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 38 Publications

8 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.

  • 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.
Targets
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 MnviT4lv[XOnIFHzd4F6 Mom0NlAhdWmw MVPEUXNQ MVPJcohq[mm2aX;uJI9nKEqDS{KgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gSXBQNWmwZIXj[YQhW1SDVEWgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjBzMt88US=> NHfDVHgzOjZ7OEC4OC=>
TF1 MVjLbY5ie2ViQYPzZZk> MWSyNEBucW5? NITDXpZFVVOR NWn2U5ZTUW6qaXLpeIlwdiCxZjDKRWsyKGmwIHj1cYFvKFSIMTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKEmONj3pcoR2[2WmIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNlTPxE1? NXmzbldCOjJ4OUiwPFQ>
Human T cell NH[4VW9McW6jc3WgRZN{[Xl? M124WmlvcGmkaYTpc44hd2ZiSlHLN{8yKGmwIHj1cYFvKFRiY3XscJMh\XiycnXzd4lv\yCFREOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDJUFIue3SrbYXsZZRm\CCVVFHUOYEheGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCyN:69VQ>? M4X6[|I{PTRyNkS4
Human monocyte NXf6R3JkU2mwYYPlJGF{e2G7 MoPCTY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJI1wdm:leYTld{BmgHC{ZYPzbY5oKEOGMUSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDHUU1EW0Zvc4TpcZVt[XSnZDDTWGFVPWFicHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlAzPs7:TR?= NIC1W3gzOzV2ME[0PC=>
Human monocyte M{nMTWtqdmG|ZTDBd5NigQ>? MmTrTY5pcWKrdHnvckBw\iCMQVuyM|EhcW5iaIXtZY4hdW:wb3P5eIV{KGW6cILld5NqdmdiQ1SxOEBie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGlHVmejbX3hMZN1cW23bHH0[YQhW1SDVEGgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjB|Md88US=> MnrHNlM2PDB4NEi=
HEL NEDZc5hEgXSxdH;4bYMhSXO|YYm= NWDYclZ[PSEQvF2= MVq0PEBp MnfOR5l1d3SxeHnjJIlv\GW6PUGyMlIm MXeyOVk{OTN2OR?=
SET-2 MmXPR5l1d3SxeHnjJGF{e2G7 Ml\SOUDPxE1? MVK0PEBp NXHTSm52S3m2b4TvfIlkKGmwZHX4QVE5Njdn M2DTOlI2QTNzM{S5
HT93A NHHkUG9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXnsVlQ2OzJyIH7N M3rXWlUh\A>? Mnr3SG1UVw>? NUXYUXVJUW6qaXLpeIlwdiCxZjDHR3MuTiCrbnT1Z4VlKGe{YX71cI9kgXSrYzDkbYZn\XKnboTpZZRqd25? M1[3UFI2QDB3OU[y
CMK NH\YfY1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2m2XWlvcGmkaYTpc44hd2ZiQ13LJINienK7aX7nJJRp\SCMQVuzRVU4OlZibYX0ZZRqd25iY3XscEBxem:uaX\ldoF1cW:w NULHbmVmOjV|NUKxNlQ>
CMK Ml3rS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkXXTY5pcWKrdHnvckBw\iCFTVugZ4FzenmrbnegeIhmKEqDS{PBOlNFKG23dHH0bY9vKGOnbHygdJJwdGmoZYLheIlwdiC5aYToJGlEPTBib3[gNE4yPjNizszN NHzKOJEzPTN3MkGyOC=>
CMK M2LrS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEnUbVBKdmirYnn0bY9vKG:oIFPNT{Bk[XK{eXnu[{B1cGViV2SgTmFMKGOnbHygdJJwdGmoZYLheIlwdiC5aYToJGlEPTBib3[gNE4xPzVizszN M2rRTlI2OzV{MUK0
NCI-H460 NETaRoZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Moi3SG1UVw>? NHLRXJVKSzVyPUCuNVMh|ryP M{\vPFI2OjF|Nkew
NCI-H358 NE\4RpFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYXEUXNQ M4XZSGlEPTB;MD6xJO69VQ>? NYLxWoNFOjV{MUO2O|A>
A549 NGXE[mFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnXPSG1UVw>? NGnSNFVKSzVyPUCuNFQh|ryP Mn\6NlUzOTN4N{C=
A549/DDP NX;XW5ZvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWL4XFZ4TE2VTx?= NYPPVJBjUUN3ME2wMlIzKM7:TR?= NWTobId7OjV{MUO2O|A>
NCI-H1299 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHNXmtFVVOR NIjhR29KSzVyPUCuNlgh|ryP Ml7ZNlUzOTN4N{C=
NCI-H2347 MnHLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFXPc2dFVVOR MXjJR|UxRTBwMUeg{txO MlPFNlUzOTN4N{C=
A549/DDP NHe4PYNHfW6ldHnvckBCe3OjeR?= MVyzNEBvVQ>? MlHOOFghcA>? MWjEUXNQ MXnEc5dvNXKnZ4XsZZRqd25ib3[gV3RCXDNicHjvd5Bpd3K7bHH0bY9v NXvRbFVCOjV{MUO2O|A>
NCI-H1299 Ml\JSpVv[3Srb36gRZN{[Xl? M3e1NFMxKG6P Mm\GOFghcA>? NVXZOHhDTE2VTx?= NY\tR|g3TG:5bj3y[Yd2dGG2aX;uJI9nKFOWQWSzJJBpd3OyaH;yfYxifGmxbh?= NUP6WXV3OjV{MUO2O|A>
NCI-H2347 NVPhenhTTnWwY4Tpc44hSXO|YYm= NUjMe2dYOzBibl2= Mlj5OFghcA>? MkXZSG1UVw>? MXnE[YNz\WG|ZTDpckBD[2x{IHX4dJJme3Orb36= M1;WS|I2OjF|Nkew
A549/DDP MYLBdI9xfG:|aYOgRZN{[Xl? MWWzNEBvVQ>? MWC0PEBp MXvEUXNQ MXTJcoR2[3Srb36gc4Yh[XCxcITvd4l{ MXKyOVIyOzZ5MB?=
NCI-H1299 MWDBdI9xfG:|aYOgRZN{[Xl? NUnL[WFYOzBibl2= M4fzOlQ5KGh? MU\EUXNQ M1O1cGlv\HWldHnvckBw\iCjcH;weI9{cXN? M2q3VFI2OjF|Nkew
NCI-H2347 MYXBdI9xfG:|aYOgRZN{[Xl? MYCzNEBvVQ>? MnzWOFghcA>? Ml7uSG1UVw>? NHTqTplKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| MonxNlUzOTN4N{C=
Hep3B NH:4N49HfW6ldHnvckBCe3OjeR?= MWSxJO69VQ>? NEXpfpIyPiCq MYXEUXNQ M{Dq[GlueGGrcnXzJJRp\SClYYDhZ4l1gSCxZjDJTGNCNWG|c3;jbYF1\WRiZ4CxN|AhdXW2YX70d{B1dyCjY4TpeoUhW1SDVEOge4l1cCCLQ{WwJI9nKH53MDFOwG0> M4T1XlI1PTBzNki5
HepG2 MVXGeY5kfGmxbjDBd5NigQ>? MWSxJO69VQ>? MUCxOkBp MWjEUXNQ M2fOSWlueGGrcnXzJJRp\SClYYDhZ4l1gSCxZjDJTGNCNWG|c3;jbYF1\WRiZ4CxN|AhdXW2YX70d{B1dyC|aXfuZYwhfG9iU2TBWFM> MkXHNlQ2ODF4OEm=
Huh7 NXPTSXJMTnWwY4Tpc44hSXO|YYm= NIOzTlcyKM7:TR?= NVvPeXpkOTZiaB?= MWDEUXNQ MnvtTY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKHOrZ37hcEB1dyCVVFHUNy=> M4H6[lI1PTBzNki5
BaF3 NFrhbFJMcW6jc3WgRZN{[Xl? NV7ZUFFzQDBibl2= NWWxd4VkPiCq NW[zU2VETE2VTx?= NWnIN5pSWmWmdXPld{B1cGVicHjvd5Bpd3K7bHH0bY9vKG:owrDTWGFVPSCrbjDKRWszXjZzN1[tcZV1[XSnZDDCRWY{NUWST2KgZ4VtdA>? MYCyOFI{Pzd7MR?=
DLD-1 MVjLbY5ie2ViQYPzZZk> NXfhS4VpOjVizszN NGPaWVY1QCCq NYW1R2FlTE2VTx?= M3u4eGlvcGmkaYTpc44hd2ZiSlHLNUBxcG:|cHjvdplt[XSrb36= NHPReWYzPDB3MEW1NC=>
RKO Mmi1T4lv[XOnIFHzd4F6 MXOyOUDPxE1? NU\4PZljPDhiaB?= MoX0SG1UVw>? NXrsUJdWUW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> MWKyOFA2ODV3MB?=
DLD-1 MWXLbY5ie2ViQYPzZZk> MWOyOUDPxE1? MXy0PEBp NV\CV4NJTE2VTx?= NGXpbGRKdmirYnn0bY9vKG:oIFrBT|IheGixc4Doc5J6dGG2aX;u M3u4SlI1ODVyNUWw
RKO NYPSflVmU2mwYYPlJGF{e2G7 NVrYUnVDOjVizszN MVO0PEBp NGfkTVBFVVOR M{\MeIRw\XNibn;0JIlvcGmkaYSgTmFMOSCyaH;zdIhwenmuYYTpc44> MWWyOFA2ODV3MB?=
DLD-1 MnTsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlLGOVAh|ryP NGfy[|Q1QCCq NILVXW1FVVOR M{fj[GlEPTB;MUWuOVEh|ryP MU[yOFA2ODV3MB?=
RKO NUHqZnZXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWS1NEDPxE1? Mo\DOFghcA>? NUjOW2ozTE2VTx?= MX;JR|UxRTF2Lke2JO69VQ>? M1P5UFI1ODVyNUWw
DLD-1 NFXHRVlCeG:ydH;zbZMhSXO|YYm= MVyyOUDPxE1? NIroUIg1QCCq NV3lRm9ETE2VTx?= MnvVTY5lfWOnczDhdI9xfG:|aYOgZpkh[WO2aY\heIlv\yClYYPwZZNmKDN? NH;K[4kzPDB3MEW1NC=>
RKO MWPBdI9xfG:|aYOgRZN{[Xl? MlfNNlUh|ryP M2PsblQ5KGh? M4WyWWROW09? NXr6XmxIUW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= MknuNlQxPTB3NUC=
HuH7 NGO4XVlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX61NEDPxE1? NEnHelA1QCCq NX3XXlJHTE2VTx?= MWC+PFImKHKnZIXjeIlwdg>? MljpNlM6PDF6M{K=
SNU182 NV\aWJhNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH\VbWI2OCEQvF2= NUftSJRCPDhiaB?= NIjUPVJFVVOR NYGwRpN1RjZ2JTDy[YR2[3Srb36= M{GzXlI{QTRzOEOy
SNU423 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnrSOVAh|ryP NFr5WXk1QCCq MlHUSG1UVw>? NFr1U4c,QDFnIILl[JVkfGmxbh?= MYSyN|k1OTh|Mh?=
HuH7 MoXCSpVv[3Srb36gRZN{[Xl? NVK1T5hxPTBizszN Mn7lNlQhcA>? Ml7HSG1UVw>? NWDTNWgyUW6qaXLpeIlwdiCxZjDTWGFVOSCjbnSgV3RCXDNicHjvd5Bpd3K7bHH0bY9vKHOrZ37p[olk[W62bIm= NX3BSGVuOjN7NEG4N|I>
SNU182 MV7GeY5kfGmxbjDBd5NigQ>? M1;sPFUxKM7:TR?= Ml;GNlQhcA>? NEDpeWNFVVOR NFv2N2VKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= NX7tRnZTOjN7NEG4N|I>
SNU423 Mn;hSpVv[3Srb36gRZN{[Xl? MlrXOVAh|ryP NH;HZYszPCCq MVzEUXNQ Ml\FTY5pcWKrdHnvckBw\iCVVFHUNUBidmRiU2TBWFMheGixc4Doc5J6dGG2aX;uJJNq\26rZnnjZY51dHl? NEDi[mwzOzl2MUizNi=>

... 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]

Protocol

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:
2% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.
5mg/mL

* 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
Formula

C17H18N6

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

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01712659 Recruiting T Cell Leukemia, Adult|Leukemia, Adult T-Cell|T Cell Leukemia, HTLV I Associated National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) October 3, 2012 Phase 2
NCT02913261 Recruiting Corticosteroid Refractory Acute Graft vs Host Disease Novartis Pharmaceuticals|Novartis February 28, 2017 Phase 3
NCT02973711 Not yet recruiting Leukemia, Chronic Myeloid University of Michigan Cancer Center February 2017 Phase 1|Phase 2
NCT03012230 Not yet recruiting Estrogen Receptor Negative|HER2/Neu Negative|Progesterone Receptor Negative|Stage IV Breast Cancer|Triple-Negative Breast Carcinoma Mayo Clinic|National Cancer Institute (NCI) February 2017 Phase 1
NCT02928978 Not yet recruiting Ductal Carcinoma In Situ|Atypical Lobular Hyperplasia|Atypical Ductal Hyperplasia|Lobular Carcinoma In Situ Julie Nangia|Incyte Corporation|Translational Breast Cancer Research Consortium|Baylor Breast Care Center January 2017 Phase 2
NCT02966353 Not yet recruiting Primary Myelofibrosis (PMF)|Post-Polycythemia Vera-Myelofibrosis (PPV-MF)|Post-Essential Thrombocythemia Myelofibrosis (PET-MF) Novartis Pharmaceuticals|Novartis January 2017 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. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=24711661.

JAK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID