The FDA has been evaluating reports of suicidal thoughts or actions in patients treated with glucagon-like peptide-1 receptor agonists (GLP-1 RAs). A preliminary evaluation has not found evidence that the use of these medicines causes suicidal thoughts or actions, but the FDA is continuing to investigate this issue. Patients should not stop taking GLP-1 RAs without consulting their health care provider. Health care providers should monitor for and advise patients using GLP-1 RAs to report new or worsening depression, suicidal thoughts, or any unusual changes in mood or behavior.
Further information may be found at https://www.fda.gov/drugs/drug-safety-and-availability/update-fdas-ongoing-evaluation-reports-suicidal-thoughts-or-actions-patients-taking-certain-type.
In male and female rats, dulaglutide causes a dose-related and treatment-duration-dependent increase in the incidence of thyroid C-cell tumors (adenomas and carcinomas) after lifetime exposure. It is unknown whether dulaglutide causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans as human relevance of dulaglutide-induced rodent thyroid C-cell tumors has not been determined.
Dulaglutide is contraindicated in patients with a personal or family history of MTC and in patients with multiple endocrine neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with use of dulaglutide and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound monitoring is of uncertain value for early detection of MTC in patients treated with dulaglutide.
Diabetes mellitus (DM), type 2; adjunct to diet and exercise:
Note: Glucagon-like peptide-1 (GLP-1) receptor agonists may be considered an additional therapeutic option in pediatric patients with type 2 DM who are ≥3 months post-diagnosis with an HbA1c of ≥6.5% while on metformin therapy (maximized) in addition to a healthy lifestyle (eg, diet and exercise) with or without insulin (Ref).
Children ≥10 years and Adolescents <18 years: SUBQ: Initial: 0.75 mg once weekly; if additional glycemic control needed after 4 weeks, may increase to 1.5 mg once weekly (Ref).
Adolescents ≥18 years: SUBQ: Initial: 0.75 mg once weekly; if additional glycemic control needed after 4 weeks, may increase to 1.5 mg once weekly. If additional glycemic control is needed, may titrate in 1.5 mg increments after at least 4 weeks at current dose up to a maximum weekly dose: 4.5 mg/dose.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Children ≥10 years and Adolescents: SUBQ:
Mild to severe impairment: No dosage adjustment necessary. Use caution when initiating or escalating doses; new-onset or worsening of existing renal failure has been reported, most commonly in patients experiencing volume depletion from GI losses (eg, vomiting, diarrhea, dehydration).
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
(For additional information see "Dulaglutide: Drug information")
Dosage guidance:
Clinical considerations: May require a dose reduction of insulin and/or insulin secretagogues (sulfonylureas, meglitinides) to avoid hypoglycemia (Ref).
Diabetes mellitus, type 2, treatment:
Note: May be used as an adjunctive agent or alternative monotherapy for select patients, including those in whom initial therapy with lifestyle intervention and metformin failed, or who cannot take metformin. May be preferred in patients who have or are at risk for atherosclerotic cardiovascular disease, when weight loss is desired, and/or in patients with an HbA1c relatively far from goal (eg, HbA1c 9% to 10%) and type 1 diabetes is not likely (Ref). Due to lack of additive glycemic benefit, avoid concomitant use with a dipeptidyl peptidase-4 inhibitor (Ref).
SUBQ: Initial: 0.75 mg once weekly; may increase to 1.5 mg once weekly after 4 to 8 weeks if needed to achieve glycemic goals (Ref). If additional glycemic control is needed, may further increase to 3 mg once weekly after at least 4 weeks on the 1.5 mg weekly dose and then to a maximum of 4.5 mg once weekly after at least 4 weeks on the 3 mg weekly dose.
Missed doses: Missed dose should be administered as soon as possible within 3 days; resume usual schedule thereafter. If there are <3 days until next scheduled dose, omit 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.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function: Mild to severe impairment: No dosage adjustment necessary (Ref). Use caution when initiating or escalating doses; new onset or worsening of existing renal failure has been reported, most commonly in patients experiencing volume depletion from GI losses (eg, vomiting, diarrhea, dehydration).
Hemodialysis, intermittent (thrice weekly): Unlikely to be dialyzable (Ref): No supplemental dose or dosage adjustment necessary; use with caution due to limited clinical evidence (Ref).
Peritoneal dialysis: Unlikely to be dialyzable (Ref): No dosage adjustment necessary; use with caution due to limited clinical evidence (Ref).
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
Acute kidney injury (AKI), which sometimes requires dialysis, has been reported with dulaglutide and other glucagon-like peptide 1 receptor agonists. Interstitial nephritis has been reported (Ref). According to the manufacturer, AKI secondary to dulaglutide was seen mostly in patients who had experienced nausea, vomiting, diarrhea, or dehydration. In a post-hoc analysis of multiple clinical trials, dulaglutide was not associated with an increase in adverse effects reflecting potential acute kidney failure (Ref).
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 GI 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
An increased incidence of diabetic retinopathy (DR) was noted during the REWIND study, a clinical trial evaluating the impact of dulaglutide on cardiovascular outcomes in patients with type 2 diabetes (Ref); the proportion of patients with DR complications was larger among patients with a prior history of DR. In addition, rapid reductions in HbA1c are associated with an early worsening of DR (Ref); in an analysis of DR complications due to another 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). Clinicians should note that this effect has been observed with SUBQ dulaglutide, exenatide, and semaglutide but not other GLP-1 receptor agonists (Ref).
Mechanism: Unknown; in general, worsening of preexisting DR is a known consequence of rapid improvement of hyperglycemia, especially in patients with uncontrolled diabetes (Ref). Although unlikely, a direct toxic effect or potential angiogenic action of dulaglutide 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 diabetic retinopathy
• In general, the risk of early worsening of DR is increased when intensive treatment is initiated in patients with long-standing poor glycemic control (Ref)
Gallbladder disease and biliary tract disease, including cholelithiasis, acute cholecystitis, and cholestasis, have been reported with glucagon-like peptide-1 (GLP-1) receptor agonists, including dulaglutide (Ref); some have required hospitalization or cholecystectomy (Ref). Resolution of biliary stones following discontinuation has been documented with other GLP-1 receptor agonists (eg, liraglutide) (Ref); one patient with dulaglutide-associated cholecystitis successfully continued dulaglutide therapy post-cholecystectomy without recurrent complications (Ref).
Mechanism: Dose- and time-related (Ref); not fully understood. Animal studies and in vitro data have demonstrated that GLP-1 enhances the proliferation 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); one case report, acute cholecystitis developed after 16 months of treatment with dulaglutide (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 other GLP-1 receptor agonists used for weight loss (eg, liraglutide, semaglutide) (Ref)
GI effects, mainly diarrhea, nausea, and vomiting, are the most common adverse reactions associated with glucagon-like peptide 1 (GLP-1) receptor agonists, including dulaglutide (Ref). Symptoms may sometimes be severe. Abdominal pain, decreased appetite, and dyspepsia may also occur. GI effects tend to occur during dose escalation and decrease over time (Ref); may result in treatment discontinuation.
In general, long-acting GLP-1 receptor agonists (eg, dulaglutide, once-weekly exenatide, liraglutide, semaglutide) are associated with less nausea and vomiting but more diarrhea when compared to their short-acting counterparts (Ref). Dulaglutide may be associated with a lower risk of diarrhea when compared to liraglutide (Ref). In the SUSTAIN-7 trial comparing once-weekly semaglutide to once-weekly dulaglutide, rates of GI effects were similar for both doses of semaglutide (0.5 mg and 1 mg) and high-dose dulaglutide (1.5 mg) (Ref).
Mechanism: Dose-related; however, the exact mechanism is not fully understood. May be a result of delayed gastric emptying or activation of 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). In a post-hoc analysis of 2 clinical trials, GI effects were most common during the first 2 weeks of treatment and the incidence declined rapidly thereafter (Ref).
Risk factors:
• Dose; generally greater with higher doses
• In general, rapid titration of GLP-1 receptor agonists is associated with a 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 (Ref). Exendin-based GLP-1 receptor agonists (eg, exenatide, lixisenatide) are associated with a doubling of reporting odds of anaphylactic reaction compared with human-analogue GLP-1 receptor agonists (eg, liraglutide, dulaglutide, semaglutide) (Ref).
Delayed hypersensitivity reactions such as a morbilliform rash (Ref) and injection site reactions (Ref) have been documented.
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).
Note: The risk of immune-mediated adverse effects is low with dulaglutide, despite the formation of neutralizing antibodies (Ref).
Onset:
Immediate hypersensitivity reactions: Rapid; generally occur within 1 hour of administration but may occur up to 6 hours after exposure (Ref).
Delayed hypersensitivity reactions: Variable; typically maculopapular (morbilliform, exanthematous) eruptions occur 4 to 14 days after drug initiation (Ref), although has been reported up to 5 weeks after starting dulaglutide (Ref).
Risk factors:
• Cross-reactivity between GLP-1 receptor agonists is unknown (Ref). Until further studies are available, dulaglutide 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 to GLP-1 receptor agonists (Ref).
In the early stages of drug development, thyroid C-cell tumors were noted to have developed during animal studies with dulaglutide. It is unknown whether dulaglutide causes thyroid C-cell tumors in humans, as the human relevance of dulaglutide-induced rodent thyroid C-cell tumors has not been determined. According to the manufacturer, one human cases of medullary thyroid carcinoma (MTC) was reported with dulaglutide during clinical trials in a patient with pretreatment calcitonin levels ~8 times the upper limit of normal. In addition, a single case of C-cell hyperplasia with elevated calcitonin levels was noted during the REWIND trial (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 glucagon-like peptide 1 (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 [DPP-4] inhibitors, glucagon-like peptide 1 [GLP-1] receptor agonists) (Ref). Acute pancreatitis was observed with dulaglutide at rates similar to placebo during the AWARD trial program and the REWIND trial (Ref).
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 unless otherwise indicated.
>10%:
Endocrine & metabolic: Hypoglycemia (≤77%; highest incidence seen with adjunctive use of insulin or sulfonylureas; severe hypoglycemia: ≤3%; highest incidence seen with adjunctive use of prandial insulin)
Gastrointestinal: Diarrhea (9% to 13%) (table 1) , nausea (12% to 21%) (table 2) , vomiting (6% to 13%) (table 3)
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
13% |
7% |
1.5 mg once weekly |
834 |
568 |
9% |
7% |
0.75 mg once weekly |
836 |
568 |
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
21% |
5% |
1.5 mg once weekly |
834 |
568 |
12% |
5% |
0.75 mg once weekly |
836 |
568 |
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
13% |
2% |
1.5 mg once weekly |
834 |
568 |
6% |
2% |
0.75 mg once weekly |
836 |
568 |
1% to 10%:
Cardiovascular: First-degree atrioventricular block (2%), prolongation P-R interval on ECG (3%), sinus tachycardia (6%), sustained tachycardia (2%)
Endocrine & metabolic: Diabetic retinopathy (2%; more common in patients with history of diabetic retinopathy at baseline) (table 4)
Drug (Dulaglutide) |
Placebo |
Dose |
Indication |
Comments |
---|---|---|---|---|
1.9% |
1.5% |
1.5 mg once weekly |
Type 2 diabetes with established cardiovascular disease or multiple cardiovascular risk factors |
N/A |
9% |
6% |
1.5 mg once weekly |
Type 2 diabetes with established cardiovascular disease or multiple cardiovascular risk factors |
Patients with a history of diabetic retinopathy at baseline |
1% |
1% |
1.5 mg once weekly |
Type 2 diabetes with established cardiovascular disease or multiple cardiovascular risk factors |
Patients without a known history of diabetic retinopathy |
Gastrointestinal: Abdominal distension (2% to 3%), abdominal pain (7% to 9%) (table 5) , constipation (4%), decreased appetite (5% to 9%) (table 6) , dyspepsia (4% to 6%) (table 7) , eructation (2%), flatulence (3%), gastroesophageal reflux disease (2%)
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
9% |
5% |
1.5 mg once weekly |
834 |
568 |
7% |
5% |
0.75 mg once weekly |
836 |
568 |
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
9% |
2% |
1.5 mg once weekly |
834 |
568 |
5% |
2% |
0.75 mg once weekly |
836 |
568 |
Drug (Dulaglutide) |
Placebo |
Dose |
Number of Patients (Dulaglutide) |
Number of Patients (Placebo) |
---|---|---|---|---|
6% |
2% |
1.5 mg once weekly |
834 |
568 |
4% |
2% |
0.75 mg once weekly |
836 |
568 |
Immunologic: Antibody development (children, adolescents, and adults: 2% to 6%; neutralizing: ≤1%)
Local: Injection-site reaction (adults: <1%; children and adolescents: 4%)
Nervous system: Fatigue (4% to 6%)
<1%:
Gastrointestinal: Cholecystitis (Butler 2021) (table 8) , pancreatitis
Drug (Dulaglutide) |
Placebo |
Comments |
---|---|---|
0.5% |
0.3% |
Serious events of acute cholecystitis |
Hypersensitivity: Hypersensitivity reaction
Frequency not defined: Gastrointestinal: Increased serum amylase, increased serum lipase
Postmarketing:
Dermatologic: Morbilliform rash (Rzepka 2020)
Gastrointestinal: Acute pancreatitis (Gerstein 2019), biliary tract disease (He 2022), cholelithiasis (Gerstein 2019; Pratley 2018), cholestasis (He 2022), gallbladder disease (He 2022), intestinal obstruction
Hepatic: Hepatitis, increased liver enzymes
Hypersensitivity: Anaphylaxis (Milicevic 2016), angioedema (Milicevic 2016)
Renal: Acute kidney injury (Tuttle 2017), interstitial nephritis (Komala 2022)
Serious hypersensitivity to dulaglutide or any component of the formulation; personal or family history of medullary thyroid carcinoma (MTC); patients with multiple endocrine neoplasia syndrome type 2 (MEN2)
Canadian labeling: Additional contraindications (not in US labeling): Pregnancy; breast-feeding
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 agonists may be redundant to surgery effects.
• GI disease: Use is not recommended in patients with preexisting severe GI disease, including severe gastroparesis.
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Renal impairment: Use with caution in patients with renal impairment.
Other warnings/precautions:
• Appropriate use: Diabetes mellitus: Not recommended for first-line therapy in patients inadequately controlled on diet and exercise alone. Do not use in patients with type 1 diabetes mellitus or for the treatment of diabetic ketoacidosis; not a substitute for insulin.
• Surgical and endoscopic procedures: Use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) has been associated with elevated residual gastric contents, which may increase the risk for adverse events during anesthesia and deep sedation (including aspiration) (Kobori 2023; Marroquin-Harris 2023; Silveira 2023). In some studies, delayed gastric emptying induced by GLP-1 RAs returned to baseline after 8 to 12 weeks of continuous therapy; therefore, risk may be higher in patients who recently initiated therapy or who use GLP-1 RAs intermittently (Raven 2024; van Zuylen 2024). Although the American Society of Anesthesiologists has suggested holding GLP-1 RAs prior to planned procedures requiring general anesthesia, the risks and benefits of this approach have not been evaluated (AGA [Hashash 2023]; ASA [Joshi 2023]). For example, in patients using GLP-1 RAs for glycemic control, holding the medication may result in perioperative hyperglycemia and increase the risk of adverse postoperative outcomes (AGA [Hashash 2023]; van Zuylen 2024). Individualize the decision to hold the GLP-1 RA based on patient-specific factors such as the indication (eg, glycemic control vs weight management), duration and frequency of therapy, presence of adverse GI symptoms, and concomitant medications that may slow gastric emptying (eg, opioids, proton pump inhibitors); may consider additional preoperative interventions (eg, clear liquid diet, full stomach precautions, gastric ultrasound) on a case-by-case basis to reduce risk (ASA [Hashash 2023]; Marroquin-Harris 2023; Raven 2024; van Zuylen 2024). Refer also to institutional protocols.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Pen-injector, Subcutaneous [preservative free]:
Trulicity: 0.75 mg/0.5 mL (0.5 mL); 1.5 mg/0.5 mL (0.5 mL); 3 mg/0.5 mL (0.5 mL); 4.5 mg/0.5 mL (0.5 mL) [contains polysorbate 80]
No
Solution Pen-injector (Trulicity Subcutaneous)
0.75 mg/0.5 mL (per 0.5 mL): $293.23
1.5 mg/0.5 mL (per 0.5 mL): $293.23
3 mg/0.5 mL (per 0.5 mL): $293.23
4.5 mg/0.5 mL (per 0.5 mL): $293.23
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution Pen-injector, Subcutaneous:
Trulicity: 0.75 mg/0.5 mL (0.5 mL); 1.5 mg/0.5 mL (0.5 mL) [contains polysorbate 80]
SUBQ: Dulaglutide is available as a single-dose device that does not require priming prior to use. Inject SUBQ into the upper arm, thigh, or abdomen; when administering within the same body region, use a different injection site. Administer once weekly on the same day each week, without regard to meals or time of day. The day of weekly administration may be changed if the last dose was administered ≥3 days before. Do not inject IV or IM. If using concomitantly with insulin, administer as separate injections (do not mix); may inject in the same body region as insulin, but not adjacent to one another.
Missed doses: Missed dose should be administered as soon as possible within 3 days; resume usual schedule thereafter. If there are <3 days until next scheduled dose, omit the missed dose and resume administration at the next scheduled weekly dose.
SUBQ: Do not inject intravenously or intramuscularly. Inject subcutaneously into the upper arm, thigh, or abdomen; when administering within the same body region, use a different injection site each week. Administer once weekly on the same day each week, without regard to meals or time of day. The day of weekly administration may be changed, as long as the last dose was administered ≥3 days before. If using concomitantly with insulin, administer as separate injections (do not mix); may inject in the same body region as insulin, but not adjacent to one another. Dulaglutide is a single-dose device that does not require priming before injection (Ref).
Store at 36°F to 46°F (2°C to 8°C). Do not freeze. Protect from light. If needed, each single-dose pen or prefilled syringe can be kept at room temperature, not to exceed 86°F (30°C) for a total of 14 days.
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/125469s046s052lbl.pdf#page=27, must be dispensed with this medication.
Adjunct treatment to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus (DM) (FDA approved in ages ≥10 years and adults); risk reduction of major cardiovascular events (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke) in patients with type 2 DM who have established cardiovascular disease or multiple cardiovascular risk factors (FDA approved in adults).
Trulicity may be confused with Tanzeum [DSC], Toujeo, Tradjenta, Tresiba
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 drug interactions program by clicking on the “Launch drug interactions program” link above.
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 drug interactions program
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
Efgartigimod Alfa: May diminish the therapeutic effect of Fc Receptor-Binding 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
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. Monitor patients for hypoglycemia. 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
Rozanolixizumab: May diminish the therapeutic effect of Fc Receptor-Binding 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
Tirzepatide: May enhance the adverse/toxic effect of Glucagon-Like Peptide-1 Agonists. Risk X: Avoid combination
Individualized medical nutrition therapy (MNT) based on ADA recommendations is an integral part of therapy.
Glucagon-like peptide-1 (GLP-1) receptor agonists are not recommended for patients with type 2 diabetes mellitus planning to become pregnant. Patients who could become pregnant should use effective contraception during therapy. Transition to a preferred therapy should be initiated prior to conception and contraception should be continued until glycemic control is achieved (ADA 2023; Alexopoulos 2019; Egan 2020)
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 201 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 2023; Blumer 2013).
Agents other than dulaglutide are currently recommended to treat diabetes mellitus in pregnancy (ADA 2023).
Plasma glucose, electrolytes, HbA1c (every 3 months; if patient is stable and meeting treatment goals, may only need twice-yearly testing; unstable patients on intensive therapy [eg, pregnancy] may need more frequent testing), (ADA 2019) renal function (in patients reporting severe GI reactions); signs/symptoms of pancreatitis.
Plasma blood glucose and HbA1c goals for patients with diabetes: Note: Postprandial blood glucose should be measured when there is a discrepancy between preprandial blood glucose concentrations and HbA1c values and to help assess glycemia for patients who receive basal/bolus or pump regimens. It is usually drawn 1 to 2 hours after starting a meal and is considered to be the "peak."
Children and Adolescents:
Blood glucose:
Type 2 diabetes:
Fasting plasma glucose: 70 to 110 mg/dL (SI: 3.9 to 6.1 mmol/L) (ISPAD [Shah 2022]).
Postprandial glucose: 70 to 140 mg/dL (SI: 3.9 to 7.8 mmol/L) (ISPAD [Shah 2022]).
HbA1c: <7%; target should be individualized; a more stringent goal (<6.5%) may be reasonable if it can be achieved without significant hypoglycemia; lower targets may also be recommended when using insulin pumps and/or continuous glucose monitoring and during the "honeymoon" phase; less aggressive goals (<7.5% or <8%) may be appropriate in patients who cannot articulate symptoms of hypoglycemia, cannot check glucose frequently, have a history of severe hypoglycemia, have extensive comorbid conditions, or lack access to analog insulins, advanced insulin delivery technology, or continuous glucose monitoring (ADA 2022; ISPAD [de Bock 2022]).
Dulaglutide is an agonist of human glucagon-like peptide-1 (GLP-1) receptor and augments glucose dependent insulin secretion and slows gastric emptying.
Bioavailability: 47% to 65%.
Distribution: Central volume, mean: 3.09 L; peripheral volume, mean: 5.98 L.
Metabolism: Degradation to amino acids by protein catabolism pathways.
Half-life elimination: ~5 days.
Time to peak, plasma: 24 to 72 hours.
Altered kidney function: Dulaglutide systemic exposure increased by 20%, 28%, 14%, and 12% for mild, moderate, and severe renal impairment, and ESRD, respectively.
Hepatic function impairment: Dulaglutide systemic exposure decreased by 23%, 33%, and 21% for mild, moderate, and severe hepatic impairment, respectively.
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