Seletalisib

Research use only, not for human use.

Seletalisib (UCB-5857)?is a potent, ATP-competitive, and selective PI3Kδ inhibitor with IC50 of 12 nM.

Seletalisib (UCB-5857)?is a potent, ATP-competitive, and selective PI3Kδ inhibitor with IC50 of 12 nM; shows significant selectivity to PI3Kδ with respect to the other class I PI3K isoforms (204-303 fold); blocks AKT phosphorylation following activation of the B-cell receptor in a B-cell line; blocks human T-cell production of several cytokines from activated T-cells, and inhibits B-cell proliferation and cytokine release; dose-dependently inhibits anti-CD3-antibody-induced interleukin 2 release in mice.Psoriasis Phase 3 Clinical(In Vitro):Seletalisib is a potent, ATP-competitive and highly selective PI3Kδ inhibitor able to block AKT phosphorylation following activation of the BCR in a B-cell line. Seletalisib inhibits N-formyl peptides (fMLP)-stimulated but not phorbol myristate acetate (PMA)-stimulated superoxide release from human neutrophils consistent with a PI3Kδ-specific activity. No indications of cytotoxicity are observed in PBMCs or other cell types treated with seletalisib. seletalisib blocks human T-cell production of several cytokines from activated T-cells. Seletalisib inhibits T-cell differentiation to Th1, Th2, and Th17 subtypes. Additionally, seletalisib inhibits B-cell proliferation and cytokine release. In human whole blood assays, seletalisib inhibits CD69 expression upon B-cell activation and anti-IgE-mediated basophil degranulation.(In Vivo):Seletalisib significantly inhibits IL-2 release following TCR stimulation in the rat. The inhibition is observed at all tested doses of seletalisib with almost complete inhibition reached at dose levels ≥1 mg/kg. Seletalisib has potent in vivo effects with an estimated IC50 value of <10 nM.

Seletalisib is a potent, ATP-competitive and highly selective PI3Kδ inhibitor able to block AKT phosphorylation following activation of the BCR in a B-cell line. Seletalisib inhibits N-formyl peptides (fMLP)-stimulated but not phorbol myristate acetate (PMA)-stimulated superoxide release from human neutrophils consistent with a PI3Kδ-specific activity. No indications of cytotoxicity are observed in PBMCs or other cell types treated with seletalisib. seletalisib blocks human T-cell production of several cytokines from activated T-cells. Seletalisib inhibits T-cell differentiation to Th1, Th2, and Th17 subtypes. Additionally, seletalisib inhibits B-cell proliferation and cytokine release. In human whole blood assays, seletalisib inhibits CD69 expression upon B-cell activation and anti-IgE-mediated basophil degranulation.

Seletalisib significantly inhibits IL-2 release following TCR stimulation in the rat. The inhibition is observed at all tested doses of seletalisib with almost complete inhibition reached at dose levels ≥1 mg/kg. Seletalisib has potent in vivo effects with an estimated IC50 value of <10 nM.

UCB-5857

PI3K/Akt/mTOR signaling

PI3K

PI3K

Inflammation/Immunology

Psoriasis

1362850-20-1

482.8451

C23H14ClF3N6O

>98% (HPLC)

DMSO: ≥83.3 mg/mL

FC(F)(F)[C@@H](C1=CC2=CC=CC(Cl)=C2N=C1C3=CC=C[N+]([O-])=C3)NC4=C5C(C=CC=N5)=NC=N4

Pyrido[3,2-d]pyrimidin-4-amine, N-[(1R)-1-[8-chloro-2-(1-oxido-3-pyridinyl)-3-quinolinyl]-2,2,2-trifluoroethyl]-

(-20℃)

With Ice Pack

≥ 2 years