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 48 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 MYLLbY5ie2ViQYPzZZk> MmXzNlAhdWmw MlPXSG1UVw>? MYDJcohq[mm2aX;uJI9nKEqDS{KgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gSXBQNWmwZIXj[YQhW1SDVEWgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjBzMt88US=> Ml\mNlI3QThyOES=
TF1 MmO2T4lv[XOnIFHzd4F6 NX;IclZbOjBibXnu M4fzOWROW09? MmfQTY5pcWKrdHnvckBw\iCMQVuxJIlvKGi3bXHuJHRHOSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGlNPi2rbnT1Z4VlKFOWQWSzJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMkVOwG0> MYKyNlY6QDB6NB?=
Human T cell NGP4SnNMcW6jc3WgRZN{[Xl? NXm4VldpUW6qaXLpeIlwdiCxZjDKRWs{NzFiaX6gbJVu[W5iVDDj[YxteyCneIDy[ZN{cW6pIFPEN{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGlNOi2|dHnteYxifGWmIGPURXQ2[SCyaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIECuNFI{|ryP NWPIN|l3OjN3NEC2OFg>
Human monocyte M2TIVmtqdmG|ZTDBd5NigQ>? NHjHW|ZKdmirYnn0bY9vKG:oIFrBT|IhcW5iaIXtZY4hdW:wb3P5eIV{KGW6cILld5NqdmdiQ1SxOEBie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGdONUOVRj3zeIlufWyjdHXkJHNVSVR3YTDwbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFAvODJ4zszN NFfYPIUzOzV2ME[0PC=>
Human monocyte MmfKT4lv[XOnIFHzd4F6 NHnId|FKdmirYnn0bY9vKG:oIFrBT|IwOSCrbjDoeY1idiCvb37vZ5l1\XNiZYjwdoV{e2mwZzDDSFE1KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUU[QZ3HtcYEue3SrbYXsZZRm\CCVVFHUNUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEOx{txO M{XKOlI{PTRyNkS4
SET-2 NFHKPYNEgXSxdH;4bYMhSXO|YYm= MV:1JO69VQ>? NXjib3RbPDhiaB?= M1\3SGN6fG:2b4jpZ{BqdmSneE2xPE44LQ>? MVqyOVk{OTN2OR?=
HT93A MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoTpN|IxKG6P MYC1JIQ> NH;lO3ZFVVOR NVvmc4lyUW6qaXLpeIlwdiCxZjDHR3MuTiCrbnT1Z4VlKGe{YX71cI9kgXSrYzDkbYZn\XKnboTpZZRqd25? NFj6Nm0zPThyNUm2Ni=>
CMK M1TWd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEjLdZpKdmirYnn0bY9vKG:oIFPNT{Bk[XK{eXnu[{B1cGViSlHLN2E2PzKYIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbh?= MV[yOVM2OjF{NB?=
CMK MkOxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhUkGNM1G2N2QhdXW2YYTpc44h[2WubDDwdo9tcW[ncnH0bY9vKHerdHigTWM2OCCxZjCwMlE3OyEQvF2= NEnVclEzPTN3MkGyOC=>
CMK NHrBZ3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX\GO|hpUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIGfUJGpCUyClZXzsJJBzd2yrZnXyZZRqd25id3n0bEBKSzVyIH;mJFAvODd3IN88US=> NITDcJczPTN3MkGyOC=>
NCI-H460 Mn\DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M37OWmROW09? M3P0fWlEPTB;MD6xN{DPxE1? M4jwNFI2OjF|Nkew
