Tirzepatide (sodium salt)

• CAS: 2023788-19-2
• Catalog Number: ALC-FP-2023788192
• Category: Featured Products
• Molecular Weight: 4813.45
• Molecular Formula: C225H348N48O68
• Solubility: Soluble in water
• Appearance: White powder
• Storage: Cool dry place( away from the light)
• Amino Acid Analysis: Asp 1.6~2.4; Tyr 1.6~2.4; Lys 1.6~2.4; lle 2.0~3.2; Leu 1.6~2.4; Val 0.8~1.2; Thr 1.6~2.4; Phe 1.6~2.4; Ser 4.0~6.0; Ala 3.2~4.8; Gly 3.2~4.8; Glu 3.2~4.8; Pro 3.2~4.8; Aib N/A; AEEA N/A
• Peptide Content: ≥85.0%
• Related Substances: Any individual impurity ≤1.0%(HPLC)
• Sample Lot No.: ANQP240921-L007
• Sequence: Tyr-{Aib}-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Ile-{Aib}-Leu-Asp-Lys-Ile-Ala-Gln-{diacid-C20-gamma-Glu-(AEEA)2-Lys}-Ala-Phe-Val-Gln-Trp-Leu-Ile-Ala-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro-Ser-NH2
• Sodium Salt: <5.0%
• Water Content: ≤10.0% (Karl Fischer)

Case Study

Tirzepatide for the Investigation of Gut Microbiota-Mediated Bone Metabolism in Obese Mice

Chen N, et al. Journal of Orthopaedic Translation, 2025, 55, 280-292.

This study explored the impact of Tirzepatide (TZP) on bone remodeling in db/db mice and in vitro bone marrow mesenchymal stem cell (BMSC) differentiation. TZP effects on osteoblast and osteoclast differentiation were evaluated via BMSC induction assays. In vivo, db/db mice received TZP, followed by 16S rRNA gene sequencing of fecal samples to identify gut microbiota alterations linked to bone mass, highlighting Lachnospiraceae depletion. Subsequent microbiota transplantation and metabolomics analysis identified evodiamine as a key metabolite suppressing osteoclastogenesis. Experimental supplementation of Lachnospiraceae reversed TZP-induced bone loss, demonstrating TZP's role in modulating bone-fat homeostasis via gut microbiota-mediated metabolites.

Tirzepatide for the Experimental Treatment of Diabetic Nephropathy via PI3K/AKT Modulation

Tian Y, et al. International Immunopharmacology, 2025, 146, 113877.

In a murine model of diabetic nephropathy (DN), tirzepatide was evaluated for its renoprotective effects. Mice received tirzepatide at one-third the semaglutide-equivalent dose, with insulin-treated and untreated DN groups as controls. Key parameters, including blood glucose, body weight, urine albumin-to-creatinine ratio (UACR), and oxidative stress biomarkers, were measured. Renal tissue RNA-seq revealed significant enrichment of the PI3K/AKT pathway, which was further validated in high-glucose-exposed podocyte cell-5 cultures. Mechanistic assays demonstrated that the antioxidative effect of tirzepatide was reversed upon PI3K inhibition, confirming pathway-dependent action. These experimental results highlight tirzepatide's potential as a targeted therapeutic agent for DN.

Tirzepatide for the Experimental Modulation of Mitochondrial Homeostasis in Parkinson's Disease Models

Tian R, et al. International Immunopharmacology, 2025, 165, 115443.

In a preclinical study, Tirzepatide was evaluated for its neuroprotective effects in MPTP-induced subacute Parkinson's disease (PD) mice. Dopaminergic neuron GLP1R and GIPR expression was first assessed using the GSE238129 dataset. Mice were administered Tirzepatide, semaglutide, or levodopa, followed by behavioral testing and brain histopathology. Mitochondrial ultrastructure and ATP levels in the substantia nigra were examined via transmission electron microscopy and biochemical assays. Western blot and immunohistochemistry quantified Drp1 and mitophagy proteins (Pink1, Parkin, p62). Complementary cellular studies employed Drp1, mitophagy, lysosomal, and autophagy modulators to validate mitochondrial functional restoration, highlighting Tirzepatide's role in modulating fission and mitophagy pathways.

Tirzepatide for the Restoration of Brown Adipose Tissue Function in Obese-Diabetic Ovariectomized Mice

Bittencourt JOA, et al. Life Sciences, 2026, 386, 124155.

This study evaluated tirzepatide, a dual GIP/GLP-1 receptor agonist, in female mice combining obesity, type 2 diabetes, and estrogen deficiency. Mice were divided into control, ovariectomy, obese-diabetic, and obese-diabetic ovariectomy groups, then treated with tirzepatide (10 nmol/kg/day) for four weeks. Body weight, relative BAT mass, and metabolic markers were assessed. Histological analyses examined adipocyte morphology, while molecular assays quantified thermogenic genes, including UCP-1 and β3-adrenergic receptor, as well as markers of mitochondrial fusion, ER stress, and autophagy. Three-way ANOVA and transcriptomic principal component analysis demonstrated that tirzepatide normalized metabolic parameters and restored BAT thermogenic function, highlighting its multifaceted therapeutic potential in postmenopausal metabolic dysfunction.

Tirzepatide for Modulating Hypothalamic Inflammation and Neuropeptide Balance in Metabolic-Menopausal Dysfunction

Marinho TS, et al. Brain Research, 2026, 1872, 150113.

Tirzepatide's central effects were assessed in female mice subjected to ovariectomy and high-fat, high-sucrose diet-induced obesity and diabetes. Mice received four weeks of tirzepatide treatment, followed by evaluation of hypothalamic inflammation, ER stress, and microglial activation using gene and protein expression analyses. Appetite-regulating neuropeptides, including AgRP, NPY, POMC, and MC4R, were quantified, alongside SOCS3 and doublecortin expression. Multivariate analysis confirmed broad hypothalamic remodeling, with reduced inflammatory markers, anti-inflammatory microglial reprogramming, and restored neuropeptide homeostasis. This experimental application demonstrated tirzepatide's capacity to coordinate molecular, cellular, and neuropeptidergic pathways, supporting its potential to recover hypothalamic circuitry under metabolic-hormonal stress.

Tirzepatide for Reducing Alcohol Consumption and Relapse-Like Behaviours in Rodent Models

Edvardsson CE, et al. eBioMedicine, 2026, 124,106119.

Rodent models of alcohol use disorder were employed to examine tirzepatide's dual GLP-1R/GIPR agonist activity. Animals underwent behavioral paradigms including locomotor activity, conditioned place preference, intermittent two-bottle choice, drinking in the dark, and alcohol deprivation effect. Molecular analyses involved microdialysis, electrophysiology, and proteomics of the lateral septum. Tirzepatide attenuated alcohol-induced reward, reduced voluntary and binge drinking, prevented relapse-like behaviors, and induced synaptic depression with histone regulatory changes. Metabolic effects, including body weight, adipose tissue mass, hepatic triglycerides, and pro-inflammatory cytokines, were also monitored. The study demonstrates tirzepatide's experimental utility in targeting both neural reward circuits and systemic metabolic consequences in AUD.