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 55 Publications

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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 NUTLW2xNU2mwYYPlJGF{e2G7 Mlf1NlAhdWmw MYXEUXNQ M2PEdWlvcGmkaYTpc44hd2ZiSlHLNkBqdiCqdX3hckBVTjFiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBGWE9vaX7keYNm\CCVVFHUOUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEGy{txO MlPpNlI3QThyOES=
TF1 M1LaVWtqdmG|ZTDBd5NigQ>? MWmyNEBucW5? NEO3WGlFVVOR NUjQZopNUW6qaXLpeIlwdiCxZjDKRWsyKGmwIHj1cYFvKFSIMTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKEmONj3pcoR2[2WmIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNlTPxE1? MU[yNlY6QDB6NB?=
Human T cell MnPXT4lv[XOnIFHzd4F6 M2LnOmlvcGmkaYTpc44hd2ZiSlHLN{8yKGmwIHj1cYFvKFRiY3XscJMh\XiycnXzd4lv\yCFREOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDJUFIue3SrbYXsZZRm\CCVVFHUOYEheGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCyN:69VQ>? NWPuSJJiOjN3NEC2OFg>
Human monocyte NVT4O2xJU2mwYYPlJGF{e2G7 MVfJcohq[mm2aX;uJI9nKEqDS{KgbY4hcHWvYX6gcY9vd2O7dHXzJIV5eHKnc4PpcochS0RzNDDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFfNMWNUTi2|dHnteYxifGWmIGPURXQ2[SCyaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIECuNFI3|ryP NIfNO4IzOzV2ME[0PC=>
Human monocyte Ml7lT4lv[XOnIFHzd4F6 M3fMemlvcGmkaYTpc44hd2ZiSlHLNk8yKGmwIHj1cYFvKG2xbn;jfZRmeyCneIDy[ZN{cW6pIFPENVQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBKTk6pYX3tZU1{fGmvdXzheIVlKFOWQWSxJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yM{JOwG0> NWPJOYFMOjN3NEC2OFg>
HEL M2TWfWN6fG:2b4jpZ{BCe3OjeR?= NYqxXlY1PSEQvF2= MXW0PEBp MXzDfZRwfG:6aXOgbY5l\Xh;MUKuNkU> NH3BNIczPTl|MUO0PS=>
SET-2 M1H6NmN6fG:2b4jpZ{BCe3OjeR?= MlT3OUDPxE1? M4XjSlQ5KGh? M4nremN6fG:2b4jpZ{BqdmSneE2xPE44LQ>? NW[wVGxWOjV7M{GzOFk>
HT93A NY\tfVlpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{DLeFMzOCCwTR?= M1z2clUh\A>? MnjpSG1UVw>? MnToTY5pcWKrdHnvckBw\iCJQ2OtSkBqdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> MVqyOVgxPTl4Mh?=
CMK MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{DwV2lvcGmkaYTpc44hd2ZiQ13LJINienK7aX7nJJRp\SCMQVuzRVU4OlZibYX0ZZRqd25iY3XscEBxem:uaX\ldoF1cW:w NYH3Z|JHOjV|NUKxNlQ>
CMK M3rpN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV\zc3RSUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPjOGIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbjD3bZRpKEmFNUCgc4YhOC5zNkOg{txO NFLMSJQzPTN3MkGyOC=>
CMK NVHre4dDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP NFzR[GgzPTN3MkGyOC=>
NCI-H460 NG\EZpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlO4SG1UVw>? Mn60TWM2OD1yLkGzJO69VQ>? MnzYNlUzOTN4N{C=
NCI-H358 NYfnVFFrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX7EUXNQ NInyRoRKSzVyPUCuNUDPxE1? NV30cmxROjV{MUO2O|A>
A549 M4G2UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUTUWYoyTE2VTx?= NHjWRopKSzVyPUCuNFQh|ryP Mn3vNlUzOTN4N{C=
A549/DDP NV;H[25ET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGj4UIFFVVOR MUfJR|UxRTBwMkKg{txO M4rXNlI2OjF|Nkew
NCI-H1299 NHvERZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYDISm1jTE2VTx?= MYTJR|UxRTBwMkig{txO MmjZNlUzOTN4N{C=
NCI-H2347 MkW2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\l[G9bTE2VTx?= NX;xVYhQUUN3ME2wMlE4KM7:TR?= NWrCXVJUOjV{MUO2O|A>
A549/DDP MVPGeY5kfGmxbjDBd5NigQ>? MVuzNEBvVQ>? Mom3OFghcA>? NIr1UJZFVVOR M{\qSGRwf25vcnXneYxifGmxbjDv[kBUXEGWMzDwbI9{eGixconsZZRqd25? MXWyOVIyOzZ5MB?=
NCI-H1299 NFvBXHlHfW6ldHnvckBCe3OjeR?= M1;ud|MxKG6P MVW0PEBp M4LINmROW09? M2XLdGRwf25vcnXneYxifGmxbjDv[kBUXEGWMzDwbI9{eGixconsZZRqd25? NELBXVMzPTJzM{[3NC=>
