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.
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 MYfLbY5ie2ViQYPzZZk> MVSyNEBucW5? MkHOSG1UVw>? MmTaTY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJHRHOSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGVRVy2rbnT1Z4VlKFOWQWS1JJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMUNOwG0> NGfHV4ozOjZ7OEC4OC=>
TF1 MWTLbY5ie2ViQYPzZZk> MmTrNlAhdWmw M{XVW2ROW09? MXvJcohq[mm2aX;uJI9nKEqDS{GgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWw3NWmwZIXj[YQhW1SDVEOgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjB{NN88US=> MVqyNlY6QDB6NB?=
Human T cell NXfyU2FwU2mwYYPlJGF{e2G7 NIC3[VFKdmirYnn0bY9vKG:oIFrBT|MwOSCrbjDoeY1idiCWIHPlcIx{KGW6cILld5NqdmdiQ1SzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWwzNXO2aX31cIF1\WRiU2TBWFViKHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNlPPxE1? NF\ufWUzOzV2ME[0PC=>
Human monocyte NFX4fFlMcW6jc3WgRZN{[Xl? NXvI[mZ{UW6qaXLpeIlwdiCxZjDKRWszKGmwIHj1cYFvKG2xbn;jfZRmeyCneIDy[ZN{cW6pIFPENVQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBIVS2FU1[td5RqdXWuYYTl[EBUXEGWNXGgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjB{Nt88US=> MkfaNlM2PDB4NEi=
Human monocyte NWXYS|NPU2mwYYPlJGF{e2G7 NGHSU2xKdmirYnn0bY9vKG:oIFrBT|IwOSCrbjDoeY1idiCvb37vZ5l1\XNiZYjwdoV{e2mwZzDDSFE1KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUU[QZ3HtcYEue3SrbYXsZZRm\CCVVFHUNUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEOx{txO NXrZTpVZOjN3NEC2OFg>
HEL MmnNR5l1d3SxeHnjJGF{e2G7 M1nCflUh|ryP MnPZOFghcA>? MXTDfZRwfG:6aXOgbY5l\Xh;MUKuNkU> NWPWPWJ{OjV7M{GzOFk>
SET-2 NUDiTI9wS3m2b4TvfIlkKEG|c3H5 NGfnV4o2KM7:TR?= NWL5UW5[PDhiaB?= M4fHNGN6fG:2b4jpZ{BqdmSneE2xPE44LQ>? MV6yOVk{OTN2OR?=
HT93A MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHPQZlE{OjBibl2= M{PTUlUh\A>? NE\KUHZFVVOR M{HSe2lvcGmkaYTpc44hd2ZiR1PTMWYhcW6mdXPl[EBoemGwdXzvZ5l1cWNiZHnm[oVz\W62aXH0bY9v M174VFI2QDB3OU[y
CMK Mo\mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUHvR|JUUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPTd{VjDteZRifGmxbjDj[YxtKHC{b3zp[oVz[XSrb36= MonDNlU{PTJzMkS=
CMK M{j5TGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3P0SGlvcGmkaYTpc44hd2ZiQ13LJINienK7aX7nJJRp\SCMQVuzRVY{TCCvdYTheIlwdiClZXzsJJBzd2yrZnXyZZRqd25id3n0bEBKSzVyIH;mJFAvOTZ|IN88US=> MkTVNlU{PTJzMkS=
CMK NFjqTpVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1XWN2lvcGmkaYTpc44hd2ZiQ13LJINienK7aX7nJJRp\SCZVDDKRWsh[2WubDDwdo9tcW[ncnH0bY9vKHerdHigTWM2OCCxZjCwMlA4PSEQvF2= NHuyb5YzPTN3MkGyOC=>
