Ruxolitinib (INCB018424)

Catalog No.S1378

Ruxolitinib (INCB018424) Chemical Structure

Molecular Weight(MW): 306.37

Ruxolitinib (INCB018424) is the first potent, selective, JAK1/2 inhibitor to enter the clinic with IC50 of 3.3 nM/2.8 nM in cell-free assays, >130-fold selectivity for JAK1/2 versus JAK3.

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Cited by 43 Publications

9 Customer Reviews

  • a, Phospho- and total STAT1 in MDA-MB-453 cells treated with abemaciclib with or without ruxolitinib for 7 days.

    Nature, 2017, 548(7668):471-475. Ruxolitinib (INCB018424) purchased from Selleck.

    j,k, Gene expression ofMYOCD (j) and ACTA2 ( SMA, k) after applying inhibitors of key components involved in the DDR2 downstream signalling pathway to HSCs cultured within 3D collagen matrix subjected to stretching (ST) (n=3, one-way ANOVA, **P=0.0036, ****P<0.0001). l,m, Expression of SMA was significantly reduced after treatment with related inhibitors in early-stage FμNs. (n=4, one-way ANOVA, ***P=0.001, ****P<0.0001). JAK2-i: INCB018424

    Nature Materials, 2017, 16:1252-1261.. Ruxolitinib (INCB018424) purchased from Selleck.

  • Representative images of human neutrophils from healthy controls stimulated with PMA (10 nM) after 150 min of ex vivo pretreatment with DMSO, ruxolitinib (300 nM), or GSK484 (PAD4 inhibitor,10 μM). Scale bar, 50 μm.

    Science, 2018, 10(436), doi: 10.1126/scitranslmed.aan8292. Ruxolitinib (INCB018424) purchased from Selleck.

    Scratching behavior (I), ear thickness measurement (J), representative H&E histopathology (K), and histology score (L) of vehicle control and Rux-treated mice on day 7, n R 10 mice per group. Scale bars indicate 100 mm. Data are represented as mean ± SEM.

    Cell, 2017, 171(1):217-228. Ruxolitinib (INCB018424) purchased from Selleck.

  • STAT3 phosphorylation as determined by phospho flow, mixed lymphocyte reactions containing BALB/c spleen-derived CD4+ T cells co-cultured with or without C57BL/6 BM-derived DC preactivated with 20 ng/mL LPS.

    Blood 2014 123(24), 3832-42. Ruxolitinib (INCB018424) purchased from Selleck.

    BMDMs were isolated from wild-type mice and incubated in the different concentrations of Ruxolitinib for 1 h before stimulation with 500 U/ml IFN-β for 30 min. Levels of GAPDH as well as total and phospho-Tyr705 STAT3 were determined by immunoblotting.

    J Immunol 2012 189(6), 2784-92. Ruxolitinib (INCB018424) purchased from Selleck.

  • Miniscule 10 PFU amount of VA7-EGFP results in productive infection only in CT26LacZ cells whereas the self-limiting infection can be rescued with JAK/STAT inhibitor Ruxolitinib in CT26WT cells counteracting also the effects of exogenous IFNβ (100 U/ml) pre-treatment. Scale bar: 200 um.

    Gene Ther 2014 10.1038/gt.2014.83. Ruxolitinib (INCB018424) purchased from Selleck.

    INCB018424 administration reverses the protective effects of ALA on ONC retinas. A-C: Representative micrographs (200× magnification) of retinal whole mounts obtained from three groups stained with anti-RNA-binding protein with multiple splicing (Rbpms) antibody (green). Sampling location: 2 mm temporal to the optic disc. Sampling field size: 439 × 330 μm2 (20× objective lens). Scale bar: 50 μm. D: Quantitative analysis of Rbpms-positive cells under different experimental conditions (mean ± standard error of the mean [SEM], n = 6 per group). The average number of Rbpms-positive cells/mm2 was calculated. ONC = optic nerve crush animal; ALA-ONC = alpha lipoic acid (ALA) animal pretreated 1 day before ONC; ALA-ONC+I = ALA animal pretreated 1 day before ONC, followed by INCB018424. *** p<0.001, ** p<0.01 compared to the ONC group, ### p<0.001 compared to the ALA-ONC group at the same time point

    Mol Vis, 2016, 22:1122-1136. Ruxolitinib (INCB018424) purchased from Selleck.


    HS578T cells were treated with indicated amount of inhibitor for 18 hr. The cells were lysed by cell lysis buffer (20 mM Tris-Cl (pH 8.0); 0.5 M NaCl; 0.25% Triton X-100; 1 mM EDTA; 1 mM EGTA; 10 mM β-glycerophosphate; 10 mM NaF; 300 µM Na3VO4; 1 mM benzamidine) containing 1 mM DTT and 2 µM PMSF. Western blot analyses were performed using cleared cell lysates resolved on sodium dodecyl sulfate (SDS)-polyacrylamide gels, transferred onto polyvinylidene difluoride (PVDF) membranes (Millipore, Billerica, MA), and probed with specific antibodies using standard procedures. Chemiluminescence reagent was purchased from  Thermo Scientific (Rockford, IL). Horseradish peroxidase-conjugated secondary antibodies from Sigma (St. Louis, MO).

    Yong Weon Yi Georgetown University. Ruxolitinib (INCB018424) purchased from Selleck.

Purity & Quality Control

Choose Selective JAK Inhibitors

Biological Activity

Description Ruxolitinib (INCB018424) is the first potent, selective, JAK1/2 inhibitor to enter the clinic with IC50 of 3.3 nM/2.8 nM in cell-free assays, >130-fold selectivity for JAK1/2 versus JAK3.
JAK2 [1]
(Cell-free assay)
JAK1 [1]
(Cell-free assay)
2.8 nM 3.3 nM
In vitro

INCB018424 potently and selectively inhibits JAK2V617F-mediated signaling and proliferation in Ba/F3 cells and HEL cells. INCB018424 markedly increases apoptosis in a dose dependent manner in Ba/F3 cells. INCB018424 (64 nM) results in a doubling of cells with depolarized mitochondria in Ba/F3 cells. INCB018424 inhibits proliferating of erythroid progenitors from normal donors and polycythemia vera patients with IC50 of 407 nM and 223 nM, respectively. INCB018424 demonstrates remarkable potency against erythroid colony formation with IC50 of 67nM. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
TF1 NGPnW5pMcW6jc3WgRZN{[Xl? MXGyNEBucW5? NU\WWWVXTE2VTx?= NETxRm1KdmirYnn0bY9vKG:oIFrBT|IhcW5iaIXtZY4hXEZzIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhTVCRLXnu[JVk\WRiU2TBWFUheGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCxNu69VQ>? MWOyNlY6QDB6NB?=
TF1 M2PBWmtqdmG|ZTDBd5NigQ>? M1LYRlIxKG2rbh?= M3TtZmROW09? MknrTY5pcWKrdHnvckBw\iCMQVuxJIlvKGi3bXHuJHRHOSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGlNPi2rbnT1Z4VlKFOWQWSzJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMkVOwG0> NG\2b3czOjZ7OEC4OC=>
Human T cell NGrCOY9McW6jc3WgRZN{[Xl? MVPJcohq[mm2aX;uJI9nKEqDS{OvNUBqdiCqdX3hckBVKGOnbHzzJIV5eHKnc4PpcochS0R|IHHzd4V{e2WmIHHzJIlvcGmkaYTpc44hd2ZiSVyyMZN1cW23bHH0[YQhW1SDVEXhJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMkROwG0> M3XaSFI{PTRyNkS4
Human monocyte NI[wZmhMcW6jc3WgRZN{[Xl? MWnJcohq[mm2aX;uJI9nKEqDS{KgbY4hcHWvYX6gcY9vd2O7dHXzJIV5eHKnc4PpcochS0RzNDDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFfNMWNUTi2|dHnteYxifGWmIGPURXQ2[SCyaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIECuNFI3|ryP NFjNTYMzOzV2ME[0PC=>
Human monocyte MluzT4lv[XOnIFHzd4F6 NGfvdHpKdmirYnn0bY9vKG:oIFrBT|IwOSCrbjDoeY1idiCvb37vZ5l1\XNiZYjwdoV{e2mwZzDDSFE1KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUU[QZ3HtcYEue3SrbYXsZZRm\CCVVFHUNUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEOx{txO NYqxfpFvOjN3NEC2OFg>
HEL MXjDfZRwfG:6aXOgRZN{[Xl? MX61JO69VQ>? NESwWZA1QCCq M1vldGN6fG:2b4jpZ{BqdmSneE2xNk4zLQ>? M2XmVlI2QTNzM{S5
SET-2 MWjDfZRwfG:6aXOgRZN{[Xl? M3T4eVUh|ryP NYLH[Wo2PDhiaB?= NGLFcm9EgXSxdH;4bYMhcW6mZYi9NVgvPyV? NHT1Z3MzPTl|MUO0PS=>
HT93A NFzveJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4DjR|MzOCCwTR?= M1[zcFUh\A>? M3vWNmROW09? MX3Jcohq[mm2aX;uJI9nKEeFUz3GJIlv\HWlZXSg[5JidnWub3P5eIlkKGSrZn\ldoVvfGmjdHnvci=> NVqwd29NOjV6MEW5OlI>
CMK NFXLZZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlXjTY5pcWKrdHnvckBw\iCFTVugZ4FzenmrbnegeIhmKEqDS{PBOVczXiCvdYTheIlwdiClZXzsJJBzd2yrZnXyZZRqd25? MX[yOVM2OjF{NB?=
CMK MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIXkTo9KdmirYnn0bY9vKG:oIFPNT{Bk[XK{eXnu[{B1cGViSlHLN2E3O0RibYX0ZZRqd25iY3XscEBxem:uaX\ldoF1cW:wIIfpeIghUUN3MDDv[kAxNjF4MzFOwG0> MljrNlU{PTJzMkS=
CMK MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP M2P2eVI2OzV{MUK0
NCI-H460 MnzYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkfJSG1UVw>? NVTrZnI6UUN3ME2wMlE{KM7:TR?= M37n[FI2OjF|Nkew
NCI-H358 NGT5OXVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2DaU2ROW09? Mo\iTWM2OD1yLkGg{txO NVvpc5RHOjV{MUO2O|A>
A549 MkDES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYDEUXNQ MUnJR|UxRTBwMESg{txO M{DDVlI2OjF|Nkew
A549/DDP NFTF[nJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWfEUXNQ NIS5T4JKSzVyPUCuNlIh|ryP MW[yOVIyOzZ5MB?=
NCI-H1299 MnTDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\HVGROW09? M3uy[WlEPTB;MD6yPEDPxE1? MX[yOVIyOzZ5MB?=
NCI-H2347 NFHHNHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2DhUGROW09? M33NS2lEPTB;MD6xO{DPxE1? NHztb|QzPTJzM{[3NC=>
A549/DDP M{PNT2Z2dmO2aX;uJGF{e2G7 MWmzNEBvVQ>? NUnLeWpTPDhiaB?= NVHNWmhPTE2VTx?= MmrCSI94di2{ZXf1cIF1cW:wIH;mJHNVSVR|IIDoc5NxcG:{eXzheIlwdg>? NF6xRpgzPTJzM{[3NC=>
NCI-H1299 NX3DelZ6TnWwY4Tpc44hSXO|YYm= MY[zNEBvVQ>? MmTZOFghcA>? MYrEUXNQ NUWxUIlrTG:5bj3y[Yd2dGG2aX;uJI9nKFOWQWSzJJBpd3OyaH;yfYxifGmxbh?= MXyyOVIyOzZ5MB?=
NCI-H2347 MULGeY5kfGmxbjDBd5NigQ>? NY\jWIpQOzBibl2= Mk\rOFghcA>? NVf1XGhCTE2VTx?= NFKwOnVF\WO{ZXHz[UBqdiCEY3yyJIV5eHKnc4Ppc44> NETJdYQzPTJzM{[3NC=>
A549/DDP MnzKRZBweHSxc3nzJGF{e2G7 Mn:1N|Ahdk1? M1PFVFQ5KGh? M4nWZ2ROW09? Mn\DTY5lfWO2aX;uJI9nKGGyb4D0c5Nqew>? MYSyOVIyOzZ5MB?=
NCI-H2347 MlrLRZBweHSxc3nzJGF{e2G7 MW[zNEBvVQ>? NUjEXZV2PDhiaB?= MYPEUXNQ M4SzfWlv\HWldHnvckBw\iCjcH;weI9{cXN? M13IclI2OjF|Nkew
Huh7 MknpSpVv[3Srb36gRZN{[Xl? MmLiNUDPxE1? MYSxOkBp NHjvcXpFVVOR MVXJcZBicXKnczD0bIUh[2GyYXPpeJkhd2ZiSVjDRU1ie3OxY3nheIVlKGeyMUOwJI12fGGwdIOgeI8he2mpbnHsJJRwKFOWQWSz M{jPPVI1PTBzNki5
BaF3 MVTLbY5ie2ViQYPzZZk> NIDjS3E5OCCwTR?= M1y0dFYhcA>? MorYSG1UVw>? NWWyfZFxWmWmdXPld{B1cGVicHjvd5Bpd3K7bHH0bY9vKG:owrDTWGFVPSCrbjDKRWszXjZzN1[tcZV1[XSnZDDCRWY{NUWST2KgZ4VtdA>? M1HOSlI1OjN5N{mx
DLD-1 Mkm1T4lv[XOnIFHzd4F6 MViyOUDPxE1? M2DKNVQ5KGh? M3XrUmROW09? NUXMUIlKUW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> M1r0XFI1ODVyNUWw
RKO MlLnT4lv[XOnIFHzd4F6 M{O0blI2KM7:TR?= MknBOFghcA>? M3jsTGROW09? MnjuTY5pcWKrdHnvckBw\iCMQVuxJJBpd3OyaH;yfYxifGmxbh?= NI[zWHEzPDB3MEW1NC=>
DLD-1 NH3DRWVMcW6jc3WgRZN{[Xl? M4q4eFI2KM7:TR?= MmWyOFghcA>? M3vsV2ROW09? NHLh[opKdmirYnn0bY9vKG:oIFrBT|IheGixc4Doc5J6dGG2aX;u Mk\XNlQxPTB3NUC=
RKO NUL4emVuU2mwYYPlJGF{e2G7 Mk\kNlUh|ryP M3nRRVQ5KGh? NFHGdo9FVVOR NHLvdXdld2W|IH7veEBqdmirYnn0JGpCUzFicHjvd5Bpd3K7bHH0bY9v M37tNlI1ODVyNUWw
DLD-1 Ml3xRZBweHSxc3nzJGF{e2G7 MXSyOUDPxE1? MXS0PEBp NFv1d|VFVVOR MorPTY5lfWOnczDhdI9xfG:|aYOgZpkh[WO2aY\heIlv\yClYYPwZZNmKDN? M3z0SVI1ODVyNUWw
RKO M3vDVmFxd3C2b4Ppd{BCe3OjeR?= MmL1NlUh|ryP NGXTT4U1QCCq NXXBN4FyTE2VTx?= NYfKT|hYUW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= MmXDNlQxPTB3NUC=
HuH7 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXXsUW0xPTBizszN NUHtcpFOPDhiaB?= Ml\RSG1UVw>? MWq+PFImKHKnZIXjeIlwdg>? NUTpXmk{OjN7NEG4N|I>
SNU182 NUO5ZXFtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjLd|k2OCEQvF2= MWS0PEBp NXTXNpNLTE2VTx?= Mn7OQlY1LSC{ZXT1Z5Rqd25? MXmyN|k1OTh|Mh?=
SNU423 NXuzcFZmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3S3VFUxKM7:TR?= M4HOTVQ5KGh? NFz4SpRFVVOR NHW2dmU,QDFnIILl[JVkfGmxbh?= NIrhVoQzOzl2MUizNi=>
HuH7 NXLBNVJVTnWwY4Tpc44hSXO|YYm= NFLWPZU2OCEQvF2= NXjZbllbOjRiaB?= M2PldGROW09? NH3jXWJKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= MVmyN|k1OTh|Mh?=
SNU182 NYHDXWJmTnWwY4Tpc44hSXO|YYm= MVW1NEDPxE1? Mlu2NlQhcA>? NX7k[25pTE2VTx?= NF7zSnNKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= M17XOFI{QTRzOEOy
SNU423 NXzGUJRCTnWwY4Tpc44hSXO|YYm= MkexOVAh|ryP M4Lrd|I1KGh? M2f0b2ROW09? MVnJcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? NV3HdJpCOjN7NEG4N|I>

... Click to View More Cell Line Experimental Data

In vivo INCB018424 (180 mg/kg, orally, twice a day) results in survive rate of greater than 90% by day 22 in a JAK2V617F-driven mouse model. INCB018424 (180 mg/kg, orally, twice a day) markedly reduces splenomegaly and circulating levels of inflammatory cytokines, and preferentially eliminated neoplastic cells, resulting in significantly prolonged survival without myelosuppressive or immunosuppressive effects in a JAK2V617F-driven mouse model. [1] The primary end point is reached in 41.9% of patients in the Ruxolitinib group as compared with 0.7% in the placebo group in the double-blind trial of myelofibrosis. Ruxolitinib results in maintaining of reduction in spleen volume and improvement of 50% or more in the total symptom score. [2] A total of 28% of the patients in the Ruxolitinib (15 mg twice daily) group has at least a 35% reduction in spleen volume at week 48 in patients with myelofibrosis, as compared with 0% in the group receiving the best available therapy. The mean palpable spleen length has decreased by 56% with Ruxolitinib but has increased by 4% with the best available therapy at week 48. Patients in the ruxolitinib group has an improvement in overall quality-of-life measures and a reduction in symptoms associated with myelofibrosis. [3]


Kinase Assay:[1]
+ Expand

Binding assay:

Recombinant proteins are expressed using Sf21 cells and baculovirus vectors and purified with affinity chromatography. JAK kinase assays use a homogeneous time-resolved fluorescence assay with the peptide substrate (-EQEDEPEGDYFEWLE). Each enzyme reaction is carried out with Ruxolitinib or control, JAK enzyme, 500 nM peptide, adenosine triphosphate (ATP; 1mM), and 2% dimethyl sulfoxide (DMSO) for 1 hour. The 50% inhibitory concentration (IC50) is calculated as INCB018424 concentration required for inhibition of 50% of the fluorescent signal.
Cell Research:[1]
+ Expand
  • Cell lines: Ba/F3 and HEL cells
  • Concentrations: 3 μM
  • Incubation Time: 48 hours
  • Method: Cells are seeded at 2 × 103/well of white bottom 96-well plates, treated with INCB018424 from DMSO stocks (0.2% final DMSO concentration), and incubated for 48 hours at 37 ℃ with 5% CO2. Viability is measured by cellular ATP determination using the Cell-Titer Glo luciferase reagent or viable cell counting. Values are transformed to percent inhibition relative to vehicle control, and IC50 curves are fitted according to nonlinear regression analysis of the data using PRISM GraphPad.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: JAK2V617F-driven mouse model
  • Formulation: 5% dimethyl acetamide, 0.5% methocellulose
  • Dosages: 180 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 61 mg/mL (199.1 mM)
Ethanol 61 mg/mL (199.1 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 306.37


CAS No. 941678-49-5
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03571321 Not yet recruiting Acute Lymphoblastic Leukemia|ALL Childhood|ALL University of Chicago|Incyte Corporation September 5 2019 Phase 1
NCT03722407 Not yet recruiting Chronic Myelomonocytic Leukemia|Leukemia H. Lee Moffitt Cancer Center and Research Institute|Incyte Corporation February 1 2019 Phase 2
NCT03558607 Recruiting Secondary Acute Myelogenous Leukemia Evolving From Myeloproliferative Disorder Seoul National University Hospital February 1 2019 Phase 1|Phase 2
NCT03613428 Not yet recruiting Acute T Cell Leukemia Sichuan University December 1 2018 Phase 1|Phase 2
NCT03701698 Not yet recruiting Acute GVHD Shanghai General Hospital Shanghai Jiao Tong University School of Medicine November 1 2018 Phase 2
NCT03395340 Recruiting Graft Versus Host Disease|JNS Kinase|Topical Administration National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)|National Institutes of Health Clinical Center (CC) November 20 2018 Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

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Frequently Asked Questions

  • Question 1:

    What is the difference between S2902 and S1378 which seem to have same structure formula according to the product information?

  • Answer:

    These two chemicals are the two different chiral forms of Ruxolitinib. S2902 S-Ruxolitinib is the S form and S1378 Ruxolitinib is the D form. One of the carbon atoms in this molecule is asymmetric, making the two molecules mirror images of each other. The biological activities of these two molecules can be very different because of the confirmation differences.

  • Question 2:

    How about the half-life of the compound (Ruxolitinib)? How long is the duration of the inhibitory effect on JAK-STAT signaling?

  • Answer:

    The half-life of this compound in body is about 2~3 hours according to previous study. Generally, it is longer in vitro culture medium than in vivo. In paper, Ruxolitinib was also used for 24hours.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID