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 39 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 NX7ZS|F3U2mwYYPlJGF{e2G7 NWX0dnh4OjBibXnu M4nrdWROW09? NFnF[VlKdmirYnn0bY9vKG:oIFrBT|IhcW5iaIXtZY4hXEZzIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhTVCRLXnu[JVk\WRiU2TBWFUheGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCxNu69VQ>? M2nTdFIzPjl6MEi0
TF1 MVvLbY5ie2ViQYPzZZk> NWeyfml5OjBibXnu NX7N[lhyTE2VTx?= MUHJcohq[mm2aX;uJI9nKEqDS{GgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWw3NWmwZIXj[YQhW1SDVEOgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjB{NN88US=> MnzINlI3QThyOES=
Human T cell M2nTR2tqdmG|ZTDBd5NigQ>? MYLJcohq[mm2aX;uJI9nKEqDS{OvNUBqdiCqdX3hckBVKGOnbHzzJIV5eHKnc4PpcochS0R|IHHzd4V{e2WmIHHzJIlvcGmkaYTpc44hd2ZiSVyyMZN1cW23bHH0[YQhW1SDVEXhJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMkROwG0> Ml76NlM2PDB4NEi=
Human monocyte NHnGdldMcW6jc3WgRZN{[Xl? Mlz2TY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJI1wdm:leYTld{BmgHC{ZYPzbY5oKEOGMUSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDHUU1EW0Zvc4TpcZVt[XSnZDDTWGFVPWFicHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlAzPs7:TR?= MX[yN|U1ODZ2OB?=
Human monocyte MlXwT4lv[XOnIFHzd4F6 M{n1[mlvcGmkaYTpc44hd2ZiSlHLNk8yKGmwIHj1cYFvKG2xbn;jfZRmeyCneIDy[ZN{cW6pIFPENVQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBKTk6pYX3tZU1{fGmvdXzheIVlKFOWQWSxJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yM{JOwG0> MnvyNlM2PDB4NEi=
HEL MnfZR5l1d3SxeHnjJGF{e2G7 Mo[zOUDPxE1? NGDxPIw1QCCq M2DqTGN6fG:2b4jpZ{BqdmSneE2xNk4zLQ>? M3ThblI2QTNzM{S5
SET-2 NVK1fVRtS3m2b4TvfIlkKEG|c3H5 Mn3FOUDPxE1? NXXq[FZEPDhiaB?= NXHoSWFqS3m2b4TvfIlkKGmwZHX4QVE5Njdn MXOyOVk{OTN2OR?=
HT93A MkHHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVfn[XpwOzJyIH7N NYf1ZYVVPSCm Moq0SG1UVw>? M2nWT2lvcGmkaYTpc44hd2ZiR1PTMWYhcW6mdXPl[EBoemGwdXzvZ5l1cWNiZHnm[oVz\W62aXH0bY9v M{PTPFI2QDB3OU[y
CMK MnvzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUK3ellbUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPTd{VjDteZRifGmxbjDj[YxtKHC{b3zp[oVz[XSrb36= M3[5W|I2OzV{MUK0
CMK MnTvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVvRV|hyUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPjOGIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbjD3bZRpKEmFNUCgc4YhOC5zNkOg{txO M4rCTFI2OzV{MUK0
CMK M2GyUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWrJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP NVXFZmpxOjV|NUKxNlQ>
NCI-H460 NE\yPHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\TNIx[TE2VTx?= NVHLR286UUN3ME2wMlE{KM7:TR?= NUPtfZF[OjV{MUO2O|A>
A549 M4jYS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NY\LbW9uTE2VTx?= MVvJR|UxRTBwMESg{txO MVmyOVIyOzZ5MB?=
A549/DDP M3XlfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2PlZmROW09? Mn\KTWM2OD1yLkKyJO69VQ>? MXuyOVIyOzZ5MB?=
NCI-H1299 Mn;ZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWHHZodpTE2VTx?= MnXITWM2OD1yLkK4JO69VQ>? M1;wXFI2OjF|Nkew
NCI-H2347 MnPIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1z0fGROW09? NYTkNW9JUUN3ME2wMlE4KM7:TR?= M2n1U|I2OjF|Nkew
A549/DDP MlHuSpVv[3Srb36gRZN{[Xl? M2HycFMxKG6P NF\1b5U1QCCq NWDX[IN2TE2VTx?= M2HmfmRwf25vcnXneYxifGmxbjDv[kBUXEGWMzDwbI9{eGixconsZZRqd25? M3LQVlI2OjF|Nkew
NCI-H1299 NIPPPFdHfW6ldHnvckBCe3OjeR?= NYDienBUOzBibl2= MWO0PEBp NVHCd3N4TE2VTx?= MoGwSI94di2{ZXf1cIF1cW:wIH;mJHNVSVR|IIDoc5NxcG:{eXzheIlwdg>? NGDBbo0zPTJzM{[3NC=>
NCI-H2347 MVrGeY5kfGmxbjDBd5NigQ>? NILpW5o{OCCwTR?= MlrNOFghcA>? MonqSG1UVw>? MnXrSIVkemWjc3WgbY4hSmOuMjDlfJBz\XO|aX;u MYqyOVIyOzZ5MB?=
A549/DDP M3T6emFxd3C2b4Ppd{BCe3OjeR?= MoDFN|Ahdk1? NUnEN5MxPDhiaB?= NXHX[ZZnTE2VTx?= M3vKTGlv\HWldHnvckBw\iCjcH;weI9{cXN? MmHwNlUzOTN4N{C=
NCI-H1299 MoDYRZBweHSxc3nzJGF{e2G7 MofNN|Ahdk1? M{m5RVQ5KGh? Ml\DSG1UVw>? MoO1TY5lfWO2aX;uJI9nKGGyb4D0c5Nqew>? MXeyOVIyOzZ5MB?=
NCI-H2347 NV;p[WoxSXCxcITvd4l{KEG|c3H5 M1LDb|MxKG6P NIP2b2M1QCCq MmDtSG1UVw>? M4Tkd2lv\HWldHnvckBw\iCjcH;weI9{cXN? M1XDSVI2OjF|Nkew
HepG2 NIHPZZFHfW6ldHnvckBCe3OjeR?= MlPmNUDPxE1? MWCxOkBp MoLiSG1UVw>? NFvtWY1KdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9ic3nncoFtKHSxIGPURXQ{ MnLrNlQ2ODF4OEm=
DLD-1 M4XLZmtqdmG|ZTDBd5NigQ>? MUeyOUDPxE1? NWLNUFhoPDhiaB?= MkHaSG1UVw>? NELhO2NKdmirYnn0bY9vKG:oIFrBT|EheGixc4Doc5J6dGG2aX;u NIfxToczPDB3MEW1NC=>
RKO NUW2VI9ZU2mwYYPlJGF{e2G7 MX6yOUDPxE1? MWm0PEBp MnjiSG1UVw>? MXfJcohq[mm2aX;uJI9nKEqDS{GgdIhwe3Cqb4L5cIF1cW:w NUfxU|lHOjRyNUC1OVA>
DLD-1 M4fxbWtqdmG|ZTDBd5NigQ>? Mmj5NlUh|ryP MX:0PEBp MXPEUXNQ MVPJcohq[mm2aX;uJI9nKEqDS{KgdIhwe3Cqb4L5cIF1cW:w MnfBNlQxPTB3NUC=
RKO NWfzNlZtU2mwYYPlJGF{e2G7 MnKxNlUh|ryP Mn\zOFghcA>? MVjEUXNQ MkHB[I9meyCwb4SgbY5pcWKrdDDKRWsyKHCqb4PwbI9zgWyjdHnvci=> Mn3YNlQxPTB3NUC=
DLD-1 NF71e|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWrC[XV4PTBizszN NEnTfmU1QCCq Mm\nSG1UVw>? NFjKRWRKSzVyPUG1MlUyKM7:TR?= MmP3NlQxPTB3NUC=
DLD-1 NV\G[pdpSXCxcITvd4l{KEG|c3H5 M4XkSlI2KM7:TR?= M4ftZlQ5KGh? NWToRVl2TE2VTx?= M{iwRmlv\HWlZYOgZZBweHSxc3nzJIJ6KGGldHn2ZZRqdmdiY3HzdIF{\SB| NYLxWXZOOjRyNUC1OVA>
RKO MVjBdI9xfG:|aYOgRZN{[Xl? MXiyOUDPxE1? M2izblQ5KGh? NGe0UG9FVVOR Ml\uTY5lfWOnczDhdI9xfG:|aYOgZpkh[WO2aY\heIlv\yClYYPwZZNmKDN? NVjoSWl6OjRyNUC1OVA>
HuH7 NGm5bZVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXj5eXl[PTBizszN MWW0PEBp M1fJN2ROW09? NEe1OI8,QDJnIILl[JVkfGmxbh?= MWiyN|k1OTh|Mh?=
SNU182 NGHBeo5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXL3elgxPTBizszN MVO0PEBp MlvLSG1UVw>? M4j6S|43PCVicnXkeYN1cW:w NFzpR|QzOzl2MUizNi=>
SNU423 MlL4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmHsOVAh|ryP M4Dje|Q5KGh? Mli4SG1UVw>? NUf1bIVpRjhzJTDy[YR2[3Srb36= M2\iSVI{QTRzOEOy
HuH7 M2PIc2Z2dmO2aX;uJGF{e2G7 MUC1NEDPxE1? NXT4c5RNOjRiaB?= NYjGc4RjTE2VTx?= NVKzNHFrUW6qaXLpeIlwdiCxZjDTWGFVOSCjbnSgV3RCXDNicHjvd5Bpd3K7bHH0bY9vKHOrZ37p[olk[W62bIm= MVGyN|k1OTh|Mh?=
SNU182 M{DYSWZ2dmO2aX;uJGF{e2G7 NEDI[HA2OCEQvF2= M13SNVI1KGh? MnjtSG1UVw>? M2\Ld2lvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 NWDOVZB5OjN7NEG4N|I>
SNU423 NFTBXIZHfW6ldHnvckBCe3OjeR?= MXy1NEDPxE1? NYfOUVZoOjRiaB?= NYrjeoNwTE2VTx?= MU\Jcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? NVPtOZZUOjN7NEG4N|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]
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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
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

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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