Ozempic
(semaglutide)Dosage & Administration
Ozempic Prescribing Information
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- In rodents, semaglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures. It is unknown whether OZEMPIC causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans as human relevance of semaglutide-induced rodent thyroid C-cell tumors has not been determined [see Warnings and Precautions , Nonclinical Toxicology ].
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- OZEMPIC is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2) [see Contraindications ]. Counsel patients regarding the potential risk for MTC with the use of OZEMPIC and inform them of symptoms of thyroid tumors (e.g. a mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for early detection of MTC in patients treated with OZEMPIC [see Contraindications , Warnings and Precautions ].
OZEMPIC is indicated:
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- as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
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- to reduce the risk of major adverse cardiovascular events (cardiovascular death, non-fatal myocardial infarction or non-fatal stroke) in adults with type 2 diabetes mellitus and established cardiovascular disease.
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- to reduce the risk of sustained eGFR decline, end-stage kidney disease, and cardiovascular death in adults with type 2 diabetes mellitus and chronic kidney disease.
Important Administration Instructions
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- Inspect OZEMPIC visually before use. It should appear clear and colorless. Do not use OZEMPIC if particulate matter and coloration is seen.
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- Administer OZEMPIC once weekly, on the same day each week, at any time of the day, with or without meals.
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- Inject OZEMPIC subcutaneously in the abdomen, thigh, or upper arm. Instruct patients to use a different injection site each week when injecting in the same body region.
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- When using OZEMPIC with insulin, instruct patients to administer as separate injections and to never mix the products. It is acceptable to inject OZEMPIC and insulin in the same body region, but the injections should not be adjacent to each other.
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- The day of weekly administration can be changed if necessary as long as the time between two doses is at least 2 days (>48 hours).
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- If a dose is missed, administer OZEMPIC as soon as possible within 5 days after the missed dose. If more than 5 days have passed, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule.
Recommended Dosage
Recommended Initiation Dosage
Initiate OZEMPIC with a dosage of 0.25 mg injected subcutaneously once weekly for 4 weeks. Follow the dosage escalation below to reduce the risk of gastrointestinal adverse reactions [see Warnings and Precautions , Adverse Reactions ].
After 4 weeks on the 0.25 mg dosage, increase the dosage to 0.5 mg once weekly.
Recommended Maintenance and Maximum Dosages for Glycemic Control
The recommended maintenance dosage is 0.5 mg, 1 mg, or 2 mg, injected subcutaneously once weekly, based on glycemic control.
If additional glycemic control is needed after at least 4 weeks on the:
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- 0.5 mg dosage, the dosage may be increased to 1 mg once weekly.
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- 1 mg dosage, the dosage may be increased to 2 mg once weekly.
The maximum recommended dosage is 2 mg once weekly.
Recommended Maintenance Dosage in Patients with Type 2 Diabetes Mellitus and Chronic Kidney Disease
Increase the dosage to the maintenance dosage, 1 mg once weekly, after at least 4 weeks on the 0.5 mg dosage.
Injection: clear, colorless solution available in 3 prefilled, disposable, single-patient-use pens:
Dose per Injection | Total Strength per Total Volume | Strength per mL |
0.25 mg 0.5 mg | 2 mg / 3 mL | 0.68 mg/mL |
1 mg | 4 mg / 3 mL | 1.34 mg/mL |
2 mg | 8 mg / 3 mL | 2.68 mg/mL |
The 2 mg/1.5 mL (1.34 mg/mL) strength is not currently marketed by Novo Nordisk Inc.
Hepatic Impairment
No dose adjustment of OZEMPIC is recommended for patients with hepatic impairment. In a study in subjects with different degrees of hepatic impairment, no clinically relevant change in semaglutide pharmacokinetics (PK) was observed [see Clinical Pharmacology ].
OZEMPIC is contraindicated in patients with:
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- A personal or family history of MTC or in patients with MEN 2 [see Warnings and Precautions ].
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- A serious hypersensitivity reaction to semaglutide or to any of the excipients in OZEMPIC. Serious hypersensitivity reactions including anaphylaxis and angioedema have been reported with OZEMPIC [see Warnings and Precautions ( 5.8)].
Hypersensitivity Reactions
Serious hypersensitivity reactions (e.g., anaphylaxis, angioedema) have been reported in patients treated with OZEMPIC. If hypersensitivity reactions occur, discontinue use of OZEMPIC; treat promptly per standard of care, and monitor until signs and symptoms resolve. Do not use in patients with a previous hypersensitivity to OZEMPIC [see Contraindications , Adverse Reactions ].
Anaphylaxis and angioedema have been reported with other GLP-1 receptor agonists. Use caution in a patient with a history of angioedema or anaphylaxis with another GLP-1 receptor agonist because it is unknown whether such patients will be predisposed to anaphylaxis with OZEMPIC.
Postmarketing Experience
The following adverse reactions have been reported during post-approval use of semaglutide, the active ingredient of OZEMPIC. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Gastrointestinal Disorders: Ileus
Hypersensitivity: anaphylaxis, angioedema, rash, urticaria.
Hepatobiliary: cholecystitis, cholecystectomy
Neurologic: dysesthesia
Pulmonary: Pulmonary aspiration has occurred in patients receiving GLP-1 receptor agonists undergoing elective surgeries or procedures requiring general anesthesia or deep sedation.
Skin and Subcutaneous Tissue: alopecia.
Oral Medications
OZEMPIC causes a delay of gastric emptying, and thereby has the potential to impact the absorption of concomitantly administered oral medications. In clinical pharmacology trials, semaglutide did not affect the absorption of orally administered medications to any clinically relevant degree [see Clinical Pharmacology ]. Nonetheless, caution should be exercised when oral medications are concomitantly administered with OZEMPIC.
OZEMPIC (semaglutide) injection, for subcutaneous use, contains semaglutide, a human GLP-1 receptor agonist (or GLP-1 analog). The peptide backbone is produced by yeast fermentation. The main protraction mechanism of semaglutide is albumin binding, facilitated by modification of position 26 lysine with a hydrophilic spacer and a C18 fatty di-acid. Furthermore, semaglutide is modified in position 8 to provide stabilization against degradation by the enzyme dipeptidyl-peptidase 4 (DPP-4). A minor modification was made in position 34 to ensure the attachment of only one fatty di-acid. The molecular formula is C187H291N45O59 and the molecular weight is 4113.58 g/mol.
Structural formula:

OZEMPIC is a sterile, aqueous, clear, colorless solution. Each 3 mL prefilled single-patient use pen contains semaglutide 2 mg (0.68 mg/mL), 4 mg (1.34 mg/mL), or 8 mg (2.68 mg/mL). Each 1 mL of OZEMPIC solution also contains the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injections. OZEMPIC has a pH of approximately 7.4. Hydrochloric acid or sodium hydroxide may be added to adjust pH. The 2 mg/1.5 mL (1.34 mg/mL) strength is not currently marketed by Novo Nordisk Inc.
Mechanism of Action
Semaglutide is a GLP-1 analogue with 94% sequence homology to human GLP-1. Semaglutide acts as a GLP-1 receptor agonist that selectively binds to and activates the GLP-1 receptor, the target for native GLP-1.
GLP-1 is a physiological hormone that has multiple actions on glucose, mediated by the GLP-1 receptors.
The principal mechanism of protraction resulting in the long half-life of semaglutide is albumin binding, which results in decreased renal clearance and protection from metabolic degradation. Furthermore, semaglutide is stabilized against degradation by the DPP-4 enzyme.
Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated, and glucagon secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phase.
The mechanism of kidney-related risk reduction has not been established.
Pharmacodynamics
Semaglutide lowers fasting and postprandial blood glucose and reduces body weight. All pharmacodynamic evaluations were performed after 12 weeks of treatment (including dose escalation) at steady state with semaglutide 1 mg.
Fasting and Postprandial Glucose
Semaglutide reduces fasting and postprandial glucose concentrations. In patients with type 2 diabetes, treatment with semaglutide 1 mg resulted in reductions in glucose in terms of absolute change from baseline and relative reduction compared to placebo of 29 mg/dL (22%) for fasting glucose, 74 mg/dL (36%) for 2-hour postprandial glucose, and 30 mg/dL (22%) for mean 24-hour glucose concentration (see Figure 1).
Figure 1. Mean 24-hour Plasma Glucose Profiles (standardized meals) in Patients with Type 2 Diabetes before (Baseline) and after 12 Weeks of Treatment with Semaglutide or Placebo
Insulin Secretion
Both first-and second-phase insulin secretion are increased in patients with type 2 diabetes treated with OZEMPIC compared with placebo.
Glucagon Secretion
Semaglutide lowers the fasting and postprandial glucagon concentrations. In patients with type 2 diabetes, treatment with semaglutide resulted in the following relative reductions in glucagon compared to placebo, fasting glucagon (8%), postprandial glucagon response (14 to 15%), and mean 24-hour glucagon concentration (12%).
Glucose dependent insulin and glucagon secretion
Semaglutide lowers high blood glucose concentrations by stimulating insulin secretion and lowering glucagon secretion in a glucose-dependent manner. With semaglutide, the insulin secretion rate in patients with type 2 diabetes was similar to that of healthy subjects (see Figure 2).
Figure 2. Mean Insulin Secretion Rate Versus Glucose Concentration in Patients with Type 2 Diabetes during Graded Glucose Infusion before (Baseline) and after 12 Weeks of Treatment with Semaglutide or Placebo and in Untreated Healthy Subjects
During induced hypoglycemia, semaglutide did not alter the counter regulatory responses of increased glucagon compared to placebo and did not impair the decrease of C-peptide in patients with type 2 diabetes.
Gastric emptying
Semaglutide causes a delay of early postprandial gastric emptying, thereby reducing the rate at which glucose appears in the circulation postprandially.
Cardiac electrophysiology (QTc)
The effect of semaglutide on cardiac repolarization was tested in a thorough QTc trial. Semaglutide does not prolong QTc intervals at doses up to 1.5 mg at steady-state.
Pharmacokinetics
Absorption
Absolute bioavailability of semaglutide is 89%. Maximum concentration of semaglutide is reached 1 to 3 days post dose.
Similar exposure is achieved with subcutaneous administration of semaglutide in the abdomen, thigh, or upper arm.
In patients with type 2 diabetes, semaglutide exposure increases in a dose-proportional manner for once-weekly doses of 0.5 mg, 1 mg and 2 mg. Steady-state exposure is achieved following 4 to 5 weeks of once-weekly administration. In patients with type 2 diabetes, the mean population-PK estimated steady-state concentrations following once weekly subcutaneous administration of 0.5 mg and 1 mg semaglutide were approximately 65 ng/mL and 123 ng/mL, respectively. In the trial comparing semaglutide 1 mg and 2 mg, the mean steady state concentrations were 111.1 ng/mL and 222.1 ng/mL, respectively.
Distribution
The mean apparent volume of distribution of semaglutide following subcutaneous administration in patients with type 2 diabetes is approximately 12.5L. Semaglutide is extensively bound to plasma albumin (>99%).
Elimination
The apparent clearance of semaglutide in patients with type 2 diabetes is approximately 0.05 L/h. With an elimination half-life of approximately 1 week, semaglutide will be present in the circulation for about 5 weeks after the last dose.
Metabolism
The primary route of elimination for semaglutide is metabolism following proteolytic cleavage of the peptide backbone and sequential beta-oxidation of the fatty acid sidechain.
Excretion
The primary excretion routes of semaglutide-related material are via the urine and feces. Approximately 3% of the dose is excreted in the urine as intact semaglutide.
Specific Populations
Based on a population pharmacokinetic analysis, age, sex, race, and ethnicity, and renal impairment do not have a clinically meaningful effect on the pharmacokinetics of semaglutide. The exposure of semaglutide decreases with an increase in body weight. However, semaglutide doses of 0.5 mg and 1 mg provide adequate systemic exposure over the body weight range of 40 to 198 kg evaluated in the clinical trials. The effects of intrinsic factors on the pharmacokinetics of semaglutide are shown in Figure 3.
Figure 3. Impact of Intrinsic Factors on Semaglutide Exposure

Patients with Renal impairment - Renal impairment does not impact the pharmacokinetics of semaglutide in a clinically relevant manner. This was shown in a study with a single dose of 0.5 mg semaglutide in patients with different degrees of renal impairment (mild, moderate, severe, or kidney failure) compared with subjects with normal renal function. This was also shown for subjects with both type 2 diabetes and renal impairment based on data from clinical studies (Figure 3).
Patients with Hepatic impairment - Hepatic impairment does not have any impact on the exposure of semaglutide. The pharmacokinetics of semaglutide were evaluated in patients with different degrees of hepatic impairment (mild, moderate, severe) compared with subjects with normal hepatic function in a study with a single-dose of 0.5 mg semaglutide.
Pediatric Patients- Semaglutide has not been studied in pediatric patients.
Drug Interaction Studies
In vitro studies have shown very low potential for semaglutide to inhibit or induce CYP enzymes, and to inhibit drug transporters.
The delay of gastric emptying with semaglutide may influence the absorption of concomitantly administered oral medicinal products [see Drug Interactions ]. The potential effect of semaglutide on the absorption of co-administered oral medications was studied in trials at semaglutide 1 mg steady-state exposure.
No clinically relevant drug-drug interaction with semaglutide (Figure 4) was observed based on the evaluated medications; therefore, no dose adjustment is required when co-administered with semaglutide. In a separate study, no apparent effect on the rate of gastric emptying was observed with semaglutide 2.4 mg.
Figure 4. Impact of Semaglutide on the Exposure of Co-administered Oral Medications
Relative exposure in terms of AUC and Cmax for each medication when given with semaglutide compared to without semaglutide. Metformin and oral contraceptive drug (ethinylestradiol/levonorgestrel) were assessed at steady state. Warfarin (S-warfarin/R-warfarin), digoxin and atorvastatin were assessed after a single dose.
Abbreviations: AUC: area under the curve. Cmax: maximum concentration. CI: confidence interval.
Immunogenicity
The observed incidence of anti-drug antibodies is highly dependent on the sensitivity and specificity of the assay. Differences in assay methods preclude meaningful comparisons of the incidence of anti-drug antibodies (ADAs) in the studies described below with the incidence of ADAs in other studies, including those of semaglutide or of other semaglutide products.
Across the placebo- and active-controlled glycemic control trials, 32 out of 3,150 (1%) OZEMPIC-treated patients developed ADAs to the active ingredient in OZEMPIC (i.e., semaglutide). Of the 32 semaglutide- treated patients that developed semaglutide ADAs, 19 patients (0.6% of the overall population) developed antibodies cross-reacting with native GLP-1. The in vitro neutralizing activity of the antibodies is uncertain at this time.
Carcinogenesis, Mutagenesis, Impairment of Fertility
In a 2-year carcinogenicity study in CD-1 mice, subcutaneous doses of 0.3, 1 and 3 mg/kg/day [2-, 11-, and 30-fold the maximum recommended human dose (MRHD) of 2 mg/week, based on AUC] were administered to the males, and 0.1, 0.3 and 1 mg/kg/day (1-, 2-, and 7-fold MRHD) were administered to the females. A statistically significant increase in thyroid C-cell adenomas and a numerical increase in C-cell carcinomas were observed in males and females at clinically relevant exposures.
- In a 2-year carcinogenicity study in Sprague Dawley rats, subcutaneous doses of 0.0025, 0.01, 0.025 and 0.1 mg/kg/day were administered (below quantification, 0.2-, 0.5-, and 3-fold the exposure at the MRHD). A statistically significant increase in thyroid C-cell adenomas was observed in males and females at all dose levels, and a statistically significant increase in thyroid C-cell carcinomas was observed in males at ≥0.01 mg/kg/day, at clinically relevant exposures.
Human relevance of thyroid C-cell tumors in rats is unknown and could not be determined by clinical studies or nonclinical studies [see Boxed Warning, Warnings and Precautions ].
Semaglutide was not mutagenic or clastogenic in a standard battery of genotoxicity tests (bacterial mutagenicity (Ames), human lymphocyte chromosome aberration, rat bone marrow micronucleus).
In a combined fertility and embryo-fetal development study in rats, subcutaneous doses of 0.01, 0.03 and 0.09 mg/kg/day (0.06-, 0.2-, and 0.6-fold the MRHD) were administered to male and female rats. Males were dosed for 4 weeks prior to mating, and females were dosed for 2 weeks prior to mating and throughout organogenesis until Gestation Day 17. No effects were observed on male fertility. In females, an increase in estrus cycle length was observed at all dose levels, together with a small reduction in numbers of corpora lutea at ≥0.03 mg/kg/day. These effects were likely an adaptive response secondary to the pharmacological effect of semaglutide on food consumption and body weight.
Kidney Outcomes Trial of OZEMPIC in Adults with Type 2 Diabetes Mellitus and Chronic Kidney Disease
FLOW (NCT03819153) was a randomized, double-blind, placebo-controlled, event driven trial in adults with type 2 diabetes mellitus and chronic kidney disease (eGFR 25 to 75 mL/min/1.73 m2 with urine albumin-to- creatinine ratio [UACR] >100 mg/g and <5000 mg/g). All patients needed to have an HbA1c ≤10% at screening and be receiving standard of care background therapy, including a maximum tolerated labeled dose of a renin- angiotensin-aldosterone system (RAAS) blocking agent including an angiotensin converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB), unless such treatment was contraindicated or not tolerated. The trial excluded patients with congenital or hereditary kidney diseases including polycystic kidney disease, autoimmune kidney diseases including glomerulonephritis or congenital urinary tract malformations.
A total of 3,533 patients were randomized to receive OZEMPIC 1 mg once weekly or placebo and were followed for a median of 41 months. The mean age of the study population was 67 years, and 70% of patients were male. Approximately 66% of the trial population was White, 24% Asian, and 5% Black or African American. At baseline, the mean eGFR was 47 mL/min/1.73m2, with 11% of patients having an eGFR <30 mL/min/1.73m2. Median baseline UACR was 568 mg/g with 69% of patients with a UACR >300 mg/g. At baseline, 95% of patients were treated with an ACE inhibitor or ARB, 16% were on sodium-glucose cotransporter 2 (SGLT2) inhibitors, 76% were on a statin, and 50% were on an antiplatelet agent.
OZEMPIC was superior to placebo in reducing the incidence of the primary composite endpoint of a sustained decline in eGFR of ≥50%, sustained eGFR <15 mL/min/1.73 m2, chronic renal replacement therapy, renal death, CV death (HR 0.76 [95% CI 0.66, 0.88], p=0.0003) as shown in Table 10 and Figure 7. The treatment effect reflected a reduction in a sustained decline in eGFR of ≥50%, progression to kidney failure and CV death. There were few renal deaths during the trial.
OZEMPIC also reduced the annual rate of change in eGFR (Figure 9), the incidence of a composite cardiovascular endpoint, consisting of non-fatal myocardial infarction (MI), non-fatal stroke, and cardiovascular death, and the incidence of all-cause death (Table 10 and Figure 8).
The treatment effect on the primary composite endpoint was generally consistent across the pre-specified subgroups examined, including age, biological sex, eGFR and UACR. The treatment benefit on the primary composite endpoint was not evident in patients taking SGLT2 inhibitors at baseline, but there were few events in these patients.
Table 10: Analyses of the Primary and Secondary Endpoints and their Individual Components in FLOW Trial
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1 Cox proportional hazards model with treatment as factor and stratified by baseline use of SGLT2-inhibitor at baseline (yes or no).
2 Two-sided p-value for the test of no difference. The significance level was 0.03224.
3 Sustained was defined as having 2 consecutive measurements ≥28 days apart fulfilling the criteria.
Figure 7. Cumulative Incidence: Time to First Occurrence of the Primary Composite Endpoint - Sustained Decline in eGFR ≥50%, Sustained eGFR<15 mL/min/1.73m2, Chronic Renal Replacement Therapy, Renal Death or CV Death

Cumulative incidence estimates are based on time from randomization to first composite renal event with non-CV and non-renal death modelled as competing risk. The x-axis is truncated at 52 months where approximately 5% of the population was in the trial.
Sustained was defined as having 2 consecutive measurements ≥28 days apart fulfilling the criteria.
Figure 8. Cumulative incidence: Time to First Occurrence of MACE in FLOW Trial
- Cumulative incidence estimates are based on time from randomization to first EAC-confirmed MACE with non-CV death modelled as competing risk. The x-axis is truncated at 52 months where approximately 5% of the population was in the trial.
Figure 9. Observed Mean Plot: eGFR (mL/min/1.73m2) by Week in FLOW Trial
- Observed data from the in-trial period until week 104. Error bars are +/- 1.96 *standard error of the mean eGFR, which was calculated using the CKD-EPI 2009 formula.
- CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration, eGFR: estimated glomerular filtration rate.
How Supplied
Injection: clear, colorless solution of 0.68 mg/mL, 1.34 mg/mL or 2.68 mg/mL of semaglutide available in prefilled, disposable, single-patient-use pens in the following packaging configurations:
Dose per Injection | Use For | Total Strength per Total Volume | Doses per Pen | Carton Contents | NDC |
0.25 mg 0.5 mg | Initiation Maintenance | 2 mg/3 mL | 4 doses of 0.25 mg and 2 doses of 0.5 mg or 4 doses of 0.5 mg | 1 pen 6 NovoFine® Plus needles | 0169-4181-13 |
1 mg | Maintenance | 4 mg/3 mL | 4 doses of 1 mg | 1 pen 4 NovoFine® Plus needles | 0169-4130-13 |
2 mg | Maintenance | 8 mg/3 mL | 4 doses of 2 mg | 1 pen 4 NovoFine® Plus needles | 0169-4772-12 |
The 2 mg/1.5 mL (1.34 mg/mL) strength (NDC 0169-4132-12) is not currently marketed by Novo Nordisk Inc.
Each OZEMPIC pen is for use by a single patient. An OZEMPIC pen must never be shared between patients, even if the needle is changed [see Warnings and Precautions ].
Recommended Storage
Prior to first use, OZEMPIC should be stored in a refrigerator between 36ºF to 46ºF (2ºC to 8ºC). Do not store in the freezer or directly adjacent to the refrigerator cooling element. Do not freeze OZEMPIC and do not use OZEMPIC if it has been frozen.
After first use of the OZEMPIC pen, the pen can be stored for 56 days at controlled room temperature (59°F to 86°F; 15°C to 30°C) or in a refrigerator (36°F to 46°F; 2°C to 8°C). Do not freeze. Keep the pen cap on when not in use. OZEMPIC should be protected from excessive heat and sunlight.
Always remove and safely discard the needle after each injection and store the OZEMPIC pen without an injection needle attached. Always use a new needle for each injection.
Recommended Storage Conditions for the OZEMPIC Pen
Prior to first use | After first use | |
Refrigerated 36°F to 46°F (2°C to 8°C) | Room Temperature 59°F to 86°F (15°C to 30°C) | Refrigerated 36°F to 46°F (2°C to 8°C) |
Until expiration date | 56 days |
INSTRUCTIONS FOR USE OZEMPIC® [oh-ZEM-pick] (semaglutide) injection, for subcutaneous use 2 mg dose (pen delivers doses in 2 mg increments only) | |
Supplies you will need to give your OZEMPIC injection:
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Step 1. Prepare your pen with a new needle | |
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Do not reuse or share your needles with other people. You may give other people a serious infection, or get a serious infection from them. Never use a bent or damaged needle. | |
Step 2. First Time Use for Each New Pen: Check the OZEMPIC flow | |
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If no drop appears, you will not inject any OZEMPIC, even though the dose counter may move. This may mean that there is a blocked or damaged needle. A small drop may remain at the needle tip, but it will not be injected. Only check the OZEMPIC flow before your first injection with each new pen. | |
Step 3. Select your dose | |
The dashed line in the dose counter | ![]() |
You will hear a “click” every time you turn the dose selector. Do not set the dose by counting the number of clicks you hear. Only doses of 2 mg can be selected with the dose selector. 2 mg must line up exactly with the dose pointer to make sure that you get a correct dose. The dose selector changes the dose. Only the dose counter and dose pointer will show that 2 mg has been selected. You can only select 2 mg for each dose. When your pen contains less than 2 mg, the dose counter stops before 2 mg is shown. The dose selector clicks differently when turned forward or backward. Do not count the pen clicks. | |
How much OZEMPIC is left? | |
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Step 4. Inject your dose | |
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How to identify a blocked or damaged needle?
How to handle a blocked needle? Change the needle as described in Step 5, and repeat all steps starting with Step 1: “Prepare your pen with a new needle”. Never touch the dose counter when you inject. This can stop the injection. You may see a drop of OZEMPIC at the needle tip after injecting. This is normal and does not affect your dose. | |
Step 5. After your injection | |
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Always remove the needle from your pen. This will reduce the risk of contamination, infection, leakage of OZEMPIC, and blocked needles leading to the wrong dose. If the needle is blocked, you will not inject any OZEMPIC. Always dispose of the needle after each injection. | |
Disposing of used OZEMPIC pens and needles:
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Caring for your pen | |
How should I store my OZEMPIC pen?
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For more information go to www.OZEMPIC.com
Manufactured by:
Novo Nordisk A/S
DK-2880 Bagsvaerd
Denmark
For information about OZEMPIC contact:
Novo Nordisk Inc.
800 Scudders Mill Road
Plainsboro, NJ 08536
1-888-693-6742
Version: 2
OZEMPIC® and NovoFine® are registered trademarks of Novo Nordisk A/S.
PATENT Information: https://novonordisk-us.com/products/product-patents.html
© 2023 Novo Nordisk
This Instructions for Use has been approved by the U.S. Food and Drug Administration.
Revised: September 2023

Mechanism of Action
Semaglutide is a GLP-1 analogue with 94% sequence homology to human GLP-1. Semaglutide acts as a GLP-1 receptor agonist that selectively binds to and activates the GLP-1 receptor, the target for native GLP-1.
GLP-1 is a physiological hormone that has multiple actions on glucose, mediated by the GLP-1 receptors.
The principal mechanism of protraction resulting in the long half-life of semaglutide is albumin binding, which results in decreased renal clearance and protection from metabolic degradation. Furthermore, semaglutide is stabilized against degradation by the DPP-4 enzyme.
Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Thus, when blood glucose is high, insulin secretion is stimulated, and glucagon secretion is inhibited. The mechanism of blood glucose lowering also involves a minor delay in gastric emptying in the early postprandial phase.
The mechanism of kidney-related risk reduction has not been established.