Galvus

Galvus

vildagliptin

Manufacturer:

Novartis Indonesia
Full Prescribing Info
Contents
Vildagliptin.
Description
Vildagliptin is 1-[(3-hydroxy-adamant-1-ylamino)-acetyl]-pyrrolidine-2(S)-carbonitrile.
Action
Pharmacology: Pharmacodynamics: Vildagliptin, a member of the islet enhancer class, is a potent and selective dipeptidyl-peptidase-4 (DPP-4) inhibitor that improves glycemic control.
The administration of vildagliptin results in rapid and complete inhibition of DPP-4 activity. In patients with type 2 diabetes, administration of vildagliptin led to inhibition of DPP-4 enzyme activity for a 24-hr period. Vildagliptin inhibition of DPP-4 results in increased fasting and postprandial endogenous levels of the incretin hormones GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic polypeptide).
By increasing the endogenous levels of these incretin hormones, vildagliptin enhances the sensitivity of β cells to glucose resulting in improved glucose-dependent insulin secretion. Treatment with 50-100 mg daily in patients with type 2 diabetes significantly improved markers of β cell function. The degree of improvement in β cell function is dependent on the initial degree of impairment; in non-diabetic (normal glycemic) individuals, vildagliptin does not stimulate insulin secretion or reduce glucose levels.
By increasing endogenous GLP-1 levels, vildagliptin enhances the sensitivity of α cells to glucose, resulting in more glucose-appropriate glucagon secretion. The reduction in inappropriate glucagon during meals in turn attenuates insulin resistance.
The enhanced increase in the insulin/glucagon ratio during hyperglycemia due to increased incretin hormone levels results in a decrease in fasting and postprandial hepatic glucose production leading to reduced glycemia.
The known effect of increased GLP-1 levels to delay gastric emptying is not observed with vildagliptin treatment. In addition, a reduction in postprandial lipemia that is not associated with vildagliptin's incretin-mediated effect to improve islet function, has been observed.
Pharmacokinetics: Linearity: Vildagliptin is rapidly absorbed with an absolute oral bioavailability of 85%. Peak plasma concentrations for vildagliptin and the area under the plasma concentration versus time curve (AUC) increased in an approximately dose-proportional manner over the therapeutic dose range.
Absorption: Following oral administration in the fasting state, vildagliptin is rapidly absorbed with peak plasma concentrations observed at 1.75 hrs. Co-administration with food slightly decreases the rate of absorption of vildagliptin, as characterized by a 19% decrease in peak concentrations and a delay in the time to peak plasma concentration to 2.5 hrs. There is no change in the extent of absorption and food does not alter the overall exposure (AUC).
Distribution: The plasma protein-binding of vildagliptin is low (9.3%) and vildagliptin distributes equally between plasma and red blood cells. The mean volume of distribution of vildagliptin at steady-state after IV administration (Vss) is 71 L, suggesting extravascular distribution.
Metabolism: Metabolism is the major elimination pathway for vildagliptin in humans, accounting for 69% of the dose. The major metabolite, LAY151, is pharmacologically inactive and is the hydrolysis product of the cyano moiety, accounting for 57% of the dose, followed by the amide hydrolysis product (4% of the dose). DPP-4 contributes partially to the hydrolysis of vildagliptin as shown in an in vivo study using DPP-4-deficient rats. Vildagliptin is not metabolized by cytochrome P-450 enzymes to any quantifiable extent. In vitro studies demonstrated that vildagliptin does not inhibit or induce cytochrome P-450 enzymes.
Excretion and Elimination: Following oral administration [14C]-vildagliptin, approximately 85% of the dose is excreted into the urine and 15% of the dose is recovered in the feces. Renal excretion of the unchanged vildagliptin accounts for 23% of the dose after oral administration. After an IV administration to healthy subjects, the total plasma and renal clearances of vildagliptin are 41 L/hr and 13 L/hr, respectively. The mean elimination half-life after IV administration is approximately 2 hrs. The elimination half-life after oral administration is approximately 3 hrs and is independent of dose.
Special Populations: Gender: No differences in the pharmacokinetics of Galvus were observed between male and female subjects with a diverse range of age and body mass index (BMI). DPP-4 inhibition by Galvus was unaffected by gender.
