Erepdekinra

Erepdekinra presents a peptide architecture featuring varied residue types that shape solubility, charge distribution, and folding pathways. Researchers examine its structural transitions to assess binding determinants. Its adaptable conformation aids studies of molecular recognition. Applications span ligand-design models, peptide optimization, and structural biochemistry.

Designed for biological research and industrial applications, not intended for individual clinical or medical purposes.
Erepdekinra(CAS 2641313-47-3)

CAT No: R2515

CAS No:2641313-47-3

Synonyms/Alias:Erepdekinra;Erepdekinra [INN];UNII-C28VQU7LB4;C28VQU7LB4;2641313-47-3;DA-63256;

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cGMP Peptide
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  • Drug master files (DMF) filing
M.F/Formula
C88H130N22O22
M.W/Mr.
1848.1
Sequence
One Letter Code:VHVTIPADLWDWINK
Three Letter Code:Ac-Val-His-Val-Thr-Ile-Pro-Ala-Asp-Leu-Trp-Asp-Trp-Ile-Asn-Lys-NH2

Erepdekinra, a recombinant human interleukin-1 receptor antagonist (IL-1Ra), represents a significant advancement in the field of cytokine research and immunology. As a biologically active protein, Erepdekinra is engineered to modulate inflammatory pathways by competitively inhibiting the binding of interleukin-1 (IL-1) to its receptor, thus preventing downstream signaling events that lead to inflammation. Its molecular design ensures high specificity for the IL-1 receptor, making it an invaluable tool for dissecting the complex roles of IL-1 in various physiological and pathological contexts. Researchers appreciate Erepdekinra for its stability, reproducibility, and compatibility with a range of in vitro and in vivo experimental models, facilitating detailed studies into cytokine signaling and immune regulation.

Immunological research: In the field of immunology, Erepdekinra is widely utilized to explore the intricate mechanisms of IL-1-mediated immune responses. By blocking IL-1 activity, scientists can delineate the contributions of this cytokine to innate and adaptive immunity, assess its involvement in immune cell activation, and investigate its role in the development of inflammatory responses. The use of this IL-1 receptor antagonist in cell-based assays and animal models allows for the precise modulation of inflammatory signaling, enabling the identification of downstream effectors and cross-talk with other cytokine pathways. Such studies are instrumental in expanding our understanding of immune system regulation and the pathogenesis of immune-mediated conditions.

Inflammation modeling: Erepdekinra serves as a critical reagent in the modeling of inflammatory diseases in laboratory settings. Researchers employ this antagonist to simulate or mitigate inflammatory processes in cultured cells or animal models, thereby elucidating the cellular and molecular events triggered by IL-1. Its application enables the assessment of gene expression changes, cytokine release profiles, and cellular phenotypes in response to IL-1 blockade. This approach is particularly valuable for distinguishing IL-1-dependent pathways from other pro-inflammatory mechanisms, aiding in the development of targeted anti-inflammatory strategies and the discovery of novel therapeutic targets.

Signal transduction studies: The ability of Erepdekinra to selectively inhibit IL-1 receptor signaling makes it an essential tool for dissecting intracellular signaling cascades. Scientists leverage this protein to investigate the activation of NF-κB, MAPK, and other signaling pathways downstream of IL-1, as well as to map the molecular interactions involved in cytokine receptor engagement. By comparing cellular responses in the presence and absence of IL-1Ra, researchers can clarify the specific contributions of IL-1 to signal transduction events, transcriptional regulation, and post-translational modifications. Such insights are crucial for advancing the field of cell signaling and for identifying intervention points in inflammatory signaling networks.

Pharmacological research: Erepdekinra is integral to the preclinical evaluation of anti-inflammatory agents and biologics targeting the IL-1 pathway. By serving as a reference antagonist in pharmacological assays, it enables the benchmarking of novel compounds and the assessment of their efficacy in blocking IL-1-mediated effects. Its use in dose-response studies, combination treatments, and mechanistic evaluations provides a robust framework for understanding the pharmacodynamics of IL-1 inhibition and for optimizing candidate molecules for further development. This application supports the rational design of next-generation immunomodulatory drugs.

Biomarker discovery: The implementation of Erepdekinra in experimental systems facilitates the identification and validation of biomarkers associated with IL-1-driven inflammation. By modulating IL-1 signaling in vitro and in vivo, researchers can monitor changes in gene expression, protein secretion, and metabolic profiles that reflect the activity of this cytokine pathway. These biomarker studies are essential for advancing personalized approaches to disease research and for establishing reliable indicators of inflammatory status in experimental models. The use of IL-1 receptor antagonists such as Erepdekinra thus underpins a wide range of scientific investigations, supporting both basic research and translational applications in immunology and inflammation biology.

InChI
InChI=1S/C88H130N22O22/c1-14-45(9)71(86(130)105-62(35-66(90)113)78(122)98-57(74(91)118)27-20-21-29-89)107-81(125)60(33-51-39-94-56-26-19-17-24-54(51)56)102-80(124)64(37-68(116)117)103-77(121)59(32-50-38-93-55-25-18-16-23-53(50)55)101-76(120)58(31-42(3)4)100-79(123)63(36-67(114)115)99-75(119)47(11)96-83(127)65-28-22-30-110(65)88(132)72(46(10)15-2)108-87(131)73(48(12)111)109-85(129)70(44(7)8)106-82(126)61(34-52-40-92-41-95-52)104-84(128)69(43(5)6)97-49(13)112/h16-19,23-26,38-48,57-65,69-73,93-94,111H,14-15,20-22,27-37,89H2,1-13H3,(H2,90,113)(H2,91,118)(H,92,95)(H,96,127)(H,97,112)(H,98,122)(H,99,119)(H,100,123)(H,101,120)(H,102,124)(H,103,121)(H,104,128)(H,105,130)(H,106,126)(H,107,125)(H,108,131)(H,109,129)(H,114,115)(H,116,117)/t45-,46-,47-,48+,57-,58-,59-,60-,61-,62-,63-,64-,65-,69-,70-,71-,72-,73-/m0/s1
InChI Key
YIXJTJKQQNLLRJ-FGAVTVSPSA-N

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