ATI 2341

ATI 2341

CAT.NO: P200220

CAS No: 1337878-62-2

Purity: 95%

Molar Mass: 2256.8

Chemical Formula: C104H178N26O25S2

Categories: , , ,

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Description

Product Name: ATI 2341

CAS No: 1337878-62-2

Purity: 95%

Molar Mass: 2256.8

Chemical Formula: C104H178N26O25S2

Storage: Store at -20 degrees Celsius

Sequence: 1-Oxohexadecyl-MGYQKKLRSMTDKYRL

Target: CXCR4

Application:

ATI 2341 is a selective peptide agonist for the chemokine receptor CXCR4, known for its role in mediating cell migration and immune responses. By specifically binding to CXCR4, ATI 2341 induces receptor internalization and signaling, influencing processes such as hematopoiesis, immune cell trafficking, and tumor metastasis. This peptide is widely used in research to study CXCR4-related pathways and their implications in cancer, HIV infection, and inflammatory diseases. ATI 2341's ability to modulate CXCR4 activity offers potential therapeutic applications in targeting metastatic cancer cells and enhancing immune system function, making it a critical tool in biomedical research and drug development.

Current Research:

ATI-2341 is a synthetic peptide that functions as a potent and selective allosteric agonist of the C-X-C chemokine receptor type 4 (CXCR4). By preferentially activating Gαi proteins over Gα13, ATI-2341 modulates intracellular signaling pathways, leading to the inhibition of cyclic adenosine monophosphate (cAMP) production and the induction of calcium mobilization. This biased signaling profile has positioned ATI-2341 as a valuable tool in immunological research and a potential therapeutic agent.

Mechanism of Action

ATI-2341 binds to CXCR4, inducing conformational changes that favor the activation of inhibitory heterotrimeric G proteins (Gαi). This interaction results in the suppression of adenylate cyclase activity, thereby reducing cAMP levels, and promotes the release of intracellular calcium stores. The allosteric nature of ATI-2341's binding allows for modulation of receptor activity distinct from that of endogenous ligands, offering insights into receptor dynamics and signaling specificity.

Applications in Research

Chemotaxis Studies: ATI-2341 has been shown to induce chemotaxis in CXCR4-expressing cells, making it a useful agent for investigating cell migration mechanisms and the role of CXCR4 in immune cell trafficking.

Hematopoietic Stem Cell Mobilization: In vivo studies have demonstrated that ATI-2341 effectively mobilizes polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs) from the bone marrow into peripheral circulation. This property suggests potential therapeutic applications in enhancing stem cell yields for transplantation procedures.

Biased Signaling Research: The ability of ATI-2341 to selectively activate Gαi over Gα13 and β-arrestin pathways provides a model for studying biased agonism at CXCR4. This facilitates a deeper understanding of how specific signaling cascades can be differentially regulated, which is crucial for the development of targeted therapeutics.

Therapeutic Potential

The selective activation of CXCR4 by ATI-2341 holds promise for therapeutic strategies aimed at modulating immune responses, particularly in conditions where CXCR4 plays a pivotal role, such as HIV infection, cancer metastasis, and inflammatory diseases. By influencing cell migration and survival pathways, ATI-2341 could contribute to novel treatments that require precise control over immune cell dynamics.

Conclusion

ATI-2341 serves as a potent and selective allosteric agonist of CXCR4, offering significant utility in both basic research and potential clinical applications. Its unique mechanism of action and ability to modulate specific signaling pathways make it an invaluable tool for advancing our understanding of chemokine receptor biology and for the development of targeted therapeutic interventions.

Reference:

Lv, Y., Ye, L., & Zheng, X. (2022). ATI-2341 Trifluoroacetic Acid (TFA) Promotes Menstrual Blood-Derived Mesenchymal Stem Cell Recruitment and Enhances Uterine Repair Through Gi Pathway in Asherman’s Syndrome. Journal of Biomaterials and Tissue Engineering, 12(3), 506-513.

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