|| See TERMINOLOGY & ABBREVIATIONS ||
|Content & Description||
Tablets may contain the following excipients: Anhydrous lactose, microcrystalline cellulose, sodium starch glycolate and magnesium stearate.
|Indication(s)||Adjunct to diet and exercise to improve glycaemic control in patients with type 2 diabetes mellitus: As monotherapy or in dual combination with metformin, a sulphonylurea, a thiazolidinedione or insulin when diet, exercise and a single antidiabetic agent do not result in adequate glycaemic control.|
|Dosage||The management of antidiabetic therapy should be individualized.
Recommended Dose: 50 or 100 mg daily for monotherapy and in dual combination with metformin, a thiazolidinedione (TZD) or insulin.
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 sulphonylurea (SU), 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.
If tighter glycaemic control is required on top of the maximum recommended daily dose of vildagliptin, the addition of other antidiabetic drugs eg, metformin, an SU, a TZD or insulin may be considered. The safety and efficacy of vildagliptin as triple oral therapy in combination with other antidiabetic drugs has not been established.
Doses >100 mg are not recommended.
Renal Impairment: No dosage adjustment of Vildagliptin is required in patients with mild renal impairment (creatinine clearance ≥50 mL/min).
Elderly: In patients treated with Vildagliptin ≥65 years and ≥75 years, 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: Special Populations under Actions).
|Administration||May be taken with or without food.|
|Overdosage||Symptoms: In healthy subjects (7-14 subjects/treatment group), Vildagliptin was administered in once-daily doses of 25 mg, 50 mg, 100 mg, 200 mg, 400 mg 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 paraesthesia, fever, oedema and transient increase in lipase levels [2x upper limit of normal (ULN)]. At 600 mg, 1 subject experienced oedema of the feet and hands, and an excessive increase in creatine phosphokinase (CPK) levels, accompanied by elevations of aspartate aminotransferase (AST), C-reactive protein and myoglobin. Three additional subjects in this dose group presented with oedema of both feet, accompanied by paraesthesia in 2 cases. All symptoms and laboratory abnormalities resolved after study drug discontinuation.
Treatment: Vildagliptin is not dialyzable, however the major hydrolysis metabolite (LAY151) can be removed by haemodialysis.
|Contraindications||Known hypersensitivity to vildagliptin or to any of the excipients of Vildagliptin.
Vildagliptin should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis, as it would not be effective in these settings.
Vildagliptin tablets contain lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take Vildagliptin.
Use in lactation: As it is not known whether vildagliptin is excreted in human milk, Vildagliptin should not be administered to breastfeeding women.
|Special Precautions||Vildagliptin is not a substitute for insulin in insulin-requiring patients.
Renal Impairment: There is limited experience in patients with moderate or severe renal impairment and in patients with end-stage renal disease (ESRD) on haemodilysis (see Pharmacokinetics: Special Populations under Actions and Precautions). Therefore, the use of Vildagliptin is not recommended in these patients.
Hepatic Impairment: Vildagliptin is not recommended in patients with hepatic impairment, including patients with a pre-treatment alanine aminotransferase (ALT) or aspartate aminotransferase (AST) >2.5x 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 Vildagliptin. Vildagliptin is not recommended in patients with a pre-treatment ALT or AST >2.5x the upper limit of normal. LFTs should be monitored during Vildagliptin 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 LFTs until the abnormality(ies) return to normal. Should an increase in AST or ALT of ≥3x upper limit of normal persist, withdrawal of therapy with Vildagliptin is recommended. Patients who develop jaundice or other signs suggestive of liver dysfunction should discontinue Vildagliptin and contact the physician immediately. Following withdrawal of treatment with Vildagliptin and LFT normalization, vildagliptin treatment should not be reinitiated.
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: 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 foetus.
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.
Use in children: Vildagliptin has not been studied in patients <18 years, therefore the use of Vildagliptin is not recommended for use in children <18 years (see Pharmacokinetics: Special Populations under Actions).
|Adverse Drug Reaction(s)||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 alanine aminotransferase (ALT) or aspartate aminotransferase (AST) elevations ≥3x upper limit of normal (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, nonprogressive in nature and not associated with cholestasis or jaundice.
Adverse reactions reported in patients who received Vildagliptin 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, <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, hypoglycaemia 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.
Vildagliptin is weight neutral when administered as monotherapy.
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 hypoglycaemia 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 hypoglycaemic events were reported in the vildagliptin arms.
Vildagliptin is weight neutral when administered in combination with metformin.
Combination with a Sulphonylurea: 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 versus 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% versus 0.6% for placebo + glimepiride. No severe hypoglycaemic events were reported in the vildagliptin arms.
At the recommended dose of 50 mg, Vildagliptin is weight neutral when administered in combination with glimepiride.
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 hypoglycaemia events were reported in patients receiving vildagliptin 50 mg once daily + pioglitazone 45 mg, hypoglycaemia 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 hypoglycaemic events were reported in the vildagliptin arms. In the pioglitazone add-on study, the change in body weight compared to placebo was +0.1 kg and +1.3 kg for Vildagliptin 50 mg daily and Vildagliptin 50 mg twice daily, respectively.
The incidence of peripheral oedema 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 oedema 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% versus pioglitazone 30 mg 9.3%).
Combination with Insulin: In clinical trials, there was no increased risk of hypoglycaemia regarding the incidence or severity of hypoglycaemia compared to placebo when Vildagliptin was added to insulin. (Vildagliptin + insulin: 22.9% versus placebo + insulin: 29.6%).
Vildagliptin 50 mg twice daily in combination with insulin had a mean change in body weight of +0.9 kg versus placebo.
Post-Marketing Experience: During post-marketing experience the following additional adverse drug reaction have been reported (frequency not known): Urticaria, pancreatitis.
|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 induces 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.|
|Pharmacology||Pharmacodynamics: Vildagliptin, a member of the islet enhancer class, is a potent and selective dipeptidyl-peptidase-4 (DPP-4) inhibitor that improves glycaemic 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 glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).
By increasing the endogenous levels of these incretin hormones, vildagliptin enhances the sensitivity of Î²-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 Î²-cell function. The degree of improvement in Î²-cell function is dependent on the initial degree of impairment; in nondiabetic (normal glycaemic) individuals, vildagliptin does not stimulate insulin secretion or reduce glucose levels.
By increasing endogenous GLP-1 levels, vildagliptin enhances the sensitivity of Î±-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 hyperglycaemia due to increased incretin hormone levels results in a decrease in fasting and postprandial hepatic glucose production, leading to reduced glycaemia.
The known effect of increased GLP-1 levels to delay gastric emptying is not observed with vildagliptin treatment. In addition, a reduction in postprandial lipaemia that is not associated with vildagliptin's incretin madiated effect to improve islet function has been observed.
Clinical Experience: More than 15,000 patients with type 2 diabetes participated in double-blind, placebo- or active-controlled clinical trials of up to >2 years treatment duration. In these studies, vildagliptin was administered to >9000 patients at daily doses of 50 mg once daily, 50 mg twice daily or 100 mg once daily. More than 5000 male and >4000 female patients received vildagliptin 50 mg once daily or 100 mg daily. More than 1900 patients receiving vildagliptin 50 mg once daily or 100 mg daily were ≥65 years. In these trials, vildagliptin was administered as monotherapy in drug-naive patients with type 2 diabetes or in combination with other antidiabetics in patients not adequately controlled by other antidiabetic medicinal products.
Overall, vildagliptin improved glycaemic control when given as monotherapy or when used in combination with metformin, a sulphonylurea (SU), and a thiazolidinedione (TZD), as measured by clinically relevant reductions in HbA1c from baseline at study endpoint.
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 non-inferiority 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 oedema was lower in the vildagliptin group than in the rosiglitazone group (2.1% versus 4.1%, respectively).
In a 24-week trial (LAF2354), vildagliptin (50 mg twice daily) was compared to pioglitazone (30 mg once daily) in patients inadequately controlled with metformin. Mean reductions from baseline HbA1c of 8.4% were -0.9% with vildagliptin added to metformin and -1% with pioglitazone added to metformin. The decrease in HbA1c from baseline >9% was greater (-1.5%) in both treatment groups. Patients receiving pioglitazone in addition to metformin experienced an increase in weight of 1.9 kg. Patients receiving vildagliptin in addition to metformin experienced an increase in weight of 0.3 kg. In a 28-week extension, HbA1c reductions were similar between treatment groups and the body weight difference further increased.
In a long-term trial of up to >2 years (LAF2308), vildagliptin (100 mg/day) was compared to glimepiride (up to 6 mg/day) in patients treated with metformin. After 1-year mean reductions in HbA1c were -0.4% with vildagliptin added to metformin and -0.5% with glimepiride added to metformin. Body weight change with vildagliptin was -0.2 kg versus +1.6 kg with glimepiride. The incidence of hypoglycemia was significantly lower in the vildagliptin group (1.7%) than in the glimepiride group (16.2%). At study endpoint (2 years), the HbA1c was similar to baseline values in both treatment groups and the body weight changes and hypoglycemia differences were maintained.
In a long-term trial of 2 years (LAF2310), vildagliptin (50 mg twice daily) was compared to gliclazide (up to 320 mg/day). After 2 years, mean reduction in HbA1c was -0.5% for vildagliptin and -0.6% for gliclazide. Vildagliptin had less weight gain (0.75 kg) and fewer hypoglycemic events (0.7%) than gliclazide (1.6 kg and 1.7%, respectively).
Pharmacokinetics: Linearity: Vildagliptin is rapidly absorbed with an absolute oral bioavailability of 85%. Peak plasma concentrations for vildagliptin and the area under the plasma concentrations 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: It is the major elimination pathway for vildagliptin in humans, accounting for 69% of the dose. The major matabolite, 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 vitrostudies demonstrated that vildagliptin does not inhibit or induce cytochrome P-450 enzymes.
Excretion and Elimination: Following oral administration of [14C]-vildagliptin, approximately 85% of the dose is excreted into the urine and 15% of the dose is recovered in the faeces. 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 t½ after IV administration is approximately 2 hrs. The elimination t ½ after oral administration is approximately 3 hrs and is independent of dose.
Special Populations: Gender: No differences in the pharmacokinetics of Vildagliptin were observed between male and female subjects with a diverse range of age and body mass index (BMI). DPP-4 inhibition by Vildagliptin was unaffected by gender.
Obesity: Body mass index does not show any impact on the pharmacokinetic parameters of Vildagliptin. DPP-4 inhibition by Vildagliptin was unaffected by BMI.
Hepatic Impairment: The effect of impaired hepatic function on the pharmacokinetics of Vildagliptin 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 Vildagliptin (100 mg) after a single dose in subjects with mild and moderate hepatic impairment was decreased (20% and 8%, respectively), while the exposure to Vildagliptin for subjects with severe impairment was increased by 22%. The maximum change (increase or decrease) in the exposure to Vildagliptin is approximately 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 Vildagliptin.
The use of vildagliptin is not recommended in patients with hepatic impairment including patients with a pre-treatment alanine transaminase (ALT) or aspartate aminotransferase (AST) >2.5x the upper limit of normal.
Renal Impairment: In subjects with mild, moderate and severe renal impairment, systemic exposure to vildagliptin was increased (Cmax 8-66%; AUC 32-134%) and total body clearance was reduced compared to subjects with normal renal function.
Elderly: In otherwise healthy elderly subjects (≥70 years), the overall exposure to Vildagliptin (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 Vildagliptin is not affected by age in the age groups studied.
Paediatric: No pharmacokinetic data available.
Ethnic Group: There was no evidence that ethnicity affects the pharmacokinetics of Vildagliptin.
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 tumour 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 tumour 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 haemangiosarcoma 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 haemangiosarcoma 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 vivomouse 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 skin, 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 the monkeys treated at 160 mg/kg/day during a 4-week recovery period. Skin lesions have not been observed in other animal species. A few cases were observed in humans treated with vildagliptin.
|ATC Classification||A10BH02 - vildagliptin; Belongs to the class of dipeptidyl peptidase 4 (DPP-4) inhibitors. Used in the treatment of diabetes.|
|Brand Name||Manufacturer/Marketer||Composition||Dosage Form||Pack Size & Price|
|DIALIPTIN||Drug International Ltd||Vildagliptin INN 50mg||Film Coated Tablet||20's: 400.00 MRP|
|GALVAN||Aristopharma Ltd.||Vildagliptin INN 50mg||Film Coated Tablet||20's: 300.00 MRP|
|GALVUS||Novartis (Bangladesh) Ltd.||Vildagliptin INN 50mg||Film Coated Tablet||28', MRP 700.00|
|VIGLITA 50||Square Pharmaceuticals Ltd.||Vildagliptin 50mg||Tablet||2x10|
|| See SUMMARY OF PRODUCT CHARACTERISTICS from Brand Manufacturer |||Manufacturer's|
|| Back to top ||
*Trademark name & prescribing information are the property of their respective Manufacturers.