Wegovy Hd (semaglutide)

No dosing information is available for this tab.

Semaglutide is administered orally or by subcutaneous injection.

No dosing information is available for this tab.

In vitro studies have demonstrated that semaglutide has a very low potential to inhibit or induce cytochrome P-450 (CYP) enzymes or to inhibit drug transporters.

There are no contraindication interactions for this drug.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Antidiabetic Agents/Gatifloxacin

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: The exact mechanism is unknown.

CLINICAL EFFECTS: Concurrent use of gatifloxacin may result in hypoglycemia and/or hyperglycemia.(1-4) Hypoglycemia is more common during the first three days of concurrent therapy. Hyperglycemia is more common after the first three days of concurrent therapy.(2)

PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.(2)

PATIENT MANAGEMENT: Patients receiving concurrent gatifloxacin should be closely monitored for hypoglycemia during the first three days of concurrent therapy and for hyperglycemia after the first three days of concurrent therapy. Patients should be instructed to discontinue gatifloxacin if hypoglycemia or hyperglycemia occur.(2)

DISCUSSION: Hypoglycemia has been reported with gatifloxacin and glyburide(1,5,6) or glimepiride.(7) In a study in patients with type 2 diabetes mellitus, concurrent gatifloxacin (400 mg daily for 10 days) had no effect on the pharmacokinetics of glyburide (steady state daily regimen); however, pharmacodynamic interactions have been reported.(2) Health Canada has received 19 reports of hypoglycemia in patients taking gatifloxacin. Seventeen of these involved concurrent hypoglycemic agents. Health Canada has received 2 reports of hyperglycemia in patients taking gatifloxacin and hypoglycemic agents. Health Canada has received 2 reports of patients experiencing hypoglycemia and hyperglycemia during concurrent gatifloxacin and hypoglycemic agents.(3) In a study, 13 reports of dysglycemia were reported in patients taking gatifloxacin. Ten of these patients had diabetes mellitus and were on concurrent hypoglycemic agents. Of these ten patients, nine patients experienced hypoglycemia, while one patient experienced hyperglycemia.(8)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Antidiabetic Agents/Gymnema

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Gymnema has been shown to increase the number of insulin-secreting beta cells in animals. It has also been shown to increase the activity of enzymes responsible for glucose uptake and utilization and inhibit peripheral utilization of glucose.(1)

CLINICAL EFFECTS: Use of gymnema may result in decreased requirements of antidiabetic agents.(2-4)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Diabetic patients should be carefully monitored if gymnema is initiated or discontinued from concurrent therapy. The dosage of the patient's antidiabetic agent(s) may need to be adjusted.(2)

DISCUSSION: In a study in 22 non-insulin-dependent patients, patients had decreased blood glucose, glycosylated hemoglobin, and glycosylated plasma proteins during gymnema therapy. Patients were able to decrease the dosage of their conventional antidiabetic therapy and five patients were able to discontinue their conventional antidiabetic therapy.(3) In a study in 27 insulin-dependent patients, patients had decreased insulin requirements, fasting blood glucose, glycosylated hemoglobin, and glycosylated plasma protein levels.(4)

Glp-1 Receptor Agonists/Anesthesia Agents

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: GLP-1 receptor agonists can cause delayed gastric emptying.(1,2)

CLINICAL EFFECTS: Gastric contents may remain in the stomach after preoperative fasting, which could increase the risk of regurgitation and aspiration.(1,2)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The American Society of Anesthesiologists (ASA) recommends the following for patients receiving elective procedures: - For patients on daily dosing, consider holding GLP-1 agonists on the day of the procedure. For patients on weekly dosing, consider holding GLP-1 agonists a week prior to the procedure. - Consult an endocrinologist for patients taking GLP-1 agonists for diabetes management if the GLP-1 agonist is held longer than the dosing schedule to avoid hyperglycemia. - For patients requiring urgent or emergent procedures, proceed and treat the patient as 'full stomach.'(3)

DISCUSSION: In one case report, a 31-year-old patient taking semaglutide followed preoperative fasting guidelines but food residue was discovered upon endoscopy, leading to cancellation of the surgical procedure.(4) In a case report, a semaglutide-treated patient experienced regurgitation upon induction of general anesthesia despite a 20 hour preoperative fasting period. The patient received semaglutide two days before the scheduled procedure.(5) A case report of a 42-year-old patient after fasting for 18 hours showed substantial gastric content upon endoscopy. The patient experienced intraoperative pulmonary aspiration of gastric contents which were suctioned from the trachea and bronchi using bronchoscopy.(6)

Glp-1 Receptor Agonists/Lithium

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The exact mechanism is unknown but may be related to nausea, vomiting, and/or diarrhea caused by volume depletion resulting in the decreased renal clearance of lithium. Weight loss may also cause stable doses of lithium to be too high for weight-based dosing.(1-6)

CLINICAL EFFECTS: Lithium has a narrow therapeutic range; even modest, unintended increases in lithium concentration may result in lithium toxicity. Early symptoms of lithium toxicity may include: lethargy, muscle weakness or stiffness, new onset or coarsening of hand tremor, vomiting, diarrhea, confusion, ataxia, blurred vision, tinnitus and nystagmus. Severe toxicity may produce multiple organ dysfunction (e.g. seizures, coma, renal failure, cardiac arrhythmias, cardiovascular collapse) and may be fatal.

PREDISPOSING FACTORS: Risk factors for lithium toxicity include: renal impairment or worsening of existing renal disease, dehydration, low sodium diet, and concomitant use of multiple medications which may impair renal elimination of lithium (e.g. ARBs, ACE Inhibitors, NSAIDs, diuretics). Patients who require higher therapeutic lithium levels to maintain symptom control are particularly susceptible to these factors.

PATIENT MANAGEMENT: The manufacturer of semaglutide states consider increased clinical or laboratory monitoring for medications that have a narrow therapeutic index or that require clinical monitoring.(1) An expert review article on the interaction between GLP-1 agonists and lithium states that clinicians may need to monitor lithium more closely when a GLP-1 agonist is initiated, whether clinically or through therapeutic drug monitoring. A cautious approach might be to consider monitoring at the following time points when there is a plan to introduce a GLP-1 agonist with lithium: 1. Before GLP-1 agonist initiation, 2. Near 1 week after starting a GLP-1 agonist, 3. Near 1 weak after each dose increases (i.e., several monthly intervals for weekly subcutaneous semaglutide and tirzepatide), and 4. Longitudinally, at more frequent intervals than guidelines recommend during the first year after GLP-1 agonist initiation, when weight loss begins to plateau. Increased monitoring may also be considered when switching between GLP-1 agonists.(7) Monitor closely to decrease the risk for lithium toxicity. Evaluate renal function and most recent lithium levels. If renal function is not stable, it would be prudent to withhold combination therapy until renal function is stable. Counsel patient to assure they know signs and symptoms of lithium toxicity and understand the importance of follow-up laboratory testing.

DISCUSSION: The impact of GLP-1 agonists on the pharmacokinetics of lithium has not been investigated in clinical studies. Literature is limited to a small number of case reports. In a case report, a 23-year-old male established on semaglutide was started on lithium and titrated to 1800 mg daily, corresponding to a lithium level of 0.9mEq/L. The patient was then switched from semaglutide to tirzepatide 5 mg weekly. Four days after his first dose of tirzepatide, he reported early symptoms of potential lithium toxicity, which progressed significantly after his second dose. Symptoms corresponded to a 15-hour post-dose level of 1.7 mEq/L, despite no changes in renal function, hydration status, or other concurrent medications. Management with intravenous fluids was sufficient, and close monitoring of lithium levels and tapering of the lithium dose prevented future toxicity. The patient remained on tirzepatide and a maintenance dose of lithium extended-release 1200 mg daily, with a lithium level measured 15-hour post-dose of 0.6mEq/L. The patient's weight remained the same from the start of tirzepatide therapy.(8) In a case report, a 62-year-old male stable on lithium for 6 years (lithium ER 600 mg daily) started semaglutide 0.25 mg twice weekly 2 to 3 weeks prior to visiting the emergency department. Patient had multiple comorbidities and medications were unchanged except for semaglutide. 6 weeks prior to visiting the ED, the patient was instructed to decrease his fluid intake due to urinary proteinuria symptoms. Lithium level was 1.8mmol/L in ED. Both lithium and semaglutide were discontinued. Lithium was restarted at 300 mg, increased to lithium ER 450 mg 10 days later and lithium levels increased to 0.8 and 0.9mmol/L. Further dose adjustment back to 300 mg resulted in a steady lithium serum level of 0.6mmol/L. No significant changes to kidney function were observed. Semaglutide was not reintroduced.(9) In another case report, a 23-year-old female was admitted to hospital for lithium toxicity. Medication list included lithium carbonate ER 900 mg and she was reported as restarting semaglutide recently. Further questioning revealed inconsistent semaglutide use over the previous 2 years, with unclear timing of a recent restart. Her lithium level on admission was found to be 2.1mmol/L. Both lithium and semaglutide were discontinued. Lithium ER had been a long-standing medication at 900 mg dose since she was 9 years old with no previous incidents of clinical lithium toxicity. She was recorded as having significant side effects to semaglutide, including nausea and vomiting. At the time of discharge, 4 days after admission, the lithium level was 0.5mmol/L and it was recommended to avoid combining lithium and semaglutide in the future. No significant changes to kidney function were observed.(9) In a case report, a 22-year-old-male stable on 2100 mg lithium carbonate ER daily was initiated on semaglutide for weight management. Patient had regular monitoring of his lithium level prior to and during dose escalation with semaglutide. During the semaglutide increase and tapering of his lithium dose, there were no report of nausea, vomiting, diarrhea, decreased oral/fluid intake, and no medication changes were made. There were no changes in mental status, symptoms concerning psychiatric decompensation, or symptoms of lithium toxicity.(9) In a 40-week study of patients with stable bipolar disorder, liraglutide resulted in a significantly greater weight loss as compared with placebo. 7 of the 60 participants were on lithium, no instances of lithium toxicity was reported and liraglutide was well tolerated.(10)

Glp-1 Receptor Agonists/Thyroid Preparations

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The exact mechanism is unknown but may be related to decreased GI motility resulting in increased absorption of levothyroxine. Weight loss may also cause stable doses of levothyroxine to be too high for weight-based dosing.(1)

CLINICAL EFFECTS: Concurrent administration of GLP-1 receptor agonists and thyroid preparations may increase the clinical effects of the thyroid agent, resulting in symptoms of hyperthyroidism.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Patients taking thyroid preparations and GLP-1 receptor agonists should be monitored for changes in thyroid function. Symptoms of hyperthyroidism include weight loss, rapid heartbeat, nervousness, sweating, tremor, fatigue, and difficulty sleeping. The dosage of levothyroxine may need to be adjusted accordingly.

DISCUSSION: In an open-label, one-sequence, crossover, 2-part trial examining the effect of administering 14 mg oral semaglutide and levothyroxine together, a 33% increase in levothyroxine AUC was identified. The trial also examined the impact of SNAC , the absorption enhancer in oral GLP-1 receptor agonists, and found that SNAC alone did not impact absorption of levothyroxine.(2) In a single-center, prospective trial, participants with diabetes without thyroid disease were given exenatide and TSH levels were measured. After 6 months of treatment, mean TSH concentration decreased from 2.3 to 1.8 without impact to T4 and T3. The mechanism that was proposed was that exenatide can increase the sensitivity of the hypothalamus or pituitary gland to the thyroid hormone negative feedback or increase the number of receptors on the hypothalamus or pituitary gland. No relationship was found between weight change and TSH level.(3) In a case report, a post-thyroidectomy patient on a stable dose of levothyroxine (125 mcg daily) started concurrent subcutaneous semaglutide therapy. Five months after starting treatments together, she started experiencing palpitations, perspiration, and heat intolerance. The levothyroxine dose was decreased to 88 mcg daily resulting in a resolution of symptoms.(4) In another case report, a 43-year-old female patient was on a stable dose of levothyroxine (200 mcg) and started on subcutaneous semaglutide. After 5 months, her TSH level dropped to 0.01 ng/dL and levothyroxine was reduced to 150 mcg daily.(5)

Selected Antidiabetic Agents/Chloroquine; Hydroxychloroquine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The exact mechanism is unknown. Chloroquine and hydroxychloroquine may increase insulin sensitivity by inhibiting insulin metabolism and inflammation and increasing cellular uptake of glucose and glycogen synthesis.(1,2) These effects may result in additive hypoglycemia with anti-diabetic agents.

CLINICAL EFFECTS: Concurrent use of chloroquine or hydroxychloroquine and antidiabetic agents may result in severe hypoglycemia.(3) Hypoglycemia can lead to coma.

PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.

PATIENT MANAGEMENT: Patients maintained on antidiabetic agents who require concurrent therapy with chloroquine or hydroxychloroquine should be closely monitored for hypoglycemia. A decrease in the dose of insulin or other anti-diabetic medications may be required. Patients should be advised of the risk and symptoms of hypoglycemia and to contact their doctor if hypoglycemia occurs.(3) Signs of hypoglycemia may include confusion, dizziness, feeling shaky, unusual hunger, headaches, irritability, pounding heart or very fast pulse, pale skin, sweating, trembling, weakness, or unusual anxiety.

DISCUSSION: Hydroxychloroquine has been shown to cause severe hypoglycemia including loss of consciousness that could be life threatening.(3) Concomitant hypoglycemic agents may increase the risk and/or severity of this effect. A 77 year old man who was stable on twice daily insulin suffered two episodes of hypoglycemic coma 2 weeks after starting prednisone 5 mg daily and hydroxychloroquine 400 mg daily for rheumatoid arthritis. His insulin dosage required a decrease of 37%.(4) Many studies have investigated the glucose-lowering effect of hydroxychloroquine. In a clinical trial of type II diabetics on maximal doses of sulfonylureas, addition of hydroxychloroquine lowered hemoglobin A1C (HbA1C) up to 1% more than placebo.(5) Another clinical trial of type II diabetics on metformin and glimepiride or gliclazide found that hydroxychloroquine 400 mg daily reduced fasting blood glucose (FBG), post-prandial glucose (PPG), and HbA1C to a similar degree as pioglitazone 15 mg daily at 24 weeks.(6) In a prospective observational study, 250 uncontrolled type II diabetics on metformin, glimepiride, pioglitazone, sitagliptin, and a SGLT-2 inhibitor received hydroxychloroquine 400 mg daily for 48 weeks. HbA1C decreased from 8.83% to 6.44%, FBG decreased by 40.78%, and PPG decreased by 58.95%. The doses of metformin were reduced by 50%, glimepiride and sitagliptin by 75%, and SGLT-2 inhibitors were discontinued in most patients.(7)

Selected Antidiabetic Agents/Selected Quinolones

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: The exact mechanism is unknown.

CLINICAL EFFECTS: Concurrent use of quinolones and antidiabetic agents may result in severe hypoglycemia.(1-7) Hypoglycemia can lead to coma.

PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.(5)

PATIENT MANAGEMENT: Patients maintained on antidiabetic agents who require concurrent therapy with a quinolone should be closely monitored for hypoglycemia.(1-4) Patients should be instructed to discontinue quinolone use and contact their doctor if hypoglycemia occurs.(2,4) Signs of hypoglycemia may include confusion, dizziness, feeling shaky, unusual hunger, headaches, irritability, pounding heart or very fast pulse, pale skin, sweating, trembling, weakness, or unusual anxiety.

DISCUSSION: Hypoglycemia has been reported with concurrent ciprofloxacin and glyburide,(1,8,9) levofloxacin and glyburide,(2,10,11) norfloxacin and glyburide,(3) levofloxacin and glipizide (12) as well as levofloxacin and metformin-glibenclamide.(14) There has been one report of fatal hypoglycemia with concurrent levofloxacin and glyburide(9) and one of the above reports of hypoglycemia with concurrent levofloxacin and glyburide resulted in hypoxic brain injury.(11) A review of postmarketing adverse event data for the fluoroquinolones and hypoglycemic coma identified 56 reports in FAERS search from October 1987- April 2017 and 11 additional cases in the medical literature. Most patients had risk factors for hypoglycemia. 41 patients were taking one or more hypoglycemic drugs. 13 deaths occurred (some of these patients had renal insufficiency). 9 patients did not fully recover and had resultant disability.(13)

*Patients with personal or family history of medullary thyroid carcinoma (MTC) or in patients with multiple endocrine neoplasia syndrome type 2 (MEN 2).

*Patients with prior serious hypersensitivity reaction to semaglutide or any ingredient in the formulation.

• Acute pancreatitis

• Family history of medullary thyroid carcinoma
• Gastroparesis
• Medullary thyroid carcinoma
• Multiple endocrine neoplasia type 2

• Diabetic retinopathy
• Hypoglycemic disorder
• Kidney disease with likely reduction in glomerular filtration rate (GFr)
• Kidney disease with reduction in glomerular filtration rate (GFr)

Adverse effects reported in at least 5% of patients receiving subcutaneous semaglutide (Ozempic(R)) in placebo-controlled clinical trials include nausea, vomiting, diarrhea, abdominal pain, and constipation.

Adverse effects reported in at least 5% of patients receiving oral semaglutide in placebo-controlled clinical trials include nausea, abdominal pain, diarrhea, decreased appetite, vomiting, and constipation.

Adverse effects reported in at least 5% of patients receiving subcutaneous semaglutide (Wegovy(R)): nausea, diarrhea, vomiting, constipation, abdominal pain, headache, fatigue, dyspepsia, dizziness, abdominal distension, eructation, hypoglycemia in patients with type 2 diabetes, flatulence, gastroenteritis, gastroesophageal reflux disease, and nasopharyngitis.

Less Frequent

• Hypoglycemic disorder

Rare or Very Rare

• Acute kidney injury
• Acute pancreatitis
• Anaphylaxis
• Angioedema
• Appendicitis
• Biliary calculus
• Cholecystitis
• Gastrointestinal obstruction
• Ileus
• Kidney disease with reduction in glomerular filtration rate (GFr)
• Necrotizing pancreatitis

More Frequent

• Acute abdominal pain
• Diarrhea
• Gastroenteritis
• Headache disorder
• Nausea
• Pharyngitis
• Vomiting

Less Frequent

• Dyspepsia
• Eructation
• Fatigue
• Flatulence
• Gastroesophageal reflux disease
• Influenza
• Sinusitis

Rare or Very Rare

• Alopecia
• Constipation
• Dizziness
• Dysesthesia
• Dysgeusia
• Elevated serum amylase
• Elevated serum lipase
• Fecal impaction
• Gastritis
• Hemorrhoids
• Hiccups
• Injection site sequelae
• Photophobia
• Skin rash
• Tachycardia
• Urolithiasis
• Urticaria

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Safety and efficacy of semaglutide for type 2 diabetes mellitus (Ozempic(R), Rybelsus(R)) have not been established in children or adolescents <18 years of age.

The safety and efficacy of semaglutide (Wegovy(R)) as an adjunct to a reduced calorie diet and increased physical activity for chronic weight management have been established in pediatric patients >=12 years of age with a BMI corresponding to >=95th percentile standardized for age and sex. Use of semaglutide for this indication is supported by a 68-week, double-blind, placebo-controlled clinical trial in pediatric patients and from studies in adult patients with obesity. There are insufficient data in pediatric patients with type 2 diabetes treated with Wegovy(R) for obesity to determine if there is an increased risk of hypoglycemia with the drug similar to that reported in adults. Inform patients of the risk of hypoglycemia and educate them on the signs and symptoms of hypoglycemia. When initiating Wegovy(R) in pediatric patients >=12 years of age with type 2 diabetes, consider reducing the dose of the concomitantly administered insulin secretagogue (such as sulfonylureas) or insulin to reduce the risk of hypoglycemia.

Data are lacking on the use of semaglutide in pregnant women. However, reproduction studies in animals have shown teratogenic effects. Poorly controlled diabetes mellitus during pregnancy increases maternal risk for diabetic ketoacidosis, pre-eclampsia, spontaneous abortion, preterm delivery, and delivery complications. In addition, poorly controlled diabetes mellitus during pregnancy increases the risk of major fetal birth defects, stillbirth, and macrosomia-related morbidity.

Embryofetal mortality, structural abnormalities (e.g., visceral and skeletal abnormalities), and alterations to growth were observed in the offspring of rats who were administered semaglutide during organogenesis at dosages resulting in systemic exposures lower than the maximum recommended human dosage. In reproduction studies in rabbits and monkeys, early pregnancy loss and structural abnormalities (e.g., visceral and skeletal abnormalities) were observed at dosages below the maximum recommended human dosage and at dosages at least 5 times greater than the maximum recommended human dosage.

Salcaprozate sodium (SNAC), an absorption enhancer contained in semaglutide oral tablets, crosses the placenta and reaches fetal tissues in rats. In a prenatal and postnatal development study in pregnant Sprague Dawley rats, SNAC was administered orally at 1000 mg/kg per day (exposure levels were not measured) on gestation day 7 through lactation day 20. An increase in the length of gestation and number of stillbirths and a decrease in pup viability were observed.

The manufacturers of the semaglutide preparations used for diabetic management state the drug should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Semaglutide should be discontinued in women for at least 2 months before a planned pregnancy due to the drug's long half-life. The manufacturer of the semaglutide preparation used for weight control management states that weight loss offers no benefit to a pregnant patient and may cause fetal harm; if a patient becomes pregnant while receiving the drug, treatment should be discontinued.

A pregnancy exposure registry has been established to monitor pregnancy outcomes in women exposed to Wegovy(R); encourage pregnant women exposed to the drug to contact 1-800-727-6500.

Semaglutide is distributed into milk in rats at concentrations 3-12 fold lower than in maternal plasma. It is not known whether semaglutide is distributed into milk in humans or what the effects of the drug are on the breast-fed infant or on milk production. The benefits of breast-feeding and the importance of semaglutide to the woman should be considered along with any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.

SNAC, an absorption enhancer contained in semaglutide oral tablets, and/or its metabolites are concentrated in the milk of lactating rats. SNAC and/or its metabolites were detected in milk of lactating rats following a single maternal administration on lactation day 10. Mean levels of SNAC and/or its metabolites in milk were approximately 2-12 fold higher than in maternal plasma. There are no data on the presence of SNAC in human milk; however, substances present in animal milk are likely to be present in human milk. Since the activity of UGT2B7, an enzyme involved in SNAC clearance, is lower in infants than in adults, higher SNAC plasma concentrations may occur in neonates and infants. Because of the unknown potential for serious adverse reactions in the breast-fed infant due to the possible accumulation of SNAC from breast-feeding and because there are alternative formulations of semaglutide (e.g., injection) that can be used during lactation, patients should be advised that breast-feeding is not recommended during treatment with oral semaglutide.

The manufacturers make no special population dosage recommendations for geriatric patients.

In the pool of placebo- and active-controlled glycemic control clinical trials, 23.6% of patients receiving subcutaneous semaglutide and 29.9% of those receiving oral semaglutide were 65 years of age and older; 3.2% of those receiving subcutaneous semaglutide and 4.8% of those receiving oral semaglutide were 75 years of age and older. In a cardiovascular outcome trial (SUSTAIN-6) of subcutaneous semaglutide, 48% of patients were 65 years of age and older and 9.6% were 75 years of age and older; in a cardiovascular outcomes trial of oral semaglutide (PIONEER 6), 43.4 or 12.3% of patients were at least 65 or at least 75 years of age, respectively. In the trials of subcutaneous semaglutide (Wegovy), 8.8% of patients receiving the drug were 65-75 years of age and 0.9% were >=75 years of age. No substantial differences in safety and efficacy relative to younger adults were observed in these patients, but increased sensitivity in some geriatric individuals cannot be ruled out.