Trajenta, 5 mg 30 pcs.

Name: Trajenta, 5 mg 30 pcs.
SKU: 215843
Availability: InStock

€43.02

EAN: 9006968009636 SKU: 215843 Categories: Diabetes, Hypoglycemic drugs, Medicine

Description

Trajenta is an inhibitor of the enzyme dipeptidyl peptidase-4 (DPP-4), which is involved in the inactivation of the hormones incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide type 1 (GFP-1). These hormones are degraded by the enzyme DPP-4. Incretins maintain glucose concentration at the necessary physiological level.

In a 24-hour period, basal concentrations of GIP and GFP-1 are at low levels, which rise rapidly in response to food intake.

The hormones activate insulin biosynthesis and production by pancreatic beta cells when blood glucose concentrations are normal or high. GFP-1 decreases the production of glucagon by pancreatic alpha cells, resulting in reduced glucose production in the liver.

Indications

Active ingredient

Composition

1 tablet contains:

The active ingredient:

linagliptin 5 mg;

Associates:

mannitol – 130.9 mg,

Pregelatinized starch – 18 mg,

Corn starch – 18 mg,

copovidone – 5.4 mg,

magnesium stearate – 2.7 mg;

Shell composition:

opadray pink (02F34337) – 5 mg (hypromellose 2910 – 2.5 mg, titanium dioxide (E171) – 1.25 mg, talc – 875 Âµg, macrogol 6000 – 250 Âµg, iron oxide red dye (E172) – 125 Âµg).

How to take, the dosage

The recommended dose of Trazenta is 5 mg (1 tablet) once daily, orally.

Trazenta can be taken regardless of meals at any time of day.

If a patient misses their next dose, they should take the medication as soon as they remember. Do not take a double dose on the same day.

Interaction

In vitro evaluation of drug interactions

Linagliptin is a weak competitive inhibitor of CYP3A4 isoenzyme.

Linagliptin does not inhibit other CYP isoenzymes and is not their inducer.

Linagliptin is a substrate for P-glycoprotein and inhibits to a small extent the P-glycoprotein-mediated transport of digoxin.

The evaluation of in vivo drug interactions

. Linagliptin has no clinically significant effect on the pharmacokinetics of metformin, glibenclamide, simvastatin, pioglitazone, warfarin, digoxin and oral contraceptive drugs as proven in vivo and is based on the low ability of linagliptin to lead to drug interactions with CYP3A4, CYP2C9, CYP2C8 substrates, P-glycoprotein and organic cation transport molecules.

Metformin. Co-administration of metformin (multiple daily doses of 850 mg 3 times/day) and linagliptin at a dose of 10 mg once daily. (above the therapeutic dose) in healthy volunteers did not lead to clinically significant changes in the pharmacokinetics of linagliptin or metformin. Thus, linagliptin is not an inhibitor of organic cation transport.

Sulfonylurea derivatives. Pharmacokinetics of linagliptin (5 mg) did not change when co-administered with glibenclamide (single dose of gliburide 1.75 mg) and multiple oral doses of linagliptin (5 mg each). However, there was a clinically insignificant 14% decrease in the AUC and Cmax values of glibenclamide. Since glibenclamide is metabolized primarily by CYP2C9, these data also support the conclusion that linagliptin is not a CYP2C9 inhibitor. No clinically significant interactions are expected with other sulfonylurea derivatives (e.g., glipizide and glimepiride), which, like glibenclamide, are primarily metabolized with CYP2C9.

Thiazolidinediones. Co-administration of several doses of linagliptin 10 mg/day. (above the therapeutic dose) and pioglitazone 45 mg/day. (multiple doses), which is a substrate for CYP2C8 and CYP3A4, had no clinically significant effect on the pharmacokinetics of linagliptin or pioglitazone or the active metabolites of pioglitazone. This indicates that in vivo linagliptin is not an inhibitor of CYP2C8-mediated metabolism and supports the conclusion that there is no significant inhibitory effect of linagliptin in vivo on CYP3A4.

