329902-61-6
Chemical Structure
gp91 ds-tat
- CAS No.: 329902-61-6
- Formula:C98H190N50O22S
- Molecular Weight:2452.94
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
Biological Activity: 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].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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gp91 ds-tat | 99.00% | 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. | ||||||||||||||||||||
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- [1]. Malaviya P, et al. Role of ferroptosis in mitochondrial damage in diabetic retinopathy. Free Radic Biol Med. 2024 Nov 20;225:821-832. [Content Brief]
- [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 Alzheimer’s disease. bioRxiv [Preprint]. 2023 Feb 15:2023.02.15.528710. [Content Brief]
- [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. [Content Brief]
Keywords
