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, also known as peptide inhibitor of c-Jun N-terminal kinase (JNK), is a synthetic peptide compound designed to selectively block the activity of JNK enzymes within cellular signaling pathways. As a member of the cell-permeable peptide family, XG 102 exhibits high specificity for its target, making it a valuable molecular tool for dissecting the roles of JNK in various biological processes. With its robust inhibitory properties, this compound has garnered significant interest in the research community, particularly for studies focused on stress response, apoptosis, and neurodegenerative mechanisms. Its ability to modulate intracellular signaling without broadly affecting other kinases positions XG 102 as a preferred reagent for elucidating the complex interactions and regulatory checkpoints associated with JNK-mediated pathways.
Signal Transduction Research: XG 102 is extensively utilized in the investigation of intracellular signaling networks, particularly those involving stress-activated protein kinases. By specifically inhibiting JNK activity, researchers can delineate the downstream effects of JNK signaling in response to various stimuli, such as oxidative stress, cytokines, or environmental insults. The compound enables precise mapping of phosphorylation cascades, facilitating the identification of JNK-dependent transcription factors and gene expression profiles. Such studies are critical for understanding how cells integrate external signals to execute adaptive or maladaptive responses, and XG 102 serves as a powerful molecular probe in these experimental settings.
Neurobiology and Neuroprotection: In neuroscience research, the peptide inhibitor is widely employed to explore the contributions of JNK signaling to neuronal survival, synaptic plasticity, and neurodegeneration. By blocking JNK activation, investigators can assess the impact on neuronal apoptosis, axonal transport, and the modulation of neuroinflammatory mediators. These insights are particularly relevant for unraveling the molecular underpinnings of neurodegenerative processes and identifying potential therapeutic targets for ameliorating neuronal damage. The use of XG 102 in in vitro and in vivo models has advanced the understanding of how stress-activated kinases influence neural cell fate and function.
Inflammation and Immune Regulation: XG 102 finds application in immunological studies aimed at dissecting the regulatory roles of JNK in inflammation and immune cell activation. By inhibiting JNK, researchers can evaluate changes in cytokine production, immune cell migration, and the expression of pro-inflammatory genes. This approach is instrumental in clarifying the signaling mechanisms that drive pathological inflammation versus normal immune responses. The peptide's selective action allows for the dissection of JNK-dependent pathways without confounding effects from other kinases, making it a valuable asset in immunology research.
Cell Death and Apoptosis Studies: The compound is frequently used to investigate the molecular mechanisms governing programmed cell death. By selectively blocking JNK-mediated signaling, XG 102 enables researchers to determine the extent to which JNK contributes to apoptosis under various experimental conditions. Such studies are vital for identifying the checkpoints and effector molecules involved in cell fate decisions, especially in the context of stress-induced apoptosis. The ability to modulate this pathway with high specificity aids in the development of strategies to protect cells from unwanted death or, conversely, to enhance the elimination of damaged cells.
Metabolic and Cardiovascular Research: XG 102 also plays a significant role in the study of metabolic and cardiovascular systems, where JNK signaling is implicated in the regulation of insulin sensitivity, lipid metabolism, and vascular function. By employing this peptide inhibitor, researchers can dissect how JNK activity influences metabolic homeostasis, endothelial responses, and the development of metabolic or vascular dysfunctions. These investigations contribute to a broader understanding of the interplay between stress signaling pathways and systemic physiological outcomes, highlighting the versatility of XG 102 as a research tool across diverse biological disciplines.
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4. Autoinhibition and phosphorylation-induced activation of phospholipase C-γ isozymes
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