For research use only. Not for human consumption. Not medical advice — consult a licensed clinician.

GLP-1 / Metabolic

Liraglutide

Also known as: Victoza

Liraglutide is an FDA-approved GLP-1 receptor agonist marketed as Victoza (type 2 diabetes, approved 2010) and Saxenda (chronic weight management, approved 2014). It was the first GLP-1 analog approved for obesity and carries an FDA boxed warning for the risk of thyroid C-cell tumors. Pediatric indications include type 2 diabetes in patients ≥10 years (Victoza) and obesity in patients ≥12 years with BMI ≥95th percentile (Saxenda).

Where to buy · live market data

Who's worth your money for Liraglutide

Every current seller, ranked by independent evidence — Merit Score, latest COA purity, and live $/mg (size-normalized). Prices refresh daily. Rankings are never paid.

Average price

$3.33/mg

Sellers

1

45-day trend

-71.4%

1 of 1 sellers have a current price· 1 stale hidden

  • No fresh prices — all 1 listing are older than 7 days.

Prices observed from public storefronts (last 24h), normalized to $/mg. "Evidence" is Merit's 0–100 Merit Score, derived only from observable verification evidence (methodology on /about); "Purity" is the latest independent COA. Some buy links are affiliate links — Merit may earn a commission at no extra cost to you, and where a vendor offers one, the code shown gets you a discount at their checkout. Affiliate status never affects price data, ranking, or the Merit Score (full policy on /disclosure). Research use only.

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Compound reference

About Liraglutide

CAS

204656-20-2

Molecular formula

C172H265N43O51

Sequence

HAEGTFTSDVSSYLEGQAAKEFIAWLVRGR

Typical dose range

0.6–1.8 mg/day subcutaneous (diabetes); 0.6–3.0 mg/day subcutaneous (obesity/weight management)

Half-life

~13 hours

Independent evidence

No COAs on file for Liraglutide

No independent third-party test has been located or submitted yet. Absence isn't a red flag — just no evidence catalogued for Liraglutide so far; we add COAs as we find them.

Research depth

20 citations indexed for Liraglutide

All research on Liraglutide →

in-vitro · 2026

Liraglutide Attenuates Hepatocyte Ferroptosis in an In Vitro Model of Metabolic Dysfunction-Associated Steatotic Liver Disease

This study examined the potential of liraglutide to attenuate ferroptosis in an in vitro model of metabolic dysfunction-associated steatotic liver disease (MASLD). HepG2 cells were allocated into three groups: control (Con), free fatty acid (FFA)-treated, and FFA with liraglutide treatment (FFA+LI).

case-report · 2026

Successful Reversal of Tamoxifen-Associated Weight Gain and Metabolic Dysfunction with Liraglutide in a Breast Cancer Survivor: A Case Report

Introduction: Adjuvant endocrine therapy for breast cancer - particularly tamoxifen - is commonly associated with weight gain, increased adiposity, and metabolic dysfunction. Lifestyle measures often fail to reverse these effects.

animal · 2026

Effects of liraglutide on gut bacterial community dynamics

Liraglutide, a GLP-1 receptor agonist, is used to induce weight loss. However, limited information exists on liraglutide's effects on the gut bacterial community and their restoration after washout.

Study · 2026

Psychiatric and eye disorders associated with use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs)

Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) semaglutide, liraglutide, and dulaglutide are indicated for diabetes. Semaglutide and liraglutide were also approved for therapy of obesity or weight control. Apprehension has been expressed about the possible link between GLP-1 RAs and suicidality.

in-vitro · 2026

An Orthogonal Framework for Higher-Order Structural and In Vitro Functional Comparability of Chemically Synthesized Liraglutide Relative to an rDNA-Origin Reference Product

Purpose Synthetic peptide test products referencing recombinant-origin products present unique regulatory challenges in demonstrating higher-order structural (HOS) comparability beyond primary sequence sameness.

animal · 2026

Liraglutide reprograms vascular smooth muscle cell metabolism to suppress extracellular matrix remodeling in diabetic atherosclerosis

Background Metabolic reprogramming contributes to vascular dysfunction in diabetic atherosclerosis, but the mechanisms linking hyperglycemia-induced metabolic alterations to extracellular matrix remodeling in vascular smooth muscle cells remain incompletely understood.