Osempic solution for subcutaneous injection 1.34mg/ml cartridges in 3ml syringe pens, complete with 4 needles.

Composition

1 ml of the drug contains: Active ingredient: semaglutide 1.34 mg; excipients: disodium hydrophosphate dihydrate, propylene glycol, phenol, hydrochloric acid (for pH correction), sodium hydroxide (for pH correction), water for injection.

Pharmacological action

Semaglutide is a GLP-1 receptor agonist (GLP-1P) produced by recombinant DNA biotechnology using a Saccharomyces cerevisiae strain with subsequent purification.

Semaglutide is an analog of GLP-1, which has 94% homology with human GLP-1. Semaglutide acts as an agonist of GLP-1P, which selectively binds and activates GLP-1P. GLP-1P serves as a target for native GLP-1.

GLP-1 is a physiological hormone that has several effects on the regulation of glucose concentration and appetite, as well as on the cardiovascular system (CVS). The effect on glucose concentration and appetite is specifically mediated by GLP-1P located in the pancreas and brain Pharmacological concentrations of semaglutide reduce blood glucose concentration and body weight through a combination of the effects described below.

GLP-1s are also present in specific areas of the heart, blood vessels, immune system, and kidneys, where their activation can have cardiovascular (SS) and microcirculatory effects. Unlike native GLP-1, the extended half-life of semaglutide (about 1 week) allows it to be applied subcutaneously (subcutaneously) once a week. Binding to albumin is the main mechanism of long-term action of semaglutide, which leads to a decrease in its excretion by the kidneys and protects against metabolic breakdown. In addition, semaglutide is stable against cleavage by the enzyme dipeptidyl peptidase-4.

Semaglutide reduces blood glucose concentration by glucose-dependent stimulation of insulin secretion and suppression of glucagon secretion. Thus, when the concentration of blood glucose increases, insulin secretion is stimulated and glucagon secretion is suppressed. The mechanism of lowering the level of glycemia also includes a slight delay in gastric emptying in the early postprandial phase. During hypoglycemia, semaglutide reduces insulin secretion and does not reduce glucagon secretion.

Semaglutide reduces total body weight and adipose tissue mass by reducing energy consumption. This mechanism affects overall loss of appetite, including increased satiety signals and decreased hunger signals, as well as improved control of food intake and reduced food cravings. Insulin resistance is also reduced, possibly by reducing body weight. In addition, semaglutide reduces the preference for eating high-fat foods.

In animal studies, it has been shown that semaglutide is absorbed by specific brain regions and enhances key satiety signals and weakens key hunger signals. By targeting isolated areas of brain tissue, semaglutide activates neurons associated with satiety and suppresses neurons associated with hunger.

In clinical trials (CI), semaglutide had a positive effect on plasma lipids, reduced systolic blood pressure (BP), and reduced inflammation. In animal studies, semaglutide suppresses the development of atherosclerosis, preventing further development of aortic plaques and reducing inflammation in the plaques.

All pharmacodynamic studies were performed after 12 weeks of therapy (including the period of dose increase) at a steady-state concentration of semaglutide 1 mg 1 time per week.

Fasting blood glucose levels and postprandial blood glucose levels

Semaglutide reduces fasting glucose and postprandial glucose concentrations. Compared to placebo, semaglutide 1 mg therapy in patients with type 2 diabetes mellitus (DM2) resulted in a decrease in glucose concentration in terms of absolute change from baseline (mmol/l) and relative decrease compared to placebo (%) in: fasting glucose concentration (1.6 mmol/l; 22%); glucose concentration 2 hours after meals (4.1 mmol/l; 37%); average daily glucose concentration (1.7 mmol/l; 22%) and postprandial peaks of glucose concentration for 3 meals (0.6-1.1 mmol/l). Semaglutide reduced fasting glucose concentrations after the first dose.

Pancreatic beta cell function and insulin secretion

Semaglutide improves the function of pancreatic beta cells. After intravenous glucose injection to patients with DM2, semaglutide improved the first and second phase of the insulin response with a threefold and twofold increase, respectively, and increased the maximum secretory activity of pancreatic beta cells after the arginine stimulation test. In addition, compared with placebo, semaglutide therapy increases fasting insulin concentrations.

Glucagon secretion

Semaglutide reduces fasting glucagon concentrations and postprandial glucagon concentrations. In patients with DM2, semaglutide leads to a relative decrease in the concentration of glucagon compared to placebo: fasting glucagon concentration (8-21%), postprandial glucagon response (14-15%) and average daily glucagon concentration (12%).

Glucose-dependent insulin secretion and glucose-dependent glucagon secretion

Semaglutide reduced high blood glucose concentrations by stimulating insulin secretion and reducing glucagon secretion in a glucose-dependent manner. The rate of insulin secretion after use of semaglutide to patients with DM2 was comparable to that in healthy volunteers. During induced hypoglycemia, semaglutide compared with placebo did not alter the counterregulatory response of increased glucagon concentrations, nor did it worsen the decrease in C-peptide concentrations in patients with DM2.

Emptying the stomach

Semaglutide caused a slight delay in early postprandial gastric emptying, thereby reducing the rate of postprandial glucose entry into the blood.

Body weight and body composition

There was a greater reduction in body weight when using semaglutide compared to the studied comparison drugs (placebo, sitagliptin, delayed-release exenatide (SV), dulaglutide and insulin glargine). Body weight loss during the use of semaglutide was mainly due to the loss of adipose tissue, exceeding the loss of muscle mass by 3 times.

Appetite, calorie intake, and food choices

Compared to placebo, semaglutide reduced calorie intake by 18-35% during three consecutive meals ad libitum. This was facilitated by semaglutide-stimulated appetite suppression both on an empty stomach and after meals, improved control of food intake, and reduced cravings for food, especially high-fat ones.

Fasting lipids and postprandial lipids

Compared to placebo, semaglutide reduced fasting concentrations of triglycerides and very low-density lipoprotein (VLDL) cholesterol by 12% and 21%, respectively. Postprandial increases in triglyceride and VLDL cholesterol levels in response to high-fat meals decreased by more than 40%.

Electrophysiology of the heart (EFs)

The effect of semaglutide on the repolarization process in the heart was tested in the EFs study. The use of semaglutide in doses exceeding therapeutic values (at steady-state concentrations up to 1.5 mg) did not lead to prolongation of the corrected QT interval.

Clinical efficacy and safety

Both improved glycemic control and reduced SS morbidity and mortality are integral parts of DM2 management.

The efficacy and safety of Ozempik®in doses of 0.5 mg and 1 mg were evaluated in six randomized controlled phase 3a CI. Of these, five CI as the main goal evaluated the effectiveness of glycemic control, while one CI evaluated the quality of the main goal of SS outcome. In addition, two phase 3 CI studies of Ozempik® were conducted in Japanese patients.

Treatment with Ozempik® demonstrated sustained, statistically superior, and clinically significant improvements in HbA1cand weight loss for up to 2 years compared to placebo and active control treatment (sitagliptin, insulin glargine, exenatide SV, and dulaglutide).

Age, gender, race, ethnicity, baseline body mass index (BMI) and body mass index (kg), duration of diabetes mellitus (DM), and renal failure did not affect the efficacy of Ozempik®.

Monotherapy

Monotherapy with the drug Asemic®in doses of 0.5 mg and 1 mg 1 time a week for 30 weeks compared with placebo resulted in a statistically more significant decline in HbA₁ (-1,5%,1.6 million% vs 0%, respectively), and fasting plasma glucose (FPG) (-2,5 mmol/l, down 2.3 mmol/l revised 0.6 mmol/l, respectively) and body mass (-3,7 kg -4,5 kg and 1.0 kg, respectively).

Ozempik®compared to sitagliptin, both in combination with 1-2 oral hypoglycemic drugs (PHPs) (metformin and / or thiazolidinedione group drugs)

Therapy with the drug Asemic®0.5 mg and 1 mg 1 time a week for 56 weeks compared with sitagliptin led to a sustained and statistically more significant decline in HbA₁ (-1,3%,1.6 million% vs. -0.5%, respectively), GPN (of-2.1 mmol/l, -2,6 mmol/l vs -1,1 mmol/l, respectively) and body mass (-4,3 kg, -6,1 kg vs -1,9 kg, respectively).