NCI-H2347 MUTGeY5kfGmxbjDBd5NigQ>? NUXFW3NCOzBibl2= M3jJWFQ5KGh? NUTpV5QyTE2VTx?= M1rTWmRm[3KnYYPlJIlvKEKlbEKg[ZhxemW|c3nvci=> NHv1dJkzPTJzM{[3NC=>
A549/DDP M2\vUWFxd3C2b4Ppd{BCe3OjeR?= NXPOTVM5OzBibl2= NFP0fXY1QCCq M{L4UGROW09? NXzZSHM3UW6mdXP0bY9vKG:oIHHwc5B1d3Orcx?= MVqyOVIyOzZ5MB?=
NCI-H1299 NWr6PW5VSXCxcITvd4l{KEG|c3H5 NGHtSIE{OCCwTR?= NHPPS4M1QCCq M3vidGROW09? M3vpe2lv\HWldHnvckBw\iCjcH;weI9{cXN? NVfKeoxFOjV{MUO2O|A>
NCI-H2347 Ml;VRZBweHSxc3nzJGF{e2G7 NHXlN5M{OCCwTR?= MYq0PEBp NYX1NVhuTE2VTx?= NVrodYZqUW6mdXP0bY9vKG:oIHHwc5B1d3Orcx?= NHX0U|MzPTJzM{[3NC=>
Hep3B NHvMd5JHfW6ldHnvckBCe3OjeR?= MnHTNUDPxE1? NYryfoNNOTZiaB?= NFrPfoxFVVOR MnW0TY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKGGldHn2[UBUXEGWMzD3bZRpKEmFNUCgc4YhhjVyIN88US=> Mn;mNlQ2ODF4OEm=
HepG2 MXPGeY5kfGmxbjDBd5NigQ>? M4TPcFEh|ryP M3rsVlE3KGh? MoP3SG1UVw>? NYDPb2dNUW2yYXny[ZMhfGinIHPhdIFkcXS7IH;mJGlJS0FvYYPzc4Nq[XSnZDDndFE{OCCvdYThcpR{KHSxIIPp[45idCC2bzDTWGFVOw>? NF3tbpMzPDVyMU[4PS=>
Huh7 M1\ve2Z2dmO2aX;uJGF{e2G7 M1jO[VEh|ryP Mn\mNVYhcA>? MkGxSG1UVw>? MnPzTY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKHOrZ37hcEB1dyCVVFHUNy=> MmP4NlQ2ODF4OEm=
BaF3 MUPLbY5ie2ViQYPzZZk> M1fPdlgxKG6P MVu2JIg> Ml3xSG1UVw>? NEPEdJpT\WS3Y3XzJJRp\SCyaH;zdIhwenmuYYTpc44hd2cEoGPURXQ2KGmwIFrBT|JXPjF5Rj3teZRifGWmIFLBSlMuTVCRUjDj[Yxt NVKxOnFYOjR{M{e3PVE>
DLD-1 M1jsNmtqdmG|ZTDBd5NigQ>? MlK1NlUh|ryP MkSzOFghcA>? NEXZNIxFVVOR NVvC[HZqUW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> MYOyOFA2ODV3MB?=
RKO M{PmV2tqdmG|ZTDBd5NigQ>? MlnTNlUh|ryP M13RblQ5KGh? Mny5SG1UVw>? M3zlWGlvcGmkaYTpc44hd2ZiSlHLNUBxcG:|cHjvdplt[XSrb36= Mm\uNlQxPTB3NUC=
DLD-1 NI\GWFhMcW6jc3WgRZN{[Xl? MYqyOUDPxE1? NVvtWVFTPDhiaB?= NYTiVJJQTE2VTx?= NYnrN2JNUW6qaXLpeIlwdiCxZjDKRWszKHCqb4PwbI9zgWyjdHnvci=> MWqyOFA2ODV3MB?=
RKO NGHQZpFMcW6jc3WgRZN{[Xl? NVXVNWx4OjVizszN MV60PEBp NVXpRnJRTE2VTx?= MV7kc4V{KG6xdDDpcohq[mm2IFrBT|EheGixc4Doc5J6dGG2aX;u MYCyOFA2ODV3MB?=
DLD-1 M2jJPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV;uRYtqPTBizszN MVG0PEBp M1SzTmROW09? M4PwbGlEPTB;MUWuOVEh|ryP MXWyOFA2ODV3MB?=
RKO MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3K0cFUxKM7:TR?= MYW0PEBp MW\EUXNQ NH\3XI9KSzVyPUG0Mlc3KM7:TR?= NYX2do9kOjRyNUC1OVA>
DLD-1 Ml;4RZBweHSxc3nzJGF{e2G7 MkLvNlUh|ryP MUS0PEBp M1u0c2ROW09? M{PSWGlv\HWlZYOgZZBweHSxc3nzJIJ6KGGldHn2ZZRqdmdiY3HzdIF{\SB| MlPrNlQxPTB3NUC=
RKO NUjQUmEzSXCxcITvd4l{KEG|c3H5 NFW5bWozPSEQvF2= NUP4XFU3PDhiaB?= M2PvTWROW09? MkHsTY5lfWOnczDhdI9xfG:|aYOgZpkh[WO2aY\heIlv\yClYYPwZZNmKDN? M1frbFI1ODVyNUWw
HuH7 Mn73S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEDzcJc2OCEQvF2= MXy0PEBp M{XpSGROW09? MX2+PFImKHKnZIXjeIlwdg>? MmToNlM6PDF6M{K=
SNU182 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1XSS|UxKM7:TR?= MofkOFghcA>? MoDhSG1UVw>? NYH2dJJ1RjZ2JTDy[YR2[3Srb36= NVSxOpZCOjN7NEG4N|I>
SNU423 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzuOVAh|ryP NFHISIg1QCCq M3TaPGROW09? M4jZPF45OSVicnXkeYN1cW:w MW[yN|k1OTh|Mh?=
HuH7 NWLmfW1STnWwY4Tpc44hSXO|YYm= MXG1NEDPxE1? M4Oxb|I1KGh? Mn7HSG1UVw>? NIn3bXNKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= MoLxNlM6PDF6M{K=
SNU182 NHvKNVRHfW6ldHnvckBCe3OjeR?= MlrpOVAh|ryP MXOyOEBp MojwSG1UVw>? NYDL[ZVqUW6qaXLpeIlwdiCxZjDTWGFVOSCjbnSgV3RCXDNicHjvd5Bpd3K7bHH0bY9vKHOrZ37p[olk[W62bIm= NVzWdmlNOjN7NEG4N|I>
SNU423 NF\QTlZHfW6ldHnvckBCe3OjeR?= NES4OZA2OCEQvF2= MmPWNlQhcA>? NWTJfXBpTE2VTx?= M3u0R2lvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 M4\WTlI{QTRzOEOy

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
cleaved PARP / cleaved caspase3; 

PubMed: 29849942     


OVCAR-8 and MDAH 2774 cells were incubated with various concentrations of ruxolitinib for 48 h. Apoptosis was determined by using cleaved poly-ADP ribose polymerase (PARP) and cleaved caspase-3 by Western blot.

p-JAK2 / p-AKT / p-MAPK / Bcl-xl / MCL-1; 

PubMed: 29849942     


OVCAR-8 and MDAH2774 cells were treated with ruxolitinib (20 μM), paclitaxel (10 nM) or the combination for 24 h. Whole cells were collected and determined for the change of STAT3, AKT and ERK pathways and expression of BCL-XL and MCL-1 by Western blot.

c-Myc / c-Jun / Cyclin B / Cyclin D / Bcl-2 / HIF-1α; 

PubMed: 30930994     


Effects of ruxolitinib on the expression of downstream target genes of the JAK-STAT pathway. The protein levels of c-Myc, c-Jun, Cyclin B1, Cyclin D1, Bcl-2 and HIF-1α were determined in MCF-7 and TAMR-MCF-7 cells 24 h following ruxolitinib treatment (0.1-10 μM). 

p-STAT3; 

PubMed: 29849942     


Dose-dependent inhibition of STAT3 phosphorylation. Human ovarian cancer cells, OVCAR-8, MDAH2774, and SKOV3, were treated with the indicated concentrations of ruxolitinib for 24 h. Phosphorylation of STAT3 was analyzed by Western blot. 

29849942 30930994
Growth inhibition assay
Cell viability; 

PubMed: 29849942     


Dose dependent inhibition of cell viability. Human ovarian cancer cell lines were treated with the indicated concentrations of ruxolitinib. Cell viability was determined 72 h later. The IC50 was determined by the Chou-Talalay method. *P<0.05; ***P<0.0005, ruxolitinib vs control in OVCAR-8 cells; #P<0.05; ##P<0.005; ###P<0.0005, ruxolitinib vs control in SKOV-3 cells; ^^P<0.005; ^^^P<0.0005, ruxolitinib vs control in MDAH2774 cells.

Cell apoptosis; 

PubMed: 29849942     


OVCAR-8 and MDAH 2774 cells were incubated with various concentrations of ruxolitinib for 48 h. Apoptosis was determined by flow cytometry using annexin V and PI staining.

Cell proliferation; 

PubMed: 29515770     


Cells were plated into 48 well plates and cell growth was measured every 48 hours via MTS assay following ruxolitinib treatment (0, 1, 10 and 100 uM) in L-428 (left) and HDLM-2 (middle) HL cells, and Karpas-1106P PMBL cells (right).

29849942 29515770
Immunofluorescence
α-tubulin; 

PubMed: 26356819     


Confocal analysis of HEL cells, treated or not with different concentration of ruxolitinib (100 and 300 nM), displaying α-Tubulin (green) and DAPI (blue) staining; MERGE shows the overlapped images. Scale bars are shown in the figure (10 μm). Note more diffuse microtubule networks in ruxolutinib-treated cells.

26356819
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

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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