N-α-Formyl-DL-phenylalanine (BAT-006021)

DL-Amino Acids
Catalog number
CAS number
Molecular Formula
Molecular Weight
1.235 g/cm3
Melting Point
167 ºC
Boiling Point
449.7 ºC
Store at -20 °C
InChI Key
Canonical SMILES
1.Chelation of Free Zn(2+) Impairs Chemotaxis, Phagocytosis, Oxidative Burst, Degranulation, and Cytokine Production by Neutrophil Granulocytes.
Hasan R1, Rink L1, Haase H2,3. Biol Trace Elem Res. 2016 May;171(1):79-88. doi: 10.1007/s12011-015-0515-0. Epub 2015 Sep 23.
Neutrophil granulocytes are the largest leukocyte population in the blood and major players in the innate immune response. Impaired neutrophil function has been reported in in vivo studies with zinc-deficient human subjects and experimental animals. Moreover, in vitro formation of neutrophil extracellular traps has been shown to depend on free intracellular Zn(2+). This study investigates the requirement of Zn(2+) for several other essential neutrophil functions, such as chemotaxis, phagocytosis, cytokine production, and degranulation. To exclude artifacts resulting from indirect effects of zinc deprivation, such as impaired hematopoietic development and influences of other immune cells, direct effects of zinc deprivation were tested in vitro using cells isolated from healthy human donors. Chelation of Zn(2+) by the membrane permeable chelator N,N,N',N'-tetrakis-(2-pyridylmethyl)-ethylenediamine (TPEN) reduced granulocyte migration toward N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLF) and IL-8, indicating a role of free intracellular Zn(2+) in chemotaxis.
2.Mechanisms of the Macrolide-Induced Inhibition of Superoxide Generation by Neutrophils.
Nozoe K1, Aida Y2, Fukuda T1, Sanui T1, Nishimura F1. Inflammation. 2016 Mar 17. [Epub ahead of print]
The effect of macrolides on the superoxide (O2 -) production by neutrophils was studied. Resting neutrophils become primed by lipopolysaccharide (LPS) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), and primed neutrophils generate O2 - in response to fMLP or adhesion, respectively. Both LPS-primed fMLP-stimulated O2 - generation by macrolide-treated neutrophils and adhesion-stimulated O2 - generation by macrolide-treated fMLP-primed neutrophils were inhibited. Macrolide inhibition of O2 - generation was dependent on serum or pH. Serum could be substituted by NaHCO3. The intensity of inhibition was azithromycin = roxithromycin > clarithromycin > erythromycin, in that order. Non-antimicrobial derivatives of erythromycin, that is, EM703 and EM900, inhibited O2 - generation at pH 7.4. NH4Cl abolished the activity of azithromycin (AZ) only when added to neutrophils with AZ but not after incubation with AZ, suggesting that NH4Cl prevented the influx of AZ.
3.Chamomile decoction extract inhibits human neutrophils ROS production and attenuates alcohol-induced haematological parameters changes and erythrocytes oxidative stress in rat.
Jabri MA1,2,3, Sani M4, Rtibi K2, Marzouki L2, El-Benna J3, Sakly M1, Sebai H1,2. Lipids Health Dis. 2016 Mar 31;15(1):65. doi: 10.1186/s12944-016-0233-4.
BACKGROUND: The aim of this study was to evaluate the protective effects of subacute pre-treatment with chamomile (Matricaria recutita L.) decoction extract (CDE) against stimulated neutrophils ROS production as well as ethanol (EtOH)-induced haematological changes and erythrocytes oxidative stress in rat.
4.Mitochondrial damage-associated molecular patterns as potential proinflammatory mediators in post-platelet transfusion adverse effects.
Yasui K1, Matsuyama N1, Kuroishi A1, Tani Y1, Furuta RA1, Hirayama F1. Transfusion. 2016 Feb 26. doi: 10.1111/trf.13535. [Epub ahead of print]
BACKGROUND: Platelet concentrates (PCs) are the most common blood components eliciting nonhemolytic transfusion reactions (NHTRs), such as allergic transfusion reactions and febrile reactions. However, the precise mechanisms of NHTRs in PC transfusion remain largely unknown. Previous studies reported that mitochondria-derived damage-associated molecular patterns (DAMPs) could be important mediators of innate cell inflammation. Platelets (PLTs) represent a major reservoir of mitochondria in the blood circulation. The aim of this study was to determine the possible involvement of mitochondrial DAMPs in NHTRs.
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