Treatment with Ozempik ® 0.5 mg and 1 mg compared with sitagliptin significantly reduced systolic blood pressure from the initial value of 132.6 mm Hg (-5.1 mm Hg, -5.6 mm Hg, versus -2.3 mm Hg, respectively). There were no changes in diastolic blood pressure.

Ozempik®preparation compared to dellagloria, both in combination with metforminonline drug Asemic® 0.5 mg compared to dellagloria 0.75 mg, both 1 time per week for 40 weeks, led to a sustained and statistically superior reduction of HbA₁ (-1.5% vs. 1.1% fall), GPN (down 2.2 mmol/l vs -1,9 mmol/l) and body weight (forecast to be minus 4.6 kg vs -2,3 kg), respectively.

Therapy with the drug Asemic®1 mg compared to dellagloria both 1.5 mg 1 time a week for 40 weeks, led to a sustained and statistically superior reduction of HbA₁ (-l,8% versus 1.4%), FPG (and 2.8 mmol/l vs of -2.2 mmol/l) and body weight (-6.5 kg vs. -3.0 kg), respectively.

Ozempik®preparation compared to exenatide SV, both in combination with metformin or metformin together with a sulfonylurea derivative

Therapy with the drug Asemic®1 mg 1 time; a week for 56 weeks compared with exenatide TV 2.0 mg led to a sustained and statistically more significant decline in HbA₁ (-U5% vs -0,9%), FPG (and 2.8 mmol/l vs -2.0 mmol/l) and body weight (-5,6 kg vs -1,9 kg), respectively. Ozempik®compared to insulin glargine, both in combination with 1-2 PHGP (metformin monotherapy or metformin with a sulfonylurea derivative)

Treatment with Ozempik®at doses of 0.5 mg and 1 mg once a week compared with insulin glargine for 30 weeks resulted in a statistically more significant reduction in HbA1c (-1.2%, -1.6% vs. -0.8%, respectively) and body weight (-3.5 kg, -5.2 kg vs. +1.2 kg, respectively).

The decrease in HDN was statistically more significant for Ozempik ® 1 mg compared to insulin glargine (-2.7 mmol / l vs. -2.1 mmol/L). There was no statistically more significant decrease in GPN for Ozempik® 0.5 mg (-2.0 mmol / l vs. -2.1 mmol/L).

Percentage of patients with severe or confirmed (

More patients achieved an HbA score_{of 1 s}

Ozempik®preparation compared to placebo, both in combination with basal insulinoterapia drug Asemic® in doses of 0.5 mg and 1 mg compared to placebo for 30 weeks led to a statistically more significant decline in HbA₁ (-1,4%, -1,8% vs. -0.1%, respectively), GPN (1.6 million mmol/l, -2,4 mmol/l vs. -0.5 mmol/l, respectively) and body mass (-3,7 kg, -6,4 kg versus 1.4 kg, respectively).

The incidence of severe or confirmed episodes of hypoglycemia did not differ significantly between Ozempik and placebo. Proportion of patients with_{HbA1c score <}8% at screening who reported severe or confirmed ( compared to placebo and comparable in patients with HbA1c >8% at screening.

Combination with monotherapy with a sulfonylurea derivative

At the 30th week of CI, a subgroup of 123 patients on monotherapy with a sulfonylurea derivative was evaluated. At week 30, HbA1c decreased by 1.6% and 1.5% with Ozempic ® at 0.5 mg and 1 mg, respectively, and increased by 0.1% with placebo.

Combination with pre-mixed insulin ± 1-2 PHGP

At the 30th week of CI, a subgroup of 867 patients receiving pre-mixed insulin therapy (with or without 2 PHPs) was evaluated. At week 30, HbA1c decreased by 1.3% and 1.8% with Ozempic ® at 0.5 mg and 1 mg, respectively, and decreased by 0.4% with placebo.

Ratio of patients who achieved the target HbA reduction_{of 1 s}

Up to 79% of patients achieved their treatment goals for reducing HbA1c compared to patients treated with sitagliptin, exenatide SV, insulin glargine, dulaglutide, and placebo. The proportion of patients who achieved increased HbA_{1 with}less than 7% without severe or confirmed hypoglycemia and without weight gain was significantly greater in the drug Asemic®in doses of 0.5 mg and 1 mg (66% and 74%, respectively) compared with patients treated with sitagliptin (27%), exenatide STAR (29%), insulin glargine (16%), dulapuri 0.75 mg (44%) and dulapuri 1.5 mg (58%).

Body weight

Monotherapy with Ozempik®1 mg or therapy in combination with 1-2 medications resulted in statistically greater weight loss (loss was up to 6.5 kg) compared to placebo, sitagliptin, exenatide SV, insulin glargine or dulaglutide. Weight loss was sustained for up to 2 years.

After one year of therapy, a greater number of patients who received Ozempik®0.5 mg (46% and 13%) and 1 mg (up to 62% and 24%) achieved weight loss of ≥5% and ≥10% compared to patients who were treated with active reference drugs sitagliptin and exenatide SV (up to 18% and up to 4%).

In a 40-week CI, a greater number of patients treated with Ozempik®0.5 mg achieved weight loss of ≥5% and ≥10% (44% and 14%) compared to patients treated with dulaglutide 0.75 mg (23% and 3%). Weight loss ≥5% and ≥10% was achieved by a greater number of patients treated with Ozempik® 1 mg (up to 63% and 27%) compared to patients treated with dulaglutide 1.5 mg (30% and 8%).

In the CC CI, a greater number of patients who received Ozempik® 0.5 mg (36% and 13%) and 1 mg (47% and 20%) achieved weight loss of ≥5% and ≥10% compared to patients who received placebo 0.5 mg (18% and 6%) and 1 mg (19% and 7%).

GPN and postprandial increase in glucose concentration

During all three daily meals, Ozempik ® 0.5 mg and 1 mg showed a significant decrease in GPN concentration to 2.8 mmol / L and a decrease in postprandial increase in glucose concentration to 1.2 mmol/l (the difference between pre-and post-meal values obtained after three meals).

Pancreatic beta cell function and insulin resistance

During treatment with Ozempik ® 0.5 mg and 1 mg, there was an improvement in the function of pancreatic beta cells and a decrease in insulin resistance, which is confirmed by the evaluation of homeostatic models of pancreatic beta cell function (HOMA-IR) and insulin resistance (HOMA-IR).

Lipids

An improvement in the fasting blood lipid profile was observed during CI of Ozempik®, mainly in the group receiving the 1 mg dose.

Assessment of the effect on CVS

3,297 patients with DM2 and high SS risk were randomized to a double-blind CI lasting 104 weeks to receive Ozempik ® 0.5 mg or 1 mg once a week or placebo 0.5 mg or 1 mg in addition to standard therapy for SS diseases for the next two years.

Treatment with Ozempik® resulted in a 26% reduction in the risk of a primary combined outcome, including death due to SS pathology, non-fatal myocardial infarction (MI), and non-fatal stroke. First of all, this was due to a significant decrease in the non-fatal stroke rate (39%) and a slight decrease in the non-fatal MI rate (26%), but no changes in the frequency of death due to SS pathology.

The risk of revascularization of the myocardium or peripheral arteries significantly decreased, while the risk of unstable angina requiring hospitalization and the risk of hospitalization due to heart failure decreased slightly.

Microcirculatory outcomes included 158 new or worse cases of nephropathy. The relative risk for the time to onset of nephropathy (new cases of persistent macroalbuminuria, persistent doubling of serum creatinine, need for continuous renal replacement therapy, and death due to kidney disease) was 0.64.

In addition to standard therapy for SS diseases, treatment with Ozempik®at doses of 0.5 mg and 1 mg compared with placebo 0.5 mg and 1 mg for 104 weeks resulted in a significant and sustained decrease from baseline values of HbA_{1 s} (-1.1% and -1.4% vs. -0.4% and -0.4%, respectively).

Blood pressure

A significant decrease in mean systolic blood pressure was observed when Ozempik® 0.5 mg (3.5-5.1 mmHg) and Ozempik®1 mg (5.4-7.3 mmHg) were used in combination with PHGP or basal insulin. There was no significant difference in diastolic blood pressure between Ozempik® and the reference drugs.

Pharmacokinetics

The drug is suitable for use once a week, since the half-life of semaglutide is approximately 1 week.

Absorption rate

The time to reach the maximum concentration (cmax) in plasma was from 1 to 3 days after use of the drug dose.

Steady-state drug concentration (AUC_{τ / 24}) was reached after 4-5 weeks of a single weekly application of the drug. After subcutaneous use of semaglutide in doses of 0.5 mg and 1 mg, the average steady-state concentrations in patients with DM2 were about 16 nmol / l and 30 nmol/l, respectively.

Exposure to semaglutide doses of 0.5 mg and 1 mg increases in proportion to the administered dose. When subcutaneous injection of semaglutide into the anterior abdominal wall, thigh or shoulder, a similar exposure is achieved.

The absolute bioavailability of semaglutide after subcutaneous use was 89%.

Distribution

The average volume of distribution of semaglutide in tissues after subcutaneous use to patients with DM2 was approximately 12.5 l. Semaglutide was significantly bound to plasma albumin (>99%).

Metabolism

Semaglutide is metabolized by proteolytic cleavage of the peptide base of the protein and subsequent beta-oxidation of the side chain fatty acid.

Elimination

The gastrointestinal tract and kidneys are the main routes of elimination of semaglutide and its metabolites,2/3 of the administered dose of semaglutide is excreted by the kidneys,1/3-through the intestines. Approximately 3% of the administered dose is excreted by the kidneys as unchanged semaglutide.

In patients with DM2, semaglutide clearance was about 0.05 l/h. With an elimination half-life of approximately 1 week, semaglutide will be present in the general bloodstream for approximately 5 weeks after the last dose of the drug is administered.

Special patient groups

There is no need to adjust the dose of semaglutide depending on age, gender, race and ethnicity, body weight, the presence of renal or hepatic insufficiency.

Age group

Based on the data obtained during the phase 3a CI, which included patients aged 20 to 86 years, it was shown that age did not affect the pharmacokinetics of semaglutide.

Gender

Gender did not affect the pharmacokinetics of semaglutide.

Race

The pharmacokinetics of semaglutide were not affected by race (white, black, or African-American, Asian).

Ethnicity

Ethnicity (Latin American) did not affect the pharmacokinetics of semaglutide.

Body weight

Body weight affected semaglutide exposure. Higher body weight results in lower exposure. Doses of semaglutide equal to 0.5 mg and 1 mg provide sufficient exposure to the drug in the body weight range from 40 to 198 kg.

Kidney failure

Renal failure did not have a clinically significant effect on the pharmacokinetics of semaglutide. This has been shown in patients with varying degrees of renal insufficiency (mild, moderate, severe, or in patients on dialysis). Compared to patients with normal renal function, a single dose of semaglutide of 0.5 mg was used in the study. This has also been shown based on phase 3 a CI data for patients with DM2 and renal insufficiency, although experience with end-stage renal disease has been limited.

Liver failure

Hepatic insufficiency did not affect semaglutide exposure. The pharmacokinetic properties of semaglutide were evaluated in a study of a single dose of semaglutide equal to 0.5 mg in patients with varying degrees of hepatic insufficiency (mild, moderate, severe) by

Children and teenagers

Studies of semaglutide in children and adolescents under 18 years of age have not been conducted.

Indications

Ozempik® is indicated for use in adult patients with type 2 diabetes mellitus on the background of diet and exercise to improve glycemic control as a dietary supplement. :* monotherapy;• combined therapy with other oral hypoglycaemic drugs (PHPs) – metformin, metformin and a sulfonylurea derivative, metformin and / or thiazolidinedione, in patients who did not achieve adequate glycemic control during previous therapy;• combined therapy with insulin in patients who did not achieve adequate glycemic control on therapy with Ozempik® and metformin. Ozempik®is indicated for reducing the risk of major cardiovascular events* in patients with type 2 diabetes mellitus and high cardiovascular risk as an adjunct to standard treatment for cardiovascular diseases. * major cardiovascular events include: death due to cardiovascular disease, non-fatal myocardial infarction, non-fatal stroke.

Contraindications

• Hypersensitivity to semaglutide or any of the excipients of the drug;
• a history of medullary thyroid cancer, including in the family;
• multiple endocrine neoplasia (MEN) type 2; type
• 1 diabetes mellitus (DM1); diabetic ketoacidosis.

The use of Ozempik® is contraindicated in the following groups of patients and in the following conditions/diseases due to the lack of data on efficacy and safety and limited experience with its use:

• pregnancy and lactation:
• under 18 years of age;
• severe hepatic insufficiency;
• end-stage renal failure (creatinine clearance <15 ml/min);
• chronic heart failure (CHF) of functional class IV (according to the NYHA classification (New York Heart Association)).

With caution

Ozempik® is recommended to be used with caution in patients with renal insufficiency and in patients with a history of pancreatitis

Side effects

From the immune system: rarely – anaphylactic reactions.

From the side of metabolism and nutrition: very often – hypoglycemia when used together with insulin or a sulfonylurea derivative; often-hypoglycemia when used together with other GHPs, decreased appetite.

From the nervous system: often – dizziness, infrequently-dysgeusia.

From the side of the organ of vision: often-complications of diabetic retinopathy.

From the cardiovascular system: increased heart rate.

From the gastrointestinal tract: very often-nausea, diarrhea; often-vomiting, abdominal pain, bloating, constipation, dyspepsia, gastritis, gastroesophageal reflux disease, belching, flatulence.

From the liver and biliary tract: often-cholelithiasis.

Local reactions: reactions at the injection site.

Systemic reactions: fatigue.

Laboratory and instrumental data: often-increased lipase activity, increased amylase activity, weight loss.

From the immune system: rarely – anaphylactic reactions. From the side of metabolism and nutrition: very often – hypoglycemia when co-administered with insulin or a sulfonylurea derivative;often-hypoglycemia when co-administered with other PHPs, reduced appetite. From the nervous system: often – dizziness, infrequently-dysgeusia. From the side of the organ of vision: often-complications of diabetic retinopathy. From the cardiovascular system: increased heart rate. From the gastrointestinal tract: very often-nausea, diarrhea; often-vomiting, abdominal pain, bloating, constipation, dyspepsia, gastritis, gastroesophageal reflux disease, belching, flatulence. From the liver and biliary tract: often-cholelithiasis. Local reactions: reactions at the injection site. Systemic reactions: fatigue. Laboratory and instrumental data: often-increased ilipase activity, increased amylase activity, weight loss.

Interaction

Delayed gastric emptying when using semaglutide may affect the absorption of concomitant oral medications. Semaglutide should be used with caution in patients receiving oral medications that require rapid absorption in the gastrointestinal tract.

Substances added to the drug can cause degradation of semaglutide. Do not mix with other medicines, including infusion solutions.

How to take, course of use and dosage

Ozempik® is used once a week at any time, regardless of food intake. Ozempik® is administered subcutaneously in the abdomen, thigh, or shoulder. The injection site may change without dose adjustment. Ozempik®should not be administered intravenously or intramuscularly. Further information on the method of application can be found in the “User’s Guide”section. If necessary, the day of weekly use can be changed, provided that the time interval between two injections is at least 3 days (>72 hours).

Dosage The initial dose of Ozempik® is 0.25 mg once a week. After 4 weeks of use, the dose should be increased to 0.5 mg once a week. To further improve glycemic control after at least 4 weeks of using the drug at a dose of 0.5 mg once a week, the dose can be increased to 1 mg once a week. The dose of Ozempik 0.25 mg is not therapeutic. Ozempik®can be used as monotherapy or in combination with one or more hypoglycemic drugs (see the section “Clinical efficacy and safety”). If Ozempik is added to previous metformin and/or thiazolidinedione therapy, metformin and/or thiazolidinedione therapy can be continued at the same doses. When Ozempik®is added to therapy with a sulfonylurea derivative or insulin, a reduction in the dose of the sulfonylurea derivative or insulin should be considered in order to reduce the risk of hypoglycemia (see the section “Special instructions”). The use of Ozempik® does not require self-monitoring of blood glucose concentration. When using Ozempik®in combination with a sulfonylurea derivative or insulin, such self-monitoring of blood glucose concentration may be required to adjust the dose of the sulfonylurea derivative or insulin. Missed dose If a dose is missed, Ozempik® should be administered as soon as possible within 5 days of the scheduled dose. If the skip duration is longer than 5 days, the missed dose does not need to be administered. The next dose of Ozempik®should be administered on the usual scheduled day. In each case, patients can resume their usual one-time weekly use schedule.

Use of the drug in special clinical groups of patients

Elderly patients (≥65 years)

No age-dependent dose adjustment is required. Experience with semaglutide in patients aged 75 years and older is limited.

Patients with hepatic insufficiency

No dose adjustment is required in patients with hepatic insufficiency. Experience with semaglutide in patients with severe hepatic insufficiency is limited; the use of Ozempik® in such patients is contraindicated.

Patients with renal insufficiency

No dose adjustment is required in patients with renal insufficiency. There is no experience of using the drug in patients with end-stage renal failure; the use of Ozempik® in such patients is contraindicated.

Children and teenagers

The use of Ozempik® in children and adolescents under 18 years of age is contraindicated due to the lack of data on safety and efficacy.

Overdose

Overdoses of up to 4 mg in a single dose and up to 4 mg per week have been reported during CI. The most common HP reported was nausea. All patients recovered without complications. There is no specific antidote for overdose of Ozempik®. In case of overdose, appropriate symptomatic therapy is recommended. Given the long elimination period of the drug (approximately 1 week), an extended period of monitoring and treatment of overdose symptoms may be required.

Special instructions

Its use is contraindicated in patients with DM1 or for the treatment of diabetic ketoacidosis. The drug does not replace insulin.

The use of GLP-1 P agonists may be associated with gastrointestinal HP. This should be taken into account when treating patients with renal insufficiency, as nausea, vomiting and diarrhea can lead to dehydration and deterioration of renal function.

Cases of acute pancreatitis have been reported with the use of GI-1 P agonists. Patients should be informed about the characteristic symptoms of acute pancreatitis. Caution should be exercised in patients with a history of pancreatitis.

Patients receiving the drug in combination with a sulfonylurea derivative or insulin may have an increased risk of hypoglycemia.

Caution should be exercised when using semaglutide in patients with diabetic retinopathy receiving insulin therapy. Such patients should be constantly monitored and treated in accordance with the clinical guidelines..

Cases of medullary thyroid cancer (MCT) have been reported in the post-marketing period of using another GTIP-1 analog, liraglutide. The available data are not sufficient to establish or exclude a causal relationship between the occurrence of breast cancer and the use of GGP-1 analogues. It is necessary to inform the patient about the risk of breast cancer and about the symptoms of a thyroid tumor (the appearance of a lump in the neck, dysphagia, shortness of breath, persistent hoarseness of the voice).

A significant increase in the concentration of calcitonin in the blood plasma may indicate breast cancer (in patients with breast cancer, the concentration of calcitonin in the blood plasma is usually >50 ng/l). If an increase in the concentration of calcitonin in the blood plasma is detected, a further examination of the patient should be carried out. Patients with nodules in the thyroid gland detected during a medical examination or during an ultrasound of the thyroid gland should also be additionally examined. The use of semaglutide in patients with a personal or family history of breast cancer or MENG type 2 syndrome is contraindicated.

Influence on the ability to drive vehicles and mechanisms

The drug does not affect or slightly affects the ability to drive vehicles or work with mechanisms. Patients should be warned to take precautions to avoid developing hypoglycemia while driving vehicles and when working with machinery, especially in combination with a sulfonylurea derivative or insulin.

Storage conditions

Store at a temperature of 2 °C to 8 °C (in the refrigerator), but not near the freezer. Protect from light. Do not freeze it. Store the syringe pen containing the drug used or carried as a spare at a temperature not exceeding 30 °C or at a temperature from 2 °C to 8 °C (in the refrigerator) for 6 weeks. Do not freeze it. After use, cover the pen with a cap to protect it from light. Ozempik® should be protected from exposure to excessive heat and light. Keep out of reach of children.

Shelf

life is 3 years. Do not use after the expiration date indicated on the label of the syringe pen and packaging.

Active ingredient

Semaglutide

Conditions of release from pharmacies

By prescription

Dosage form

solution for injection