Ritonavir. Co-administration of linagliptin (single oral administration of 5 mg) and ritonavir (multiple oral administration of 200 mg), an active inhibitor of P-glycoprotein and CYP3A4 isoenzyme, increased the AUC and Cmax of linagliptin by approximately 2-fold and 3-fold, respectively. However, these changes in the pharmacokinetics of linagliptin were not considered significant. Therefore, no significant interactions with other P-glycoprotein and CYP3A4 inhibitors are expected clinically, and no dose changes are required.

Rifampicin. Multiple co-administration of linagliptin and rifampicin, an active inducer of P-glycoprotein and CYP3A4 isoenzyme, resulted in a reduction of 39.6% and 43.8% in the AUC and Cmax values of linagliptin, respectively, and a reduction of approximately 30% in the inhibition of basal dipeptidyl peptidase-4 activity. Thus, it is expected that the clinical efficacy of linagliptin used in combination with active P-glycoprotein inducers will be maintained, although it may not be fully apparent.
Digoxin. Co-administration in healthy volunteers of linagliptin (5 mg/day) and digoxin (0.25 mg/day) had no effect on digoxin pharmacokinetics. Thus, linagliptin in vivo is not an inhibitor of transport mediated by P-glycoprotein.

Warfarin. Linagliptin administered repeatedly at a dose of 5 mg/day did not alter the pharmacokinetics of warfarin, which is a substrate for CYP2C9, indicating that linagliptin has no ability to inhibit CYP2C9.

Simvastatin. Linagliptin used repeatedly in healthy volunteers at a dose of 10 mg/day. (above the therapeutic dose), had minimal effect on the pharmacokinetic parameters of simvastatin, which is a sensitive substrate for CYP3A4. After linagliptin 10 mg dose together with simvastatin used in daily dose of 40 mg for 6 days AUC of simvastatin was increased by 34% and Cmax was increased by 10%. Thus, linagliptin is a weak inhibitor of metabolism mediated by CYP3A4. Dose changes in concomitant administration with drugs that are metabolized with participation of CYP3A4 are considered to be inadvisable.

The oral contraceptive drugs. Co-administration of linagliptin at a dose of 5 mg with levonorgestrel or ethinylestradiol did not alter the pharmacokinetics of these drugs.

Special Instructions

Trazenta is contraindicated in patients with type 1 diabetes mellitus or for the treatment of diabetic ketoacidosis.
The incidence of hypoglycemia when using linagliptin as monotherapy was comparable to placebo.

In clinical trials it has been reported that the incidence of hypoglycemia when using linagliptin in combination with drugs that are not thought to cause hypoglycemia (metformin, thiazolidinedione derivatives) was similar to the corresponding effect of placebo.

Sulfonylurea derivatives are known to cause hypoglycemia. Therefore, caution should be exercised when using linagliptin in combination with sulfonylurea derivatives. If necessary, it is possible to reduce the dose of sulfonylurea derivatives.

Special clinical studies on the use of linagliptin in combination with insulin have not been conducted.
The use of linagliptin does not increase the risk of cardiovascular disease.

Linagliptin in combination therapy with other oral hypoglycemic drugs has been used in patients with severe renal insufficiency.

Linagliptin provided a significant decrease in glycosylated hemoglobin concentration and fasting glucose concentration.
No dose adjustment is required for use in patients with impaired renal, hepatic function and in elderly patients.

Impact on ability to drive and operate vehicles

There have been no studies of the effect of Trazenta on the ability to drive and operate vehicles. However, due to the possible development of dizziness, caution should be exercised when driving vehicles and operating machinery.

Contraindications

Individual intolerance to the components of Tragent, type 1 diabetes, diabetic ketoacidosis

Side effects

The following side effects have been observed during monotherapy with linagliptin:

Immune system: hypersensitivity reactions.

Respiratory system: cough.

Digestive system: pancreatitis.