110954-19-3
110954-19-3
Chemical Structure
Aspartyl-alanyl-diketopiperazine
Synonym(s): DA-DKP
- CAS No.: 110954-19-3
- Formula:C7H10N2O4
- Molecular Weight:186.17
IUPAC Name: 2-((2S,5S)-5-methyl-3,6-dioxopiperazin-2-yl)acetic acid
InChIKey: RVLCUCVJZVRNDC-IMJSIDKUSA-N
SMILES: O=C(O)C[C@@H](C(N[C@H]1C)=O)NC1=O
Biological Activity: Aspartyl-alanyl-diketopiperazine (DA-DKP) is an immunomodulatory molecule generated by cleavage and cyclization from the N-terminus of human albumin and can modulate the inflammatory immune response through a molecular pathway implicated in T- lymphocyte anergy[1][2].
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Aspartyl-alanyl-diketopiperazine | 98.87% | Aspartyl-alanyl-diketopiperazine (DA-DKP) is an immunomodulatory molecule generated by cleavage and cyclization from the N-terminus of human albumin and can modulate the inflammatory immune response through a molecular pathway implicated in T- lymphocyte anergy. | ||||||||||||||||||||
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Aspartyl-alanyl-diketopiperazine (Standard) | ≥98% | Aspartyl-alanyl-diketopiperazine (DA-DKP) (Standard) is the analytical standard of Aspartyl-alanyl-diketopiperazine (HY-107091). This product is intended for research and analytical applications. Aspartyl-alanyl-diketopiperazine is an immunomodulatory molecule and anti-inflammatory agent. Aspartyl-alanyl-diketopiperazine increases the level of active Rap1 in activated human T lymphocytes and reduces the phosphorylation levels of Ras, ATF-2, c-jun, MEK1, MEKK1, ERK1, JNK1,2,3, p38MAPK and MEF-2. Aspartyl-alanyl-diketopiperazine inhibits the production of pro-inflammatory cytokines, including the levels of IFN-γ and TNF-α. Aspartyl-alanyl-diketopiperazine can be used in studies of inflammatory immune responses. | ||||||||||||||||||||
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References
- [1]. Bar-Or D, et al. Dipeptidyl peptidase IV activity in commercial solutions of human serum albumin. Anal Biochem. 2013 Oct 1;441(1):13-7. [Content Brief]
- [2]. Shimonkevitz R, et al. A diketopiperazine fragment of human serum albumin modulates T-lymphocyte cytokine production through rap1. J Trauma. 2008 Jan;64(1):35-41. [Content Brief]
