1881277-32-2
Chemical Structure
Resolvin D1-d5
Synonym(s): RvD1-d5
- CAS No.: 1881277-32-2
- Formula:C22H27D5O5
- Molecular Weight:381.52
IUPAC Name: (4Z,7S,8R,9E,11E,13Z,15E,17S,19Z)-7,8,17-trihydroxydocosa-4,9,11,13,15,19-hexaenoic-21,21,22,22,22-d5 acid
InChIKey: OIWTWACQMDFHJG-CLQVKFETSA-N
SMILES: O[C@H](/C=C/C=C\C=C\C=C\[C@H]([C@H](C/C=C\CCC(O)=O)O)O)C/C=C\C([2H])(C([2H])([2H])[2H])[2H]
Biological Activity: Resolvin D1-d5 is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages[1][2].
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Resolvin D1-d5 | 99.2% | Resolvin D1-d5 is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages. | ||||||||||||||||||||
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Resolvin D1 | 99.6% | Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α–mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages. | ||||||||||||||||||||
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References
- [1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
- [2]. Schmid M, et al. Resolvin D1 Polarizes Primary Human Macrophages toward a Proresolution Phenotype through GPR32. J Immunol. 2016 Apr 15;196(8):3429-37. [Content Brief]
