PSMα3 TFA 

PSMα3 TFA is an inhibitor of NF-κB p65 and p38 MAPK. PSMα3 TFA forms membrane pores and binds to residues of human insulin B chain to inhibit insulin aggregation. PSMα3 TFA forms α-type amyloid-like fibrils to exert cytotoxic effects, and acts as a functional amyloid virulence determinant of Staphylococcus aureus. PSMα3 TFA is applicable to research related to spondyloarthritis, rheumatoid arthritis, insulin-derived amyloidosis, and Staphylococcus aureus infection^[1][2][3].

PSMα3 TFA (10 μM; 6-24 h) alters surface molecule expression in TLR4-stimulated human moDCs, enhancing early HLA-DR expression and reducing CD40 and CD80 expression at 6 and 24 h, respectively, while showing a trend to reduce PD-L1 upregulation at 24 h^[1].
PSMα3 TFA (10 μM; 6-24 h) significantly impairs pro- and anti-inflammatory cytokine secretion by TLR4-stimulated human moDCs, reducing TNF, IL-12, and IL-10 production at 6 and 24 h, respectively^[1].
PSMα3 TFA (10 μM; 1 h) reduces NF-κB and p38 phosphorylation in a non-significant trend in TLR4-stimulated human moDCs after 1 h of treatment^[1].
PSMα3 TFA (10 μM; 24 h) significantly reduces OVA uptake by immature human moDCs after 24 h of treatment, and shows a non-significant trend to further reduce OVA uptake in TLR2- or TLR4-stimulated moDCs^[1].
PSMα3 TFA (2.5-10 μM; 10 min) induces concentration-dependent transient pore formation in human moDCs after 10 min of treatment, as measured by LDH release, without reducing cell viability^[1].
PSMα3 TFA (10 μM; 24 h moDC pretreatment) in combination with TLR2/TLR4 ligands reduces the frequency of T-bet⁺ Th1 cells and IFN-γ secretion in co-cultured human naïve CD4⁺ T cells, while increasing IL-13 secretion when used to pretreat moDCs^[1].
PSMα3 TFA (10 μM; 1-2 d) significantly increases IDO production by TLR4-stimulated human moDCs after 1 and 2 d of treatment^[1].
Synthetic PSMα3 TFA (0.0625-10 mg/mL; up to 7 days) maintains a stable α-helical conformation in aqueous solution and does not form amyloid fibrils after incubation for up to 7 days at 37 °C, with only minor oligomer formation observed under specific non-standard pre-treatment and incubation conditions^[2].
PSMα3 TFA forms a unique cross-α amyloid-like fibril structure, solved at 1.45 Å resolution, with amphipathic α-helices stacked perpendicular to the fibril axis into tight self-associating sheets^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

2749.15

C₁₃₀H₁₉₃F₃N₂₈O₃₂S

{f}-Met-Glu-Phe-Val-Ala-Lys-Leu-Phe-Lys-Phe-Phe-Lys-Asp-Leu-Leu-Gly-Lys-Phe-Leu-Gly-Asn-Asn

{f}-MEFVAKLFKFFKDLLGKFLGNN

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Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Richardson JR, et, al. Staphylococcus aureus PSM Peptides Modulate Human Monocyte-Derived Dendritic Cells to Prime Regulatory T Cells. Front Immunol. 2018 Nov 13;9:2603.  [Content Brief]

  [2]. Kalitnik A, et al. Cytotoxic Staphylococcus aureus PSMα3 inhibits the aggregation of human insulin in vitro. Phys Chem Chem Phys. 2024 May 29;26(21):15587-15599.  [Content Brief]

  [3]. Tayeb-Fligelman E, et, al. The cytotoxic Staphylococcus aureus PSMα3 reveals a cross-α amyloid-like fibril. Science. 2017 Feb 24;355(6327):831-833.  [Content Brief]