Obesity: BMI does not show any impact on the pharmacokinetic parameters of Galvus. DPP-4 inhibition by Galvus was unaffected by BMI.
Hepatic Impairment: The effect of impaired hepatic function on the pharmacokinetics of Galvus was studied in subjects with mild, moderate and severe hepatic impairment based on the Child-Pugh scores (ranging from 6 for mild to 12 for severe) in comparison to subjects with normal hepatic function. The exposure to Galvus (100 mg) after a single dose in subjects with mild and moderate hepatic impairment was decreased (20% and 8%, respectively), while the exposure to Galvus for subjects with severe impairment was increased by 22%. The maximum change (increase or decrease) in the exposure to Galvus is ~30%, which is not considered to be clinically relevant. There was no correlation between the severity of hepatic function impairment and changes in exposure to Galvus.
The use of vildagliptin is not recommended in patients with hepatic impairment including patients with a pre-treatment ALT or AST >2.5 times the upper limit of normal.
Renal Impairment: In subjects with mild, moderate and severe renal impairment, and end-stage renal disease (ESRD) patients on hemodialysis, systemic exposure to vildagliptin was increased (Cmax 8-66%; AUC 32-134%) compared to subjects with normal renal function. Exposure to the inactive metabolite (LAY151) increased with increasing severity of renal impairment (AUC 1.6- to 6.7-fold). Changes in exposure to vildagliptin did not correlate with severity of renal impairment, whereas changes in exposure to the inactive metabolite did correlate. Elimination half-life of vildagliptin was not affected by renal impairment. No dosage adjustment is required in patients with mild renal impairment. Due to limited experience, the use of Galvus is not recommended in patients with moderate or severe renal impairment or in patients with ESRD on hemodialysis (see Precautions).
Elderly: In otherwise healthy elderly subjects (≥70 years), the overall exposure to Galvus (100 mg once daily) was increased by 32% with an 18% increase in peak plasma concentration compared to younger healthy subjects (18-40 years). These changes are not considered to be clinically relevant. DPP-4 inhibition by Galvus is not affected by age in the age groups studied.
Pediatric: No pharmacokinetic data available.
Ethnic Group: There was no evidence that ethnicity affects the pharmacokinetics of Galvus.
Clinical Experience: A total of 5795 patients with type 2 diabetes participated in 13 double-blind, placebo- or active-controlled clinical trials of at least 12-week treatment duration. In these studies, vildagliptin was administered to 3784 patients at daily doses of 50 mg once daily (n=1102), 50 mg twice daily (n=2027) or 100 mg once daily (n=655). The number of male and female patients receiving vildagliptin 50 mg once daily or 100 mg daily was 2069 and 1715, respectively. The number of patients receiving vildagliptin 50 mg once daily or 100 mg daily who were ≥65 years was 664 and 121 of the patients were ≥75 years. In these trials, vildagliptin was administered as monotherapy in drug-naive patients with type 2 diabetes or in combination in patients not adequately controlled by other antidiabetic medicinal products.
Overall, vildagliptin improved glycemic control when given as monotheraphy or when used in combination with metformin, a sulfonylurea and a thiazolidinedione as measured by clinically relevant reductions in HbA1c from baseline at study endpoint (see table).
In clinical trials, the magnitude of HbA1c reductions with vildagliptin was greater in patients with higher baseline HbA1c.
In a 52-week trial (LAF2309), vildagliptin (100 mg/day) reduced baseline HbA1c by -1% compared to -1.4% for metformin (titrated to 2 g/day); statistical noninferiority was not achieved. Patients treated with vildagliptin reported significantly lower incidences of gastrointestinal adverse reactions versus those treated with metformin.
In a 24-week trial (LAF2327), vildagliptin (100 mg/day) was compared to rosiglitazone (8 mg once daily). Mean reductions were -1.1% with vildagliptin and -1.3% with rosiglitazone in patients with mean baseline HBA1c of 8.7%. Patients receiving rosiglitazone experienced a mean increase in weight (+1.6 kg) while those receiving vildagliptin experienced no weight gain (-0.3 kg). The incidence of peripheral edema was lower in the vildagliptin group than in the rosiglitazone group (2.1% vs 4.1%, respectively). (See table.)


Click on icon to see table/diagram/image


Toxicology: Preclinical Safety Data: A 2-year carcinogenicity study was conducted in rats at oral doses up to 900 mg/kg (approximately 200 times the human exposure at the maximum recommended dose). No increases in tumor incidence attributable to vildagliptin were observed. A 2-year carcinogenicity study was conducted in mice at oral doses up to 1000 mg/kg (up to 240 times the human exposure at the maximum recommended dose). Mammary tumor incidence was increased in female mice at approximately 150 times the maximum anticipated human exposure to vildagliptin; it was not increased at approximately 60 times the maximum human exposure. The incidence of hemangiosarcoma was increased in male mice treated at 42-240 times the maximum human exposure to vildagliptin and in female mice at 150 times the maximum human exposure. No significant increases in hemangiosarcoma incidences were observed at approximately 16 times the maximum human exposure to vildagliptin in males and approximately 60 times the maximum human exposure in females.
Vildagliptin was not mutagenic in a variety of mutagenicity tests including a bacterial reverse mutation Ames assay and a human lymphocyte chromosomal aberration assay. Oral bone marrow micronucleus tests in both rats and mice did not reveal clastogenic or aneugenic potential up to 2000 mg/kg or approximately 400 times the maximum human exposure. An in vivo mouse liver comet assay using the same dose was also negative.
In a 13-week toxicology study in cynomolgus monkeys, skin lesions have been recorded at doses ≥5 mg/kg/day. These were consistently located on the extremities (hands, feet, ears and tail). At 5 mg/kg/day (approximately equivalent to human AUC exposure at the 100 mg dose), only blisters were observed. They were reversible despite continued treatment and were not associated with histopathological abnormalities. Flaking and peeling skin, scabs and tail sores with correlating histopathological changes were noted at doses ≥20 mg/kg/day (approximately 3 times human AUC exposure at the 100-mg dose). Necrotic lesions of the tail were observed at ≥80 mg/kg/day. It should be noted that vildagliptin exhibits a significantly higher pharmacological potency in monkeys compared with humans. Skin lesions were not reversible in monkeys treated at 160 mg/kg/day during a 4-week recovery period. Skin lesions have not been observed in other animal species or in humans treated with vildagliptin.
Indications/Uses
Adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus: As monotherapy or in dual combination with metformin, sulfonylurea (SU) and thiazolidinedione (TZD) when diet, exercise and a single antidiabetic agent do not result in adequate glycemic control.
Dosage/Direction for Use
The management of antidiabetic therapy should be individualized.
Monotherapy: Recommended Dose: 50 or 100 mg daily. The 50-mg dose should be administered once daily in the morning. The 100-mg dose should be administered as 2 divided doses of 50 mg given in the morning and evening.
Combination Therapy: Combination therapy with other antidiabetic drugs eg, metformin, SU or TZD may be given if a tighter glycemic control is required on the top of the maximum recommended daily dose of Galvus 100 mg as monotherapy.
The recommended dose of Galvus is 50 mg or 100 mg daily in dual combination with metformin, SU or TZD. The 50-mg dose should be administered once daily in the morning. The 100-mg dose should be administered as 2 divided doses of 50 mg given in the morning and evening.
When used in dual combination with a sulfonylurea, the recommended dose of vildagliptin is 50 mg once daily administered in the morning. In this patient population, vildagliptin 100 mg daily was no more effective than vildagliptin 50 mg once daily.
Galvus can be administered with or without meal.
Children: Galvus has not been studied in patients <18 years, therefore, the use of Galvus in pediatric patients is not recommended (see Pharmacokinetics under Actions).
Hepatic or Renal Impairment: Galvus is not recommended in patients with hepatic impairment including patients with a pre-treatment ALT or AST >2.5 times the upper limit of normal.
In patients with mild renal impairment, the recommended dose of Galvus is 50 mg once daily in the morning or 50 mg twice daily given in the morning and evening. Galvus is, however, not recommended in patients with moderate or severe renal impairment or end-stage renal disease (ESRD) on hemodialysis (see Pharmacokinetics under Actions and Precautions).
There is limited data on the use of combination therapy in patients with renal and hepatic impairment. Therefore, the use of Galvus is not recommended in these patients.
Elderly: In patients ≥65 and ≥75 years treated with Galvus, no differences were observed in the overall safety, tolerability or efficacy between this elderly population and younger patients. No dosage adjustments are, therefore, necessary in the elderly patients (see Pharmacokinetics under Actions).
Overdosage
Symptoms: In healthy subjects (7-14 subjects per treatment group), Galvus was administered in once-daily doses of 25, 50, 100, 200, 400 and 600 mg for up to 10 consecutive days. Doses up to 200 mg were well tolerated. At 400 mg, there were 3 cases of muscle pain and individual cases of mild and transient paresthesia, fever, edema and transient increase in lipase levels (2 times ULN). At 600 mg, 1 subject experienced edema of the feet and hands, and an excessive increase in creatinine phosphokinase (CPK) levels, accompanied by elevations of aspartate aminotransferase (AST), C-reactive protein and myoglobin. Three additional subjects in this dose group presented with edema of both feet, accompanied by paresthesia in 2 cases. All symptoms and laboratory abnormalities resolved after study drug discontinuation.
Management: Galvus is not dialyzable, however, the major hydrolysis metabolite (LAY151) can be removed by hemodialysis.
Contraindications
Known hypersensitivity to vildagliptin or to any of the excipients. Galvus is also contraindicated in patients with moderate and severe renal and hepatic impairment.
Galvus is not a substitute for insulin in insulin-requiring patients. Galvus should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis.
Special Precautions
Renal Impairment: There is limited experience in patients with moderate or severe renal impairment and in patients with end-stage renal disease (ESRD) on hemodialysis. Therefore, the use of Galvus is not recommended in these patients.
Hepatic Impairment: Galvus is not recommended in patients with hepatic impairment, including patients with a pre-treatment ALT or AST >2.5 times the upper limit of normal.
Liver Enzyme Monitoring: Rare cases of hepatic dysfunction (including hepatitis) have been reported. In these cases, the patients were generally asymptomatic without clinical sequelae and liver function tests (LFTs) returned to normal after discontinuation of treatment. LFTs should be performed prior to the initiation of treatment with Galvus. Galvus is not recommended in patients with a pre-treatment ALT or AST >2.5 times the upper limit of normal. LFTs should be monitored during Galvus treatment at 3-month intervals during the 1st year and periodically thereafter. Patients who develop increased transaminase levels should be monitored with a 2nd liver function evaluation to confirm the finding and be followed thereafter with frequent liver function tests until the abnormalities return to normal. Should an increase in AST or ALT of 3 times upper limit of normal or greater persist, withdrawal of therapy with Galvus is recommended. Patients who develop jaundice or other signs suggestive of liver dysfunction should discontinue Galvus and contact their physician immediately. Following withdrawal of treatment with Galvus and LFT normalization, vildagliptin treatment should not be reinitiated.
Others: Galvus tablets contain lactose. Patients with rare hereditary problems of galactose intolerance, Lapp lactase deficiency or glucose-galactose malabsorption should not take Galvus.
Effects on the Ability to Drive or Operate Machinery: No studies on the effects on the ability to drive and use machines have been performed. Patients who may experience dizziness should therefore, avoid driving vehicles or using machines.
Use in pregnancy & lactation: Fertility studies have been performed in rats at doses up to 200 times the human dose and have revealed no evidence of impaired fertility or early embryonic development due to vildagliptin. Vildagliptin was not teratogenic in either rats or rabbits. There are, however, no adequate and well-controlled studies in pregnant women and therefore, vildagliptin should not be used during pregnancy unless the benefit to the mother outweighs the potential risk to the fetus.
Animal studies are not always predictive of human response. Because current information strongly suggests that abnormal blood glucose levels during pregnancy are associated with a higher incidence of congenital anomalies as well as increased neonatal morbidity and mortality, most experts recommend that insulin monotherapy be used during pregnancy to maintain blood glucose levels as close to normal as possible.
As it is not known whether vildagliptin is excreted in human milk, Galvus should not be administered to breastfeeding women.
Use In Pregnancy & Lactation
Fertility studies have been performed in rats at doses up to 200 times the human dose and have revealed no evidence of impaired fertility or early embryonic development due to vildagliptin. Vildagliptin was not teratogenic in either rats or rabbits. There are, however, no adequate and well-controlled studies in pregnant women and therefore, vildagliptin should not be used during pregnancy unless the benefit to the mother outweighs the potential risk to the fetus.
