteric-coated granules with dissimilar pH-dependent dissolution profiles [see Clinical Pharmacology (12.3)].
DEXILANT delayed-release capsules are available in ii dosage strengths: 30 and 60 mg, per capsule. Each capsule contains enteric-coated granules consisting of dexlansoprazole (agile ingredient) and the following inactive ingredients: sugar spheres, magnesium carbonate, sucrose, low-substituted hydroxypropyl cellulose, titanium dioxide, hydroxypropyl cellulose, hypromellose 2910, talc, methacrylic acrid copolymers, polyethylene glycol 8000, triethyl citrate, polysorbate 80, and colloidal silicon dioxide. The components of the capsule shell include the following inactive ingredients: hypromellose, carrageenan and potassium chloride. Based on the capsule shell color, blue contains FD&C Blueish No. two aluminum lake; grayness contains blackness ferric oxide; and both comprise titanium dioxide.
Clinical Pharmacology
mechanism of activity
Dexlansoprazole belongs to a class of antisecretory compounds, the substituted benzimidazoles, that suppress gastric acid secretion past specific inhibition of the (H+, Grand+)-ATPase at the secretory surface of the gastric parietal cell. Considering this enzyme is regarded as the acid (proton) pump within the parietal cell, dexlansoprazole has been characterized as a gastric proton-pump inhibitor, in that it blocks the final footstep of acid production.
pharmacodynamics
Antisecretory Activity
The effects of DEXILANT threescore mg (n=20) or lansoprazole xxx mg (n=23) once daily for five days on 24 60 minutes intragastric pH were assessed in healthy subjects in a multiple-dose crossover study. The results are summarized in Table 5.
| DEXILANT 60 mg | Lansoprazole 30 mg |
|---|---|
| Hateful Intragastric pH | |
| 4.55 | 4.13 |
| % Time Intragastric pH >4 (hours) | |
| 71 | 60 |
Serum Gastrin Effects
The effect of dexlansoprazole on serum gastrin concentrations was evaluated in approximately 3460 patients in clinical trials up to eight weeks and in 1023 patients for upward to half-dozen to 12 months. The mean fasting gastrin concentrations increased from baseline during handling with 30 and 60 mg DEXILANT. In patients treated for more than half dozen months, hateful serum gastrin levels increased during approximately the starting time iii months of treatment and were stable for the remainder of handling. Mean serum gastrin levels returned to pre-treatment levels within i calendar month of discontinuation of treatment.
Increased gastrin causes enterochromaffin-like cell hyperplasia and increased serum CgA levels. The increased CgA levels may cause false positive results in diagnostic investigations for neuroendocrine tumors [see Warnings and Precautions (5.eight)].
Enterochromaffin-Like Cell (ECL) Effects
In that location were no reports of ECL jail cell hyperplasia in gastric biopsy specimens obtained from 653 patients treated with DEXILANT 30, 60, or 90 mg for upwardly to 12 months.
During lifetime exposure of rats dosed daily with up to 150 mg/kg/solar day of lansoprazole, marked hypergastrinemia was observed followed by ECL cell proliferation and germination of carcinoid tumors, especially in female rats [come across Nonclinical Toxicology (13.one)].
Cardiac Electrophysiology
At a dose 5 times the maximum recommended dose, dexlansoprazole does not prolong the QT interval to whatever clinically relevant extent.
pharmacokinetics
The dual delayed-release conception of DEXILANT results in a dexlansoprazole plasma concentration-time contour with ii distinct peaks; the first summit occurs one to 2 hours later on assistants, followed by a second top within 4 to 5 hours (come across Figure 1 ). Dexlansoprazole is eliminated with a half-life of approximately one to two hours in good for you subjects and in patients with symptomatic GERD. No accumulation of dexlansoprazole occurs later multiple, one time daily doses of DEXILANT xxx or 60 mg although mean AUCt and Cmax values of dexlansoprazole were slightly college (less than 10%) on 24-hour interval 5 than on Solar day 1.
| Figure 1: Hateful Plasma Dexlansoprazole Concentration – Fourth dimension Contour Following Oral Assistants of 30 or 60 mg DEXILANT In one case Daily for v Days in Good for you Developed Subjects |
 |
The pharmacokinetics of dexlansoprazole are highly variable, with per centum coefficient of variation (%CV) values for Cmax, AUC, and CL/F of greater than 30% (see Table 6).
| Dose (mg) | Cmax (ng/mL) | AUC24 (ng∙h/mL) | CL/F (Fifty/h) |
|---|---|---|---|
| thirty | 658 (40%) | 3275 (47%) | eleven.4 (48%) |
| lx | 1397 (51%) | 6529 (60%) | 11.half-dozen (46%) |
Absorption
Later oral administration of DEXILANT 30 or threescore mg to good for you subjects and symptomatic GERD patients, hateful Cmax and AUC values of dexlansoprazole increased approximately dose proportionally (come across Effigy 1 ).
When granules of DEXILANT 60 mg are mixed with water and dosed via NG tube or orally via syringe, the bioavailability (Cmax and AUC) of dexlansoprazole was like to that when DEXILANT 60 mg was administered every bit an intact capsule [run into Dosage and Administration (2.3)].
Effect on Food
In food-effect studies in salubrious subjects receiving DEXILANT nether various fed conditions compared to fasting, increases in Cmax ranged from 12 to 55%, increases in AUC ranged from ix to 37%, and Tmax varied (ranging from a decrease of 0.7 hours to an increment of three hours) [see Dosage and Assistants (2.3)].
Distribution
Plasma protein binding of dexlansoprazole ranged from 96 to 99% in healthy subjects and was independent of concentration from 0.01 to twenty mcg/mL. The apparent volume of distribution (Vz/F) after multiple doses in symptomatic GERD patients was forty Fifty.
Elimination
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 past 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 (*i/*i), 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.
Excretion
Following the administration of DEXILANT, no unchanged dexlansoprazole is excreted in urine. Following the administration of [14C] dexlansoprazole to six healthy male subjects, approximately l.7% (standard deviation (SD): 9.0%) of the administered radioactive decay was excreted in urine and 47.6% (SD: seven.3%) in the feces. Apparent clearance (CL/F) in healthy subjects was 11.4 to 11.6 L/hour, respectively, after 5 days of 30 or sixty mg once daily administration.
Specific Populations
Age: Pediatric Population
The pharmacokinetics of dexlansoprazole in patients under the historic period of 12 years accept non been studied.
Patients 12 to 17 Years of Age
- The pharmacokinetics of dexlansoprazole were studied in 36 patients 12 to 17 years of age with symptomatic GERD in a multi-center trial. Patients were randomized to receive DEXILANT 30 or 60 mg once daily for seven days. The dexlansoprazole mean Cmax and AUC in patients 12 to 17 years of age were 105 and 88%, respectively, compared to those observed in adults at the 30 mg dose, and were 81 and 78%, respectively, at the lx mg dose (encounter Tables 6 and 7).
| Dose | Cmax (ng/mL) | AUCtau (ng∙h/mL) | CL/F (L/h) |
|---|---|---|---|
| 30 mg | 691 | 2886 | 12.8 |
| 60 mg | 1136 | 5120 | 15.3 |
Historic period: Geriatric Population
The last elimination half-life of dexlansoprazole is significantly increased in geriatric subjects compared to younger subjects (2.2 and 1.v hours, respectively). Dexlansoprazole exhibited higher systemic exposure (AUC) in geriatric subjects (34% college) than younger subjects [see Use in Specific Populations (8.v)].
Sex
In a written report of 12 male and 12 female healthy subjects who received a single dose of DEXILANT 60 mg, females had higher systemic exposure (AUC) (43% higher) than males. This difference in exposure betwixt males and female does not represent a pregnant prophylactic business.
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 exist altered in patients with renal impairment, and no studies were conducted in patients with renal damage. In addition, the pharmacokinetics of lansoprazole were not clinically dissimilar in patients with mild, moderate or severe renal impairment compared to good for you subjects with normal renal function.
Hepatic Impairment
In a written report of 12 patients with moderate hepatic impairment (Child-Pugh Class B) who received a single dose of lx mg DEXILANT, the systemic exposure (AUC) of bound and unbound dexlansoprazole was approximately two times greater compared to subjects with normal hepatic function. This deviation in exposure was not due to a departure in protein binding. No studies have been conducted in patients with astringent hepatic damage (Child-Pugh Class C) [see Dosage and Administration (2.2), Utilize in Specific Populations (eight.6)].
Drug-Drug Interactions
Effect of Dexlansoprazole on Other Drugs
Cytochrome P 450 Interactions
Dexlansoprazole is metabolized, in part, past CYP2C19 and CYP3A4 [see Clinical Pharmacology (12.3)].
In vitro studies have shown that dexlansoprazole is not likely to inhibit CYP isoforms 1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 2E1 or 3A4. As such, no clinically relevant interactions with drugs metabolized by these CYP enzymes would exist expected. Furthermore, in vivo studies showed that DEXILANT did not have an impact on the pharmacokinetics of co-administered phenytoin (CYP2C9 substrate) or theophylline (CYP1A2 substrate). The subjects' CYP1A2 genotypes in the drug-drug interaction report with theophylline were not determined. Although in vitro studies indicated that DEXILANT has the potential to inhibit CYP2C19 in vivo, an in vivo drug-drug interaction study in mainly CYP2C19 extensive and intermediate metabolizers has shown that DEXILANT does not affect the pharmacokinetics of diazepam (CYP2C19 substrate).
Clopidogrel
Clopidogrel is metabolized to its active metabolite in part by CYP2C19. A study of healthy subjects who were CYP2C19 extensive metabolizers, receiving in one case daily administration of clopidogrel 75 mg alone or concomitantly with DEXILANT 60 mg (n=40), for ix days was conducted. The mean AUC of the active metabolite of clopidogrel was reduced by approximately 9% (mean AUC ratio was 91%, with 90% CI of 86 to 97%) when DEXILANT was co-administered compared to assistants of clopidogrel alone. Pharmacodynamic parameters were also measured and demonstrated that the change in inhibition of platelet aggregation (induced past 5 mcM ADP) was related to the alter in the exposure to clopidogrel active metabolite. The consequence on exposure to the active metabolite of clopidogrel and on clopidogrel-induced platelet inhibition is not considered clinically of import.
Event of Other Drugs on Dexlansoprazole
Because dexlansoprazole is metabolized by CYP2C19 and CYP3A4, inducers and inhibitors of these enzymes may potentially change exposure of dexlansoprazole.
pharmacogenomics
Effect of CYP2C19 Polymorphism on Systemic Exposure of Dexlansoprazole
Systemic exposure of dexlansoprazole is mostly higher in intermediate and poor metabolizers. In male Japanese subjects who received a single dose of DEXILANT 30 or threescore mg (Due north=2 to 6 subjects/grouping), hateful dexlansoprazole Cmax and AUC values were up to two times college in intermediate compared to extensive metabolizers; in poor metabolizers, hateful Cmax was upwards to iv 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 volition be affected by CYP2C19 phenotypes besides.
Nonclinical Toxicology
carcinogenesis, mutagenesis, impairment of fertility
The carcinogenic potential of dexlansoprazole was assessed using lansoprazole studies. In 2 24 month carcinogenicity studies, Sprague-Dawley rats were treated orally with lansoprazole at doses of v to 150 mg/kg/solar day, nearly one to twoscore times the exposure on a trunk surface (mg/mtwo) ground of a l kg person of average height [1.46 m2 body expanse (BSA)] given the recommended homo dose of lansoprazole 30 mg/mean solar day.
Lansoprazole produced dose-related gastric ECL cell hyperplasia and ECL cell carcinoids in both male and female rats [see Clinical Pharmacology (12.2)].
In rats, lansoprazole likewise increased the incidence of intestinal metaplasia of the gastric epithelium in both sexes. In male rats, lansoprazole produced a dose-related increment of testicular interstitial jail cell adenomas. The incidence of these adenomas in rats receiving doses of 15 to 150 mg/kg/day (four to xl times the recommended human lansoprazole dose based on BSA) exceeded the low groundwork incidence (range = i.4 to x%) for this strain of rat.
In a 24 month carcinogenicity written report, CD-1 mice were treated orally with lansoprazole doses of fifteen to 600 mg/kg/day, two to fourscore times the recommended homo lansoprazole dose based on BSA. Lansoprazole produced a dose-related increased incidence of gastric ECL cell hyperplasia. It also produced an increased incidence of liver tumors (hepatocellular adenoma plus carcinoma). The tumor incidences in male person mice treated with 300 and 600 mg lansoprazole/kg/day (40 to fourscore times the recommended human lansoprazole dose based on BSA) and female person mice treated with 150 to 600 mg lansoprazole/kg/twenty-four hour period (20 to fourscore times the recommended human being lansoprazole dose based on BSA) exceeded the ranges of background incidences in historical controls for this strain of mice. Lansoprazole handling produced adenoma of rete testis in male person mice receiving 75 to 600 mg/kg/day (10 to 80 times the recommended human lansoprazole dose based on BSA).
A 26 calendar week p53 (+/-) transgenic mouse carcinogenicity study of lansoprazole was non positive.
Lansoprazole was positive in the Ames test and the in vitro human lymphocyte chromosomal abnormality assay. Lansoprazole was not genotoxic in the ex vivo rat hepatocyte unscheduled DNA synthesis (UDS) exam, the in vivo mouse micronucleus test or the rat os marrow cell chromosomal aberration test.
Dexlansoprazole was positive in the Ames test and in the in vitro chromosome aberration test using Chinese hamster lung cells. Dexlansoprazole was negative in the in vivo mouse micronucleus test.
The potential effects of dexlansoprazole on fertility and reproductive performance were assessed using lansoprazole studies. Lansoprazole at oral doses up to 150 mg/kg/twenty-four hours (40 times the recommended man lansoprazole dose based on BSA) was found to have no event on fertility and reproductive performance of male and female rats.
Clinical Studies
healing of erosive esophagitis in adults
Two multi-center, double-bullheaded, active-controlled, randomized, 8 week studies were conducted in patients with endoscopically confirmed EE. Severity of the disease was classified based on the Los Angeles Nomenclature Grading System (Grades A-D). Patients were randomized to ane of the following three handling groups: DEXILANT 60 mg one time daily, DEXILANT xc mg once daily or lansoprazole xxx mg one time daily. Patients who were H. pylori positive or who had Barrett's Esophagus and/or definite dysplastic changes at baseline were excluded from these studies. A total of 4092 patients were enrolled and ranged in historic period from xviii to ninety years (median age 48 years) with 54% male. Race was distributed as follows: 87% Caucasian, 5% Black and 8% Other. Based on the Los Angeles Classification, 71% of patients had balmy EE (Grades A and B) and 29% of patients had moderate to severe EE (Grades C and D) before treatment.
The studies were designed to exam not-inferiority. If non-inferiority was demonstrated then superiority would be tested. Although non-inferiority was demonstrated in both studies, the finding of superiority in one study was not replicated in the other.
The proportion of patients with healed EE at Week four or viii is presented below in Table 8.
| Study | Number of Patients (N) Patients with at least one post-baseline endoscopy. | Treatment Grouping (daily) | Calendar week iv % Healed | Week 8 Main efficacy endpoint. % Healed | (95% CI) for the Treatment Difference (DEXILANT–Lansoprazole) by Week 8 |
|---|---|---|---|---|---|
| CI = Confidence interval | |||||
| 1 | 657 | DEXILANT sixty mg | 70 | 87 | (-1.5, 6.one) Demonstrated not-inferiority to lansoprazole. |
| 648 | Lansoprazole xxx mg | 65 | 85 | ||
| two | 639 | DEXILANT lx mg | 66 | 85 | (2.2, 10.5) |
| 656 | Lansoprazole thirty mg | 65 | 79 | ||
DEXILANT xc mg once daily was studied and did non provide additional clinical benefit over DEXILANT 60 mg one time daily.
maintenance of healed erosive esophagitis & relief of heartburn in adults
A multi-center, double-blind, placebo-controlled, randomized study was conducted in patients who successfully completed an EE study and showed endoscopically confirmed healed EE. Maintenance of healing and symptom resolution over a half-dozen calendar month period was evaluated with DEXILANT 30 or lx mg once daily compared to placebo. A total of 445 patients were enrolled and ranged in age from 18 to 85 years (median age 49 years), with 52% female. Race was distributed equally follows: 90% Caucasian, v% Black and 5% Other.
Sixty six percentage of patients treated with thirty mg of DEXILANT remained healed over the 6 calendar month time period every bit confirmed by endoscopy (see Table 9).
| Number of Patients (N) Patients with at least one post-baseline endoscopy | Treatment Group (daily) | Maintenance Rate (%) |
|---|---|---|
| 125 | DEXILANT thirty mg | 66.4 Statistically significant vs placebo |
| 119 | Placebo | xiv.3 |
DEXILANT 60 mg once daily was studied and did non provide boosted clinical benefit over DEXILANT 30 mg once daily.
The effect of DEXILANT xxx mg on maintenance of relief of heartburn was also evaluated. Upon entry into the maintenance written report, a majority of patients' baseline heartburn severity was rated every bit none. DEXILANT 30 mg demonstrated a statistically significantly higher percentage of 24 hour heartburn-free periods compared to placebo over the six month treatment flow (come across Table 10). The majority of patients treated with placebo discontinued due to relapse of EE betwixt Calendar month 2 and Month half-dozen.
| Overall Handling Secondary efficacy endpoint | Month ane | Month half dozen | ||||
|---|---|---|---|---|---|---|
| Handling Group (daily) | N | Heartburn-Free 24 hr Periods (%) | Due north | Heartburn-Gratuitous 24 hour Periods (%) | Northward | Heartburn-Complimentary 24 hour Periods (%) |
| DEXILANT xxx mg | 132 | 96.i Statistically pregnant vs placebo | 126 | 96.7 | 80 | 98.3 |
| Placebo | 141 | 28.6 | 117 | 28.6 | 23 | 73.3 |
treatment of symptomatic non-erosive gerd in adults
A multi-centre, double-blind, placebo-controlled, randomized, four week study was conducted in patients with a diagnosis of symptomatic not-erosive GERD made primarily by presentation of symptoms. These patients who identified heartburn as their chief symptom, had a history of heartburn for half dozen months or longer, had heartburn on at least four of seven days immediately prior to randomization and had no esophageal erosions every bit confirmed by endoscopy. However, patients with symptoms which were not acid-related may non have been excluded using these inclusion criteria. Patients were randomized to one of the following handling groups: DEXILANT 30 mg daily, 60 mg daily, or placebo. A total of 947 patients were enrolled and ranged in historic period from 18 to 86 years (median age 48 years) with 71% female. Race was distributed as follows: 82% Caucasian, 14% Black and 4% Other.
DEXILANT 30 mg provided statistically significantly greater percent of days with heartburn-free 24 hour periods over placebo every bit assessed by daily diary over 4 weeks (meet Tabular array eleven). DEXILANT 60 mg once daily was studied and provided no additional clinical benefit over DEXILANT thirty mg once daily.
| N | Treatment Grouping (daily) | Heartburn-Free 24 hr Periods (%) |
|---|---|---|
| 312 | DEXILANT xxx mg | 54.9 Statistically significant vs placebo |
| 310 | Placebo | eighteen.5 |
A higher percentage of patients on DEXILANT thirty mg had heartburn-free 24 hr periods compared to placebo every bit early as the beginning three days of treatment and this was sustained throughout the treatment period (per centum of patients on Twenty-four hours 3: DEXILANT 38% vs placebo 15%; on 24-hour interval 28: DEXILANT 63% vs placebo 40%).
pediatric gerd
Use of DEXILANT in patients 12 to 17 years of age is supported by testify from acceptable and well-controlled studies of DEXILANT capsules in adults, with boosted safety, efficacy, and pharmacokinetic data from studies performed in pediatric patients.
Healing of EE, Maintenance of Healed EE and Relief of Heartburn
In a multi-center, 36 calendar week trial, 62 patients 12 to 17 years of age with a documented history of GERD for at least three months and endoscopically-proven erosive esophagitis (EE) were enrolled to evaluate the healing of EE, maintenance of healed EE and relief of heartburn, followed by an boosted 12 weeks without treatment. The median historic period was xv years, with males bookkeeping for 61% of the patients. Based on the Los Angeles Classification Grading Scale, 97% of patients had mild EE (Grades A and B), and 3% of patients had moderate to severe EE (Grades C and D) earlier treatment.
In the first eight weeks, 62 patients were treated with DEXILANT 60 mg once daily to evaluate the healing of EE. Of the 62 patients, 58 patients completed the eight calendar week trial, and 51 (88%) patients achieved healing of EE, as confirmed by endoscopy, over viii weeks of treatment (encounter Tabular array 12).
| DEXILANT sixty mg | |
|---|---|
| Proportion of randomized patients healed | 51/62 (82%) Reported are the exact confidence limits. |
| Proportion of evaluable patients healed Includes only patients who underwent post-baseline endoscopy. due north (%) | 51/58 (88%) |
After the initial eight weeks of treatment, all 51 patients with healed EE were randomized to receive handling with DEXILANT 30 mg or placebo, in one case daily for an additional 16 weeks to evaluate maintenance of healing and symptom resolution. Maintenance of healing was assessed by endoscopy at Calendar week 24. Of the 51 patients randomized, xiii patients discontinued early. Of these, five patients did not undergo post-baseline endoscopy. Eighteen of 22 (82%) evaluable patients treated with DEXILANT 30 mg remained healed over the 16 week handling period as confirmed by endoscopy, compared with 14 of 24 (58%) in placebo (see Table 13).
| DEXILANT 30 mg | Placebo | |
|---|---|---|
| Proportion of randomized patients who maintained healing of EE | xviii/25 (72%) Reported are the exact confidence limits. | xiv/26 (54%) |
| Proportion of evaluable patients who maintained healing of EE Includes patients with at least one post-baseline endoscopy. n (%) | xviii/22 (82%) | xiv/24 (58%) |
Relief of heartburn was assessed in randomized patients during the 16 week maintenance period. The median pct of 24 hour heartburn-free periods was 87% for those receiving DEXILANT xxx mg compared to 68% for those receiving placebo.
Out of the 32 patients who maintained healing of EE at the end of the xvi week maintenance period, 27 patients (16 treated with DEXILANT and 11 treated with placebo during the double-blind phase) were followed for an additional 12 weeks without therapy. Twenty four of the 27 patients completed the 12 week follow-up menses. I patient required handling with acid suppression therapy.
Treatment of Symptomatic Non-Erosive GERD
In a single-arm, open-label, multi-middle trial, 104 pediatric patients 12 to 17 years of historic period with symptomatic non-erosive GERD were treated with DEXILANT 30 mg in one case daily, for four weeks to evaluate safety and effectiveness. Patients had a documented history of GERD symptoms for at least three months prior to screening, reported heartburn on at least three out of seven days during screening, and had no esophageal erosions as confirmed by endoscopy. The median age was 15 years, with females accounting for seventy% of the patients. During the four week treatment menses, the median per centum of 24 hr heartburn free periods was 47%.
Source: https://www.healthgrades.com/drugs/feed/dexilant/pharmacology
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