NCI-H358 NX3SUoZIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoLDSG1UVw>? NFrsZ5hKSzVyPUCuNUDPxE1? M1HwOlI2OjF|Nkew
A549 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLoSG1UVw>? NXPlbpo1UUN3ME2wMlA1KM7:TR?= NGHPbHAzPTJzM{[3NC=>
A549/DDP NXf0[2NUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3XLUGROW09? MYnJR|UxRTBwMkKg{txO Ml25NlUzOTN4N{C=
A549/DDP M4jJR2Z2dmO2aX;uJGF{e2G7 MmHyN|Ahdk1? MnjpOFghcA>? M{PNVGROW09? NFXpWGdFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w NEHxfpozPTJzM{[3NC=>
NCI-H1299 NVn6dnNJTnWwY4Tpc44hSXO|YYm= NInjUFc{OCCwTR?= MVK0PEBp NXXCUGhrTE2VTx?= NUXJeFhvTG:5bj3y[Yd2dGG2aX;uJI9nKFOWQWSzJJBpd3OyaH;yfYxifGmxbh?= NIPVbpAzPTJzM{[3NC=>
NCI-H2347 MnHlSpVv[3Srb36gRZN{[Xl? NYnIfI1UOzBibl2= MXO0PEBp NXX3d|dOTE2VTx?= NE\rOGdF\WO{ZXHz[UBqdiCEY3yyJIV5eHKnc4Ppc44> Mki1NlUzOTN4N{C=
A549/DDP MYTBdI9xfG:|aYOgRZN{[Xl? NVHkTXhHOzBibl2= MYK0PEBp M1u5OGROW09? NHz1NoRKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| M3fkVVI2OjF|Nkew
NCI-H1299 NYjQXIN7SXCxcITvd4l{KEG|c3H5 MYmzNEBvVQ>? NV\tVnNuPDhiaB?= NED2c4hFVVOR M3\xR2lv\HWldHnvckBw\iCjcH;weI9{cXN? MnvENlUzOTN4N{C=
NCI-H2347 MkjNRZBweHSxc3nzJGF{e2G7 Ml\CN|Ahdk1? NFGzUZE1QCCq Mly5SG1UVw>? NFfhfZJKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| NEC5cY8zPTJzM{[3NC=>
Hep3B M3jUWWZ2dmO2aX;uJGF{e2G7 MUWxJO69VQ>? Mn[xNVYhcA>? NYW1TppPTE2VTx?= NEHXe2dKdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9iYXP0bZZmKFOWQWSzJJdqfGhiSVO1NEBw\iC-NUCg{txO NUXjdIY5OjR3MEG2PFk>
HepG2 MXfGeY5kfGmxbjDBd5NigQ>? M2TGcVEh|ryP MWexOkBp M{\GdGROW09? NGXpdHJKdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9ic3nncoFtKHSxIGPURXQ{ M3nTXVI1PTBzNki5
Huh7 NWftSI45TnWwY4Tpc44hSXO|YYm= MWqxJO69VQ>? M1ziPVE3KGh? NGjzRnBFVVOR MV;JcZBicXKnczD0bIUh[2GyYXPpeJkhd2ZiSVjDRU1ie3OxY3nheIVlKGeyMUOwJI12fGGwdIOgeI8he2mpbnHsJJRwKFOWQWSz MXuyOFUxOTZ6OR?=
DLD-1 NYGxc5NyU2mwYYPlJGF{e2G7 MlnpNlUh|ryP Mn3oOFghcA>? M2nzdGROW09? NV;mVGxrUW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> M1fVblI1ODVyNUWw
RKO NVPsZ5BTU2mwYYPlJGF{e2G7 MoO2NlUh|ryP M1SxU|Q5KGh? NYD4eXJCTE2VTx?= NIPlR3FKdmirYnn0bY9vKG:oIFrBT|EheGixc4Doc5J6dGG2aX;u M4jHUVI1ODVyNUWw
DLD-1 NX75S5pkU2mwYYPlJGF{e2G7 MlPLNlUh|ryP NVXRVlFsPDhiaB?= MWTEUXNQ NVTSc5dXUW6qaXLpeIlwdiCxZjDKRWszKHCqb4PwbI9zgWyjdHnvci=> M37n[FI1ODVyNUWw
RKO MVLLbY5ie2ViQYPzZZk> MWGyOUDPxE1? MlOwOFghcA>? NHfRNFJFVVOR MoH5[I9meyCwb4SgbY5pcWKrdDDKRWsyKHCqb4PwbI9zgWyjdHnvci=> Ml\INlQxPTB3NUC=
DLD-1 NYHzPJVKSXCxcITvd4l{KEG|c3H5 NV;wT3R[OjVizszN M3n5OFQ5KGh? M2TGT2ROW09? NYXDZW5CUW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= M2[wclI1ODVyNUWw
HuH7 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFzJXpc2OCEQvF2= MUK0PEBp MknkSG1UVw>? MnOwQlgzLSC{ZXT1Z5Rqd25? NVTpNWp1OjN7NEG4N|I>
SNU423 NIjkOFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4[1N|UxKM7:TR?= NHLxWFA1QCCq NULrXWRuTE2VTx?= MY[+PFEmKHKnZIXjeIlwdg>? M{HxPFI{QTRzOEOy
HuH7 MUTGeY5kfGmxbjDBd5NigQ>? MX[1NEDPxE1? NF;YVVczPCCq MWPEUXNQ MXfJcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? NYTidYFyOjN7NEG4N|I>
SNU182 NUG3c3lTTnWwY4Tpc44hSXO|YYm= NVjZ[oluPTBizszN MljHNlQhcA>? MUnEUXNQ NXTOdpd[UW6qaXLpeIlwdiCxZjDTWGFVOSCjbnSgV3RCXDNicHjvd5Bpd3K7bHH0bY9vKHOrZ37p[olk[W62bIm= MUmyN|k1OTh|Mh?=
SNU423 Ml3aSpVv[3Srb36gRZN{[Xl? NGfRR5E2OCEQvF2= M4ja[VI1KGh? MYLEUXNQ MYrJcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? M1G2UFI{QTRzOEOy

... 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
NCT03571321 Not yet recruiting Acute Lymphoblastic Leukemia|ALL Childhood|ALL University of Chicago|Incyte Corporation September 5 2019 Phase 1
NCT03801434 Not yet recruiting BCR-JAK2 Fusion Protein Expression|Blasts 20 Percent or Less of Peripheral Blood White Cells|Blasts More Than 5 Percent of Bone Marrow Nucleated Cells|Blasts More Than 5 Percent of Peripheral Blood White Cells|Blasts Under 20 Percent of Bone Marrow Nucleated Cells|Chronic Eosinophilic Leukemia Not Otherwise Specified|Eosinophilia|Hepatomegaly|Hypereosinophilic Syndrome|JAK2 Gene Mutation|Splenomegaly|TEL-JAK2 Fusion Protein Expression Stanford University|Incyte Corporation June 19 2019 Phase 2
NCT03801434 Not yet recruiting BCR-JAK2 Fusion Protein Expression|Blasts 20 Percent or Less of Peripheral Blood White Cells|Blasts More Than 5 Percent of Bone Marrow Nucleated Cells|Blasts More Than 5 Percent of Peripheral Blood White Cells|Blasts Under 20 Percent of Bone Marrow Nucleated Cells|Chronic Eosinophilic Leukemia Not Otherwise Specified|Eosinophilia|Hepatomegaly|Hypereosinophilic Syndrome|JAK2 Gene Mutation|Splenomegaly|TEL-JAK2 Fusion Protein Expression Stanford University|Incyte Corporation June 19 2019 Phase 2
NCT03610971 Not yet recruiting Chronic Phase Chronic Myeloid Leukemia|Chronic Myeloid Leukemia Chronic Phase H. Lee Moffitt Cancer Center and Research Institute|H. Jean Khoury Cure CML Consortium|Incyte Corporation May 2019 Phase 2
NCT03722407 Not yet recruiting Chronic Myelomonocytic Leukemia|Leukemia H. Lee Moffitt Cancer Center and Research Institute|Incyte Corporation May 1 2019 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