Dulaglutide is a once-weekly glucagon-like peptide-1 (GLP-1) receptor agonist sold by Eli Lilly as Trulicity. GLP-1 is a gut hormone that raises insulin release after meals, lowers glucagon and slows stomach emptying. Unlike most drugs in its class, dulaglutide is not a small modified peptide but a large fusion protein: two GLP-1-like chains attached to part of a human antibody. FDA approved it on September 18, 2014, and the EU authorized it in November 2014.
Its most important fact is what it is approved for: blood sugar control in type 2 diabetes, and reducing heart attacks, strokes and cardiovascular deaths in adults with type 2 diabetes at cardiovascular risk. That second indication rests on REWIND, a 9,901-person trial in which most participants did not yet have established heart disease. Dulaglutide is not approved for weight management, and in head-to-head trials it lowered weight less than semaglutide.
This page summarizes what the FDA label, clinical trials and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | GLP-1 receptor agonist (GLP-1 analog fused to a modified human IgG4 Fc fragment) |
| Brand / approval | Trulicity (Eli Lilly); FDA BLA 125469, approved September 18, 2014; EU authorization November 21, 2014 |
| Route | Subcutaneous injection once weekly, any time of day, with or without food |
| Strengths | Single-dose pens of 0.75, 1.5, 3 and 4.5 mg (each in 0.5 mL) |
| Labeled dosing | Adults: start 0.75 mg/week, up to 4.5 mg/week; children 10 years and older: up to 1.5 mg/week |
| Half-life (label) | About 5 days; steady state reached in 2–4 weeks |
| Size | About 63 kilodaltons, made in Chinese hamster ovary cell culture |
| Boxed warning | Thyroid C-cell tumors in rats; contraindicated with a personal or family history of medullary thyroid carcinoma or MEN 2 |
| US status | Prescription biologic; not a controlled substance |
| WADA status | Not named on the 2026 Prohibited List |
What it is
Native GLP-1 lasts only minutes in the blood, because the enzyme dipeptidyl peptidase-4 (DPP-4) breaks it down quickly and the kidneys clear it (Glaesner et al., Diabetes Metab Res Rev 2010). Lilly’s solution, developed under the code LY2189265, was to fuse a GLP-1 analog to the Fc portion of an antibody to extend how long it stays active.
According to the Trulicity label, the molecule has these features:
| Feature | What it does |
|---|---|
| Two identical chains joined by disulfide bonds | Each chain carries one GLP-1 analog at its start, linked by a short peptide to an antibody Fc fragment |
| GLP-1 analog 90% homologous to human GLP-1 (7-37) | Changes in the region that DPP-4 attacks make it resistant to that enzyme |
| Modified IgG4 Fc fragment | Changes reduce binding to high-affinity Fc receptors and the formation of “half-antibodies”; further changes were made in a region with a potential T-cell epitope (a site the immune system might recognize) |
| Total size about 63 kDa | Made in mammalian (Chinese hamster ovary) cell culture rather than by peptide synthesis |
In the original laboratory and animal work, the fusion protein kept full GLP-1 receptor activity in cell assays. Its half-life was 1.5–2 days in rats and cynomolgus monkeys, and in monkeys it raised glucose-dependent insulin secretion for up to a week after one dose (Glaesner et al., 2010).
This design differs from the other GLP-1 drugs in the library. Exenatide is a lizard-venom peptide that resists DPP-4 naturally but needs twice-daily dosing or a slow-release depot. Liraglutide and semaglutide are modified GLP-1 peptides; their pages explain how they were made long-acting. Tirzepatide adds a second target, the GIP receptor.
The label describes the same mechanism as other GLP-1 drugs. Dulaglutide:
- raises insulin release from pancreatic beta cells only when glucose is elevated (both first- and second-phase insulin secretion increased);
- lowers glucagon secretion;
- slows stomach emptying, an effect that is largest after the first dose and fades with later doses.