NCI-H460 NVnYbphHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkPoSG1UVw>? M{XEUWlEPTB;MD6xN{DPxE1? M3nJT|I2OjF|Nkew
NCI-H358 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml2zSG1UVw>? NF61Xm1KSzVyPUCuNUDPxE1? M3\XSlI2OjF|Nkew
A549 M1raZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUH0O3RxTE2VTx?= M1vVemlEPTB;MD6wOEDPxE1? NGTQSFQzPTJzM{[3NC=>
A549/DDP MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWPBXpVzTE2VTx?= MlfGTWM2OD1yLkKyJO69VQ>? MXeyOVIyOzZ5MB?=
NCI-H1299 NEfWSHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUD2SFUxTE2VTx?= MWfJR|UxRTBwMkig{txO Mm\NNlUzOTN4N{C=
NCI-H2347 M1TnNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYHEUXNQ NF7zSolKSzVyPUCuNVch|ryP NUDDVYV2OjV{MUO2O|A>
A549/DDP NIXHN5RHfW6ldHnvckBCe3OjeR?= NFzJT|Q{OCCwTR?= NGfJTYw1QCCq NInvVWpFVVOR MV;Ec5dvNXKnZ4XsZZRqd25ib3[gV3RCXDNicHjvd5Bpd3K7bHH0bY9v Mn\MNlUzOTN4N{C=
NCI-H1299 NVzYV2NrTnWwY4Tpc44hSXO|YYm= MWqzNEBvVQ>? NH3LZYc1QCCq MlvpSG1UVw>? NGrK[mJFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w NEDJ[XozPTJzM{[3NC=>
NCI-H2347 MoDnSpVv[3Srb36gRZN{[Xl? NGLRVo0{OCCwTR?= NXnveFR4PDhiaB?= MYfEUXNQ MWfE[YNz\WG|ZTDpckBD[2x{IHX4dJJme3Orb36= NEOwZ48zPTJzM{[3NC=>
A549/DDP NID1U4lCeG:ydH;zbZMhSXO|YYm= MnHtN|Ahdk1? NV7XRollPDhiaB?= MWPEUXNQ NITldpNKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| MVqyOVIyOzZ5MB?=
NCI-H1299 MonBRZBweHSxc3nzJGF{e2G7 M4XJUlMxKG6P MVW0PEBp M{LrTGROW09? NGjIXVJKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| MYeyOVIyOzZ5MB?=
NCI-H2347 M1nN[WFxd3C2b4Ppd{BCe3OjeR?= MmHJN|Ahdk1? NH7VZXU1QCCq M2Tz[2ROW09? MoPSTY5lfWO2aX;uJI9nKGGyb4D0c5Nqew>? NVmwVJRTOjV{MUO2O|A>
Hep3B MVrGeY5kfGmxbjDBd5NigQ>? NV[4cY46OSEQvF2= M{f0XVE3KGh? M4T1d2ROW09? M2e0ZmlueGGrcnXzJJRp\SClYYDhZ4l1gSCxZjDJTGNCNWG|c3;jbYF1\WRiZ4CxN|AhdXW2YX70d{B1dyCjY4TpeoUhW1SDVEOge4l1cCCLQ{WwJI9nKH53MDFOwG0> MX6yOFUxOTZ6OR?=
HepG2 MoXqSpVv[3Srb36gRZN{[Xl? MXWxJO69VQ>? NUnPdJBHOTZiaB?= NGH6boxFVVOR MWXJcZBicXKnczD0bIUh[2GyYXPpeJkhd2ZiSVjDRU1ie3OxY3nheIVlKGeyMUOwJI12fGGwdIOgeI8he2mpbnHsJJRwKFOWQWSz MViyOFUxOTZ6OR?=
Huh7 M1PZbWZ2dmO2aX;uJGF{e2G7 NXHVeWk2OSEQvF2= M2TCSFE3KGh? MULEUXNQ Moi2TY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKHOrZ37hcEB1dyCVVFHUNy=> MmfmNlQ2ODF4OEm=
BaF3 M4fX[GtqdmG|ZTDBd5NigQ>? NX;GOnV7QDBibl2= NXzvbIRqPiCq MYHEUXNQ MlvEVoVlfWOnczD0bIUheGixc4Doc5J6dGG2aX;uJI9nyqCVVFHUOUBqdiCMQVuyWlYyP0ZvbYX0ZZRm\CCEQV[zMWVRV1JiY3XscC=> NEH3O4QzPDJ|N{e5NS=>
DLD-1 M4fyZmtqdmG|ZTDBd5NigQ>? NGTVdJAzPSEQvF2= NEPWSYw1QCCq MVXEUXNQ NYLiOVJtUW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> NGLoTXYzPDB3MEW1NC=>
RKO NGe0THNMcW6jc3WgRZN{[Xl? NVqxfJVWOjVizszN NGTRZVE1QCCq Mn;6SG1UVw>? NHfqVmRKdmirYnn0bY9vKG:oIFrBT|EheGixc4Doc5J6dGG2aX;u Mkf4NlQxPTB3NUC=
DLD-1 MkPiT4lv[XOnIFHzd4F6 M1vjXFI2KM7:TR?= NVzTZ4JrPDhiaB?= MVjEUXNQ M2XXT2lvcGmkaYTpc44hd2ZiSlHLNkBxcG:|cHjvdplt[XSrb36= MYWyOFA2ODV3MB?=
RKO MknjT4lv[XOnIFHzd4F6 NXTGeno5OjVizszN NHfLdJA1QCCq MXnEUXNQ M3zxOoRw\XNibn;0JIlvcGmkaYSgTmFMOSCyaH;zdIhwenmuYYTpc44> MVOyOFA2ODV3MB?=
DLD-1 Mn7tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX21NEDPxE1? M4TyNVQ5KGh? MXTEUXNQ Mo\OTWM2OD1zNT61NUDPxE1? MVeyOFA2ODV3MB?=
RKO MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1jvZ|UxKM7:TR?= MnHXOFghcA>? NES5Xm1FVVOR MnPOTWM2OD1zND63OkDPxE1? MXOyOFA2ODV3MB?=
DLD-1 M37MeWFxd3C2b4Ppd{BCe3OjeR?= M2LFTVI2KM7:TR?= M1zrOFQ5KGh? MWXEUXNQ MYTJcoR2[2W|IHHwc5B1d3OrczDifUBi[3SrdnH0bY5oKGOjc4Dhd4UhOw>? NFPyXZIzPDB3MEW1NC=>
RKO NHK0fIJCeG:ydH;zbZMhSXO|YYm= M1\lZlI2KM7:TR?= NED0SVU1QCCq NVHxZ3ZWTE2VTx?= MVLJcoR2[2W|IHHwc5B1d3OrczDifUBi[3SrdnH0bY5oKGOjc4Dhd4UhOw>? NVLEOWt[OjRyNUC1OVA>
HuH7 M4TzdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWnufIVPPTBizszN NFTQfow1QCCq NGPibXNFVVOR NGGweXE,QDJnIILl[JVkfGmxbh?= MVGyN|k1OTh|Mh?=
SNU182 NHTM[XVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2LZ[FUxKM7:TR?= MnzvOFghcA>? NX30Z4Y5TE2VTx?= NFvvXpo,PjRnIILl[JVkfGmxbh?= NW\ZRXVROjN7NEG4N|I>
SNU423 NEPi[VJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV[1NEDPxE1? M4rvTFQ5KGh? MnntSG1UVw>? MkC0QlgyLSC{ZXT1Z5Rqd25? NHr1d3MzOzl2MUizNi=>
HuH7 MmrnSpVv[3Srb36gRZN{[Xl? NWLWc|lSPTBizszN MoSyNlQhcA>? MnPQSG1UVw>? NFrvTIpKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= MmL2NlM6PDF6M{K=
SNU182 NIW3SHBHfW6ldHnvckBCe3OjeR?= NIH6fY02OCEQvF2= MYiyOEBp MmDySG1UVw>? MkPrTY5pcWKrdHnvckBw\iCVVFHUNUBidmRiU2TBWFMheGixc4Doc5J6dGG2aX;uJJNq\26rZnnjZY51dHl? NEjCZ3QzOzl2MUizNi=>
SNU423 NXGzdVlSTnWwY4Tpc44hSXO|YYm= MXe1NEDPxE1? NIXHeWEzPCCq MV\EUXNQ MW\Jcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? NETIb4kzOzl2MUizNi=>

... 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(Data is from Selleck tests instead of citations):
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
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. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=24711661.

JAK Signaling Pathway Map

JAK Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID