Ruxolitinib (INCB018424)

For research use only.

Catalog No.S1378

309 publications

Ruxolitinib (INCB018424) Chemical Structure

CAS No. 941678-49-5

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.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 208 In stock
USD 160 In stock
USD 230 In stock
USD 320 In stock
USD 800 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Selleck's Ruxolitinib (INCB018424) has been cited by 309 publications

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. 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 MYTLbY5ie2ViQYPzZZk> MX6yNEBucW5? MVLEUXNQ M3f0TGlvcGmkaYTpc44hd2ZiSlHLNkBqdiCqdX3hckBVTjFiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBGWE9vaX7keYNm\CCVVFHUOUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEGy{txO M37QdlIzPjl6MEi0
TF1 MlG5T4lv[XOnIFHzd4F6 NVX4eXAyOjBibXnu M1HoNmROW09? MVTJcohq[mm2aX;uJI9nKEqDS{GgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWw3NWmwZIXj[YQhW1SDVEOgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjB{NN88US=> NV7HTFZMOjJ4OUiwPFQ>
Human T cell MUXLbY5ie2ViQYPzZZk> NXzibXJiUW6qaXLpeIlwdiCxZjDKRWs{NzFiaX6gbJVu[W5iVDDj[YxteyCneIDy[ZN{cW6pIFPEN{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGlNOi2|dHnteYxifGWmIGPURXQ2[SCyaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIECuNFI{|ryP MliyNlM2PDB4NEi=
Human monocyte NYLucFJEU2mwYYPlJGF{e2G7 MkjlTY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJI1wdm:leYTld{BmgHC{ZYPzbY5oKEOGMUSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDHUU1EW0Zvc4TpcZVt[XSnZDDTWGFVPWFicHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlAzPs7:TR?= NVjuWI9YOjN3NEC2OFg>
Human monocyte MXTLbY5ie2ViQYPzZZk> M2rLTmlvcGmkaYTpc44hd2ZiSlHLNk8yKGmwIHj1cYFvKG2xbn;jfZRmeyCneIDy[ZN{cW6pIFPENVQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBKTk6pYX3tZU1{fGmvdXzheIVlKFOWQWSxJJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yM{JOwG0> MV:yN|U1ODZ2OB?=
HEL MnznR5l1d3SxeHnjJGF{e2G7 MUG1JO69VQ>? MWK0PEBp NF65OFVEgXSxdH;4bYMhcW6mZYi9NVIvOiV? NWPxToNxOjV7M{GzOFk>
SET-2 Mnq3R5l1d3SxeHnjJGF{e2G7 NXzUTmpCPSEQvF2= M1fIXFQ5KGh? MnXTR5l1d3SxeHnjJIlv\GW6PUG4Mlcm NX\tVHpSOjV7M{GzOFk>
HT93A MnnIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUezNlAhdk1? M4fSR|Uh\A>? MnPMSG1UVw>? NVXPNmZOUW6qaXLpeIlwdiCxZjDHR3MuTiCrbnT1Z4VlKGe{YX71cI9kgXSrYzDkbYZn\XKnboTpZZRqd25? NUG3NmRjOjV6MEW5OlI>
CMK NX\BZXVVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn;UTY5pcWKrdHnvckBw\iCFTVugZ4FzenmrbnegeIhmKEqDS{PBOVczXiCvdYTheIlwdiClZXzsJJBzd2yrZnXyZZRqd25? Moq3NlU{PTJzMkS=
CMK M2T5NWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYXBXooyUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPjOGIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbjD3bZRpKEmFNUCgc4YhOC5zNkOg{txO M1myNlI2OzV{MUK0
CMK MoewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP MnvGNlU{PTJzMkS=
NCI-H460 M2mxZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrEUXNQ NGLyNmhKSzVyPUCuNVMh|ryP M2O3OlI2OjF|Nkew
NCI-H358 NEPaTY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHjUbGZFVVOR M{CySGlEPTB;MD6xJO69VQ>? NH6xW4MzPTJzM{[3NC=>
A549 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NU\aUJNKTE2VTx?= NInjc4NKSzVyPUCuNFQh|ryP NFjRfZgzPTJzM{[3NC=>
A549/DDP NGHPVotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIDpepFFVVOR NFnKXXNKSzVyPUCuNlIh|ryP M{\yT|I2OjF|Nkew
NCI-H1299 NF;UTYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTEUXNQ MofLTWM2OD1yLkK4JO69VQ>? M3XmOVI2OjF|Nkew
NCI-H2347 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWPEUXNQ MXPJR|UxRTBwMUeg{txO MV[yOVIyOzZ5MB?=
A549/DDP M4HMbGZ2dmO2aX;uJGF{e2G7 MYezNEBvVQ>? NWHvdmNPPDhiaB?= MmnFSG1UVw>? MlSySI94di2{ZXf1cIF1cW:wIH;mJHNVSVR|IIDoc5NxcG:{eXzheIlwdg>? MUOyOVIyOzZ5MB?=
NCI-H1299 MYfGeY5kfGmxbjDBd5NigQ>? NHO0dWc{OCCwTR?= NFHTOWQ1QCCq MULEUXNQ MVPEc5dvNXKnZ4XsZZRqd25ib3[gV3RCXDNicHjvd5Bpd3K7bHH0bY9v MUSyOVIyOzZ5MB?=
NCI-H2347 M1H4WmZ2dmO2aX;uJGF{e2G7 NITzNnE{OCCwTR?= MY[0PEBp MlLySG1UVw>? NVXvOJR4TGWlcnXhd4UhcW5iQnPsNkBmgHC{ZYPzbY9v MU[yOVIyOzZ5MB?=
A549/DDP NVnmdWxZSXCxcITvd4l{KEG|c3H5 M4iySVMxKG6P MmTPOFghcA>? MoDiSG1UVw>? NWDWbVF6UW6mdXP0bY9vKG:oIHHwc5B1d3Orcx?= M1\sWlI2OjF|Nkew
NCI-H1299 NYHMTHZvSXCxcITvd4l{KEG|c3H5 M{nUcFMxKG6P NWXsVpRYPDhiaB?= MmPKSG1UVw>? NUDMUJJyUW6mdXP0bY9vKG:oIHHwc5B1d3Orcx?= M1rSTlI2OjF|Nkew
NCI-H2347 M3PBNGFxd3C2b4Ppd{BCe3OjeR?= M3GyNVMxKG6P NU\RfGNjPDhiaB?= NX7qb3N[TE2VTx?= M4HjXWlv\HWldHnvckBw\iCjcH;weI9{cXN? NIi3bYgzPTJzM{[3NC=>
Hep3B MV7GeY5kfGmxbjDBd5NigQ>? NYrRWHVrOSEQvF2= MYOxOkBp M4jGRmROW09? MlL2TY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKGGldHn2[UBUXEGWMzD3bZRpKEmFNUCgc4YhhjVyIN88US=> M3rpbFI1PTBzNki5
HepG2 MYnGeY5kfGmxbjDBd5NigQ>? M2ixZlEh|ryP NEi5XJQyPiCq MULEUXNQ MUTJcZBicXKnczD0bIUh[2GyYXPpeJkhd2ZiSVjDRU1ie3OxY3nheIVlKGeyMUOwJI12fGGwdIOgeI8he2mpbnHsJJRwKFOWQWSz NUnqZpd6OjR3MEG2PFk>
Huh7 NV3uWGVrTnWwY4Tpc44hSXO|YYm= NVm5TpZ6OSEQvF2= M2nzeFE3KGh? M1uyd2ROW09? NYHBPWgxUW2yYXny[ZMhfGinIHPhdIFkcXS7IH;mJGlJS0FvYYPzc4Nq[XSnZDDndFE{OCCvdYThcpR{KHSxIIPp[45idCC2bzDTWGFVOw>? MYeyOFUxOTZ6OR?=
BaF3 MYrLbY5ie2ViQYPzZZk> NXq1PVlQQDBibl2= NFLOVJk3KGh? NFHFcnhFVVOR NYfyOFlGWmWmdXPld{B1cGVicHjvd5Bpd3K7bHH0bY9vKG:owrDTWGFVPSCrbjDKRWszXjZzN1[tcZV1[XSnZDDCRWY{NUWST2KgZ4VtdA>? NEj5WpAzPDJ|N{e5NS=>
DLD-1 MmrPT4lv[XOnIFHzd4F6 M4rj[lI2KM7:TR?= M4r2[FQ5KGh? MojwSG1UVw>? MlfyTY5pcWKrdHnvckBw\iCMQVuxJJBpd3OyaH;yfYxifGmxbh?= MWOyOFA2ODV3MB?=
RKO M1;2Z2tqdmG|ZTDBd5NigQ>? NInJcHUzPSEQvF2= MYK0PEBp M{jndWROW09? M{XpbGlvcGmkaYTpc44hd2ZiSlHLNUBxcG:|cHjvdplt[XSrb36= M1jVWFI1ODVyNUWw
DLD-1 M2TQOWtqdmG|ZTDBd5NigQ>? NIXJdZQzPSEQvF2= MXi0PEBp M{faUmROW09? MXPJcohq[mm2aX;uJI9nKEqDS{KgdIhwe3Cqb4L5cIF1cW:w NGnPW|YzPDB3MEW1NC=>
RKO NGXofXFMcW6jc3WgRZN{[Xl? M3PrWFI2KM7:TR?= M4jNflQ5KGh? M4e2S2ROW09? MWLkc4V{KG6xdDDpcohq[mm2IFrBT|EheGixc4Doc5J6dGG2aX;u MVmyOFA2ODV3MB?=
DLD-1 MmLkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3Ydno2OCEQvF2= M1Th[FQ5KGh? NGXXNnRFVVOR M4fCW2lEPTB;MUWuOVEh|ryP MnH2NlQxPTB3NUC=
RKO NHnvVFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV:1NEDPxE1? NHn4VGI1QCCq M{PHfmROW09? MVTJR|UxRTF2Lke2JO69VQ>? NHLyelIzPDB3MEW1NC=>
DLD-1 MoXjRZBweHSxc3nzJGF{e2G7 NW\PVllSOjVizszN MVW0PEBp NUjkUoNvTE2VTx?= NH75PYZKdmS3Y3XzJIFxd3C2b4Ppd{BjgSCjY4TpeoF1cW6pIHPhd5Bie2ViMx?= NV7kXGRROjRyNUC1OVA>
RKO MlTRRZBweHSxc3nzJGF{e2G7 MnO1NlUh|ryP MV20PEBp NVmzfVNZTE2VTx?= NUH1U3Q5UW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= M4izdlI1ODVyNUWw
HuH7 NXm1blFrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVf4PVY4PTBizszN M2W4ZVQ5KGh? MmfSSG1UVw>? M1nTeF45OiVicnXkeYN1cW:w Mnz0NlM6PDF6M{K=
SNU182 NH;yfmJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MknWOVAh|ryP M4ruS|Q5KGh? NYLX[ZVYTE2VTx?= M{HheF43PCVicnXkeYN1cW:w NUfRd4EyOjN7NEG4N|I>
SNU423 NFfadVBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1v6bFUxKM7:TR?= NV3kdZNxPDhiaB?= MkHzSG1UVw>? MW[+PFEmKHKnZIXjeIlwdg>? MV[yN|k1OTh|Mh?=
HuH7 MVTGeY5kfGmxbjDBd5NigQ>? NFPnWYI2OCEQvF2= M{XJTlI1KGh? NITDVZZFVVOR M2PKT2lvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 M3u3TFI{QTRzOEOy
SNU182 MWjGeY5kfGmxbjDBd5NigQ>? MWW1NEDPxE1? NFLxcIYzPCCq NF;YXG9FVVOR M{TleWlvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 M3vMdFI{QTRzOEOy
SNU423 NFXBOZdHfW6ldHnvckBCe3OjeR?= MVq1NEDPxE1? NXH3dlhYOjRiaB?= NG[zXpNFVVOR MknZTY5pcWKrdHnvckBw\iCVVFHUNUBidmRiU2TBWFMheGixc4Doc5J6dGG2aX;uJJNq\26rZnnjZY51dHl? NIHoW4kzOzl2MUizNi=>

... 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]
- Collapse

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]
- Collapse
  • 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

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O
CalculateReset

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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

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

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

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

Related JAK Products

Tags: buy Ruxolitinib (INCB018424) | Ruxolitinib (INCB018424) supplier | purchase Ruxolitinib (INCB018424) | Ruxolitinib (INCB018424) cost | Ruxolitinib (INCB018424) manufacturer | order Ruxolitinib (INCB018424) | Ruxolitinib (INCB018424) distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID