Ruxolitinib [941678-49-5]

Katalog-Nummer HY-50856-5mg

Size : 5mg

Marke : MedChemExpress

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Ruxolitinib (INCB18424) est un inhibiteur de JAK1/2 qui est puissant et sélectif avec des IC50s de 3,3 nM et 2,8 nM dans les tests sans cellules, et a une sélectivité de 130 fois pour JAK1/2 sur JAK3. Ruxolitinib induit l'autophagie et tue les cellules tumorales par une mitophagie toxique.

Ruxolitinib (INCB18424) ist ein potenter und selektiver JAK1/2-Inhibitor mit IC50s von 3,3 nM und 2,8 nM in zellfreien Assays und hat eine 130-fache Selektivität für JAK1/2 gegenüber JAK3. Ruxolitinib induziert autophagy und tötet Tumorzellen durch toxische mitophagy ab.

Ruxolitinib (INCB18424) is a potent and selective JAK1/2 inhibitor with IC50s of 3.3 nM and 2.8 nM in cell-free assays, and has 130-fold selectivity for JAK1/2 over JAK3. Ruxolitinib induces autophagy and kills tumor cells through toxic mitophagy.

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Ruxolitinib Chemische Struktur

CAS. Nr. : 941678-49-5

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Proliferation Assay
IF
WB
RT-PCR
    Huh7 cells are pretreated with DMSO, 5 μM Filgotinib, 5 μM Ruxolitinib or 5 μM IFNα-IFNAR-IN-1 hydrochloride for 1 h and infected with MERS-CoV at a MOI of 1. MERS-CoV N gene copy number is quantified by RT-qPCR.
    Levels of IL-6, TNF, and MCP1 production in macrophages isolated from wild-type mice (females/20 weeks) following in vitro treatment with Ruxolitinib are determined utilizing CBA and flow cytometry.
    The expression of phosphorylated (p-) and unphosphorylated STAT1 and STAT6 in macrophages is assessed by western blotting.
    Ruxolitinib (100 mg/kg/day; intraperitoneal injection; 8 weeks) reduces the expression of proinflammatory cytokine genes in the livers of ARE-Del+/− mice. RNA is isolated from the livers of Ruxolitinib-treated mice.
    Relative cell number of LNCaP/AR cells treated with annotated treatment: 10 µM Enzalutamide (Enz), 5 µM Filgotinib (Filg), 5 µM Ruxolitinib (Ruxo), 1 µM Fludarabine (Flu), 0.2 µM Niclosamide (Nic) and DMSO for 8 days.
    A549 cells are treated with 2.5 µM BVD and 10 µM Ruxolitinib (Rux) separately or in combination for 2 days. Immunoblotting is conducted to determine pSTAT3-Y705.
    The induction of MIS target genes Id2, Id3, Smad6, and Igfbp5 was recapitulated as measured by qPCR following a 48 h incubation of ex vivo cultured ovaries from PND2 rat with 1 μM candidate MISR2 agonists Gandotinib, SP600125m, CYC-116, Ruxolitinib.
    Representative DDX4 immunofluorescence following 48 h incubation of ovaries from PND2 mice cultured ex vivo with 1 μM candidate MISR2 agonists Gandotinib, SP600125, CYC-116, Ruxolitinib.
    The xenografts treated with both Trametinib and Ruxolitinib (20 mg/kg; i.p.; every 3 days) show the expression of pSTAT3 and pERK1/2 in xenograft tumors exposed to the indicated treatment. Densitometry analyses of pSTAT3 and pERK1/2 expression normalized to STAT3 and ERK1/2 expression, respectively.
    Growth curves for DND-41, RPMI-8402 and LOUCY T-ALL cell lines. Growth medium is supplemented with DMSO, MRK-560 100 nM, Ruxolitinib 1 µM or both compounds.
    The A3A mRNA level is monitored in MCF10A cells 16 h after treatment with 3p-hpRNA and JAK inhibitors (JAKi #1: 2 μM Pacritinib, JAKi #2: 2 μM Ruxolitinib).
    The MAGE‐C3 overexpressing KYSE30 cells are treated with Ruxolitinib (2 μM, for 20 h.) and probed for STAT1 expression pSTAT1Tyr701. The pSTAT1Tyr701 expression levels are almost unchanged when exposure to Ruxolitinib in presence with IFN‐γ.
    Cxcl10 and Ccl5 mRNA levels are analyzed in TNF-α (100 ng/mL)-stimulated BMDMs for 6 h, which are pretreated with notopterol (10 mM) in the presence or absence of ruxolitinib (10 μM) or SD1029 (10 μM) for 3 h.
    Immunoblot of pSTAT1, STAT1 and β-actin levels in H69AR cells±200 ng/mL IFNg 10 min pulse followed by 24 h chase in media with DMSO, Ruxolitinib (100 nM) or MRT67307 (1 µM).
    Analysis of PIM1 RNA and protein expression in HOXA9 positive patient derived xenograft (PDX) samples ex vivo after 1 μM Ruxolitinib over 6 hours.
    Jak2 is inhibited by lentiviral expression of Jak2 shRNA or control shRNA in CWR22Pc and CWR22Rv1 cells. Alternatively, cells are treated with Jak2 inhibitors AZD1480 (0.8 μM) and Ruxolitinib (0.4 μM) (72 h), followed by Western blot analysis of Jak2 and active Stat5a/b.
    A431 cells are then treated in full growth media with vehicle, CSA (50 ng/mL), Ruxolitinib (20 μM), or both Ruxolitinib and CSA for 36 hours.
    106 autonomous Ba/F3 cells stably transduced with ALL-associated JAK3 mutant V674A or double mutant L857P/Y100A are treated with increasing concentration of Ruxolitinib (0–2 μM). Two hours after treatment, the cells are lysed and subjected to Western blot analysis. Phosphorylation of STAT5, JAK3, and JAK1 is detected using specific anti-pY694 STAT5, anti-pY980/81 JAK3, and anti-pY1034/35 JAK1 antibodies. Membranes are reprobed with anti-STAT5, anti-JAK3, anti-JAK1, and anti-β-actin an
    Ruxolitinib decreases spleen weight. Mice are sacrificed on day 21 or 24 to evaluate spleen size.
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    Ruxolitinib (INCB18424) is a potent and selective JAK1/2 inhibitor with IC50s of 3.3 nM and 2.8 nM in cell-free assays, and has 130-fold selectivity for JAK1/2 over JAK3. Ruxolitinib induces autophagy and kills tumor cells through toxic mitophagy.

    JAK2

    2.8 nM (IC50)

    JAK1

    3.3 nM (IC50)

    Tyk2

    19 nM (IC50)

    JAK3

    428 nM (IC50)

    In Vitro

    Ruxolitinib potently and selectively inhibits JAK2V617F-mediated signaling and proliferation, markedly increases apoptosis in a dose dependent manner, and at 64 nM results in a doubling of cells with depolarized mitochondria in Ba/F3 cells.
    Ruxolitinib demonstrates remarkable potency against erythroid colony formation with IC50 of 67 nM, and inhibits proliferating of erythroid progenitors from normal donors and polycythemia vera patients with IC50 values of 407 nM and 223 nM, respectively.

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

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