Animal studies are not always predictive of human response. Because current information strongly suggests that abnormal blood glucose levels during pregnancy are associated with a higher incidence of congenital anomalies as well as increased neonatal morbidity and mortality, most experts recommend that insulin monotherapy be used during pregnancy to maintain blood glucose levels as close to normal as possible.
As it is not known whether vildagliptin is excreted in human milk, Galvus should not be administered to breastfeeding women.
Adverse Reactions
Safety data were obtained from 3784 patients exposed to vildagliptin at a daily dose of 50 mg (once daily) or 100 mg (50 mg twice daily or 100 mg once daily) in controlled trials of at least 12 weeks' duration. Of these patients, 2264 patients received vildagliptin as monotherapy and 1520 patients received vildagliptin in combination with another agent. Two thousand six hundred eighty two (2682) patients were treated with vildagliptin 100 mg daily (2027 with 50 mg twice daily and 655 with 100 mg once daily) and 1102 patients were treated with vildagliptin 50 mg once daily.
The majority of adverse reactions in these trials were mild and transient, not requiring treatment discontinuations. No association was found between adverse reactions and age, ethnicity, duration of exposure or daily dose.
Rare cases of angioedema have been reported on vildagliptin at a similar rate to controls. A greater proportion of cases were reported when vildagliptin was administered in combination with an angiotensin-converting enzyme inhibitor (ACE inhibitor). The majority of events were mild in severity and resolved with ongoing vildagliptin treatment.
Rare cases of hepatic dysfunction (including hepatitis) have been reported. In these cases, the patients were generally asymptomatic without clinical sequelae and liver function tests (LFTs) returned to normal after discontinuation of treatment. In data from controlled monotherapy and add-on therapy trials up to 24 weeks in duration, the incidence of ALT or AST elevations ≥3 times ULN (classified as present on at least 2 consecutive measurements or at the final on-treatment visit) was 0.2%, 0.3% and 0.2% for vildagliptin 50 mg daily, vildagliptin 50 mg twice daily and all comparators, respectively. These elevations in transaminases were generally asymptomatic, non-progressive in nature and not associated with cholestasis or jaundice.
Adverse reactions reported in patients who received Galvus in double-blind studies as monotherapy and add-on therapies are listed as follows for each indication by system organ class and absolute frequency. Frequencies are defined as: Very common (≥1/10); common (≥1/100, <1/10); uncommon (≥1/1000, <1/100); rare (>1/10,000 to ≤1/1000); very rare (≤1/10,000). Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness.
Monotherapy: The overall incidence of withdrawals from monotherapy trials due to adverse reactions was no greater for patients treated with vildagliptin at a dose of 50 mg once daily (0.2%) or vildagliptin at a dose of 50 mg twice daily (0.1%) than for placebo (0.6%) or comparators (0.5%).
In monotherapy studies, hypoglycemia was uncommon, reported in 0.5% (2 of 409) of patients treated with vildagliptin 50 mg once daily and 0.3% (4 of 1373) of patients treated with vildagliptin 50 mg twice daily compared to 0.2% (2 of 1082) of patients in the groups treated with an active comparator or placebo, with no serious or severe events reported.
Galvus is weight neutral when administered as monotherapy.
Adverse Reactions Reported in Patients who Received Galvus 50 mg once daily (n=409) or 50 mg twice daily (n=1373) as Monotherapy in Double-Blind Studies: Nervous System Disorders: Common: Dizziness. Uncommon: Headache.
Gastrointestinal Disorders: Uncommon: Constipation, nausea, diarrhea.
General Disorders and Administration Site Conditions: Uncommon: Peripheral edema.
Infection and Infestation: Common: Nasopharyngitis.
Cardiovascular Disorders: Common: Hypertension.
Combination with Metformin: In clinical trials with the combination of vildagliptin + metformin, 0.4% of patients withdrew due to adverse reactions in the vildagliptin 50 mg once daily + metformin treatment group, and no withdrawal due to adverse reactions was reported in either the vildagliptin 50 mg twice daily + metformin or the placebo + metformin treatment groups.
In clinical trials, the incidence of hypoglycemia was uncommon in patients receiving vildagliptin 50 mg once daily in combination with metformin (0.9%), patients receiving vildagliptin 50 mg twice daily in combination with metformin (0.5%) and in patients receiving placebo + metformin (0.4%). No severe hypoglycemic events were reported in the vildagliptin arms.
Galvus is weight neutral when administered in combination with metformin.
Adverse Reactions Reported in Patients who Received Galvus 50 mg once daily (n=233) or 50 mg twice daily (n=183) in Combination with Metformin in Double-Blind Studies: Galvus in Dual Oral Therapy with Metformin: Nervous System Disorders: Common: Tremor, dizziness, headache.
Combination with a Sulfonylurea: In clinical trials with the combination of vildagliptin 50 mg + glimepiride, the overall incidence of withdrawals due to adverse reactions was 0.6% in the vildagliptin 50 mg + glimepiride treatment group vs 0% in the placebo + glimepiride treatment group.
In clinical trials, the incidence of hypoglycemia when vildagliptin 50 mg once daily was added to glimepiride was 1.2% vs 0.6% for placebo + glimepiride. No severe hypoglycemic events were reported in the vildagliptin arms.
At the recommended dose of 50 mg, Galvus is weight neutral when administered in combination with glimepiride.
Adverse Reactions Reported in Patients who Received Galvus 50 mg once daily in Combination with a Sulfonylurea in Double-Blind Studies (n=170): Nervous System Disorders: Common: Tremor, headache, dizziness.
General Disorders and Administration Site Conditions: Common: Asthenia.
Combination with a Thiazolidinedione: In clinical trials with the combination of vildagliptin and a thiazolidinedione, 0.7% of patients withdrew for adverse reactions in the vildagliptin 50 mg once daily + pioglitazone group, and there were no withdrawals due to adverse reactions reported in either the vildagliptin 50 mg twice daily + pioglitazone or the placebo + pioglitazone treatment groups.
In clinical trials, no hypoglycemic events were reported in patients receiving vildagliptin 50 mg once daily + pioglitazone 45 mg, hypoglycemia was uncommon in patients receiving vildagliptin 50 mg twice daily + pioglitazone 45 mg (0.6%) but common in patients receiving placebo + pioglitazone 45 mg (1.9%). No severe hypoglycemic events were reported in the vildagliptin arms.
In the pioglitazone add-on study, the change in the body weight compared to placebo was 0.1 kg and 1.3 kg for Galvus 50 mg daily and Galvus 50 mg twice daily, respectively.
The incidence of peripheral edema when vildagliptin was added to a maximum dose of background pioglitazone (45 mg once daily) was 8.2% as 50 mg once daily and 7%, as 50 mg twice daily compared to 2.5% for background pioglitazone alone. The incidence of edema when vildagliptin was added to pioglitazone as dual initial therapy in drug-naive patients was, however, less than for pioglitazone alone [50 mg once daily (3.5%), 50 mg twice daily (6.1%) vs pioglitazone 30 mg (9.3%)].
Adverse Reactions Reported in Patients who Received Galvus 50 mg once daily (n=146) or 50 mg twice daily (n=158) in Combination with a Thiazolidinedione in Double-Blind Studies: Investigations: Common: Increased weight.
Vascular Disorders: Common: Peripheral edema.
Drug Interactions
Vildagliptin has a low potential for drug interactions. Since vildagliptin is not a cytochrome (CYP) P-450 enzyme substrate nor does it inhibit nor induce CYP450 enzymes, it is not likely to interact with co-medications that are substrates, inhibitors or inducers of these enzymes.
Furthermore, vildagliptin does not affect metabolic clearance of co-medications metabolized by CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4/5. Drug-drug interaction studies were conducted with commonly co-prescribed medications for patients with type 2 diabetes or medications with a narrow therapeutic window. As a result of these studies, no clinically relevant interactions with other oral antidiabetics (glibenclamide, pioglitazone, metformin), amlodipine, digoxin, ramipril, simvastatin, valsartan or warfarin were observed after co-administration with vildagliptin.
Incompatibilities: Not applicable.
Storage
Do not store above 30°C. Store in original package and protect from moisture.
MIMS Class
ATC Classification
A10BH02 - vildagliptin ; Belongs to the class of dipeptidyl peptidase 4 (DPP-4) inhibitors. Used in the treatment of diabetes.
Presentation/Packing
Tab [white to light yellowish, round (diameter: 8 mm), debossed with "NVR" on one side and "FB" on the other side] 50 mg x 28's.
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