XG-102, a TAT-coupled dextrogyre peptide inhibiting the c-Jun N-terminal kinase, was shown efficient in the treatment of experimental uveitis. Research show that XG-102 peptide has potential for treating intraocular inflammation.
CAT No: 10-101-141
CAS No:1198367-70-2
Synonyms/Alias:AM 111;XG 102 peptide;D-JNKI-1
XG 102 is a synthetic peptide inhibitor recognized for its specificity in targeting c-Jun N-terminal kinase (JNK) activity within cellular systems. As a cell-permeable peptide derived from the JNK-interacting protein (JIP) scaffold, it effectively disrupts JNK-mediated signaling cascades by competitively inhibiting the interaction between JNK and its substrates. This mode of action has established XG 102 as a valuable molecular tool for dissecting the roles of JNK in diverse physiological and pathological contexts. Its unique sequence and cell-penetrating properties have made it a preferred choice among researchers investigating signal transduction, cellular stress responses, and apoptosis regulation. The compound's well-characterized mechanism and robust selectivity for JNK pathways underscore its utility in fundamental and applied biochemical research.
Signal transduction studies: XG 102 is widely employed in research focused on elucidating the intricate signaling networks mediated by the mitogen-activated protein kinase (MAPK) family, particularly the JNK pathway. By selectively inhibiting JNK activity, the peptide allows investigators to dissect the downstream effects of JNK signaling in processes such as gene expression regulation, cellular differentiation, and response to extracellular stimuli. Its application facilitates the identification of JNK-specific targets and the clarification of pathway cross-talk, enabling a more precise understanding of cellular signaling dynamics.
Apoptosis and cell death research: The peptide inhibitor is instrumental in studies probing the molecular mechanisms underlying programmed cell death. JNK activation is known to play a pivotal role in stress-induced apoptosis, and the use of XG 102 enables researchers to modulate this pathway with high specificity. Through controlled inhibition of JNK, experimental models can be used to delineate the contribution of this kinase to apoptotic processes, providing critical insights into cell fate determination and the regulation of survival pathways in various cell types.
Neurobiology and neuroprotection investigations: In the context of neuronal cell biology, XG 102 has been utilized to explore the involvement of JNK signaling in neurodegenerative processes and neuronal stress responses. By inhibiting JNK activity, the peptide offers a means to assess the role of this kinase in neuronal injury, synaptic plasticity, and neuroinflammation. Its use supports the development of mechanistic models for understanding neurobiological disorders and identifying potential molecular targets for further research.
Inflammatory signaling analysis: JNK is a central mediator of inflammatory responses, influencing the expression of pro-inflammatory cytokines and transcription factors such as AP-1. XG 102 serves as a valuable tool for dissecting the contribution of JNK to inflammatory signaling pathways in both immune and non-immune cells. Application of the peptide in experimental systems enables researchers to parse out JNK-dependent mechanisms driving inflammation, thereby advancing knowledge in immunology and inflammation biology.
Peptide functional studies and assay development: The unique structure and inhibitory properties of XG 102 make it an ideal candidate for peptide-based assay development and functional studies. Its well-characterized mode of action provides a reliable positive control for validating JNK inhibition in biochemical assays, cell-based screens, and high-content analysis platforms. Furthermore, the peptide's cell-permeable nature facilitates its integration into diverse experimental designs, supporting the advancement of peptide research methodologies and the refinement of signal transduction assays.
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