Pharmacokinetics
From the Trulicity label:
| Parameter | Value |
|---|---|
| Time to peak (steady state) | 24–72 hours, median 48 hours |
| Absolute bioavailability | 65% (0.75 mg); 47% (1.5 mg); 3 and 4.5 mg estimated to be similar to 1.5 mg |
| Dose proportionality | Concentrations rose roughly in proportion to dose from 0.75 to 4.5 mg |
| Volume of distribution | 3.09 L central; 5.98 L peripheral |
| Clearance | 0.142 L/hour |
| Elimination half-life | About 5 days |
| Steady state | Reached within 2–4 weeks; accumulation ratio about 1.56 |
| Metabolism | Presumed broken down into amino acids by general protein catabolism |
Several factors had little effect on exposure:
- Kidneys. Exposure was 20%, 28%, 14% and 12% higher in mild, moderate and severe kidney impairment and end-stage kidney disease. The label recommends no dose adjustment, unlike exenatide, which is cleared by the kidneys.
- Liver. Exposure was 21–33% lower in hepatic impairment, which the label did not consider clinically relevant, but experience is limited.
- Injection site. Abdomen, upper arm and thigh gave similar exposure.
- Children. In 128 patients aged 10 and older, exposure (AUC) was about 37% lower than in adults, which was not judged clinically meaningful.
A thorough QT study found no QTc prolongation at 4 mg and 7 mg, doses above the 4.5 mg maximum.
Approved medical use
The label lists two indications (Trulicity label):
- As an add-on to diet and exercise to improve blood sugar control in adults and children 10 years and older with type 2 diabetes.
- To reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal heart attack or nonfatal stroke) in adults with type 2 diabetes who have established cardiovascular disease or multiple cardiovascular risk factors.
FDA approved the cardiovascular indication on February 21, 2020, based on REWIND (FDA supplement approval letter).
| Population | Labeled dosing |
|---|---|
| Adults | Start 0.75 mg once weekly; may increase to 1.5 mg after 4 weeks; further increases in 1.5 mg steps after at least 4 weeks on the current dose; maximum 4.5 mg once weekly |
| Children 10 years and older | Start 0.75 mg once weekly; may increase to a maximum of 1.5 mg after at least 4 weeks |
| Missed dose | Take it if at least 3 days (72 hours) remain before the next dose; otherwise skip it |
The label says the step-up schedule is meant to reduce gastrointestinal side effects. Dulaglutide is not approved for type 1 diabetes or for weight management, and it is not approved for children under 10.
What the research shows
Blood sugar in type 2 diabetes
HbA1c is a measure of average blood sugar over about 3 months. In the label’s 26-week monotherapy trial, 807 adults were randomized to dulaglutide 0.75 mg, dulaglutide 1.5 mg or metformin 1,500–2,000 mg/day (Trulicity label):
| Arm | HbA1c change (baseline 7.6%) | Weight change |
|---|---|---|
| Dulaglutide 0.75 mg | −0.7% | −1.4 kg |
| Dulaglutide 1.5 mg | −0.8% | −2.3 kg |
| Metformin | −0.6% | −2.2 kg |
Both doses met the trial’s non-inferiority margin against metformin. In a 972-patient trial adding drugs to metformin, HbA1c at 26 weeks changed by +0.1% on placebo, −1.0% on 0.75 mg, −1.2% on 1.5 mg and −0.6% on the DPP-4 inhibitor sitagliptin. Weight fell 1.4, 2.7, 3.0 and 1.4 kg, respectively.
Higher doses (AWARD-11)
AWARD-11 randomized 1,842 adults on metformin (mean baseline HbA1c 8.6%, BMI 34.2) to 1.5, 3 or 4.5 mg weekly, double-blind, after stepping up from 0.75 mg every 4 weeks (Frias et al., Diabetes Care 2021; Trulicity label). Results at 36 weeks:
| Outcome | 1.5 mg | 3 mg | 4.5 mg |
|---|---|---|---|
| HbA1c change | −1.5% | −1.6% | −1.8% |
| Difference from 1.5 mg (95% CI) | — | −0.1% (−0.2 to 0.0) | −0.2% (−0.4 to −0.1) |
| Reached HbA1c under 7.0% | 50% | 56% | 62% |
| Weight change (baseline ≈ 95–96 kg) | −3.0 kg | −3.8 kg | −4.6 kg |
| Nausea | 13.4% | 15.6% | 16.4% |
| Vomiting | 5.6% | 8.3% | 9.3% |
| Diarrhea | 7.0% | 11.4% | 10.7% |
The 4.5 mg dose was statistically superior to 1.5 mg for both HbA1c and weight. The gains from tripling the dose were real but modest: about 0.2–0.3 percentage points of HbA1c and 1.6 kg of weight.
Compared with other GLP-1 drugs
| Trial | Comparison | n, duration | HbA1c change | Weight change | Notes |
|---|---|---|---|---|---|
| AWARD-1 (Wysham et al., Diabetes Care 2014) | Dulaglutide 1.5 mg and 0.75 mg vs exenatide 10 mcg vs placebo, on metformin plus pioglitazone | 52 weeks (primary end point 26 weeks) | −1.51% and −1.30% vs −0.99% (exenatide) and −0.46% (placebo) | Not reported in abstract | Both dulaglutide doses superior to exenatide; less hypoglycemia with 1.5 mg than exenatide |
| AWARD-6 (Dungan et al., Lancet 2014) | Dulaglutide 1.5 mg weekly vs liraglutide 1.8 mg daily | 599, 26 weeks, open-label | −1.42% vs −1.36% (difference −0.06%, 95% CI −0.19 to 0.07) | Not reported in abstract | Non-inferior; nausea 20% vs 18% |
| SUSTAIN 7 (Pratley et al., Lancet Diabetes Endocrinol 2018) | Dulaglutide 1.5 mg vs semaglutide 1.0 mg (and 0.75 mg vs 0.5 mg) | 1,201, 40 weeks, open-label | −1.4% vs −1.8% (difference −0.41%, 95% CI −0.57 to −0.25) | −3.0 kg vs −6.5 kg | Semaglutide superior at both dose pairs; GI disorders 48% (dulaglutide 1.5 mg) vs 44% (semaglutide 1.0 mg) |
Note that AWARD-6 and SUSTAIN 7 used dulaglutide 1.5 mg. We did not find a head-to-head trial of 4.5 mg against semaglutide. On weight, even dulaglutide 4.5 mg (−4.6 kg in AWARD-11) sits well below what semaglutide 1.0 mg achieved in SUSTAIN 7, although the trials are not directly comparable.
Cardiovascular outcomes (REWIND)
REWIND was a double-blind trial at 371 sites in 24 countries. It randomized 9,901 adults aged 50 or older with type 2 diabetes to dulaglutide 1.5 mg weekly or placebo, added to usual care, and followed them for a median of 5.4 years (Gerstein et al., Lancet 2019; Trulicity label).
The authors note that earlier GLP-1 outcome trials enrolled people at high cardiovascular risk with high HbA1c. REWIND’s population was broader:
- Only 31.5% had established cardiovascular disease; 62.8% had risk factors without established disease.
- Median baseline HbA1c was 7.2%, so many participants had fairly well-controlled diabetes.
- Mean age was 66 years and 46% were women.
| Outcome | Dulaglutide (n = 4,949) | Placebo (n = 4,952) | Hazard ratio (95% CI) |
|---|---|---|---|
| Major cardiovascular events (primary outcome) | 594 (12.0%) | 663 (13.4%) | 0.88 (0.79–0.99), p = 0.026 |
| Cardiovascular death | 6.4% | 7.0% | 0.91 (0.78–1.06) |
| Nonfatal heart attack | 4.1% | 4.3% | 0.96 (0.79–1.16) |
| Nonfatal stroke | 2.7% | 3.5% | 0.76 (0.61–0.95) |
| Death from any cause | 10.8% | 12.0% | 0.90 (0.80–1.01) |
Dulaglutide lowered the primary outcome by 12% relative to placebo. The label notes that the results for individual components were descriptive and not adjusted for multiple testing, so the stroke finding should not be read as proven on its own. All-cause death did not differ significantly (p = 0.067). Gastrointestinal adverse events were reported by 47.4% on dulaglutide vs 34.1% on placebo.
Dulaglutide’s proven benefit later made it the comparator in SURPASS-CVOT. In 13,299 people with type 2 diabetes and atherosclerotic disease, major cardiovascular events occurred in 12.2% on tirzepatide and 13.1% on dulaglutide 1.5 mg (HR 0.92, 95.3% CI 0.83–1.01). Tirzepatide was non-inferior but not superior (Nicholls et al., NEJM 2025). The tirzepatide page covers that trial in more detail.
Kidney outcomes
Two sources address the kidneys:
- REWIND exploratory analysis. A composite kidney outcome (new macroalbuminuria, a sustained eGFR decline of 30% or more, or chronic renal replacement therapy, meaning long-term dialysis or a transplant) occurred in 17.1% on dulaglutide vs 19.6% on placebo (HR 0.85, 95% CI 0.77–0.93). The clearest effect was on new macroalbuminuria (HR 0.77, 95% CI 0.68–0.87); the eGFR decline (HR 0.89, 95% CI 0.78–1.01) and dialysis results were not significant (Gerstein et al., Lancet 2019). Albuminuria means protein leaking into the urine, an early sign of kidney damage.
- AWARD-7. In 577 adults with type 2 diabetes and moderate to severe chronic kidney disease (stages 3–4), dulaglutide plus mealtime insulin lowered HbA1c as much as insulin glargine plus mealtime insulin over 26 weeks. At 52 weeks, eGFR was higher with dulaglutide 1.5 mg (34.0 vs 31.3 mL/min/1.73 m², p = 0.005), and symptomatic hypoglycemia was about half as frequent (4.4 vs 9.6 events per patient-year) (Tuttle et al., Lancet Diabetes Endocrinol 2018).
Dulaglutide does not carry a kidney-protection indication. The REWIND result was exploratory and AWARD-7 was open-label.
Cognition
In another exploratory REWIND analysis of 8,828 participants with cognitive testing, the prespecified cognitive outcome did not differ significantly (HR 0.93, 95% CI 0.85–1.02). Only after a post-hoc adjustment did the authors find a 14% lower hazard of substantial cognitive impairment (HR 0.86, 95% CI 0.79–0.95) (Cukierman-Yaffe et al., Lancet Neurol 2020). This is a hypothesis, not an established benefit.
Youth with type 2 diabetes
AWARD-PEDS randomized 154 participants aged 10 to under 18 to placebo, 0.75 mg or 1.5 mg for 26 weeks (Arslanian et al., NEJM 2022):
- HbA1c: rose 0.6 percentage points on placebo and fell 0.6 (0.75 mg) and 0.9 (1.5 mg) points on dulaglutide (p under 0.001).
- Reached HbA1c under 7.0%: 51% on pooled dulaglutide vs 14% on placebo.
- BMI: no difference between groups.
Weight
Dulaglutide is not approved for weight management, and all trials on its label enrolled people with type 2 diabetes. In those trials, average weight loss was about 1–3 kg at the 0.75 and 1.5 mg doses and 4.6 kg at 4.5 mg over 36 weeks. Youth in AWARD-PEDS had no change in BMI. We found no controlled trials of dulaglutide in lean or resistance-trained people. For how GLP-1 drugs affect lean mass, see the semaglutide page.
Side effects and risks
Boxed warning: thyroid C-cell tumors
In a 2-year study in rats, dulaglutide caused dose- and duration-dependent increases in thyroid C-cell tumors (adenomas and carcinomas) at 3 or more times the human exposure at 4.5 mg/week. A 6-month study in transgenic mice and a 12-month study in monkeys found no C-cell tumors or proliferative changes (Trulicity label). Whether the rat finding applies to humans is unknown.
In human trials, one case of medullary thyroid carcinoma (MTC) occurred in a patient whose calcitonin was already about 8 times the upper limit of normal before treatment, and one case of C-cell hyperplasia was reported in REWIND. Dulaglutide is contraindicated in people with a personal or family history of MTC or with multiple endocrine neoplasia type 2 (MEN 2).
Gastrointestinal effects
These are the most common side effects. In the label’s pool of placebo-controlled trials (1,670 patients on dulaglutide, mean exposure 23.8 weeks):
| Adverse reaction | Placebo (n = 568) | 0.75 mg (n = 836) | 1.5 mg (n = 834) |
|---|---|---|---|
| Nausea | 5.3% | 12.4% | 21.1% |
| Vomiting | 2.3% | 6.0% | 12.7% |
| Diarrhea | 6.7% | 8.9% | 12.6% |
| Abdominal pain | 4.9% | 6.5% | 9.4% |
| Decreased appetite | 1.6% | 4.9% | 8.6% |
| Dyspepsia | 2.3% | 4.1% | 5.8% |
| Fatigue | 2.6% | 4.2% | 5.6% |
| Any GI reaction | 21% | 32% | 41% |
| Stopped because of GI reactions | 0.2% | 1.3% | 3.5% |
Severe GI reactions occurred in 1.4% on placebo, 2.2% on 0.75 mg and 4.3% on 1.5 mg, a warning added to the label in 2026. The label does not recommend dulaglutide in severe gastroparesis (very slow stomach emptying). Postmarketing reports include ileus, intestinal obstruction and severe constipation with fecal impaction.
Kidney injury from dehydration
Acute kidney injury, sometimes needing dialysis, has been reported with GLP-1 drugs including dulaglutide. Most cases followed nausea, vomiting or diarrhea that caused dehydration.
Pancreas and gallbladder
- Pancreatitis. Adjudicated pancreatitis occurred at 1.4 cases per 1,000 patient-years on dulaglutide vs 0.88 on non-incretin comparators in the registration trials. In AWARD-11 it occurred in 0.2%, 0.3% and 0.5% on 1.5, 3 and 4.5 mg. Fatal hemorrhagic or necrotizing pancreatitis has been reported postmarketing. Pancreatic enzymes (lipase and/or amylase) rose by 14–20% on average.
- Gallbladder. In REWIND, gallstones occurred at 0.62 vs 0.56 per 100 patient-years, and serious acute cholecystitis in 0.5% vs 0.3%.
Heart rate and conduction
Dulaglutide raised heart rate by a mean of 2–4 beats per minute. Sinus tachycardia was reported in 5.6% on 1.5 mg vs 3.0% on placebo. The PR interval (the electrical delay between the heart’s upper and lower chambers) lengthened by 2–3 milliseconds, and first-degree AV block was reported in 2.3% on 1.5 mg vs 0.9% on placebo.
Hypoglycemia
On its own or with metformin, dulaglutide caused little hypoglycemia (glucose under 54 mg/dL in 0.7% on 1.5 mg with metformin, with no severe episodes). The risk rises sharply with other drugs:
| Background therapy | Glucose under 54 mg/dL (0.75 / 1.5 mg) | Severe hypoglycemia (0.75 / 1.5 mg) |
|---|---|---|
| Sulfonylurea (78 weeks) | 20% / 21% | 0% / 0.7% |
| Mealtime insulin (52 weeks) | 77% / 69% | 2.7% / 3.4% |
The label advises considering a lower sulfonylurea or insulin dose when starting dulaglutide.
Eyes
In REWIND, diabetic retinopathy complications occurred in 1.9% on dulaglutide vs 1.5% on placebo. Among people with a history of retinopathy, the rates were 8.5% vs 6.2%. The label notes that rapid improvement in blood sugar can temporarily worsen retinopathy and advises monitoring those with a history of it.
Other label warnings
- Serious allergic reactions, including anaphylaxis and angioedema, have been reported. Systemic hypersensitivity reactions occurred in 0.5% of adults in trials.
- Pulmonary aspiration during general anesthesia or deep sedation, because food may remain in the stomach.
- Antibodies. 1.6% of adults developed anti-dulaglutide antibodies (0.9% neutralizing), with no identified clinical effect.
- Pregnancy. Animal studies showed fetal harm (in rats at 6 or more times and in rabbits at 5 times human exposure), alongside reduced maternal food intake. The label says to use it in pregnancy only if the benefit justifies the risk.
Interactions
- Oral drugs. Slower stomach emptying can reduce the rate of absorption of oral medicines. At 1.5 mg, dulaglutide did not change absorption of tested drugs to a clinically relevant degree, but experience at 3 and 4.5 mg is limited. The label advises monitoring drug levels of narrow-therapeutic-index drugs such as warfarin.
- Insulin and sulfonylureas. Higher risk of hypoglycemia (see above).
- Insulin injections. Dulaglutide and insulin must be given as separate injections and never mixed.
Who should not use it
- People with a personal or family history of medullary thyroid carcinoma, or with MEN 2.
- People who have had a serious allergic reaction to dulaglutide or its ingredients.
- Not recommended in severe gastroparesis.
- Use with caution in end-stage kidney disease and in liver impairment, where clinical experience is limited.
Legal status and use outside medicine
Dulaglutide is a prescription-only biologic and is not a controlled substance in the US. It is not named on the WADA 2026 Prohibited List, and GLP-1 receptor agonists as a class are not listed. In overdoses reported in trials, effects were mainly mild to moderate nausea and vomiting and non-severe hypoglycemia, according to the label.
Key takeaways
- A fusion protein, not a small peptide. Dulaglutide links a DPP-4-resistant GLP-1 analog to an antibody Fc fragment, giving a 63 kDa molecule with a half-life of about 5 days.
- Proven cardiovascular benefit in a broad population. REWIND lowered major cardiovascular events by 12% (HR 0.88, 95% CI 0.79–0.99) in a population where only about a third had established heart disease.
- Moderate effects on blood sugar and weight. At 1.5 mg it matched liraglutide on HbA1c but lost to semaglutide 1.0 mg on both HbA1c and weight (−3.0 vs −6.5 kg). Raising the dose to 4.5 mg added about 0.2–0.3% HbA1c and 1.6 kg.
- No dose change for kidney disease. Exposure changed little with kidney impairment, and it lowered blood sugar as well as insulin glargine in moderate to severe kidney disease.
- Class-typical risks. Nausea affected 21% on 1.5 mg, and the label warns about pancreatitis, gallbladder disease, dehydration-related kidney injury, retinopathy complications and rat thyroid tumors.
- Approved for type 2 diabetes only. It is not approved for weight management, and no trials in lean or athletic people exist.
Sources
- Eli Lilly and Company. Trulicity (dulaglutide) injection, prescribing information (DailyMed version published August 2026). DailyMed.
- Food and Drug Administration. Drugs@FDA: Trulicity, BLA 125469. FDA.
- Food and Drug Administration. Supplement approval letter, BLA 125469/S-033 (cardiovascular indication based on REWIND), February 21, 2020. FDA.
- European Medicines Agency. Trulicity (dulaglutide): EPAR. EMA.
- Glaesner W, Vick AM, Millican R, et al. Engineering and characterization of the long-acting glucagon-like peptide-1 analogue LY2189265, an Fc fusion protein. Diabetes Metab Res Rev. 2010;26(4):287–296. PubMed.
- Frias JP, Bonora E, Nevarez Ruiz L, et al. Efficacy and safety of dulaglutide 3.0 mg and 4.5 mg versus dulaglutide 1.5 mg in metformin-treated patients with type 2 diabetes in a randomized controlled trial (AWARD-11). Diabetes Care. 2021;44(3):765–773. PubMed.
- Wysham C, Blevins T, Arakaki R, et al. Efficacy and safety of dulaglutide added onto pioglitazone and metformin versus exenatide in type 2 diabetes in a randomized controlled trial (AWARD-1). Diabetes Care. 2014;37(8):2159–2167. PubMed.
- Dungan KM, Povedano ST, Forst T, et al. Once-weekly dulaglutide versus once-daily liraglutide in metformin-treated patients with type 2 diabetes (AWARD-6): a randomised, open-label, phase 3, non-inferiority trial. Lancet. 2014;384(9951):1349–1357. PubMed.
- Pratley RE, Aroda VR, Lingvay I, et al. Semaglutide versus dulaglutide once weekly in patients with type 2 diabetes (SUSTAIN 7): a randomised, open-label, phase 3b trial. Lancet Diabetes Endocrinol. 2018;6(4):275–286. PubMed.
- Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121–130. PubMed.
- Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and renal outcomes in type 2 diabetes: an exploratory analysis of the REWIND randomised, placebo-controlled trial. Lancet. 2019;394(10193):131–138. PubMed.
- Nicholls SJ, Pavo I, Bhatt DL, et al. Cardiovascular outcomes with tirzepatide versus dulaglutide in type 2 diabetes. N Engl J Med. 2025;393(24):2409–2420. PubMed.
- Tuttle KR, Lakshmanan MC, Rayner B, et al. Dulaglutide versus insulin glargine in patients with type 2 diabetes and moderate-to-severe chronic kidney disease (AWARD-7): a multicentre, open-label, randomised trial. Lancet Diabetes Endocrinol. 2018;6(8):605–617. PubMed.
- Cukierman-Yaffe T, Gerstein HC, Colhoun HM, et al. Effect of dulaglutide on cognitive impairment in type 2 diabetes: an exploratory analysis of the REWIND trial. Lancet Neurol. 2020;19(7):582–590. PubMed.
- Arslanian SA, Hannon T, Zeitler P, et al. Once-weekly dulaglutide for the treatment of youths with type 2 diabetes. N Engl J Med. 2022;387(5):433–443. PubMed.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA.