Ruxolitinib (INCB018424)

For research use only.

Catalog No.S1378

285 publications

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. Ruxolitinib kills tumor cells through toxic mitophagy. Ruxolitinib induces autophagy and enhances apoptosis.

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Selleck's Ruxolitinib (INCB018424) has been cited by 285 publications

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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. Ruxolitinib kills tumor cells through toxic mitophagy. Ruxolitinib induces autophagy and enhances apoptosis.
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 MnfDT4lv[XOnIFHzd4F6 NETVbnMzOCCvaX6= Mn7xSG1UVw>? NX7DVoRnUW6qaXLpeIlwdiCxZjDKRWszKGmwIHj1cYFvKFSIMTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKEWSTz3pcoR2[2WmIGPURXQ2KHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNVLPxE1? M3nJeVIzPjl6MEi0
TF1 MUnLbY5ie2ViQYPzZZk> MYOyNEBucW5? NGPaellFVVOR M1nUe2lvcGmkaYTpc44hd2ZiSlHLNUBqdiCqdX3hckBVTjFiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBKVDZvaX7keYNm\CCVVFHUN{BxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEK0{txO M3LHXlIzPjl6MEi0
Human T cell MX7LbY5ie2ViQYPzZZk> MnLSTY5pcWKrdHnvckBw\iCMQVuzM|EhcW5iaIXtZY4hXCClZXzsd{BmgHC{ZYPzbY5oKEOGMzDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFnMNk1{fGmvdXzheIVlKFOWQWS1ZUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEKz{txO M1vBfVI{PTRyNkS4
Human monocyte MoXyT4lv[XOnIFHzd4F6 M1zxc2lvcGmkaYTpc44hd2ZiSlHLNkBqdiCqdX3hckBud26xY4n0[ZMh\XiycnXzd4lv\yCFREG0JIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gS20uS1OILYP0bY12dGG2ZXSgV3RCXDWjIIDoc5NxcG:{eXzheIlwdiC5aYToJGlEPTBib3[gNE4xOjcQvF2= MkLPNlM2PDB4NEi=
Human monocyte NGrOUG1McW6jc3WgRZN{[Xl? M3XpZmlvcGmkaYTpc44hd2ZiSlHLNk8yKGmwIHj1cYFvKG2xbn;jfZRmeyCneIDy[ZN{cW6pIFPENVQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBKTk6pYX3tZU1{fGmvdXzheIVlKFOWQWSxJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yM{JOwG0> NWKyUHNsOjN3NEC2OFg>
HEL M4\6fWN6fG:2b4jpZ{BCe3OjeR?= MlPOOUDPxE1? MlvMOFghcA>? MV3DfZRwfG:6aXOgbY5l\Xh;MUKuNkU> MUCyOVk{OTN2OR?=
SET-2 NIHn[mtEgXSxdH;4bYMhSXO|YYm= NF3OdHI2KM7:TR?= NWTZTlA6PDhiaB?= MWDDfZRwfG:6aXOgbY5l\Xh;MUiuO{U> MXeyOVk{OTN2OR?=
HT93A MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4jTflMzOCCwTR?= NWDORVV5PSCm NGK4OG5FVVOR MWHJcohq[mm2aX;uJI9nKEeFUz3GJIlv\HWlZXSg[5JidnWub3P5eIlkKGSrZn\ldoVvfGmjdHnvci=> M3\1UVI2QDB3OU[y
CMK NEXBSIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXjqV4dmUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPTd{VjDteZRifGmxbjDj[YxtKHC{b3zp[oVz[XSrb36= MmjKNlU{PTJzMkS=
CMK M4rQ[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHRNZlvUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPjOGIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbjD3bZRpKEmFNUCgc4YhOC5zNkOg{txO M4noRlI2OzV{MUK0
CMK MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYfJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP MXKyOVM2OjF{NB?=
NCI-H460 NUfIS2Z{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUTkd25vTE2VTx?= NIjGXIxKSzVyPUCuNVMh|ryP NFLRN2gzPTJzM{[3NC=>
NCI-H358 M3XLeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPuU|RFVVOR MoLHTWM2OD1yLkGg{txO NInS[XkzPTJzM{[3NC=>
A549 NIXKTpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4K4O2ROW09? MkDsTWM2OD1yLkC0JO69VQ>? MlXQNlUzOTN4N{C=
A549/DDP NEjIPWtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1OzPWROW09? NXGxRXM2UUN3ME2wMlIzKM7:TR?= NVTQO2tIOjV{MUO2O|A>
NCI-H1299 NUTjZnhLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3zXIZ6TE2VTx?= NHjSPYZKSzVyPUCuNlgh|ryP Mkm5NlUzOTN4N{C=
NCI-H2347 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLnSG1UVw>? NEHq[4tKSzVyPUCuNVch|ryP NYO2b5NTOjV{MUO2O|A>
A549/DDP NEK4cItHfW6ldHnvckBCe3OjeR?= MUmzNEBvVQ>? NYnweXl[PDhiaB?= NXz1[JhITE2VTx?= NEHH[otFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w MlHqNlUzOTN4N{C=
NCI-H1299 NG\yO2xHfW6ldHnvckBCe3OjeR?= Ml;EN|Ahdk1? MnrOOFghcA>? MYTEUXNQ NHns[FhFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w NWHaVXNjOjV{MUO2O|A>
NCI-H2347 M4Lmd2Z2dmO2aX;uJGF{e2G7 NGPNd5c{OCCwTR?= M1nhXVQ5KGh? MUDEUXNQ MkXSSIVkemWjc3WgbY4hSmOuMjDlfJBz\XO|aX;u MmHQNlUzOTN4N{C=
A549/DDP NHqwWXBCeG:ydH;zbZMhSXO|YYm= NWe2WXpiOzBibl2= MkHmOFghcA>? M2P3emROW09? M4rLS2lv\HWldHnvckBw\iCjcH;weI9{cXN? NY\INHB[OjV{MUO2O|A>
NCI-H1299 NUnJSWE{SXCxcITvd4l{KEG|c3H5 NF;BSlM{OCCwTR?= MXO0PEBp NHHjRW5FVVOR M2nGeGlv\HWldHnvckBw\iCjcH;weI9{cXN? MXuyOVIyOzZ5MB?=
NCI-H2347 MlXERZBweHSxc3nzJGF{e2G7 NVKxOWFkOzBibl2= M{XQ[FQ5KGh? NHPpOGtFVVOR MUfJcoR2[3Srb36gc4Yh[XCxcITvd4l{ NWfhdm9UOjV{MUO2O|A>
Hep3B NFHwXHlHfW6ldHnvckBCe3OjeR?= M2O3XVEh|ryP NV;oN4tmOTZiaB?= M4n3[WROW09? NGDMUJdKdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9iYXP0bZZmKFOWQWSzJJdqfGhiSVO1NEBw\iC-NUCg{txO Mon4NlQ2ODF4OEm=
HepG2 MoD0SpVv[3Srb36gRZN{[Xl? NE[3dm4yKM7:TR?= NXqwbZJWOTZiaB?= NFLjbVVFVVOR NEL1UpJKdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9ic3nncoFtKHSxIGPURXQ{ MoLONlQ2ODF4OEm=
Huh7 NHrkdFZHfW6ldHnvckBCe3OjeR?= MVexJO69VQ>? MWKxOkBp MUfEUXNQ MXrJcZBicXKnczD0bIUh[2GyYXPpeJkhd2ZiSVjDRU1ie3OxY3nheIVlKGeyMUOwJI12fGGwdIOgeI8he2mpbnHsJJRwKFOWQWSz NIS2S|czPDVyMU[4PS=>
BaF3 NGLnR5FMcW6jc3WgRZN{[Xl? NY\VUXdNQDBibl2= MV22JIg> MVfEUXNQ NGXNfpVT\WS3Y3XzJJRp\SCyaH;zdIhwenmuYYTpc44hd2cEoGPURXQ2KGmwIFrBT|JXPjF5Rj3teZRifGWmIFLBSlMuTVCRUjDj[Yxt NInjdYIzPDJ|N{e5NS=>
DLD-1 NYPS[XI{U2mwYYPlJGF{e2G7 NWDHfpZ3OjVizszN NG\YXoY1QCCq NVrQc|BFTE2VTx?= NX7mfWg2UW6qaXLpeIlwdiCxZjDKRWsyKHCqb4PwbI9zgWyjdHnvci=> NGHSUoIzPDB3MEW1NC=>
RKO NUDDPYJQU2mwYYPlJGF{e2G7 NFrCW5czPSEQvF2= MmrNOFghcA>? NG\kTWFFVVOR M4fXS2lvcGmkaYTpc44hd2ZiSlHLNUBxcG:|cHjvdplt[XSrb36= NFrlXWMzPDB3MEW1NC=>
DLD-1 MX\LbY5ie2ViQYPzZZk> Mmj1NlUh|ryP M4PDblQ5KGh? M1zS[mROW09? MU\Jcohq[mm2aX;uJI9nKEqDS{KgdIhwe3Cqb4L5cIF1cW:w NYfsUnAxOjRyNUC1OVA>
RKO M2\6dGtqdmG|ZTDBd5NigQ>? M3HXUFI2KM7:TR?= MYW0PEBp MVLEUXNQ NGjlNZdld2W|IH7veEBqdmirYnn0JGpCUzFicHjvd5Bpd3K7bHH0bY9v NInzOG8zPDB3MEW1NC=>
DLD-1 NVzTcml{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVL6e443PTBizszN NGj1TZA1QCCq MVLEUXNQ MXPJR|UxRTF3LkWxJO69VQ>? NWrxeJF3OjRyNUC1OVA>
RKO NWjHXGllT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3OOFFoPTBizszN MV[0PEBp NXrYZ|JWTE2VTx?= MlX0TWM2OD1zND63OkDPxE1? MliyNlQxPTB3NUC=
DLD-1 MYnBdI9xfG:|aYOgRZN{[Xl? NUPPRYVWOjVizszN MWW0PEBp MYrEUXNQ NFfqZXpKdmS3Y3XzJIFxd3C2b4Ppd{BjgSCjY4TpeoF1cW6pIHPhd5Bie2ViMx?= NID3NnIzPDB3MEW1NC=>
RKO MnnlRZBweHSxc3nzJGF{e2G7 NX\wO3Y5OjVizszN M3r2XVQ5KGh? NVTHPHpnTE2VTx?= NXTUXJBJUW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= MnKxNlQxPTB3NUC=
HuH7 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnvYOVAh|ryP MV20PEBp M1O3RmROW09? M{HEUl45OiVicnXkeYN1cW:w M{\oVVI{QTRzOEOy
SNU182 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFHx[WU2OCEQvF2= M2[xRVQ5KGh? MULEUXNQ MkTvQlY1LSC{ZXT1Z5Rqd25? NH2w[ZYzOzl2MUizNi=>
SNU423 M4\Oemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjXOVAh|ryP NFHnPXM1QCCq MWXEUXNQ NYGyWVR3RjhzJTDy[YR2[3Srb36= MWOyN|k1OTh|Mh?=
HuH7 M{C0NGZ2dmO2aX;uJGF{e2G7 MkL2OVAh|ryP NVHtcVcyOjRiaB?= MknPSG1UVw>? M2\wRmlvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 M{TqSlI{QTRzOEOy
SNU182 MlXFSpVv[3Srb36gRZN{[Xl? MVS1NEDPxE1? NF\rVXgzPCCq MYXEUXNQ MWXJcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? MkDHNlM6PDF6M{K=
SNU423 NYOyUY96TnWwY4Tpc44hSXO|YYm= MUW1NEDPxE1? MoHtNlQhcA>? NILM[ldFVVOR NHHWN5BKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= NF\z[4ozOzl2MUizNi=>

... 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]
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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]
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  • 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]
- Collapse
  • Animal Models: JAK2V617F-driven mouse model
  • 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
Smiles C1CCC(C1)C(CC#N)N2C=C(C=N2)C3=C4C=CNC4=NC=N3

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04485260 Not yet recruiting Drug: KRT-232|Drug: Ruxolitinib Myelofibrosis Kartos Therapeutics Inc. August 2020 Phase 1|Phase 2
NCT04359290 Recruiting Drug: Ruxolitinib administration ARDS Human|COVID Philipps University Marburg Medical Center July 1 2020 Phase 2
NCT04480086 Not yet recruiting Drug: Mivebresib|Drug: Navitoclax|Drug: Ruxolitinib Myelofibrosis (MF) AbbVie July 31 2020 Phase 1
NCT04454658 Not yet recruiting Drug: ABBV-744|Drug: Navitoclax|Drug: Ruxolitinib Myelofibrosis (MF) AbbVie July 14 2020 Phase 1
NCT04414098 Not yet recruiting Drug: INC424 / Ruxolitinib COVID-19 Marcelo Iastrebner|Novartis|Clinica Zabala June 1 2020 Phase 2
NCT03774082 Recruiting Drug: INC424 Graft vs Host Disease Novartis Pharmaceuticals|Novartis May 20 2020 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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID