Dulaglutide

Tirzepatide reduced the primary composite kidney outcome by 23% versus dulaglutide (HR 0.77, 95% CI 0.68–0.88; p=0.0002).; Reductions were consistent in low-to-moderate-risk CKD (HR 0.70, 95% CI 0.58–0.84) and high-risk CKD (HR 0.79, 95% CI 0.64–0.96).; The benefit was primarily driven by lower new-onset persistent macroalbuminuria in low-to-moderate-risk CKD and slower eGFR decline in high-risk CKD.; Annual eGFR decline was lower with tirzepatide than dulaglutide overall (difference 0.29 mL/min/1.73 m²) and in high-risk CKD (difference 0.93 mL/min/1.73 m²).

Tirzepatide was associated with lower modified MACE risk versus dulaglutide (IR 31.3 vs 39.4 per 1,000 person-years; HR 0.80, 95% CI 0.65-0.99).; The tirzepatide-dulaglutide difference appeared driven by lower all-cause mortality (HR 0.60, 95% CI 0.43-0.83).; Modified MACE rates were similar for tirzepatide versus semaglutide (IR 23.7 vs 23.2; HR 1.03, 95% CI 0.90-1.17).; In post hoc analyses, tirzepatide was associated with lower rates of pneumonia-related hospitalization compared with dulaglutide.

Primary endpoint occurred in 12.2% of tirzepatide group vs 13.1% of dulaglutide group (HR 0.92; 95.3% CI 0.83–1.01; P=0.003 for noninferiority).; Superiority of tirzepatide was not established (P=0.09).; Adverse events were similar between groups, though more gastrointestinal events occurred with tirzepatide.

Kidney failure, composite CKM events, and MACE risks were similar across liraglutide, semaglutide, and dulaglutide initiators.; Liraglutide had significantly lower all-cause death hazard vs semaglutide in intent-to-treat analysis (HR 0.83; 95% CI 0.69-0.99), which lost significance in per-protocol models.; Liraglutide was associated with lower all-cause mortality vs dulaglutide in both intent-to-treat (HR 0.69; 95% CI 0.58-0.83) and per-protocol (HR 0.50; 95% CI 0.31-0.82) analyses.; Dulaglutide vs semaglutide showed decreased risk of gallstones (HR 0.72; 95% CI 0.54-0.95) and acute cholecystitis (HR 0.62; 95% CI 0.39-0.99).

Semaglutide versus empagliflozin: composite of death, MI, or stroke HR 0.89 (95% CI, 0.78 to 1.02); rates 3.7% vs 4.5% at 2 years and 5.9% vs 6.9% at 3 years; Semaglutide versus empagliflozin: stroke HR 0.62 (95% CI, 0.43 to 0.89); death HR 0.97 (CI, 0.81 to 1.15); MI HR 0.85 (CI, 0.68 to 1.05); Dulaglutide versus empagliflozin: composite outcome HR 1.03 (95% CI, 0.90 to 1.16), with similar risks for death, MI, and stroke separately; Limitations include observational design, lack of cause-specific mortality data, and residual confounding

Semaglutide significantly reduced HbA1c compared with liraglutide (0.56; 95% CI: 0.19-0.94; p < 0.001), with no significant differences in FBS, BMI, or weight change.; Semaglutide showed superior efficacy versus dulaglutide in reducing HbA1c (3.72; 95% CI: 0.02-7.41; p = 0.05) and FBS (2.66; 95% CI: 0.26-5.07; p = 0.03), but no significant differences in weight and BMI change.; Tirzepatide exhibited a notable advantage over semaglutide in reducing HbA1c (-0.45; 95% CI: -0.88 to -0.02; p = 0.04), with no clear superiority for weight and FBS change.; Transitioning from liraglutide to semaglutide did not significantly impact HbA1c but was associated with weight loss (2.48; 95% CI: 0.45-4.51; p = 0.02) and reduced FBS (10.76; 95% CI: 0.55-20; p = 0.04).

Greater bodyweight loss corresponded to greater improvements in metabolic parameters across weight loss subgroups.; Significant but weak correlations were observed between bodyweight change and triglycerides (r=0.18-0.25), HDL cholesterol (r=-0.37 to -0.29), and systolic blood pressure (r=0.19-0.41).; Fasting serum glucose improvements had the lowest association with weight loss (36.6%-43.5%) in mediation analyses comparing tirzepatide with dulaglutide 0.75 mg.; Non-glycemic and glycemic parameter improvements appeared differentially associated with weight loss, suggesting both weight loss-associated and -unassociated effects of tirzepatide.

What is Dulaglutide?

**Mechanism of Action** Dulaglutide is a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist engineered by fusing two GLP-1 analog molecules to a modified human immunoglobulin G4 (IgG4) Fc fragment. This structure extends its half-life to approximately 5 days, enabling once-weekly subcutaneous administration.

How does Dulaglutide work?

Once-weekly GLP-1 receptor agonist fused to an IgG4 Fc fragment for extended half-life.

What is the research status of Dulaglutide?

Dulaglutide is currently classified as approved, with 1,318 research references on record. This is for research purposes only and is not medical advice.

What is the half-life of Dulaglutide?

The reported half-life of Dulaglutide is ~5 days.