In both male and female rats, tirzepatide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures. It is unknown whether tirzepatide causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans as human relevance of tirzepatide-induced rodent thyroid C-cell tumors has not been determined.
Tirzepatide is contraindicated in patients with a personal or family history of MTC or in patients with multiple endocrine neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk for MTC with the use of tirzepatide and inform them of symptoms of thyroid tumors (eg, 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 tirzepatide.
Note: Due to lack of additive glycemic benefit, avoid concomitant use with a dipeptidyl peptidase-4 inhibitor (ADA/EASD [Davies 2018]). May require a dose reduction of insulin and/or insulin secretagogues (sulfonylureas, meglitinides) to avoid hypoglycemia (AACE/ACE [Garber 2020]). Use is not recommended in patients with severe GI disease (eg, severe gastroparesis) (has not been studied).
Diabetes mellitus, type 2, treatment:
SUBQ: Initial: 2.5 mg once weekly for 4 weeks, then increase to 5 mg once weekly. May increase dose in 2.5 mg/week increments every 4 weeks if needed to achieve glycemic goals (maximum weekly dose: 15 mg/week). Note: The lower initial dose (2.5 mg weekly) is intended to reduce GI symptoms; it does not provide effective glycemic control. If changing the day of administration is necessary, allow at least 72 hours between 2 doses.
Missed dose: Missed dose should be administered as soon as possible within 4 days; resume usual schedule thereafter. If >4 days have elapsed, skip the missed dose and resume administration at the next scheduled weekly dose.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
No dosage adjustment necessary.
No dosage adjustment necessary.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Pen-injector, Subcutaneous [preservative free]:
Mounjaro: 2.5 mg/0.5 mL (0.5 mL); 5 mg/0.5 mL (0.5 mL); 7.5 mg/0.5 mL (0.5 mL); 10 mg/0.5 mL (0.5 mL); 12.5 mg/0.5 mL (0.5 mL); 15 mg/0.5 mL (0.5 mL)
No
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Mounjaro: https://pi.lilly.com/us/mounjaro-us-mg.pdf?s=mg
SUBQ: Administer by SUBQ injection into the abdomen, thigh, or upper arm at any time of day on the same day each week, with or without food. If changing the day of administration is necessary, allow ≥72 hours between 2 doses. Rotate injection sites with each dose. Do not mix with other injectable products (eg, insulin); administer as separate injections. Avoid adjacent injections if administering other agents in the same area of the body. Solution should be clear and colorless to slightly yellow; do not use if particulate matter or discoloration are seen. Tirzepatide is a single-dose device that does not require priming before injection.
Type 2 diabetes mellitus, treatment: As an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
Limitations of use: Has not been studied in patients with a history of pancreatitis; not indicated for use in patients with type 1 diabetes mellitus.
Tirzepatide may be confused with tolazamide. Mounjaro may be confused with Monjuvi.
Acute kidney injury (AKI), which sometimes requires dialysis, has been reported with glucagon-like peptide-1 (GLP-1) receptor agonists. According to the manufacturer, AKI was seen mostly in patients who had experienced nausea, vomiting, diarrhea, or dehydration secondary to GLP-1 receptor agonists.
Mechanism: Non–dose-related; exact mechanism is unknown. Pre-renal AKI may occur due to dehydration and volume contraction secondary to gastrointestinal symptoms (eg, nausea, vomiting, diarrhea) (Ref).
Onset: Varied; because the mechanism is thought to be related to volume contraction, timing may be dependent on gastrointestinal symptoms, initiation or dosage adjustment of concomitant medications, and/or comorbid conditions (Ref).
Risk factors:
• Volume contraction (eg, during periods of severe vomiting or diarrhea) (Ref)
• Co-administration of medications known to result in kidney injury during episodes of dehydration (eg, drugs that inhibit the renin-angiotensin system) (Ref)
• Preexisting kidney impairment
Diabetic retinopathy (DR) was reported with tirzepatide during the SURPASS-2 study, a clinical trial evaluating the safety and efficacy of tirzepatide compared to semaglutide in patients with type 2 diabetes (Ref); patients with a prior history of DR were excluded from this trial. In addition, rapid reductions in HbA1c are associated with an early worsening of DR (Ref). In an analysis of DR complications due to the glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide, the increased risk of DR was mainly observed in patients with preexisting DR and primarily attributable to the magnitude and rapidity of reduction in HbA1c (Ref).
Mechanism: Unknown. In general, worsening of preexisting DR is a known consequence of rapid improvement of hyperglycemia, especially in patients with uncontrolled diabetes. Although unlikely, a direct toxic effect or potential angiogenic action of tirzepatide has not been ruled out (Ref).
Onset: Varied; clinicians should note that DR is a progressive condition, and the onset of DR complications may vary.
Risk factors:
• Preexisting DR
• In general, the risk of early worsening of DR is increased when intensive treatment is initiated in patient with long-standing poor glycemic control (Ref)
Gallbladder disease and biliary tract disease, including cholelithiasis, cholecystitis, cholestasis, and cholangitis have been reported with glucagon-like peptide-1 (GLP-1) receptor agonists. Cholelithiasis, biliary colic, and cholecystectomy have been reported with tirzepatide. Resolution of biliary stones following discontinuation has been documented with the GLP-receptor agonist liraglutide (Ref).
Mechanism: Dose- and time-related (Ref); not fully understood. Animal studies and in vitro data have demonstrated that GLP-1 enhances the proliferations and functional activity of cholangiocytes, which may result in gallbladder diseases (Ref). Some authors have postulated a change in bile acid production and secretion, suppressed secretion of cholecystokinin, decreased gallbladder emptying, prolonged gallbladder refilling, weight loss, or potentially a combination of these factors (Ref).
Onset: Varied; an increased risk was seen following >26 weeks of therapy (Ref).
Risk factors:
• Higher doses (Ref)
• Longer duration of treatment (eg, >26 weeks) (Ref)
• Substantial or rapid weight loss has been associated with an increased risk with GLP-1 receptor agonists used for weight loss (eg, liraglutide, semaglutide) (Ref)
GI effects, commonly abdominal pain, constipation, decreased appetite, diarrhea, dyspepsia, nausea, and vomiting, have been reported with tirzepatide (Ref). Symptoms may sometimes be severe. GI effects tend to occur during dose escalation and decrease over time; may result in treatment discontinuation.
Mechanism: Dose-related; however, the exact mechanism is not fully understood. May be a result of delayed gastric emptying or activation centers involved in appetite regulation, satiety, and nausea (Ref).
Onset: Intermediate; nausea, vomiting, and diarrhea are most common soon after initiation (eg, the first 4 weeks of treatment) and during dose escalation (Ref).
Risk factors:
• Dose; generally greater with higher doses
• In general, rapid titration of GLP-1 receptor agonists is associated with higher risk of GI symptoms
Serious, immediate hypersensitivity reactions, including anaphylaxis and angioedema, have been reported with glucagon-like peptide-1 (GLP-1) receptor agonists. Delayed hypersensitivity reactions have also been documented (Ref).
Mechanism: Non–dose-related; immunologic.
Immediate hypersensitivity reactions: IgE-antibodies are formed against a drug allergen following initial exposure (Ref).
Delayed hypersensitivity reactions: T-cell mediated (Ref).
Onset:
Immediate hypersensitivity reactions: Rapid; generally occurs within 1 hour of administration but may occur up to 6 hours after exposure (Ref)
Delayed hypersensitivity reactions: Variable; may occur from 1 day to 6 weeks after initiation (Ref).
Risk factors:
• Cross-reactivity between GLP-1 receptor agonists is unknown (Ref). Until further studies are available, tirzepatide should be used with caution in patients with a history of anaphylaxis or angioedema to other GLP-1 receptor agonists. Skin tests have been used in patients with histories of immediate hypersensitivity reactions (Ref) and delayed hypersensitivity reactions (Ref).
Increased heart rate and sinus tachycardia (≥15 beats per minute from baseline) have been reported with tirzepatide.
Onset: Intermediate; increases in heart rate were observed within 4 weeks of initiating tirzepatide (Ref).
In the early stages of drug development, thyroid C-cell tumors were noted to have developed during animal studies with tirzepatide. It is unknown whether tirzepatide causes thyroid C-cell tumors in humans, as the human relevance of tirzepatide-induced rodent thyroid C-cell tumors has not been determined. Human cases of medullary thyroid carcinoma (MTC) have been reported with glucagon-like peptide-1 (GLP-1) receptor agonists dulaglutide and liraglutide (Ref).
Mechanism: Unknown. Animal studies have shown dose-dependent and treatment duration-dependent harmful effects in rodents but not primates, thereby indicating that proliferative C-cell effects of GLP-1 receptor agonists may be rodent-specific. Humans have far fewer C-cells than rodents, and expression of the GLP-1 receptor in human C-cells is very low (Ref).
Risk factors:
• Patients with a personal or family history of MTC or patients with multiple endocrine neoplasia syndrome type 2 (MEN 2) may be at an increased risk
Cases of acute pancreatitis (including hemorrhagic pancreatitis and necrotizing pancreatitis with some fatalities), chronic pancreatitis, and pancreatic adenocarcinoma have been reported with use of incretin-based therapies (eg, dipeptidyl peptidase 4 inhibitors, glucagon-like peptide-1 [GLP-1] receptor agonists) (Ref). In clinical trials, acute pancreatitis was observed with tirzepatide.
Mechanism: Causality has not been firmly established (Ref). GLP-1 receptor agonists directly stimulate GLP-1 receptors in pancreatic islet beta cells and exocrine duct cells which may cause an overgrowth of the cells that cover the smaller ducts, thereby resulting in hyperplasia, increased pancreatic weight, duct occlusion, back pressure, and subsequent acute or chronic pancreatic inflammation (Ref).
Onset: Not well characterized.
Risk factors:
• Patients with a prior history of pancreatitis may be at an increased risk for acute pancreatitis
• Patients with acute pancreatitis due to any cause are at an increased risk for progression to recurrent acute pancreatitis and then to chronic pancreatitis; patients with chronic pancreatitis are at an increased risk for pancreatic cancer (Ref)
• Risk factors for pancreatitis due to any cause include, but are not limited to, hypertriglyceridemia, cholelithiasis, alcohol use, and obesity (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in adults.
>10%: Gastrointestinal: Decreased appetite (5% to 11%) (table 1), diarrhea (12% to 17%) (table 2), increased serum amylase (33% to 38%), increase serum lipase (31% to 42%), nausea (12% to 18%) (table 3)
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
11% |
1% |
15 mg once weekly |
241 |
235 |
|
10% |
1% |
10 mg once weekly |
240 |
235 |
|
5% |
1% |
5 mg once weekly |
237 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
17% |
9% |
15 mg once weekly |
241 |
235 |
|
13% |
9% |
10 mg once weekly |
240 |
235 |
|
12% |
9% |
5 mg once weekly |
237 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
18% |
4% |
15 mg once weekly |
241 |
235 |
|
15% |
4% |
10 mg once weekly |
240 |
235 |
|
12% |
4% |
5 mg once weekly |
237 |
235 |
1% to 10%:
Cardiovascular: Sinus tachycardia (5% to 10%) (table 4)
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
Comments |
|---|---|---|---|---|---|
|
10% |
4% |
15 mg once weekly |
241 |
235 |
Increase from baseline in heart rate of ≥15 beats per minute |
|
6% |
4% |
10 mg once weekly |
240 |
235 |
Increase from baseline in heart rate of ≥15 beats per minute |
|
5% |
4% |
5 mg once weekly |
237 |
235 |
Increase from baseline in heart rate of ≥15 beats per minute |
Gastrointestinal: Abdominal distention (3%), abdominal pain (5% to 6%) (table 5), constipation (6% to 7%) (table 6), dyspepsia (5% to 8%) (table 7), eructation (3%), flatulence (1% to 3%), gastroesophageal reflux disease (2% to 3%), vomiting (5% to 9%) (table 8)
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
6% |
4% |
5 mg once weekly |
237 |
235 |
|
5% |
4% |
15 mg once weekly |
241 |
235 |
|
5% |
4% |
10 mg once weekly |
240 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
7% |
1% |
15 mg once weekly |
241 |
235 |
|
6% |
1% |
10 mg once weekly |
240 |
235 |
|
6% |
1% |
5 mg once weekly |
237 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
8% |
3% |
5 mg once weekly |
237 |
235 |
|
8% |
3% |
10 mg once weekly |
240 |
235 |
|
5% |
3% |
15 mg once weekly |
241 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Dose |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
9% |
2% |
15 mg once weekly |
241 |
235 |
|
5% |
2% |
10 mg once weekly |
240 |
235 |
|
5% |
2% |
5 mg once weekly |
237 |
235 |
Hypersensitivity: Hypersensitivity reaction (3%: including severe hypersensitivity reaction) (table 9)
|
Drug (Tirzepatide) |
Placebo |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|
|
3% |
2% |
718 |
235 |
Local: Injection-site reaction (3%)
<1%: Gastrointestinal: Gallbladder disease (table 10) (acute; including biliary colic, cholecystectomy, and cholelithiasis (table 11))
|
Drug (Tirzepatide) |
Placebo |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|
|
0.6% |
0% |
718 |
235 |
|
Drug (Tirzepatide) |
Placebo |
Number of Patients (Tirzepatide) |
Number of Patients (Placebo) |
|---|---|---|---|
|
0.6% |
0% |
718 |
235 |
Frequency not defined: Gastrointestinal: Acute pancreatitis
Postmarketing: Endocrine & metabolic: Diabetic retinopathy (Frias 2021)
Serious hypersensitivity to tirzepatide or any component of the formulation; a personal or family history of medullary thyroid carcinoma or in patients with multiple endocrine neoplasia syndrome type 2 (MEN 2).
Disease-related concerns:
• Bariatric surgery:
- Dehydration: Evaluate, correct, and maintain postsurgical fluid requirements and volume status prior to initiating therapy, and closely monitor the patient for the duration of therapy; acute and chronic kidney failure exacerbation may occur. A majority of cases occurred in patients with nausea, vomiting, diarrhea, and/or dehydration. Nausea is common and fluid intake may be more difficult after gastric bypass, sleeve gastrectomy, and gastric band (Mechanick 2020).
- Excessive glucagon-like peptide-1 exposure: Closely monitor for efficacy and assess for signs and symptoms of pancreatitis if therapy is initiated after surgery; gastric bypass and sleeve gastrectomy (but not gastric band) significantly increase endogenous postprandial GLP-1 concentrations (Korner 2009; Peterli 2012). Administration of exogenous GLP-1 receptor agonists may be redundant to surgery effects.
Concurrent drug therapy issues:
• Delayed gastric emptying: Tirzepatide slows gastric emptying, which may alter the absorption of other medications. Monitor narrow therapeutic index medications for increased or decreased response.
Other warnings/precautions:
• Appropriate use: Diabetes mellitus: Do not use in patients with type 1 diabetes mellitus or for the treatment of diabetic ketoacidosis; not a substitute for insulin.
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Alpha-Lipoic Acid: May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Androgens: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Beta-Blockers (Beta1 Selective): May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Beta-Blockers (Nonselective): May enhance the hypoglycemic effect of Antidiabetic Agents. Beta-Blockers (Nonselective) may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Bortezomib: May enhance the therapeutic effect of Antidiabetic Agents. Bortezomib may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Direct Acting Antiviral Agents (HCV): May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Etilefrine: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Guanethidine: May enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy
Hormonal Contraceptives: Tirzepatide may decrease the serum concentration of Hormonal Contraceptives. Management: Patients using oral hormonal contraceptives should switch to a non-oral contraceptive method, or add a barrier method of contraception, for 4 weeks after initiation of tirzepatide and for 4 weeks after each dose escalation of tirzepatide. Risk D: Consider therapy modification
Hyperglycemia-Associated Agents: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Hypoglycemia-Associated Agents: Antidiabetic Agents may enhance the hypoglycemic effect of Hypoglycemia-Associated Agents. Risk C: Monitor therapy
Insulins: Glucagon-Like Peptide-1 Agonists may enhance the hypoglycemic effect of Insulins. Management: Consider insulin dose reductions when used in combination with glucagon-like peptide-1 agonists. Risk D: Consider therapy modification
Liraglutide: May enhance the adverse/toxic effect of Glucagon-Like Peptide-1 Agonists. Risk X: Avoid combination
Maitake: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Meglitinides: Glucagon-Like Peptide-1 Agonists may enhance the hypoglycemic effect of Meglitinides. Management: Consider meglitinide dose reductions when used in combination with glucagon-like peptide-1 agonists, particularly when also used with basal insulin. Risk D: Consider therapy modification
Monoamine Oxidase Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Pegvisomant: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Prothionamide: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Quinolones: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Quinolones may diminish the therapeutic effect of Agents with Blood Glucose Lowering Effects. Specifically, if an agent is being used to treat diabetes, loss of blood sugar control may occur with quinolone use. Risk C: Monitor therapy
Ritodrine: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Salicylates: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Selective Serotonin Reuptake Inhibitors: May enhance the hypoglycemic effect of Agents with Blood Glucose Lowering Effects. Risk C: Monitor therapy
Semaglutide: May enhance the adverse/toxic effect of Glucagon-Like Peptide-1 Agonists. Risk X: Avoid combination
Sincalide: Drugs that Affect Gallbladder Function may diminish the therapeutic effect of Sincalide. Management: Consider discontinuing drugs that may affect gallbladder motility prior to the use of sincalide to stimulate gallbladder contraction. Risk D: Consider therapy modification
Sulfonylureas: Glucagon-Like Peptide-1 Agonists may enhance the hypoglycemic effect of Sulfonylureas. Management: Consider sulfonylurea dose reductions when used in combination with glucagon-like peptide-1 agonists. Risk D: Consider therapy modification
Thiazide and Thiazide-Like Diuretics: May diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Agents other than tirzepatide are currently recommended for patients with type 2 diabetes mellitus planning to become pregnant (ADA 2021).
Tirzepatide may decrease the efficacy of oral hormonal contraception due to changes in gastric emptying; contraceptives administered by a nonoral route are not affected. Because the changes in gastric emptying are largest following the first dose, patients using an oral contraceptive should add a barrier method for 4 weeks after starting tirzepatide treatment and for 4 weeks after each dose increase. Alternately, patients can be switched to nonoral contraceptive methods.
Consult drug interactions database for more detailed information specific to use of tirzepatide and specific contraceptives.
Based on data from animal reproduction studies, in utero exposure to tirzepatide may cause fetal harm.
Poorly controlled diabetes during pregnancy can be associated with an increased risk of adverse maternal and fetal outcomes, including diabetic ketoacidosis, preeclampsia, spontaneous abortion, preterm delivery, delivery complications, major malformations, stillbirth, and macrosomia (ACOG 2018). To prevent adverse outcomes, prior to conception and throughout pregnancy, maternal blood glucose and HbA1c should be kept as close to target goals as possible but without causing significant hypoglycemia (ADA 2021; Blumer 2013).
Agents other than tirzepatide are currently recommended to treat diabetes mellitus in pregnancy (ADA 2021).
It is not known if tirzepatide is present in breast milk.
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother.
Plasma glucose; GI adverse reactions (eg, nausea, vomiting, diarrhea); kidney function (at baseline and following dose increases in patients with kidney impairment reporting severe GI adverse reactions); signs/symptoms of pancreatitis (eg, persistent severe abdominal pain, which may radiate to the back and that may or may not be accompanied by vomiting); signs/symptoms of gallbladder disease; worsening of diabetic retinopathy (particularly in those with a prior history of the disease).
HbA1c: Monitor at least twice yearly in patients who have stable glycemic control and are meeting treatment goals; monitor quarterly in patients in whom treatment goals have not been met, or with therapy change. Note: In patients prone to glycemic variability (eg, patients with insulin deficiency), or in patients whose HbA1c is discordant with serum glucose levels or symptoms, consider evaluating HbA1c in combination with blood glucose levels and/or a glucose management indicator (ADA 2021; KDIGO 2020).
Recommendations for glycemic control in patients with diabetes:
Nonpregnant adults (ADA 2021):
HbA1c: <7% (a more aggressive [<6.5%] or less aggressive [<8%] HbA1c goal may be targeted based on patient-specific characteristics). Note: In patients using a continuous glucose monitoring system, a goal of time in range >70% with time below range <4% is recommended and is similar to a goal HbA1c <7%.
Preprandial capillary blood glucose: 80 to 130 mg/dL (more or less stringent goals may be appropriate based on patient-specific characteristics).
Peak postprandial capillary blood glucose (~1 to 2 hours after a meal): <180 mg/dL (more or less stringent goals may be appropriate based on patient-specific characteristics).
Older adults (≥65 years of age) (ADA 2021):
Note: Consider less strict targets in patients who are using insulin and/or insulin secretagogues (sulfonylureas, meglitinides) (ES [LeRoith 2019]).
HbA1c: <7% to 7.5% (healthy); <8% to 8.5% (complex/intermediate health). Note: Individualization may be appropriate based on patient and caregiver preferences and/or presence of cognitive impairment. In patients with very complex or poor health (ie, limited remaining life expectancy), consider making therapy decisions based on avoidance of hypoglycemia and symptomatic hyperglycemia rather than HbA1c level.
Preprandial capillary blood glucose: 80 to 130 mg/dL (healthy); 90 to 150 mg/dL (complex/intermediate health); 100 to 180 mg/dL (very complex/poor health).
Bedtime capillary blood glucose: 80 to 180 mg/dL (healthy); 100 to 180 mg/dL (complex/intermediate health); 110 to 200 mg/dL (very complex/poor health).
Classification of hypoglycemia (ADA 2021):
Level 1: 54 to 70 mg/dL; hypoglycemia alert value; initiate fast-acting carbohydrate (eg, glucose) treatment.
Level 2: <54 mg/dL; threshold for neuroglycopenic symptoms; requires immediate action.
Level 3: Hypoglycemia associated with a severe event characterized by altered mental and/or physical status requiring assistance.
Tirzepatide is a glucose-dependent insulinotropic polypeptide (GIP) receptor and glucagon-like peptide-1 (GLP-1) receptor agonist that increases glucose-dependent insulin secretion, decreases inappropriate glucagon secretion, and slows gastric emptying.
Distribution: Vdss: ~10.3 L.
Protein binding: 99% to plasma albumin.
Metabolism: By proteolytic cleavage of the peptide backbone, beta-oxidation of the C20 fatty diacid moiety, and amide hydrolysis.
Bioavailability: 80%.
Half-life elimination: ~5 days.
Time to peak: 8 to 72 hours.
Excretion: Urine and feces (as metabolites).
Clearance: 0.061 L/hour.
Solution Pen-injector (Mounjaro Subcutaneous)
2.5 mg/0.5 mL (per 0.5 mL): $292.30
5 mg/0.5 mL (per 0.5 mL): $292.30
7.5 mg/0.5 mL (per 0.5 mL): $292.30
10 mg/0.5 mL (per 0.5 mL): $292.30
12.5 mg/0.5 mL (per 0.5 mL): $292.30
15 mg/0.5 mL (per 0.5 mL): $292.30
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