Gp91 ds-tat

Gp91 ds-tat, a biological active peptide, is a NADPH oxidase 2 (Nox2) inhibitor. gp91 ds-tat blocks NADPH oxidase-dependent superoxide production. gp91 ds-tat ameliorates high glucose-induced increase in total ROS, LPOs and iron levels. gp91 ds-tat inhibits homocysteine (Hcy) -induced activation of NLRP3 inflammasomes and restores Hcy-inhibited lysosomal TRPML1 channel activity. gp91 ds-tat improves cerebrovascular and cognitive function in APP/PS1 mice. gp91 ds-tat can be used for the study of Alzheimer’s disease (AD), glomerular inflammation and cardiovascular disease[1][2][3][4].

Product Specifications

CAS Number

[329902-61-6]

UNSPSC

12352209

Target

Ferroptosis; Glutathione Peroxidase; NADPH Oxidase; Reactive Oxygen Species (ROS) ; TRP Channel

Type

Peptides

Related Pathways

Apoptosis; Immunology/Inflammation; Membrane Transporter/Ion Channel; Metabolic Enzyme/Protease; Neuronal Signaling; NF-κB

Applications

Metabolism-sugar/lipid metabolism

Field of Research

Inflammation/Immunology; Neurological Disease; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/gp91-ds-tat.html

Purity

98.24

Solubility

DMSO : 100 mg/mL (ultrasonic) |H2O : ≥ 50 mg/mL

Smiles

O=C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CS)C(N[C@@H](CO)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCC(N)=O)C(N[C@@H](CC(C)C)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CCCNC(N)=N)N

Molecular Formula

C98H190N50O22S

Molecular Weight

2452.94

References & Citations

[1]Malaviya P, et al. Role of ferroptosis in mitochondrial damage in diabetic retinopathy. Free Radic Biol Med. 2024 Nov 20;225:821-832. |[2]Ruiz-Uribe NE, et al. Vascular oxidative stress causes neutrophil arrest in brain capillaries, leading to decreased cerebral blood flow and contributing to memory impairment in a mouse model of Alzheimerâ€™s disease. bioRxiv [Preprint]. 2023 Feb 15:2023.02.15.528710.|[3]Li G, et al. Regulation of TRPML1 channel activity and inflammatory exosome release by endogenously produced reactive oxygen species in mouse podocytes. Redox Biol. 2021 Jul;43:102013.